About all

Is tsh elevated in hypothyroidism: Treatment of Hypothyroidism – American Family Physician


Treatment of Hypothyroidism – American Family Physician

1. Helfand M,
Crapo LM.
Screening for thyroid disease. Ann Intern Med.

2. Sawin CT,
Chopra D,
Azizi F,
Mannix JE,
Bacharach P.
The aging thyroid. Increased prevalence of elevated serum thyrotropin levels in the elderly. JAMA.

3. Hueston WJ. Thyroid disease. In: Rosenfeld JA, Alley N, Acheson LS, Admire JB, eds. Women’s health in primary care. Baltimore: Williams & Wilkins, 1997:617–31.

4. Farwell AP,
Braverman LE.
Inflammatory thyroid disorders. Otolaryngol Clin North Am.

5. Hay ID.
Thyroiditis: a clinical update. Mayo Clin Proc.

6. Schubert MF,
Kountz DS.
Thyroiditis. A disease with many faces. Postgrad Med.

7. Larsen PR, Davies TF, Hay ID. The thyroid gland. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of endocrinology. 9th ed. Philadelphia: Saunders, 1998:461.

8. Dong BJ,
Hauck WW,
Gambertoglio JG,
Gee L,
White JR,
Bubp JL,

et al.
Bioequivalence of generic and brand-name levothyroxine products in the treatment of hypothyroidism. JAMA.

9. Singer PA,
Cooper DS,
Levy EG,
Ladenson PW,
Braverman LE,
Daniels G,

et al.
Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of Care Committee, American Thyroid Association. JAMA.

10. Grebe SK,
Cooke RR,
Ford HC,
Fagerstrom JN,
Cordwell DP,
Lever NA,

et al.
Treatment of hypothyroidism with once weekly thyroxine. J Clin Endocrinol Metab.

11. Bunevicius R,
Kazanavicius G,
Zalinkevicius R,
Prange AJ Jr.
Effects of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism. N Engl J Med.

12. Carr D,
McLeod DT,
Parry G,
Thornes HM.
Fine adjustment of thyroxine replacement dosage: comparison of the thyrotrophin releasing hormone test using a sensitive thyrotrophin assay with measurement of free thyroid hormones and clinical assessment. Clin Endocrinol [Oxf].

13. Rosenbaum RL,
Barzel US.
Levothyroxine replacement dose for primary hypothyroidism decreases with age. Ann Intern Med.

14. Sawin CT,
Geller A,
Hershman JM,
Castelli W,
Bacharach P.
The aging thyroid. The use of thyroid hormone in older persons. JAMA.

15. Hays MT,
Nielsen KR.
Human thyroxine absorption: age effects and methodological analyses. Thyroid.

16. Wallace K,
Hoffman MT.
Thyroid dysfunction: how to manage overt and subclinical disease in older patients. Geriatrics.

17. Pines A,
Dotan I,
Tabori U,
Villa Y,
Mijatovic V,
Leno Y,

et al.
l-Thyroxine prevents the bone-conserving effect of HRT in postmenopausal women with subclinical hypothyroidism. Gynecol Endocrinol.

18. Hanna FW,
Pettit RJ,
Ammari F,
Evans WD,
Sandeman D,
Lazarus JH.
Effect of replacement doses of thyroxine on bone mineral density. Clin Endocrinol [Oxf].

19. Hussein WI,
Green R,
Jacobsen DW,
Fairman C.
Normalization of hyperhomocysteinemia with l-Thyroxine in hypothyroidism. Ann Intern Med.

20. Green R,
Chong YY,
Jacobsen DW,
Robinson K,
Gupta M.
Serum homocysteine is high in hypothyroidism: a possible link with coronary artery disease. Presented at the International Conference on Homocysteine Metabolism, from Basic Science to Clinical Medicine. Ireland, July 2–5, 1995. Ir J Med Sci.
1995;164(suppl 15):27–8.

21. Surks MI,
Sievert R.
Drugs and thyroid function. N Engl J Med.

22. Refetoff S,
Weiss RE,
Usala SJ.
The syndromes of resistance to thyroid hormone. Endocr Rev.

23. Guide to clinical and preventive services: report of the U.S. Preventive Services Task Force. 2d ed. Baltimore: Williams & Wilkins, 1996:209–18.

24. Helfand M,
Redfern CC.
Clinical guideline, part 2. Screening for thyroid disease: an update. American College of Physicians. Ann Intern Med.

Hypothyroidism – Diagnosis and treatment


In general, your doctor may test for an underactive thyroid if you are feeling increasingly tired, have dry skin, constipation and weight gain, or have had previous thyroid problems or a goiter.

Blood tests

Diagnosis of hypothyroidism is based on your symptoms and the results of blood tests that measure the level of TSH and sometimes the level of the thyroid hormone thyroxine. A low level of thyroxine and high level of TSH indicate an underactive thyroid. That’s because your pituitary produces more TSH in an effort to stimulate your thyroid gland into producing more thyroid hormone.

Doctors can diagnose thyroid disorders much earlier than in the past — often before you experience symptoms. Because the TSH test is the best screening test, your doctor will likely check TSH first and follow with a thyroid hormone test if needed.

TSH tests also play an important role in managing hypothyroidism. They help your doctor determine the right dosage of medication, both initially and over time.

In addition, TSH tests are used to help diagnose a condition called subclinical hypothyroidism, which usually causes no outward signs or symptoms. In this condition, you have normal blood levels of triiodothyronine and thyroxine, but higher than normal levels of TSH.

There are certain factors that can affect blood tests for thyroid problems. One is the blood-thinning medication called heparin. Another is biotin, a vitamin taken as a stand-alone supplement or as part of a multivitamin. Let your doctor know about any medications or supplements you take before having blood tests done.


Standard treatment for hypothyroidism involves daily use of the synthetic thyroid hormone levothyroxine (Levo-T, Synthroid, others). This oral medication restores adequate hormone levels, reversing the signs and symptoms of hypothyroidism.

You’ll likely start to feel better soon after you start treatment. The medication gradually lowers cholesterol levels elevated by the disease and may reverse any weight gain. Treatment with levothyroxine will likely be lifelong, but because the dosage you need may change, your doctor is likely to check your TSH level every year.

Determining proper dosage may take time

To determine the right dosage of levothyroxine initially, your doctor generally checks your level of TSH after six to eight weeks. After that, blood levels are generally checked six months later. Excessive amounts of the hormone can cause side effects, such as:

  • Increased appetite
  • Insomnia
  • Heart palpitations
  • Shakiness

If you have coronary artery disease or severe hypothyroidism, your doctor may start treatment with a smaller amount of medication and gradually increase the dosage. Progressive hormone replacement allows your heart to adjust to the increase in metabolism.

Levothyroxine causes virtually no side effects when used in the appropriate dose and is relatively inexpensive. If you change brands, let your doctor know to ensure you’re still receiving the right dosage.

Also, don’t skip doses or stop taking the drug because you’re feeling better. If you do, the symptoms of hypothyroidism will gradually return.

Proper absorption of levothyroxine

Certain medications, supplements and even some foods may affect your ability to absorb levothyroxine. Talk to your doctor if you eat large amounts of soy products or a high-fiber diet or you take other medications, such as:

  • Iron supplements or multivitamins that contain iron
  • Aluminum hydroxide, which is found in some antacids
  • Calcium supplements

Levothyroxine is best taken on an empty stomach at the same time every day. Ideally, you’ll take the hormone in the morning and wait an hour before eating or taking other medications. If you take it at bedtime, wait four hours after your last meal or snack.

If you miss a dose of levothyroxine, take two pills the next day.

Subclinical hypothyroidism

If you have subclinical hypothyroidism, discuss treatment with your doctor. For a relatively mild increase in TSH, you probably won’t benefit from thyroid hormone therapy, and treatment could even be harmful. On the other hand, for a higher TSH level, thyroid hormones may improve your cholesterol level, the pumping ability of your heart and your energy level.

More Information

Show more related information

Alternative medicine

Although most doctors recommend synthetic thyroxine, natural extracts containing thyroid hormone derived from the thyroid glands of pigs are available. These products contain both thyroxine and triiodothyronine. Synthetic thyroid medications contain thyroxine only, and the triiodothyronine your body needs is derived from the thyroxine.

Extracts are available by prescription only and shouldn’t be confused with the glandular concentrates sold in natural foods stores. These products aren’t regulated by the Food and Drug Administration, and their potency and purity isn’t guaranteed.

Preparing for your appointment

You’ll likely start by seeing your family doctor or a general practitioner. In some cases, you may be referred to a doctor who specializes in the body’s hormone-secreting glands (endocrinologist). Infants with hypothyroidism need immediate referral to a pediatrics endocrinologist for treatment. Children or teens need to see a pediatric endocrinologist if there is any uncertainly about starting levothyroxine or proper dosing of the hormone.

Here’s some information to help you get ready for your appointment and know what to expect from your doctor.

What you can do

  • Be aware of any pre-appointment restrictions. At the time you make the appointment, be sure to ask if there’s anything you need to do in advance.
  • Write down any symptoms you’re experiencing, including any that may seem unrelated to the reason for which you scheduled the appointment.
  • Write down key personal information, including any major stresses or recent life changes.
  • Make a list of all medications, vitamins or supplements you’re taking.
  • Take a family member or friend along, if possible. Someone who accompanies you may remember something that you missed or forgot.
  • Write down questions to ask your doctor.

Preparing a list of questions will help you make the most of your time with your doctor. For hypothyroidism, some basic questions to ask include:

  • What’s the most likely cause of my symptoms?
  • What tests do I need?
  • Is my condition likely temporary or long lasting?
  • What treatments are available, and which do you recommend?
  • I have these other health conditions. How can I best manage them together?
  • Are there restrictions I need to follow?
  • Should I see a specialist?
  • Is there a generic alternative to the medicine you’re prescribing?
  • Are there brochures or other printed material I can take with me? What websites do you recommend?

Don’t hesitate to ask any other relevant questions you have.

What to expect from your doctor

Your doctor is likely to ask you a number of questions, including:

  • When did you begin experiencing symptoms?
  • Have your symptoms been continuous or occasional?
  • How severe are your symptoms?
  • What, if anything, seems to improve your symptoms?
  • What, if anything, appears to worsen your symptoms?
  • Do you have a family history of thyroid disease?

Nov. 19, 2020

Hypothyroidism diet: Can certain foods increase thyroid function?

Is there any truth to the hypothyroidism diet? Can certain foods increase thyroid function?

Answer From Ann Kearns, M. D., Ph.D.

Generally, there’s no hypothyroidism diet. Although claims about hypothyroidism diets abound, there’s no evidence that eating or avoiding certain foods will improve thyroid function in people with hypothyroidism.

However, adequate dietary iodine is essential for normal thyroid function. In developed countries, thyroid disease from iodine deficiency has been nearly eliminated by iodine additives in salt and food. Eating a balanced diet makes taking supplemental iodine unnecessary. In fact, too much iodine can cause hyperthyroidism in some people.

Other supplements such as soy, taken in large amounts, may have an impact on thyroid hormone production but won’t cause hypothyroidism in people who are not also iodine deficient.

Avoiding dietary extremes will ensure thyroid health. If you have concerns, talk with your doctor about taking a multivitamin with minerals.

If you have hypothyroidism, take thyroid hormone replacement medication as directed by your doctor — generally with an empty stomach. It’s also important to note that too much dietary fiber can impair the absorption of thyroid hormone replacement medication. Certain foods, supplements and medications can have the same effect.

Avoid taking your thyroid hormone at the same time as:

  • Walnuts
  • Soybean flour
  • Cottonseed meal
  • Iron supplements or multivitamins containing iron
  • Calcium supplements
  • Antacids that contain aluminum, magnesium or calcium
  • Some ulcer medications, such as sucralfate (Carafate)
  • Some cholesterol-lowering drugs, such as those containing cholestyramine (Prevalite) and colestipol (Colestid)

To avoid potential interactions, eat these foods or use these products several hours before or after you take your thyroid medication.

Supplements containing biotin, common in hair and nail preparations, can interfere with the measurement of thyroid hormone. Biotin does not affect thyroid hormone levels, but supplements should be stopped for at least a week before measuring your thyroid function so that your thyroid status is accurately reflected.


Ann Kearns, M.D., Ph.D.

  • Thyroid disease: Can it affect a person’s mood?
  • Hypothyroidism: Can calcium supplements interfere with treatment?

June 01, 2021

Show references

  1. Synthroid (prescribing information). AbbVie Inc.; 2019. https://www.rxabbvie.com/pdf/synthroid.pdf. Accessed Aug. 28, 2019.
  2. Levothyroxine. IBM Micromedex. https://www.micromedexsolutions.com. Accessed Aug. 19, 2019.
  3. Ross DS. Treatment of primary hypothyroidism in adults. https://www.uptodate.com/contents/search. Accessed Aug. 19, 2019.
  4. Rakel D, ed. Hypothyroidism. In: Integrative Medicine. 4th ed. Elsevier; 2018. https://www.clinicalkey.com. Accessed Aug. 20, 2019.
  5. Carafate (prescribing information). Allergan; 2018. https://www.allergan.com/assets/pdf/carafate_pi. Accessed Aug. 28, 2019.
  6. Cholestyramine. IBM Micromedex. https://www.micromedexsolutions.com. Accessed Aug. 21, 2019.
  7. Colestipol. IBM Micromedex. https://www.micromedexsolutions.com. Accessed Aug. 21, 2019.
  8. AskMayoExpert. Hypothyroidism. Mayo Foundation for Medical Education and Research; 2019.
  9. Nippoldt TB (expert opinion). Mayo Clinic. Aug. 6, 2016.
  10. Jonklaas J, et al. Guidelines for the treatment of hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014; doi: 10.1089/thy.2014.0028.
  11. Kearns A (expert opinion). Mayo Clinic. Aug. 21, 2019.
  12. Iodine. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed Aug. 21, 2019.

See more Expert Answers

Products and Services

  1. Newsletter: Mayo Clinic Health Letter — Digital Edition
  2. Book: Mayo Clinic Family Health Book, 5th Edition


Thyroid Function Tests | American Thyroid Association


The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. The thyroid’s job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormones help the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should.


The major thyroid hormone secreted by the thyroid gland is thyroxine, also called T4 because it contains four iodine atoms. To exert its effects, T4 is converted to triiodothyronine (T3) by the removal of an iodine atom. This occurs mainly in the liver and in certain tissues where T3 acts, such as in the brain. The amount of T4 produced by the thyroid gland is controlled by another hormone, which is made in the pituitary gland located at the base of the brain, called thyroid stimulating hormone (abbreviated TSH). The amount of TSH that the pituitary sends into the bloodstream depends on the amount of T4 that the pituitary sees. If the pituitary sees very little T4, then it produces more TSH to tell the thyroid gland to produce more T4. Once the T4 in the bloodstream goes above a certain level, the pituitary’s production of TSH is shut off. In fact, the thyroid and pituitary act in many ways like a heater and a thermostat. When the heater is off and it becomes cold, the thermostat reads the temperature and turns on the heater. When the heat rises to an appropriate level, the thermostat senses this and turns off the heater. Thus, the thyroid and the pituitary, like a heater and thermostat, turn on and off. This is illustrated in the figure below.

T4 and T3 circulate almost entirely bound to specific transport proteins. If the levels of these transport proteins changes, there can be changes in how much bound T4 and T3 is measured. This frequently happens during pregnancy and with the use of birth control pills. The “free” T4 or T3 is the hormone that is unbound and able to enter and affect the body tissues.


Blood tests to measure these hormones are readily available and widely used, but not all are useful in all situations. Tests to evaluate thyroid function include the following:

The best way to initially test thyroid function is to measure the TSH level in a blood sample. Changes in TSH can serve as an “early warning system” – often occurring before the actual level of thyroid hormones in the body becomes too high or too low. A high TSH level indicates that the thyroid gland is not making enough thyroid hormone (primary hypothyroidism). The opposite situation, in which the TSH level is low, usually indicates that the thyroid is producing too much thyroid hormone (hyperthyroidism). Occasionally, a low TSH may result from an abnormality in the pituitary gland, which prevents it from making enough TSH to stimulate the thyroid (secondary hypothyroidism). In most healthy individuals, a normal TSH value means that the thyroid is functioning properly.

T4 is the main form of thyroid hormone circulating in the blood. A Total T4 measures the bound and free hormone and can change when binding proteins differ (see above). A Free T4 measures what is not bound and able to enter and affect the body tissues. Tests measuring free T4 – either a free T4 (FT4) or free T4 index (FTI) – more accurately reflect how the thyroid gland is functioning when checked with a TSH.

The finding of an elevated TSH and low FT4 or FTI indicates primary hypothyroidism due to disease in the thyroid gland. A low TSH and low FT4 or FTI indicates hypothyroidism due to a problem involving the pituitary gland. A low TSH with an elevated FT4 or FTI is found in individuals who have hyperthyroidism.

T3 tests are often useful to diagnosis hyperthyroidism or to determine the severity of the hyperthyroidism. Patients who are hyperthyroid will have an elevated T3 level. In some individuals with a low TSH, only the T3 is elevated and the FT4 or FTI is normal. T3 testing rarely is helpful in the hypothyroid patient, since it is the last test to become abnormal. Patients can be severely hypothyroid with a high TSH and low FT4 or FTI, but have a normal T3.

Measurement of free T3 is possible, but is often not reliable and therefore not typically helpful.

Reverse T3 is a biologically inactive protein that is structurally very similar to T3, but the iodine atoms are placed in different locations, which makes it inactive. Some reverse T3 is produced normally in the body, but is then rapidly degraded. In healthy, non-hospitalized people, measurement of reverse T3 does not help determine whether hypothyroidism exists or not, and is not clinically useful.


The immune system of the body normally protects us from foreign invaders such as bacteria and viruses by destroying these invaders with substances called antibodies produced by blood cells known as lymphocytes. In many patients with hypothyroidism or hyperthyroidism, lymphocytes react against the thyroid (thyroid autoimmunity) and make antibodies against thyroid cell proteins. Two common antibodies are thyroid peroxidase antibody and thyroglobulin antibody. Measuring levels of thyroid antibodies may help diagnose the cause of the thyroid problem. For example, positive anti-thyroid peroxidase and/or anti-thyroglobulin antibodies in a patient with hypothyroidism result in a diagnosis of Hashimoto’s thyroiditis. While detecting antibodies is helpful in the initial diagnosis of hypothyroidism due to autoimmune thyroiditis, following their levels over time is not helpful in detecting the development of hypothyroidism or response to therapy. TSH and FT4 are what tell us about the actual thyroid function or levels.

A different antibody that may be positive in a patient with hyperthyroidism is the stimulatory TSH receptor antibody (TSI). This antibody causes the thyroid to be overactive in Graves’ Disease. If you have Graves’ disease, your doctor might also order a thyrotropin receptor antibody test (TSHR or TRAb), which detects both stimulating and blocking antibodies. Following antibody levels in Graves’ patients may help to assess response to treatment of hyperthyroidism, to determine when it is appropriate to discontinue antithyroid medication, and to assess the risk of passing antibodies to the fetus during pregnancy.

Thyroglobulin (Tg) is a protein produced by normal thyroid cells and thyroid cancer cells. It is not a measure of thyroid function and it does not diagnose thyroid cancer when the thyroid gland is still present. It is used most often in patients who have had surgery for thyroid cancer in order to monitor them after treatment. Tg is included in this brochure of thyroid function tests to communicate that, although measured frequently in certain scenarios and individuals, Tg is not a primary measure of thyroid hormone function.


Because T4 contains iodine, the thyroid gland must pull a large amount of iodine from the bloodstream in order to make an appropriate amount of T4. The thyroid has developed a very active mechanism for doing this. Therefore, this activity can be measured by having an individual swallow a small amount of iodine, which is radioactive. The radioactivity allows the doctor to track where the iodine goes. By measuring the amount of radioactivity that is taken up by the thyroid gland (radioactive iodine uptake, RAIU), doctors may determine whether the gland is functioning normally. A very high RAIU is seen in individuals whose thyroid gland is overactive (hyperthyroidism), while a low RAIU is seen when the thyroid gland is underactive (hypothyroidism). In addition to the radioactive iodine uptake, a thyroid scan may be obtained, which shows a picture of the thyroid gland and reveals what parts of the thyroid have taken up the iodine (see Thyroid Nodules brochure).


There are many medications that can affect thyroid function testing. Some common examples include:

  • Estrogens, such as in birth control pills, or in pregnancy, cause high levels of total T4 and T3. This is because estrogens increase the level of the binding proteins. In these situations, it is better to ask both for TSH and free T4 for thyroid evaluation, which will typically be in the normal range.
  • Biotin, a commonly taken over-the-counter supplement, can cause the measurement of several thyroid function tests to appear abnormal, when they are in fact normal in the blood. Biotin should not be taken for 2 days before blood is drawn for thyroid function testing to avoid this effect.

Thyroid Blood Test Results: Understanding TSH Levels

If there’s a bright side to hypothyroidism, or an underactive thyroid, it’s that treatment usually just involves taking daily medication, and testing is limited to a simple blood test. Your hypothyroidism test results are your doctor’s blueprint for prescribing the right dose of synthetic thyroid hormone medication and tracking how well it’s working.

Thyroxine, Triiodothyronine, and TSH Levels

The main job of the thyroid gland is to make the hormone thyroxine, also known as T4 because it has four iodine molecules. The thyroid also makes the hormone triiodothyronine, known as T3 because it has three iodine molecules, but in smaller amounts, explains Cathy Doria-Medina, MD, an endocrinologist with HealthCare Partners Medical Group in Torrance, California. “The thyroid gland makes mostly T4, [and] the T4 has to be converted to T3, because T3 is the part of thyroxine that actually does the work,” she says.

The pituitary gland at the base of the brain controls hormone production in your body. It makes thyroid-stimulating hormone (TSH), which tells the thyroid gland how much T4 and T3 to produce. The TSH level in your blood reveals how much T4 your pituitary gland is asking your thyroid gland to make. If your TSH levels are abnormally high, it could mean you have an underactive thyroid, or hypothyroidism. That’s because it indicates your pituitary gland is producing more TSH in an effort to stimulate your thyroid to produce thyroid hormone, according to the Mayo Clinic.

“TSH levels go in the opposite direction of your thyroid hormone,” Dr. Doria-Medina explains. “If you’re making too little thyroid hormone, your TSH will go up. If you’re making too much thyroid hormone, your TSH will go down.”

What’s normal can vary depending on a number of factors, including the laboratory where your blood test is done, she adds. A normal range for TSH in most laboratories is 0.4 milliunits per liter (mU/L) to 4.0 mU/L.

If your TSH is higher than 4.0 mU/L on repeat tests, you probably have hypothyroidism.

Your doctor may also order a T4 test. Most of the T4 in your blood attaches to a protein, and when it does, it can’t get into your cells. Only T4 that is unattached or “free” can get into your cells to go to work. A blood test can measure how much free T4 if available.

Hypothyroidism Tests: A Measure of Treatment Success

Hypothyroidism is treated with daily medication. Taking synthetic thyroid hormone medication can bring your T4 and TSH levels back to their normal ranges. Once you’re on the right dose, your symptoms should subside.

When you first start taking medication, your doctor will need to monitor your blood to fine-tune the dosage. “Initially you will need to be tested more frequently,” Doria-Medina says. “A person who is newly diagnosed and taking medication for hypothyroidism should be tested every six weeks until the dosage is just right.”

The dose you start with is your doctor’s educated guess about what’s best for you — most likely the lowest dose possible to avoid side effects, which can include a rapid heartbeat and restlessness.

Medication for hypothyroidism is slow acting, and it can take several weeks for your body to adjust. If your TSH is still high and your symptoms haven’t subsided after 6 to 10 weeks, your doctor will likely increase the dose, and you’ll need your blood tested again after another 6 to 10 weeks.

How to Keep Hypothyroidism Under Control

Because you’ll need to take thyroid medication every day for the rest of your life, even after the right dose is found, your hormone levels will be monitored regularly to be sure that your treatment is working properly. “Eventually, most people with hypothyroidism can just be seen yearly by their doctor,” Doria-Medina says.

The American Thyroid Association recommends that you keep your TSH within a narrow range of 0.5 to 2.5 mU/L, but don’t be alarmed if your test results vary a little. Some variation is normal because your pituitary gland sends out TSH in pulses, not a steady stream. Also, factors like the time of day you’re tested can make a difference. TSH levels are likely to be higher at night and lower during the day. Some people, including those who are pregnant or those with a history of thyroid cancer, have different TSH goals. Talk to your doctor about the target TSH range that’s right for you.

If you have new or worsening symptoms or your health status changes — such as if you become pregnant, go through menopause, or are given another medicine that can interfere with the absorption of your thyroid hormones, such as anticonvulsants, certain antacids, or iron or calcium supplements — you should see your doctor and have your blood tested again, even if it’s ahead of schedule.

Hypothyroidism: Symptoms and Treatments of Hypothyroid Disease

Hypothyroidism (Underactive Thyroid)

Part 1: Too Little Thyroid Hormone

Hypothyroidism is a condition in which the thyroid gland is not able to produce enough thyroid hormone. Since the main purpose of thyroid hormone is to “run the body’s metabolism,” it is understandable that people with this condition will have symptoms associated with a slow metabolism.

While the estimates vary, approximately 10 million Americans are likely to have this common medical condition. In fact, as many as 10% of women may have some degree of thyroid hormone deficiency.  

When your thyroid gland isn’t able to produce normal amounts of thyroid hormones, you’ll receive a diagnosis of hypothyroidism. Photo: 123rf

Hypothyroidism is more common than you would believe, and millions of people are currently hypothyroid and don’t know it. For an overview of how thyroid hormone is produced and how its production is regulated, check out our thyroid hormone production page.

Causes of Hypothyroidism

There are two fairly common causes of hypothyroidism. The first is a result of previous (or currently ongoing) inflammation of the thyroid gland, which leaves a large percentage of the cells of the thyroid damaged (or dead) and incapable of producing sufficient hormone.

The most common cause of thyroid gland failure is called autoimmune thyroiditis (also called Hashimoto’s thyroiditis), a form of thyroid inflammation caused by the patient’s own immune system.

The second major cause is the broad category of “medical treatments.”  The treatment of many thyroid conditions warrants surgical removal of a portion or all of the thyroid gland. If the total mass of thyroid producing cells left within the body is not enough to meet the needs of the body, the patient will develop hypothyroidism. Remember, this is often the goal of the surgery for thyroid cancer.

But at other times, the surgery will be to remove a worrisome nodule, leaving half of the thyroid in the neck undisturbed. Sometimes, this remaining thyroid lobe and isthmus will produce enough hormone to meet the demands of the body. For other patients, however, it may become apparent years later that the remaining thyroid just can’t quite keep up with demand.

Similarly, goiters and some other thyroid conditions can be treated with radioactive iodine therapy. The aim of the radioactive iodine therapy (for benign conditions) is to kill a portion of the thyroid to prevent goiters from growing larger or producing too much hormone (hyperthyroidism).

Occasionally, the result of radioactive iodine treatment will be that too many cells are damaged so the patient often becomes hypothyroid within a year or two. However, this is usually greatly preferred over the original problem.

Learn More about Hypothyroidism: Hypothyroidism Slideshow: Causes, Symptoms, and Treatments

There are several other rare causes of hypothyroidism, one of them being a completely “normal” thyroid gland that is not making enough hormone because of a problem in the pituitary gland. If the pituitary does not produce enough thyroid stimulating hormone (TSH) then the thyroid simply does not have the “signal” to make hormone. So it doesn’t.

Symptoms of Hypothyroidism

  • Fatigue
  • Weakness
  • Weight gain or increased difficulty losing weight
  • Coarse, dry hair
  • Dry, rough pale skin
  • Hair loss
  • Cold intolerance (you can’t tolerate cold temperatures like those around you)
  • Muscle cramps and frequent muscle aches
  • Constipation
  • Depression
  • Irritability
  • Memory loss
  • Abnormal menstrual cycles
  • Decreased libido

If you have one or more of these symptoms contact your doctor.

Each individual patient may have any number of these symptoms, and they will vary with the severity of the thyroid hormone deficiency and the length of time the body has been deprived of the proper amount of hormone.

You may have one of these symptoms as your main complaint, while another will not have that problem at all and will be suffering from an entirely different symptom. Most people will have a combination of these symptoms. Occasionally, some patients with hypothyroidism have no symptoms at all, or they are just so subtle that they go unnoticed.

If you have these symptoms, you need to discuss them with your doctor. Additionally, you may need to seek the skills of an endocrinologist.  If you have already been diagnosed and treated for hypothyroidism and continue to have any or all of these symptoms, you need to discuss it with your physician. 

Potential Dangers of Having Hypothyroidism

Because the body is expecting a certain amount of thyroid hormone, the pituitary will make additional thyroid stimulating hormone (TSH) as a way to prompt the thyroid to produce more hormone.

This extra work at signaling the thyroid gland to keep producing TSH may cause it to become enlarged, leading to he formation of a goiter (termed a “compensatory goiter”). Left untreated, the symptoms of hypothyroidism will usually progress. Rarely, complications can result in severe life-threatening depression, heart failure, or coma.

Hypothyroidism can often be diagnosed with a simple blood test: the thyroid hormone panel. In some persons, however, it’s not so simple and more detailed tests are needed.  Most importantly, a good relationship with a good endocrinologist will almost surely be needed.   

Hypothyroidism is completely treatable in many patients simply by taking a small pill once a day. However, this is a simplified statement, and it’s not always so easy.  There are several types of thyroid hormone preparations and one type of medicine will not be the best therapy for all patients. 

Many factors must be considered in establishing a personalized plan for the treatment of hypothyroidism and it is different for every patient.  

Questions to Ask Your Doctor

  • What is the cause of my underactive thyroid (hypothyroidism)?
  • Do I have Hashimoto’s disease?
  • What do the results of my blood test mean?
  • How long will I need medicine for my hypothyroidism and what are the side effects?
  • What TSH level will you use as a target for me?
  • After I’m in the optimal range, how often do you suggest I come back for blood tests to make sure my dosage needs haven’t changed?
  • Am I at risk for related health problems?
  • How quickly can I expect relief from my hypothyroid symptoms?
  • Are there any lifestyle changes I can make to relieve my symptoms?

Once you have the answers to these questions, your doctor will have a better understanding of your concerns and needs, and can take all the information into consideration in formulating a thyroid management plan in discussion with you.

Updated on: 02/17/21

Hypothyroidism: Overview, Causes, and Symptoms

How Doctors Diagnose Hypothyroidism – Diagnosis of an underactive thyroid function is made based on a combination of thyroid blood test results, symptoms, and several other factors.

Hypothyroidism is evaluated and diagnosed by a physician, usually an endocrinologist or your primary care doctor. Symptoms, signs, and more critically, blood tests—are taken into consideration when evaluating the possibility of an underactive thyroid gland—all of which help identify the cause and severity of the disease.

A diagnosis is reached after a thorough review of the patient’s personal medical and family histories, any risk factors, findings on physical examination, in addition to the results of thyroid function levels. There are several types of hormones checked in a blood test to assess your thyroid status—the most definitive one is the TSH (thyroid-stimulating hormone). Often, physicians may decide to check the free thyroxine, or T4, free T4 index, or total T4 to aid in the diagnosis.

Your doctor may check your thyroid status for an underactive thyroid by reviewing thyroid hormone levels. Photo: 123rf

Why Hypothyroidism is not Diagnosed on Symptoms Alone

Many of the symptoms of hypothyroidism are fairly common complaints found in people with a normally functioning thyroid gland, so it can be hard to decipher if the symptoms are related to the thyroid. One of the best ways to figure out if your symptoms could be related to a thyroid condition is to consider how long you have been experiencing them. 

For example, have you always felt cold when others were warm? Did you just start to notice decreased energy? If you are starting to notice new signs and symptoms, it could be related to a thyroid issue. However, only a physician (eg, endocrinologist) can diagnose a thyroid problem.

What to Consider in Your Personal and Family Medical Histories

It’s important to give your physician as many details as possible about your personal medical history, as well as family history (eg, mother had hypothyroidism). Be sure to discuss:

  • Your general state of health—particularly any changes you have noticed in your general overall health.
  • Your family’s health history—especially if a close relative has been diagnosed with hypothyroidism (or any other thyroid-related issues).
  • Whether you’ve ever had thyroid surgery, or radiation to your neck to treat cancer.
  • Any medicines you may be taking that could cause hypothyroidism (eg, amiodarone, lithium, interferon alpha, interleukin-2, or prior chemotherapy).

Physical Examination—Looking for Signs of Hypothyroidism
Your physician will perform a thorough examination and look for physical signs of hypothyroidism, including:

  • Evidence of dry skin
  • Swelling around the eyes and legs
  • Slower reflexes
  • Slower heart rate

Blood Tests: Hypothyroidism can be detected by different blood tests.

  • TSH Test.  A thyroid-stimulating hormone or TSH is a blood test that measures the amount of T4 (thyroxine) that the thyroid is being signaled to make. If you have an abnormally high level of TSH, it could mean you have hypothyroidism.
  • T4 (thyroxine) Test. The thyroid gland produces T4 (thyroxine). The free T4 and the free T4 index are blood tests that, in combination with a TSH test, can let your physician know how your thyroid is functioning. 

[[wysiwyg_imageupload::]]The pituitary gland tells the thyroid how much thyroxine to produce through signaling by TSH. There are cells in the pituitary gland that decide what your body’s “set point” is. Your set point is the normal range of TSH your body needs, as determined by your pituitary gland.

As blood flows through the pituitary gland, these same cells detect if there are adequate T4 levels in the body. If your T4 level is adequate, the pituitary sends the appropriate amount of TSH to the thyroid to maintain T4 levels in the normal range. If your T4 level is too low, the pituitary sends more TSH out telling the thyroid to make more T4. If your T4 level is too high, the pituitary sends less TSH out, telling the thyroid to make less T4.

Normal and Abnormal TSH Ranges

  • 0.4 mU/L to 4.0 mU/L is considered the reference range (there may be a slight variation depending on the laboratory), and people who have a normally functioning thyroid gland usually fall within this range.
  • If TSH measures > 4.0 mU/L, a second test (T4) is performed to verify the results. TSH > 4.0/mU/L with a low T4 level indicates hypothyroidism.
  • If your TSH is > 4.0 mU/L and your T4 level is normal, this may prompt your physician to test your serum anti-thyroid peroxidase (anti-TPO) antibodies. When these antibodies are present, it may indicate an autoimmune thyroid disorder, which is a risk factor for developing hypothyroidism.  If you have these antibodies, your doctor will most likely perform and TSH test at least once per year.

An easy way to remember how the thyroid works–think about supply and demand. As the T4 level falls, the TSH rises. As the T4 level rises, the TSH falls. However, not everyone with hypothyroidism has elevated levels of TSH. 

If your pituitary gland is not working properly, it may not send out normal TSH amounts—and if this is the case—the thyroid may be healthy. However, if the amount of TSH is off, the thyroid won’t make the right amount of T4. This is rare and is known as secondary or central hypothyroidism.

Updated on: 01/22/19

What is Thyroid Hormone Replacement Therapy?

90,000 insufficient formation of thyroid hormones: causes, symptoms, diagnosis and treatment methods on the website “Alpha Health Center”

The difficulty in diagnosing hypothyroidism is that a disease characterized by a violation of the production of thyroid hormones is often hidden. It has several varieties and stages, including latent, when the symptoms of hypothyroidism are weak or not manifested at all. Because of this, it is difficult to detect pathology on your own, without contacting a specialized specialist and an appropriate examination.At the same time, with early diagnosis, the prognosis of treatment is favorable.

Clinic “Alpha-Health Center” in Samara invites you to make an appointment with an endocrinologist with more than 7 years of experience. Here you can go through a complex of laboratory tests and receive a personalized plan of therapeutic measures.

Forms and causes of the disease

Hypothyroidism is often called a disease of megacities: due to the poor environmental situation and the lack of iodine prophylaxis in large cities, it is more common than in rural areas.The disease affects people of different social status and gender. However, it is 5 times more common in women. The age of the patient is also important: after 40 years, the likelihood of developing an endocrine disorder increases.

How thyroid hypothyroidism manifests itself can be determined by its form:

  • primary;
  • secondary;
  • tertiary.

The primary form of pathology is a condition that develops as a result of damage to the thyroid gland.It is characterized by an increase in the production of a hormone called thyroid-stimulating hormone. It develops due to autoimmune disruptions, as well as as a result of previous drug treatment of diffuse and diffuse nodular goiter, or iodine deficiency. Congenital hypothyroidism is also distinguished, most often due to insufficient development of the thyroid gland.

The secondary form is the result of damage to the hypothalamic-pituitary system, that is, individual sections of the GM, in which the production of TT is disrupted and the functions of the thyroid gland deteriorate.

There is information about the tertiary form of hypothyroidism that it is a consequence of pathological lesions of the hypothalamus. Both of these forms develop due to trauma, surgery, tumors and other conditions that provoke disturbances in the hypothalamus or pituitary gland.

Characteristic features

To understand how hypothyroidism develops, it is worth considering the role played by thyroid hormones, as well as the functioning of this organ.Thyroid hormones are involved in the regulation of metabolic processes, and also stimulate the functioning of internal systems, including the nervous, immune and cardiovascular. The pathological condition of the gland will certainly affect the processes of growth and multi-vector development of the body, the activation of the functions of the adrenal glands, mammary and gonads. It is not surprising that deviations in the secretion of hormones of this gland have an extremely negative effect on health and well-being, the work of many organs and systems.

Hypothyroidism is a disease that develops gradually and is difficult to diagnose.The reason is that most of its clinical manifestations are nonspecific. Symptoms characteristic of hypothyroidism are also characteristic of other diseases, and sometimes can be attributed to general malaise, overwork, and chronic fatigue. At the same time, the severity of symptoms does not show a correlation with the severity of the disease: sometimes, in patients with laboratory signs of this syndrome, there are no external manifestations of the disease.

Rapid weight gain

A common symptom of hypothyroidism is rapid weight gain.It is associated in the overwhelming majority of cases not with the accumulation of fat reserves, but with swelling. Hypothyroidism is usually accompanied by a decrease in metabolic rate and fluid retention. It also leads to weight gain.

The increase in body weight can be associated with other reasons: decreased physical activity and eating disorders. Failures and disruptions in the work of the endocrine system that occur during hypothyroidism are accompanied by causeless weakness, lethargy, and rapid fatigue.As a result, a girl or a man pays less attention to physical activity and gains weight.

Hypothyroidism is often accompanied by an increase in the level of “bad” cholesterol. The reason lies in a decrease in the activity of lipoprotein lipase, which leads to a deterioration in the mechanism of excretion of atherogenic lipids.


With an exacerbation of hypothyroidism, symptoms of puffiness appear:

  • Puffiness and swelling of the face;
  • swelling and swelling of the nasal mucosa;
  • Difficulty in nasal breathing;
  • lip augmentation;
  • the appearance on the tongue of distinguishable imprints of the dentition;
  • hearing impairment;
  • Thickening of the vocal cords – the voice becomes harsh.

Also, with hypothyroidism, there may be swelling of the upper and / or lower eyelids of one or both eyes, inflammation of the serous membranes of the pleura, peritoneum, pericardium.

Dermatological problems

In case of hypothyroidism, symptoms can also be expressed in regular dry skin, its thickening and coarsening. Patients complain of brittle nails and splitting, hair loss. However, these symptoms can indicate both thyroid disorders and a number of other endocrine disorders.

Diagnosis of hypothyroidism in old age can be difficult due to the fact that changes in the condition of the skin, nail plates and hair are often interpreted as normal manifestations of aging. Also, these symptoms are characteristic of secondary mucinosis, dimphostasis, amyloid lysene. Despite the similarities in external manifestations, the mechanism of development of these diseases is different.

Sexual and Reproductive Function

Frequent symptoms of hypothyroidism in girls and women are irregularities in the menstrual cycle, its frequency, soreness, as well as an abundance of discharge.The disease can also manifest itself as changes in the breast and mastopathy. Hypothyroidism in women in position increases the risk of miscarriage or placental abruption.

In men, hypothyroidism often leads to erectile dysfunction and decreased libido.


The clinical symptoms of hypothyroidism often include a variety of malfunctions in the digestive system. Patients complain of decreased appetite, regular nausea and constipation.Gallbladder dysfunction often occurs. These symptoms can be a manifestation of other diseases, but if they are accompanied by any other signs of hypothyroidism, a visit to an endocrinologist is required.

Cognitive functions and psychoemotional state

What else is insidious hypothyroidism – symptoms can manifest itself in impaired cognitive functions. Patients report complaints of forgetfulness, absent-mindedness, drowsiness, tearfulness. In 8-18% of cases, hypothyroidism is associated with depression.

Violations can also manifest themselves in a decrease in tissue sensitivity, in particular, polyneuropathy and deterioration of reflexes. With a severe form of hypothyroidism and the absence of therapy, a decrease in intellectual abilities and even the development of dementia are possible. Their appearance can be prevented only with the help of timely diagnostics.

Respiratory system

According to statistics, from 10 to 80% of cases of the disease are accompanied by sleep apnea syndrome. This symptom is more common in older men.There are two explanations why hypothyroidism manifests itself in this way:

  • decrease in the activity of the respiratory center, leading to impaired ventilation of the lungs;
  • Protein sweating into the muscles of the pharynx and tongue, which is also accompanied by obstruction.

For this reason, patients with sleep apnea syndrome are shown to undergo an examination for the presence of disorders in the functioning of the endocrine system, in particular the thyroid gland.

Hypothyroidism also leads to a complication of the course and exacerbation of bronchial asthma.

Musculoskeletal system

Latent thyroid hypothyroidism, the symptoms of which are difficult to diagnose, are often similar to those of thoracic or cervical osteochondrosis. Patients complain of weakness in the hands, tingling and burning sensations, unpleasant “goosebumps” on the skin. With hypothyroidism, myalgia (muscle pain) in the upper extremities is possible.

Disorders in the work of the musculoskeletal system are rarely associated with malfunctions of the endocrine system.But if there are no other reasons for the appearance of these symptoms (injuries, the presence of other chronic pathological conditions), it is advisable to check the state of the thyroid gland.

Cardiovascular system

With hypothyroidism, patients are prescribed a planned ECG. It allows you to identify abnormalities in the work of the heart muscle and blood vessels. Typical consequences of hypothyroidism are circulatory failure, weak and infrequent pulse, low blood pressure. ECG allows not only to diagnose the syndrome, but also to notice and prevent cardiovascular complications in time.

One of the earliest symptoms of hypothyroidism in women and men is the development of diastolic arterial hypertension. The disease is accompanied by a change in the total peripheral resistance of the blood vessels. Also, hypothyroidism plays an important role in the development of coronary artery disease.

Diagnostic methods

The syndrome is diagnosed by determining the concentration of TT, or thyroid-stimulating hormone. In adult patients, its value normally varies within 0.3-4.2 μIU / ml. Also, the patient is prescribed a study to determine T4 (free thyroxine).


Treatment of hypothyroidism in most diagnosed cases consists of lifelong replacement therapy. Exceptions are cases in which a violation of TT production is associated with side effects of drugs or any other substances. The drug of choice for this disease is levothyroxine sodium.

The condition of a patient with hypothyroidism after the appointment of therapy will improve gradually.The first signs of improvement after correctly selected treatment are observed no earlier than 2-3 weeks later. A pronounced therapeutic effect is usually achieved after a few months.

Diet plays an important role in the treatment of hypothyroidism. Patients with this disease are advised to reduce the consumption of easily digestible carbohydrates – to give up bakery products, jam, honey, jam, sugar.

Self-control of the patient over his condition is no less important.In order to diagnose secondary hypothyroidism in time, it is useful to keep a diary, registering changes in body weight, blood pressure and pulse rates, and general well-being. This measure helps to reduce the risk of developing complications of hypothyroidism and eliminate the side effects of hormone replacement therapy.

Diagnostics and treatment of hypothyroidism in Samara

In the “Alpha Health Center” you can get an endocrinologist’s advice and go through the necessary complex of laboratory tests.Reception is by appointment. We work every day, seven days a week. Call us!

90,000 Top 10 Myths About Hypothyroidism | Family medical center in Solntsevo, Novo-Peredelkino, Peredelkino Blizhnee, Solntsevo Park, Moscow, pos. Western

Myth . For any thyroid disease, including hypothyroidism, it is better to avoid the sun and refuse physiotherapy and neck massage.

True . If you take the correct dose of thyroxine, and the level of TSH is maintained at a normal level, then any sports and activities, climate and food are not contraindicated for you.

Myth . If a person has hypothyroidism, then he constantly feels bad.

True . A person receiving thyroxine replacement therapy is practically no different from other healthy people. If TSH is normal (even while taking substitution therapy), the examination should be continued to look for other causes of poor health.

Myth . For any thyroid disease, including hypothyroidism, it is better to consume more iodine and iodine-containing foods.

True . Iodine is just a building block for thyroid hormones. In hypothyroidism, the body has lost the function of producing these hormones, so iodine preparations will be ineffective in this case.

Myth . A woman with hypothyroidism is categorically contraindicated in pregnancy, and when it occurs, an interruption must be performed.

True . If the dosage of drugs for the treatment of hypothyroidism is selected correctly, then women can safely plan pregnancy, carry and give birth to children.

Myth . If a pregnant woman has hypothyroidism, her baby will be born mentally retarded.

True . Correctly selected therapy for hypothyroidism does not adversely affect the development of the fetus.

Myth . If a woman is receiving substitution therapy for hypothyroidism (thyroxine), then she should not breastfeed.

True . The medicinal substance that gets into breast milk does not affect the well-being of the child and does not cause him to develop any undesirable reactions.

Myth . Being overweight is most often associated with a dysfunction of the thyroid gland.

True . In 95-98% of cases, the cause of excess weight is the wrong lifestyle (the discrepancy between intake and energy expenditure). At the same time, genetic factors play a role and, in a small percentage of cases, endocrine diseases. Despite the frequent absence of primary endocrine disease at the heart of overweight and obesity, an endocrinologist is involved in the treatment of these conditions and their complications (metabolic syndrome, diabetes mellitus).

Myth . Taking thyroxine leads to weight gain or aggressiveness.

True . If the dosage of the drug is selected correctly, then such side effects should not occur.

Myth . When taken for a long time, thyroxin preparations can cause damage to the liver, stomach and other organs.

True . Since thyroxine, which is synthesized and clothed in the form of a tablet, does not differ at all in structure from its own hormone, it has no side effects.

Myth . The reason for increasing the thyroxine dose is complaints of weakness, increased fatigue, decreased performance, and not the TSH level.

True . To adjust the thyroxine dose, it is necessary to focus only on the TSH level, which (with the exception of rare situations) should not be determined more often than once every 6-8 weeks. Against the background of persistently compensated hypothyroidism, TSH control is carried out annually.

You can make an appointment with endocrinologist Olga Sergeevna Fedorova by phone +7 (495) 644-44-66 or on the website.

Laboratory diagnostics of thyroid diseases






(μIU / ml)

T4 general

(nmol / l)

T4 free

(pmol / l)

T3 general

(nmol / l)

T3 free

(pmol / l)


11.6 – 35.9

105 – 290

21 – 49

0.84 – 3.63

Children aged

2 days

3 days

1 week

2 weeks

3 weeks

1 month

6 months

1 year

5 years

10 years

15 years

8.3 – 19.8

1.0 – 10.9

1.2 – 5.8

0.7 – 6.4

0.7 – 6.4

0.7 – 6.4

0.7 – 6.4

0.7 – 6.4

83 – 303

110 – 285

93 – 247

88 – 225

94 – 259

112 – 243

103 – 210

92 – 189

89 – 173

71 – 145

64 – 149

21 – 38

19 – 37

18 – 35

18 – 35

17 – 33

16 – 33

15 – 29

14 – 23

13 – 23

12 – 22

12 – 23

1.95 – 3.63

0.81 – 3.39

0.65 – 1.90

0.59 – 1.84

0.77 – 2.15

1.10 – 3.10

1.43 – 3.17

1.75 – 3.50

1.80 – 3.10

1.70 – 3.10

1.50 – 2.80


up to 60 years

over 60 years old

0.3 – 4.0

0.5 – 7.8

50 – 150

65 – 135

10 – 25

10 – 18

1.0 – 3.0

0.62 – 2.79

3.0 – 7.0


1 trimester

2nd trimester

3 trimester

0.3 – 4.5

0.5 – 4.6

0.8 – 5.2

79 – 227

9 – 26

6 – 21

6 – 21

1.79 – 3.80

3.2 – 5.9

3.0 – 5.2

3.0 – 5.2

NOTE: Conversion factor TSH: 1 μIU / ml = 1 mU / L.

Rates are subject to change with various standard commercial kits.


1) The study is performed in the morning on an empty stomach – at least 8 – 12 hours should elapse between the last meal and blood sampling. On the evening of the preceding day, a light dinner is recommended.It is advisable to exclude fatty, fried and alcohol from the diet 1 – 2 days before the examination. If the day before there was a feast or there was a visit to the bath or sauna, it is necessary to postpone the laboratory test for 1-2 days. Avoid smoking for 1 hour before blood sampling.

2) Do not donate blood after X-ray examinations, physiotherapy procedures.

3) It is necessary to exclude factors influencing the research results: physical stress (running, climbing stairs), emotional arousal.Before the procedure, you should rest for 10 – 15 minutes and calm down.

4) It must be remembered that the result of the study may be distorted by the action of the drugs taken or the products of their metabolism. The appointment and cancellation of any drug is accompanied by a change in laboratory parameters. Therefore, before taking the analysis, you should consult your doctor about the possibility of limiting the intake of medications to prepare for the study. It is recommended to stop taking medications before donating blood for research, that is, blood sampling is done before taking medications.

5) Taking into account the daily rhythms of changes in blood parameters, repeated studies should be carried out at the same time.

6) Different research methods and units of measurement may be used in different laboratories. In order for the assessment of the survey results to be correct and to ensure the acceptability of the results, it is advisable to conduct research in the same laboratory at the same time.

Research on thyroid hormones. For 2 – 3 days before the study, the intake of iodine-containing drugs is excluded, for 1 month – thyroid hormones (to obtain true basal levels), unless there are special instructions from an endocrinologist.However, if the purpose of the study is to control the dose of thyroid hormone drugs, blood will be drawn while taking the usual dose of . It should be borne in mind that taking levothyroxine causes a transient significantly increased content of total and free thyroxine in the blood for about 9 hours (by 15 – 20%).

Thyroglobulin test should be performed at least 6 weeks after thyroidectomy or treatment.If diagnostic procedures such as a biopsy or thyroid scan are prescribed, then the study of the level of TG in the blood must be strictly carried out before the procedures. Since patients after radical treatment of differentiated thyroid cancer receive high doses of thyroid hormones (to suppress TSH secretion), against the background of which the TG level also decreases, its concentration should be determined 2 to 3 weeks after discontinuation of suppressive thyroid hormone therapy.


TSH is a reference criterion for laboratory assessment of thyroid function.It is with him that the diagnosis should begin if there is a suspicion of deviations in the hormonal activity of the thyroid gland. TSH is a glycoprotein hormone that is produced in the anterior lobe of the pituitary gland and stimulates the synthesis and iodination of thyroglobulin, the formation and secretion of thyroid hormones. The pituitary secretion of TSH is very sensitive to changes in the concentration of T 3 and T 4 in the blood serum. A decrease or increase in this concentration by 15-20% leads to reciprocal shifts in TSH secretion (feedback principle).

The existence of a dependence of the formation and secretion of TSH on the action of drugs, the daily rhythm of changes in the level of TSH, the state of stress and the presence of somatic diseases in the patient should be taken into account when interpreting the results of the study.

The biological half-life of TSH is 15 – 20 minutes.

INDICATIONS FOR DETERMINING TSH: Diagnosis of thyroid dysfunction, various types of hypothyroidism, hyperthyroidism, delayed mental and sexual development in children, cardiac arrhythmias, myopathy, depression, alopecia, infertility, amenorrhea, hyperprolactinemia, impotence and decreased libido.

– monitoring the condition of patients on the background of hormone replacement therapy: TSH secretion is suppressed during standard therapy or during postoperative replacement therapy.

Normal or elevated TSH levels indicate an inadequate dose of the drug, incorrect hormonal therapy, or the presence of antibodies to thyroid antigens. During replacement therapy for hypothyroidism, the optimal TSH level is within the lower reference values. During replacement therapy, blood for TSH testing should be taken 24 hours after the last dose of the drug.

· screening for congenital hypothyroidism: On the 5th day of a child’s life, the level of TSH in the serum or blood stain is determined on filter paper. If the TSH level exceeds 20 mIU / L, a new blood sample must be retested. With a TSH concentration in the range of 50 to 100 mIU / L, there is a high probability of having the disease.Concentrations above 100 mIU / L are typical for congenital hypothyroidism.


In healthy newborns, there is a sharp rise in the level of TSH in the blood at birth, decreasing to the basal level by the end of the first week of life.

In women, the concentration of TSH in the blood is approximately 20% higher than in men. With age, the concentration of TSH increases slightly, the amount of hormone release at night decreases.Decreased TSH levels are often observed in the elderly, and in these cases, low sensitivity to stimulation must be taken into account.

The concentration of TSH increases during pregnancy (oral contraceptives and the menstrual cycle do not affect the dynamics of the hormone)

For TSH, daily fluctuations in secretion are characteristic: the highest values ​​of TSH in the blood reach by 24 – 4 o’clock in the morning, in the morning hours the highest level in the blood is determined at 6 – 8 o’clock. The minimum TSH values ​​are determined at 15-18 pm.The normal rhythm of TSH secretion is disrupted when awake at night. The TSH level is not affected by the interval after taking levothyroxine. It is recommended to repeat the analysis if the results obtained do not correspond to the clinical picture and parameters of other studies.

In middle-aged women and older men, the maximum peak serum TSH occurs in December.

With menopause, there may be an increase in TSH content with an intact thyroid gland.





Gestosis (preeclampsia).

Contact with lead.

Uncompensated primary adrenal insufficiency.

Subacute thyroiditis (convalescence phase).

After heavy physical exertion. Excessive TSH secretion in pituitary adenomas (thyrotropinoma): thyrotoxicosis of central genesis.

Smoking cessation.

The secretion of TSH by pituitary adenomas is not always autonomous, but is subject to partial regulation by the type of feedback. With the appointment of such patients with thyrostatic drugs (methylthiouracil, mercazolil and others) and a decrease in their level of thyroid hormones in the blood under the influence of treatment, a further increase in the content of TSH in the blood serum is observed. Primary hypothyroidism.

Syndrome of unregulated TSH secretion.

Thyroid hormone resistance syndrome.

Hashimoto’s thyroiditis with clinical and subclinical hypothyroidism.

Severe physical and mental illnesses.

Bicycle ergometer exercises.


Ectopic TSH secretion (tumors of the lung, breast).

TSH secretion is stimulated by low temperature and low blood pressure.


Secondary amenorrhea.

Hyperthyroidism of pregnant women and postpartum necrosis of the pituitary gland.

Pituitary dwarfism.


Diffuse and nodular toxic goiter.

Delayed sexual development.


Neurogenic anorexia.

General diseases in old age.

Psychological stress.

Klinefelter’s Syndrome.

Cushing’s Syndrome.

Subclinical thyrotoxicosis.

T3 toxicosis.

Heat stress.

Injury of the pituitary gland.

Transient thyrotoxicosis in autoimmune thyroiditis.

TSH-independent thyrotoxicosis.

The inhibitory effect of STH on the synthesis and release of TSH.

Chronic renal failure.

Cirrhosis of the liver.

Exogenous thyroid hormone therapy.

Endogenous depression.

Endocrine ophthalmopathy.


· In treated hyperthyroid patients, TSH may remain low for 4-6 weeks after reaching euthyroid state.

· In pregnant women and women taking contraceptives, normal TTT levels and elevated T 3 and T 4 levels occur with euthyroidism.

· The absence of primary thyroid disease can be ascertained in any patient with a normal TSH and T 4 in combination with an isolated deviation (in either direction) T 3 .

· In severe patients with normal concentrations of T 4 and T 3 , TSH production may be impaired.

· TSH secretion is suppressed during treatment with thyroxine and in postoperative replacement therapy. Normal or elevated TSH levels in these cases indicate a low dose of the drug, peripheral resistance to thyroid hormones, or the presence of antibodies to thyroid hormones.

· During hypothyroidism replacement therapy, the optimal TSH level should be below the reference values.


Basic conditions, accompanied by a rise in the level of TSH

* Secondary and tertiary hypothyroidism is accompanied in 25% of cases by a slight increase in TSH levels with reduced biological activity with a significant decrease in T 4 .

* In the syndrome of resistance to thyroid hormones, a slight increase in the level of TSH is revealed with an increased content of thyroid hormones in the blood.

* Uncompensated primary adrenal insufficiency is sometimes accompanied by an increase in TSH levels, which normalize with the appointment of glucocorticosteroids.

* With a TSH-producing pituitary adenoma, an increased level of TSH and thyroid hormones is determined.

* Chronic renal failure may be accompanied by an increase in TSH both due to a delay in the excretion of iodine (true hypothyroidism), and due to the use of drugs that increase the level of TSH in the blood and the accumulation of metabolites.

* With an exacerbation of mental illness, every fourth patient may have a transient increase in TSH levels associated with the activation of the hypothalamic-pituitary-thyroid system.

* Effect of antidopamine drugs (metoclopramide and sulpiride), amiodarone.

* Non-thyroid disease syndrome.























































Thyroxine is a thyroid hormone, the biosynthesis of which occurs in the follicular cells of the thyroid gland under the control of TSH.The main fraction of organic iodine in the blood is in the form T 4 . About 70% of T 4 is associated with thyroxine-binding globulin (TC), 20% with thyroxine-binding prealbumin (TSPA) and 10% with albumin. Only 0.02 – 0.05% T 4 circulates in the blood in a state not bound to proteins – free fraction T 4 . The concentration of T 4 in serum depends not only on the rate of secretion, but also on changes in the binding capacity of proteins. Free T 4 is 0.02 – 0.04% of total thyroxine.

Period of biological half-life T 4 – 6 days.


In healthy newborns, the concentration of free and total T 4 is higher than in adults.

The level of the hormone in men and women remains relatively constant throughout life, decreasing only after 40 years.

During pregnancy, the concentration of thyroxine increases, reaching maximum values ​​in the 3rd trimester.

During the day, the maximum concentration of thyroxine is determined from 8 to 12 hours, the minimum – from 23 to 3 hours. During the year, the maximum values ​​of T 4 are observed between September and February, the minimum in summer.


Hemolysis, repeated thawing and freezing of serum may result in decreased T results 4 .High serum bilirubin concentrations tend to overestimate the results. The presence of the preservative EDTA gives false-positive results for free T 4 . Fasting, poor dietary intake with low protein content, exposure to lead, heavy muscle exercise and exercise, excessive physical exertion, various types of stress, weight loss in obese women, surgery, hemodialysis can contribute to a decrease in total and free T values ​​ 4 . Hyperemia, obesity, interruption of heroin intake (due to an increase in transport proteins) cause an increase in T 4 , heroin reduces free T 4 in the blood serum.Smoking causes both a decrease and an overestimation of thyroxine test results. The imposition of a tourniquet when taking blood with and without “hand work” causes an increase in total and free T 4 .

Levels of T 4 in blood from the umbilical vein are lower in premature infants compared to term infants and positively correlate with birth weight of term infants. High values ​​of T 4 in newborns are caused by increased TSH, free T 4 is close to the level in adults.The values ​​increase sharply in the first hours after birth and gradually decrease by the age of 5. In men, there is a decrease during puberty, in women this is not observed.

The concentration of free T 4 , as a rule, remains within the normal range in severe diseases not associated with the thyroid gland (the concentration of total T 4 may be reduced).




HIV infection.Acute hepatitis (4 weeks) and subacute hepatitis.

Hyperthyroidism, conditions with increased TSH (pregnancy, genetic increase, acute intermittent porphyria, primary biliary cirrhosis).

Hyperestrogenism (an increase in the content of total T 4 due to an increase in TSH, while the level of free T 4 remains normal).

Diffuse toxic goiter.


Acute mental disorders.

Acute thyroiditis (isolated cases).

Postpartum thyroid dysfunction.

Thyroid hormone resistance syndrome.


Toxic adenoma.


TSH – independent thyrotoxicosis.


Secondary hypothyroidism (Sheehan’s syndrome, inflammation in the pituitary gland).

Hypothyroidism, conditions with decreased TSH (nephrotic syndrome, chronic liver disease, protein loss through the gastrointestinal tract, nutritional disorders, genetic decrease in TSH).


Primary hypothyroidism (congenital and acquired: endemic goiter, AIT, neoplastic processes in the thyroid gland).

Tertiary hypothyroidism (traumatic brain injury, inflammation in the hypothalamus).


· an isolated increase in total T 4 against the background of normal TSH and T 3 values ​​may be a rare finding. This appears to be a patient with normal thyroid function, but congenital excess hepatic production of thyroid hormone carrier proteins.

· with “isolated” T 3 – hyperthyroidism, the level of free and total T 4 – within normal limits.

· at the initial stage of hypothyroidism, the level of free T 3 decreases earlier than the total T 4 . The diagnosis is confirmed in case of an increase in TSH or an excessive response to TRH stimulation.

· normal T level 4 does not guarantee normal thyroid function. T 4 within the normal range can be with endemic goiter, suppressive or replacement therapy, with a latent form of hyperthyroidism or a latent form of hypothyroidism.

· in hypothyroidism thyroxine contributes to the normalization of TSH and T 4 . Increased concentrations of total and free T 4 and TSH concentration in the region of the lower limit of the norm are observed when selecting adequate replacement therapy.

· during thyrostatic therapy, the T level 4 in the area of ​​the upper limit of the norm indicates an adequate choice of a maintenance dose.

· an increased level of free T 4 does not always indicate a violation of thyroid function.This may be due to the use of certain medications or serious general illnesses.







































































Thyroid overdose





Hypothyroidism treated with thyroxine.

Diseases associated with an increase in free fatty acids.

Postpartum thyroid dysfunction.

Thyroid hormone resistance syndrome.

Conditions in which the level or binding capacity of TSH is reduced.


Thyrotoxic adenoma.

Toxic goiter.

TSH-independent thyrotoxicosis.

Chronic liver diseases.

Secondary hypothyroidism (Sheehan’s syndrome, inflammatory diseases in the pituitary gland, thyrotropinoma).

Low protein diet and significant iodine deficiency.

Fluctuations in free T levels 4 can be observed in euthyroid patients with acute or chronic non-thyroid diseases

Contact with lead.

Primary hypothyroidism not treated with thyroxine (congenital and acquired: endemic goiter, AIT, neoplasms in the thyroid gland, extensive resection of the thyroid gland).

Late pregnancy.

A sharp decrease in body weight in obese women.

Tertiary hypothyroidism (TBI, inflammatory processes in the hypothalamus).

Surgical interventions.


Triiodothyronine is a thyroid hormone, 58% composed of iodine.Part of serum T 3 is formed by enzymatic deiodination of T 4 in peripheral tissues, and only a small amount is formed by direct synthesis in the thyroid gland .. Less than 0.5% of T 3 circulating in serum is in free form and biologically active. The remaining T 3 is in a reversible relationship with serum proteins: TSH, TSPA and albumin. The affinity of T 3 to whey proteins is 10 times lower than T 4 . In this regard, the level of free T 3 does not have such a great diagnostic value as the level of free T 4 .At least 80% of the circulating T 3 is obtained as a result of monodeiodization of T 4 in peripheral tissues. T 3 is 4 – 5 times more active in biological systems than T 4 . Although the minimum serum T 3 concentration is 100 times lower than the T 4 concentration, most immunoassays have little cross-reactivity with T 4 . Since T 3 levels change rapidly under the influence of stress or other non-thyroid factors, measuring T 3 is not the best general test for determining thyroid status.Free T 3 is about 0.2 – 0.5% of the total T 3 .

The biological half-life T 3 is 24 hours.


differential diagnosis of thyroid diseases,

control study with isolated T 3 -toxicosis,

initial stage of thyroid hyperfunction, in particular autonomic cells,

acute hyperthyroidism after suppressive thyroxine therapy,

relapse of hyperthyroidism.

· to exclude an overdose of drugs, it is necessary to control the level of T 3 , which should be within the normal range.


The concentration of T 3 in the blood serum of newborns is 1/3 of its level observed in adults, but within 1 – 2 days it increases to the concentration detected in adults.In early childhood, the concentration of T 3 decreases slightly, and in adolescence (by the age of 11 – 15) it again reaches the level of an adult. After 65 years, there is a more significant decrease in the level of T 3 compared to T 4 . Women have lower T 3 concentrations than men, on average by 5-10%.

During pregnancy (especially in the 3rd trimester), the concentration of T 3 in the blood increases 1.5 times.After childbirth, the hormone levels return to normal within 1 week.

The indicators T 3 are characterized by seasonal fluctuations: the maximum level falls on the period from September to February, the minimum – in the summer period.




High altitude.


Increase in body weight.

Interruption of heroin use.

With iodine deficiency, there is a compensatory increase in the levels of total and free T 3 .

When applying a tourniquet for the purpose of taking blood for 3 min. without “working with the hand” it is possible to increase T 3 by about 10%.

Physical exercise.




Premature newborns.

Low-calorie diet.

Acute diseases.


Poor diet with low protein content.

After abortion.

Weight loss.

Severe somatic diseases.

Heavy physical activity in women.

Electroconvulsive therapy.





Iodine-deficient goiter.

Treated hyperthyroidism.

Initial non-thyroid failure.

Conditions with increased TSG.

T 3 – thyrotoxicosis.

Hypothyroidism (with early or mild primary hypothyroidism, T 4 decreases more than T 3 – a high ratio of T 3 / T 4 ).

Uncompensated primary adrenal insufficiency.

Acute and subacute non-thyroid diseases.

Primary, secondary and tertiary hypothyroidism.

The period of convalescence after serious illness.

Syndrome of the euthyroid patient.

Conditions with low TSG.

Severe non-thyroid pathology, including somatic and mental illnesses.

Chronic liver diseases.






























T 3 – toxicosis. Syndrome of peripheral vascular resistance.


Third trimester of pregnancy.

In non-thyroid diseases, a low level of free T 3 is a nonspecific finding.

















· with iodine deficiency, a compensatory increase in total and free T 3 is observed.Thus, the body adapts to the lack of “raw materials”. Providing a sufficient amount of iodine entails a normalization of T 3 . These persons do not require any treatment. An incorrect interpretation of an increased level of T 3 as T 3 -toxicosis, despite the normal TSH and sometimes even a reduced T 4 , can lead to unreasonable prescription of thyrostatics, which is a gross mistake.

· in hypothyroidism, the levels of total and free T 3 can be in the region of the lower limit of the norm for a long time, since the increased peripheral transformation of T 4 into T 3 compensates for the decrease in T 3 .

· normal level of T 3 can be with latent functional defects of thyroid function, with hypothyroidism, compensated transformation of T 4 into T 3 .

· During goiter treatment or postoperative thyroxine replacement therapy, TSH and T levels 3 are measured to prevent dosage.

· in the treatment of hypothyroidism with thyroxine, the increase in T 3 is significantly less compared with T 4 .With the introduction of large doses of thyroxine, TSH is suppressed to unrecorded values. To exclude an overdose of drugs, an analysis of the level of T 3 is carried out, which should be within the normal range.

· at the beginning of the course of thyrostatic therapy, the level of T 3 may increase as a result of compensation processes.

· determination of the level of T 3 in serum has low sensitivity and specificity in hypothyroidism, since the activation of the conversion of T 4 to T 3 maintains the level of T 3 within the normal range until the development of severe hypothyroidism.Patients with NTZ or in a state of energy hunger have low indicators with T 3 and o T 3 . The level of T 3 should be determined in combination with free T 4 in the diagnosis of complex and unusual manifestations of hyperthyroidism or some rare conditions. High T 3 is a frequent and early sign of recurrence of Graves’ disease. High or normal T level 3 occurs in hyperthyroidism in patients with NTZ against the background of a decrease in TSH content (less than 0.01 mIU / L).High or normal T 3 occurs in cordarone-induced hyperthyroidism.



TTG increased,

free T 4 increased or normal, free T 3 decreased or normal.

* Reception of amiodarone, iodine-containing X-ray contrast agents, large doses of propranolol.

* Severe non-thyroid pathology, including somatic and mental illnesses.

* Uncompensated primary adrenal insufficiency.

* Convalescence period.

TTG increased,

free T 4 increased or normal, clinical euthyroidism.

* Total resistance to thyroid hormones.

TTG increased,

free T 4 normal

* Recently performed thyroid hormone correction.

* Insufficient thyroid hormone therapy, patients do not complain.

TTG lowered,

free T 4 raised,

free T 3 lowered.

* Artifical thyrotoxicosis due to self-designation T 4 .

TTG lowered,

free T 4 ok.

* Excessive thyroid hormone therapy.

* Taking medications containing T 3 .

TSH normal,

free T 4 and T 3 are lowered.

* Reception of large doses of salicylates.

TTG increased,

free T 4 raised,

clinical thyrotoxicosis.

* TSH – secreting tumors.

TSH normal,

increase in the level of total T 4 at a normal level of St. T 4 .

* Familial dysalbuminemic hyperthyroxinemia.

TTG increased,

free and common T 4 reduced,

total and free T 3 reduced.

* Chronic liver diseases: chronic hepatitis, liver cirrhosis.

Abnormal concentrations of total T 4 and total T 3

* Most often are the result of disorders of the binding protein, and not the result of thyroid dysfunction. When the TSG level changes, the calculated indicators of free T 4 are more reliable than the content of total T 4 .If the indices of free hormones differ, the total T 4 and the total T 3 should be determined.



Chemical name


Mechanism of action

Thiocyanates and isothiocyanates

Plants of the cruciferous family, smoking

Inhibition of iodine-concentrating mechanisms


Yellow turnip

Obstruction of iodide organization and formation of active

thyroid hormones in the thyroid gland (the activity of goitrin is 133% of the activity of propylthiouracil).

Cyanogenic glycosides

Cassava, maize, sweet potatoes, bamboo shoots

Converted into isothiocyanates in the body


Onions, garlic

Thiourea-like antithyroid action


Millet, sorghum, beans, groundnuts

Inhibition of TPO and iodothyronine deiodinases – inhibition of peripheral metabolism of thyroid hormones.

Phenols (resorcinol)

Drinking water, coal dust, cigarette smoke

Inhibition of iodine organification in the thyroid gland and inhibition of TPO

Polycyclic aromatic hydrocarbons

Food products, drinking water, ground water

Acceleration of T4 metabolism due to activation of hepatic UDP-glucuronyl transferase and formation of T4 glucuronide

Phthalic acid esters

Plastic products, some types of fish

Inhibition of TPO and the incorporation of iodine into thyroid hormones

Polychlorinated and polybrominated biphenyls

Freshwater fish

Development of AIT


Drinking water, food

Hyperplasia of follicular epithelium, accelerated metabolism of thyroid hormones, increased activity of microsomal enzymes

High level or deficiency of lithium, selenium

They can block the proteolysis of the colloid and the release of TG from the follicles, the entry of iodine into the thyroid gland, the connection of thyroid hormones with serum proteins, and accelerate the process of their deiodination.



Variants of the syndrome of non-thyroid diseases (SNTZ)

Low level T 3

A decrease in the T level 3 is observed in 70% of hospital patients with systemic diseases with normal thyroid function.Total T 3 below normal by 60%, free T 3 – 40%. T level 4 – normal. The SNTZ variant is associated with a violation of the transformation of T 4 into T 3 due to a decrease in the activity of 5-monodeiodinase. This condition is also characteristic of fasting and is an adaptive response of the body associated with a decrease in basal metabolism.

Low level T 3 and T 4

Simultaneous decrease in the level of T 3 and T 4 often occurs in patients in intensive care units.At the same time, a low level of total T 4 is an unfavorable prognostic sign. This variant of SNTZ is associated with the presence of an inhibitor of the binding of thyroid hormones in the blood and an increase in the metabolic clearance of T 4 .

High level T 4

An increase in serum T 4 and reverse T 3 is observed in acute porphyria, chronic hepatitis, primary biliary cirrhosis.At the same time, the level of total T 3 and free T 4 is within the normal range, the level of free T 3 is at the lower limit of the norm or is reduced.





Simultaneous use may require an increase in the dose of L-thyroxine

Medicines that block receptors of both true catecholamines and pseudo-mediators formed from thyroxine.

Propranolol (anaprilin, obzidan)

Medicines that reduce the absorption of L-thyroxine.

Cholestyramine (questran)

Aluminum hydroxide

Ferrous sulfate (hemofer)

Sucralfat (Venter)


Calcium carbonate

Medicines that accelerate the metabolism of L-thyroxine in the liver


Phenytoin (diphenin)

Carbamazepine (finlepsin)


Simultaneous use may require a decrease in the dose of L-thyroxine

Medicines that reduce the level of thyroxine-binding globulin in serum


Anabolic steroids





* Decreased absorption of T 4 in the intestine: diseases of the mucous membrane of the small intestine (sprue, etc.)diarrhea in diabetes, cirrhosis of the liver, after surgery for jejuno-jejunal shunting or resection of the small intestine, pregnancy.

* Drugs that increase the excretion of unmetabolized T 4 : rifampicin, carbamazepine, phenytoin.

* Taking drugs that reduce the absorption of thyroxine: cholestyramine, aluminum hydroxide, ferrous sulfate, calcium carbonate, sucralfate, colestipol.

* Drugs blocking the conversion of T 4 to T 3 : amiodarone (cordarone), selenium deficiency.


* Aging (over 65 years of age).

* Obesity.





Iodine-containing preparations and radiopaque substances

Induction of hypothyroidism by inhibiting the synthesis and secretion of thyroid hormones – a decrease in the level of T 4 and an increase in the content of TSH.Decrease in the rate of formation of T 3 from T 4 . (Sometimes preparations containing iodine can cause the Iodine-Basedow phenomenon)

Lithium preparations

Suppress the secretion of T 4 and T 3 and reduce the conversion of T 4 to T 3 , inhibit the proteolysis of thyroglobulin.

Sulfonamides (including drugs used to treat diabetes)

They have a weak suppressive effect on the thyroid gland, inhibit the synthesis and secretion of thyroid hormones (they have structural and functional disorders of the thyroid gland).


Suppresses the secretion of TSH.

Testosterone, methyltestosterone, nandrolone

Decrease in serum TSH and total T concentration 4 and stimulate TSH synthesis.

Phenytoin, Phenobarbital, Carbamazepine

Enhances catabolism of T 4 by enzyme systems of the liver (with prolonged use, thyroid function control is required).With long-term treatment with phenytoin, the level of free T 4 and TSH may be similar to those in secondary hypothyroidism.

Oral contraceptives

May cause a significant increase in total T 4 , but not free T 4 .


Block the capture of thyroid iodine, increase

free T 4 by reducing the binding of T 4 to TSH.


Influences the synthesis of thyroid hormones, reducing the level of total and free T 4 .

Glucocorticoids (with short-term administration in high doses and with long-term therapy in medium doses)

Reduce the conversion of T 4 to T 3 by increasing the concentration of inactive reverse T 3 , inhibit the secretion of thyroid hormones and TSH and reduce its release on TRH.


Slow down the conversion of T 4 to T 3 and lower the level of T 3 .

Furosemide (in large doses)

Causes a drop in total and free T 4 followed by an increase in TSH.


Suppresses the absorption of T 4 cells.When carrying out heparin therapy, an inadequately high level of free T 4 can be detected.


The effects are multidirectional, depending on the initial supply of iodine and the state of the thyroid gland.

* Amiodarone-induced hypothyroidism is most often observed in iodine-deficient regions.Pathogenesis: Amiodarone inhibiting TSH-dependent production of cAMP, reduces the synthesis of thyroid hormones and iodine metabolism; inhibits 5-deiodinase – selenoprotein, providing the transformation of T 4 into T 3 and reverse T 3 , which leads to a decrease in the extra- and intrathyroid content of T 3 .

* Amiodarone-induced thyrotoxicosis most often occurs in iodine-deficient or areas of moderate iodine deficiency.Pathogenesis: iodine released from amiodarone leads to an increase in the synthesis of thyroid hormones in the existing zones of autonomy in the thyroid gland. It is also possible to develop destructive processes in the thyroid gland, which were caused by the action of amiodarone itself.


Before treatment, it is necessary to study the basal level of TSH and anti-TPO. The content of free T 4 and free T 3 is checked if the TSH level is changed.An increase in anti-TPO levels is a risk factor for thyroid dysfunction during therapy with cordarone.

During the first 6 months after starting therapy, the level of TSH may not correspond to the level of peripheral thyroid hormones (high level of TSH / high level of free T 4 / low level of free T 3 ). If euthyroidism persists, the TSH usually returns to normal over time.

Long-term observation. The TSH level during cordarone therapy should be determined every 6 months.It is the TSH level in such conditions that is a reliable indicator of thyroid status.

Taking amiodarone initially causes an increase in the TSH level. This is followed by the dynamics of the levels of reverse T 3 , T 4 , and T 3 . A progressive decrease in the level of T 3 reflects a disturbance in the peripheral transformation of T 4 into T 3 . An increase in the content of total and free T 4 may be associated with the stimulatory effect of TSH and / or with a decrease in clearance of T 4 .



Acute and chronic NTZ have a complex effect on the results of thyroid tests. If possible, testing should be postponed until recovery, unless there is a history or symptoms of thyroid dysfunction. In seriously ill patients, as well as with intensive drug treatment, the results of some thyroid tests cannot be interpreted.

Combined determination of the level of TSH and T 4 allows the most reliable differentiation of the true primary thyroid pathology (coincidence of changes in the level of T 4 and TSH) and transient shifts caused by NTZ themselves (discrepancy between changes in the level of T 4 and TSH).

The pathological level of free T 4 in patients with severe somatic diseases does not prove the presence of thyroid pathology. In the case of a pathological level of free T 4 , it is necessary to examine the content of total T 4 . If both indicators (free T 4 and total T 4 ) unidirectionally go beyond the normal range, thyroid pathology is possible. If the indices of free T 4 and total T 4 diverge, then this is most likely due not to thyroid dysfunction, but to a somatic illness and medication.If a pathological level of total T 4 is detected, it is necessary to correlate this result with the severity of the somatic disease. The low level of total T 4 is typical only for severely and agonizing patients. Low total T 4 in patients outside the intensive care unit suggests hypothyroidism. An increased level of total T 3 and free T 3 is a reliable indicator of hyperthyroidism in somatic diseases, but normal or low T 3 does not exclude hyperthyroidism.

Determination of TSH level in patients with NTZ. Determination of TSH and T levels 4 (free T 4 and total T 4 ) is the most effective combination for detecting thyroid dysfunction in patients with somatic pathology. In such cases, the TSH reference intervals should be expanded to 0.05-10.0 mIU / L. The TSH level can transiently decrease to subnormal values ​​in the acute phase of the disease and rise in the recovery phase.



A change in the functioning of the thyroid gland in women occurs already from the first weeks of pregnancy.It is influenced by many factors, most of which directly or indirectly stimulate the thyroid gland of a woman. This occurs mainly in the first half of pregnancy.

Thyroid stimulating hormone. Literally from the first weeks of pregnancy under the influence of chorionic gonadotropin (CG), which has structural homology with TSH, the production of thyroid hormones of the thyroid gland is stimulated. In this regard, the feedback mechanism suppresses the production of TSH, the level of which during the first half of pregnancy is reduced in about 20% of pregnant women.With multiple pregnancies, when the level of hCG reaches very high values, the level of TSH in the first half of pregnancy is significantly reduced, and sometimes suppressed, in almost all women. The lowest TSH levels are on average 10-12 weeks of gestation. Nevertheless, in some cases, it can remain somewhat reduced until late in pregnancy.

Thyroid hormones. Determining the level of total thyroid hormones during pregnancy is not informative, since it will always be increased (in general, the production of thyroid hormones during pregnancy normally increases by 30-50%).The free T level 4 in the first trimester of pregnancy is usually highly normal, but in about 10% with suppressed TSH levels, it exceeds the upper limit of the norm. As the gestation period increases, the level of free T 4 will gradually decrease and by the end of pregnancy is very often low normal. In some patients, even without thyroid pathology and receiving individual iodine prophylaxis, a borderline decrease in the level of free T 4 in combination with a normal level of TSH can be found in late pregnancy.The level of free T 3 , as a rule, changes unidirectionally with the level of free T 4 , but it turns out to be increased less often.

General principles of diagnosis of thyroid diseases during pregnancy.

* Combined determination of TSH and free T 4 is required.

* Determination of the level of total T 4 and T 3 during pregnancy is not very informative.

* The TSH level in the first half of pregnancy is normally lowered in 20-30% of women.

* The levels of general T 4 and T 3 are normally always increased (approximately 1.5 times).

* The level of free T4 in the first trimester is slightly increased in about 2% of pregnant women and in 10% of women with suppressed TSH.

* In late pregnancy, a low-normal or even borderline-reduced level of free T 4 with a normal level of TSH is often determined.


Thyroglobulin is a glycoprotein containing iodine.TG is the main component of the thyroid follicle colloid and acts as an accumulation of thyroid hormones. The synthesis of thyroid hormones occurs on the surface of TG. TG secretion is controlled by TSH.

The biological half-life of TG in blood plasma is 4 days.


An increase in the content of TG in the blood reflects a violation of the integrity of the hematofollicular barrier and is observed in diseases occurring with a violation of the structure of the gland or accompanied by iodine deficiency.The release of TG into the bloodstream increases with stimulation and structural damage to the thyroid gland. Determination of TG does not make sense in the next 2 to 3 weeks after a puncture biopsy, since the level of TG can be increased due to the passive release of the colloid into the blood when the gland is traumatized. The TG level rises shortly after thyroid surgery. Consumption of a large amount of iodine with food suppresses the release of thyroid hormones from the thyroid gland, shifting the balance between the formation and decay of TG towards its formation and accumulation in the colloid.The level of triglycerides may be elevated in case of thyroid disease, subacute thyroiditis, thyroid enlargement under the influence of TSH, and in some cases benign thyroid adenoma.

The presence of antibodies to TG can cause false negative results, therefore, in parallel with TG, it is desirable to determine antibodies to TG.

In patients with undifferentiated thyroid cancer, the concentration of TG in the blood rarely increases. In differentiated tumors with low functional activity, the level of TG increases to a lesser extent than in tumors with high functional activity.An increase in the level of TG was found in highly differentiated thyroid cancer. Determination of the TG level for the detection of metastases of thyroid carcinoma and dynamic monitoring of the condition of patients during treatment of follicular carcinoma is of great diagnostic value. It was also found that metastases of thyroid cancer have the ability to synthesize TG.

A decrease in the level of triglycerides in the blood after surgery or radiation therapy excludes the presence of metastases. On the contrary, an increase in the level of TG can serve as a sign of a generalized process.

Since patients after radical treatment of differentiated thyroid cancer receive high doses of thyroid hormones (to suppress TSH secretion), against the background of which the level of TG also decreases, its concentration should be determined 2 to 3 weeks after discontinuation of suppressive therapy with thyroid hormones.

In pediatric endocrinology, the determination of TG is of great importance in the management of children with congenital hypothyroidism for the selection of the dose of hormone replacement therapy.With aplasia of the thyroid gland, when TG in the blood is not detected, the maximum dosage is shown, while in other cases, the detection and increase in the concentration of TG suggests a reversible course of the disease, and therefore the dosage of the hormone may be reduced.


TG values ​​in newborns are increased and significantly decrease during the first 2 years of life.


– thyroid carcinoma (excluding medullary cancer),

– early detection of recurrence and metastases of highly differentiated thyroid cancer in operated patients,

– evaluation of the effectiveness of radioiodine therapy for thyroid cancer metastases (by decreasing its blood content to normal values),

– lung metastases of unknown origin,

– bone metastases of unknown origin, pathological fragility of bones,

– determination of TG cannot be carried out for the purpose of differential diagnosis of benign and malignant thyroid tumors.


Healthy faces 1.5 – 50ng / ml

Thyroid cancer:

Before surgery 125.9 + 8.5 ng / ml

After surgery without metastases and relapses 6.9 + 1.8 ng / ml

Metastases and relapses of highly differentiated 609.3 + 46.7 ng / ml

thyroid cancer in operated patients

Benign tumors (before surgery) 35.2 + 16.9 ng / ml

Thyrotoxicosis (severe form) 329.2 + 72.5 ng / ml


The thyroid gland, containing specific antigens, can lead the body’s immune system into a state of autoaggression.One of these antigens is thyroglobulin. Damage to the thyroid gland in autoimmune or neoplastic diseases can cause TG to enter the bloodstream, which, in turn, leads to the activation of the immune response and the synthesis of specific antibodies. The concentration of anti-TG varies widely and depends on the disease. Therefore, the determination of the concentration of anti-TG can be used to diagnose and monitor the treatment of thyroid diseases.


Anti-TGs are an important parameter for detecting autoimmune thyroid diseases and are carefully measured during disease follow-up.An increase in anti-TG levels is determined in Hashimoto’s thyroiditis (more than 85% of cases), Graves’ disease (more than 30% of cases), thyroid cancer (45% of cases), idiopathic myxedema (more than 95% of cases), pernicious anemia (50% of cases, low titers), SLE (about 20% of cases), subacute de Quervain thyroiditis (low titers), hypothyroidism (about 40% of cases), DTZ (about 25% of cases), a weakly positive result can be obtained with non-toxic goiter.

Estrogen-progesterone therapy for contraception increases the titer of antibodies to thyroglobulin and peroxidase. In women with AIT while taking these drugs, the antibody titer is significantly higher than in people with AIT who do not take these drugs.

An increased titer of anti-TG can be obtained in patients with non-endocrine diseases when taking drugs that affect the nature of the immune response.

In patients with Hashimoto’s thyroiditis, the titer of anti-TG during treatment, as a rule, decreases, but there may be patients in whom anti-TG can persist or be detected in waves with a period of about 2 – 3 years.The anti-TG titer in pregnant women with Graves’ or Hashimoto’s disease decreases progressively during pregnancy and rises briefly after childbirth, reaching a peak after 3 to 4 months. A normal anti-TG titer does not exclude Hashimoto’s thyroiditis. The microsomal antibody test is more sensitive for Hashimoto’s thyroiditis than the anti-TG test, especially in patients under 20 years of age.

Determination of anti-TG makes it possible to predict thyroid dysfunction in patients with other autoimmune endocrine diseases and in family members with hereditary organ-specific autoimmune diseases.Weakly positive results are usually found in other autoimmune disorders and chromosomal abnormalities such as Turner syndrome and Down syndrome.

Positive results in some patients with hyperthyroidism suggest a combination with thyroiditis. The use of anti-TG for the detection of autoimmune thyroid diseases is especially justified in iodine-deficient areas.

Children born to mothers with high titers of anti-TG may develop autoimmune thyroid diseases during their lifetime, which requires that such children be considered a risk group.

About 5 – 10% of practically healthy people can have a low titer of anti-TG without symptoms of the disease, more often in women and the elderly, which is probably associated with the identification of individuals with subclinical forms of autoimmune thyroiditis.

INDICATIONS FOR DETERMINING ANTI-TG : – newborns: high titer of anti-TG in mothers, – chronic Hashimoto’s thyroiditis, – differential diagnosis of hypothyroidism, – diffuse toxic goiter (Graves’ disease), – postoperative management of patients with highly differentiated cancer complex with TG, – in iodine-deficient areas, the assessment of the level of anti-TG in serum contributes to the diagnosis of autoimmune thyroid pathology in patients with nodular goiter.

REFERENCE LIMITS – 0 – 100 mU / ml



Anti-TPO test is used to verify autoimmune thyropathies. Possessing the ability to bind to complement, anti-TPO are directly involved in autoaggression, that is, they are an indicator of the aggression of the immune system towards its own body. Thyroid peroxidase provides the formation of an active form of iodine, which is able to be involved in the process of iodification of thyroglobulin, that is, it plays a key role in the synthesis of thyroid hormones.Antibodies to the enzyme block its activity, as a result of which the secretion of thyroid hormones, mainly thyroxine, decreases. Anti-TPO is the most sensitive test for detecting autoimmune thyroid diseases. Usually, their appearance is the first shift that is observed during the development of hypothyroidism due to Hashimoto’s thyroiditis.


Autoimmune diseases of the thyroid gland are the main factor underlying hypothyroidism and hyperthyroidism and develop in genetically susceptible individuals.Thus, the measurement of circulating anti-TPO is a marker of genetic predisposition. The presence of anti-TPO and an increased level of TSH allows predicting the development of hypothyroidism in the future.

A high concentration of anti-TPO is observed in Hashimoto’s thyroiditis (sensitivity 90-100%) and Graves’ disease (sensitivity 85%). The level of anti-TPO increases by 40 – 60% in DTZ, but in a lower titer than in the active stage of Hashimoto’s thyroiditis.

The detection of anti-TPO during pregnancy indicates the risk of developing postpartum thyroiditis in the mother and the possible impact on the development of the child.

At low concentrations, anti-TPO can occur in 5-10% of the healthy population and in patients with diseases not associated with the thyroid gland, for example, in inflammatory rheumatic diseases.

The anti-TPO titer is increased during the treatment with estrogen-progesterone drugs and taking drugs that affect the nature of the immune response.


– autoimmune thyroiditis,

– prediction of the risk of hypothyroidism with an isolated increase in TSH levels,

– prognosis of postpartum thyroiditis in women from high-risk groups,

– ophthalmopathy: enlargement of the ocular tissues (suspicion of “euthyroid Graves’ disease”).

– neonates: hyperthyroidism and high levels of anti-TPO or Graves disease in the mother,

– risk factor for thyroid dysfunction during therapy with interferon, interleukin-2, lithium preparations, cordaron,

is a risk factor for miscarriage and failure during fertilization.

REFERENCE LIMITS – 0 – 30 mU / ml.



Autoantibodies to the microsomal fraction are detected in all types of autoimmune thyroid diseases, however, they can also be detected in healthy people.Anti-MF is a cytotoxic factor that directly causes damage to thyroid cells. Microsomal antigen is a lipoprotein that makes up the membranes of the vesicles containing thyroglobulin. Autoimmune thyroiditis is a disease characterized by the formation of antibodies to various components of the thyroid gland with the development of its lymphoid infiltration and proliferation of fibrous tissue. Anti-MF can destroy the thyroid gland and reduce its functional activity.


The highest levels of anti-MF are found in patients with Hashimoto’s AIT (in 95% of patients), idiopathic mexidema, at the last stage of chronic atrophic thyroiditis, especially in elderly women, quite often in patients with an identified untreated form of Graves’ disease.Anti-MF is detected in 85% of DTZ patients, which indicates its autoimmune genesis. Anti-MF is sometimes found in thyroid cancer. Elevated anti-MF levels during the 1st trimester of pregnancy indicate a certain degree of risk of postpartum thyroiditis.


– Hashimoto’s thyroiditis,

– autoimmune nature of thyroid diseases,

– prognosis of postpartum thyroiditis in women from high-risk groups,

– a high degree of risk of thyroiditis with a hereditary predisposition to this disease, with other forms of autoimmune processes (type 1 diabetes mellitus, Addison’s disease, pernicious anemia).


Thyroid stimulating hormone receptors – membrane structures of thyrocytes (and, possibly, cells of other organs and tissues). TSH-RP are regulatory proteins that are integrated in the thyroid cell membrane and affect both the synthesis and secretion of TG and cell growth. They specifically bind the TSH of the pituitary gland and ensure the implementation of its biological action.The reason for the development of diffuse toxic goiter (Graves’ disease) is the appearance in the blood of patients of special immunoglobulins – autoantibodies that specifically compete with TSH for binding to thyrocyte receptors and are capable of exerting a stimulating effect on the thyroid gland, similar to TSH. Detection of a high level of autoantibodies to TSH receptors in the blood of patients with Graves’ disease is a prognostic harbinger of disease recurrence (sensitivity 85% and specificity 80%). Fetoplacental transfer of these antibodies is one of the causes of congenital hyperthyroidism in newborns if the mother has Graves’ disease.To obtain evidence of the reversible nature of the disease, laboratory monitoring is required to establish the elimination of antibodies to TSH-RP from the child’s body. The disappearance of antibodies in a child after medication achievement of euthyroidism and elimination of goiter serves as the basis for deciding whether to discontinue drug therapy.

Autoantibodies to TSH receptors in increased amounts can be found in patients with Hashimoto’s goiter, with subacute AIT. The level of autoantibodies progressively decreases during drug treatment of these diseases or after thyroidectomy, which can be used to monitor the effectiveness of the treatment.




· Differential diagnosis of postpartum thyroiditis and HD in postpartum thyrotoxicosis.

· Prognosis of the risk of fetal / neonatal thyrotoxicosis in women with previous thyroid radiotherapy for HD or during ongoing therapy with thionamides.

· Diagnosis of Graves’ euthyroid ophthalmopathy.

· Calculation of the duration of therapy and the risk of relapse in patients receiving therapy for HD (especially in children).

REFERENCE LIMITS : Serum TSH autoantibodies are normally up to 11 U / L.

Take tests constantly in the same laboratory – and your doctor will approximately know your personal indicators of the norm and any deviation from the norm will be immediately noticed by him.

Diseases of the thyroid gland / Diseases / Clinic EXPERT

General understanding of the thyroid gland and its functions

The thyroid gland (TG) is an endocrine organ located on the anterior surface of the neck.The gland is separated from the skin only by thin fascia (“plates” of connective tissue), therefore it is located almost under the skin. Due to its location, it is well accessible to palpation (palpation during examination), and with a significant increase it is clearly visible “by eye”, deforming the contour of the neck. The thyroid gland normally consists of two lobes connected by an isthmus. This structure resembles a butterfly.

The main task of the thyroid gland is the production of specific substances – thyroid hormones. This process takes place with the obligatory participation of iodine.The thyroid gland is the only gland that captures iodine from the bloodstream and is capable of synthesizing hormones only with an adequate supply of it.

Thyroid hormones affect the entire body. If you describe in one phrase the action of “thyroid” hormones – they regulate metabolism. With a normal content of thyroid hormones in the blood, all processes in the body proceed in a physiological rhythm. The mechanism of hormone production in adults does not depend on gender and age.


There is definitely a hereditary predisposition to thyroid diseases.It has long been noted that such diseases are more often suffered in the same family. Usually, patients already at the first visit report that the closest blood relatives had problems with the “thyroid”. Women are more susceptible to thyroid diseases (10 times more often than men).

There is a connection between the onset of thyroid disease and:

  • suffered stress
  • infection
  • intense exposure to the sun
  • unfavorable environmental conditions

Against the background of a genetic predisposition, provoking external factors trigger a pathological mechanism resulting in thyroid disease glands.

Diseases of the thyroid gland

All diseases of the thyroid gland occur either with impaired production of thyroid hormones, or without them.

In turn, thyroid malfunction occurs in the direction of

  • decrease – hypofunction, hypothyroidism
  • increase – hyperfunction, hyperthyroidism.


Primary hypothyroidism can be caused by:

  • autoimmune thyroiditis
  • removal of the thyroid gland during surgery (postoperative hypothyroidism)
  • destruction of the thyroid gland under the influence of radioactive substances (post-radiation hypothyroidism)

Thyroid disease 9000 , belonging to the category of autoimmune, when its own immune system produces antibodies that affect the work of the thyroid gland.

Typical for AIT are antibodies to thyroperoxidase (at to TPO) – more specific for the disease and antibodies to thyroglobulin (at to TG). With immune aggression, these antibodies develop a gradual decrease in the work of the thyroid gland, i.e. hypothyroidism occurs – one of the natural manifestations of AIT.

The pathological process occurring in the thyroid gland can change not only the function, but also its structure. Ultrasound of the thyroid gland determines the changes specific to AIT.Since AIT leads to hypothyroidism, the treatment of the disease is reduced to the appointment of the thyroid hormone (thyroxine) to compensate for the deficiency of hormones in the body.

Treatment is prescribed only when the thyroid gland function decreases. If the patient only has an increased level of antibodies in the blood, but the thyroid function is normal, no treatment is prescribed. Thyroid function is retained for annual monitoring and more frequent monitoring in women during pregnancy. It is also believed that the presence of an autoimmune disease of one organ can be combined with other autoimmune diseases (of other organs).Therefore, the detection of AIT often entails examination of other endocrine glands.

To establish the diagnosis of “Autoimmune thyroiditis”, it is necessary to identify at least two of the three indicators (decreased thyroid function (hypothyroidism), the presence of antibodies to the thyroid gland, a specific picture of the thyroid gland structure during ultrasound).

If only one parameter is present, then the diagnosis is put “in question” and is taken under control.

Postoperative and post-radiation hypothyroidism (AIT)

As a result of partial or complete removal / destruction of the thyroid gland (surgery or treatment with radioactive iodine), the body finds itself in conditions of thyroid hormone deficiency.The disease is detected immediately after treatment (with complete removal of the thyroid gland) or after a short time (with incomplete removal of the organ or after radioiodine therapy). The only treatment is to replenish thyroid hormones by taking thyroxine.

Causes of secondary hypothyroidism

A rare reason for a decrease in the thyroid gland is the pathology of the organs regulating its function (pituitary gland and hypothalamus). This means that it is not the thyroid gland itself that is affected, but the “bosses” above it. The cause of the pathology of the pituitary gland and hypothalamus can be tumors, trauma, cysts in this area.Very rarely, the pituitary gland can produce the “inactive” hormone TSH, which is unable to stimulate the thyroid gland to produce hormones.


Diseases occurring with an increase in the thyroid gland

Diffuse toxic goiter (DTZ, Graves ‘disease, Graves’ disease)

This is an autoimmune thyroid disease, when the immune system produces specific antibodies that stimulate thyroid stimulation (thyroid TSH receptor). The production of hormones in the thyroid gland becomes pathologically increased, clinically manifested by thyrotoxicosis (the reaction of various tissues of the body to a large amount of thyroid hormones in the thyroid gland), and in the laboratory – by an increased concentration of T3 and T4 in the blood and a reduced TSH index.Often, DTZ is combined with autoimmune endocrine ophthalmopathy (specific lesion of the eyes). These two diseases have common autoimmune roots, so it is not uncommon to combine them. There are three treatment options for this disease:

  • Conservative therapy (with tablets) for 1-1.5 years
  • Thyroid surgery
  • Radioactive iodine treatment (radioiodine therapy).

The success of the pill therapy is the least persistent (the disease can relapse in 30-70% of cases).

More often Graves’ disease occurs in young patients, more often in women.

Nodular (and multinodular) toxic goiter (UTZ, MUTZ)

The disease is the same as nodular non-toxic goiter: for an unknown reason, nodules form in the structure of the thyroid gland, but they (nodes) are pathologically active and capable of producing a high amount of thyroid hormones with the development of the clinical picture of thyrotoxicosis. Often the disease is accompanied by an abnormal heart rhythm.In addition to routinely determining the level of thyroid hormones (they will be like in Graves’ disease), the disease is also confirmed by thyroid scintigraphy to determine the autonomy of the node. Treatment – surgery or radioiodine therapy after drug preparation of the patient.

Diseases proceeding without dysfunction of the thyroid gland:

Nodular (and multinodular) non-toxic goiter (UNZ, MNZ)

Disease of unspecified etiology (causes), when nodules form in the thyroid tissue.In most cases, the nodes are small (from 1 cm to 2.5-3 cm), are benign in their cellular composition, do not impair thyroid function and do not require any treatment. Observation is carried out, an annual dynamic examination is performed.

Diffuse non-toxic goiter (DNZ)

This term describes a diffuse enlargement of the thyroid gland in size with unchanged organ function, the absence of laboratory and ultrasound data for an autoimmune process. Most often, an increase in thyroid gland is associated with iodine deficiency.When this fact is eliminated, the size of the thyroid gland returns to normal.

Malignant diseases

This is a separate group of thyroid cancer. There are papillary cancer, follicular cancer, medullary cancer, anaplastic thyroid cancer. They differ in their cellular composition, each has features of diagnosis, treatment and monitoring. The most common variants of thyroid cancer (papillary and follicular) are successfully treated, respectively, patients have a good chance of cure and a prognosis for life.More aggressive cancer – medullary and anaplastic – has its own diagnostic and therapeutic characteristics, gives a worse prognosis for treatment and survival. Patients with thyroid cancer are monitored by an oncologist and an endocrinologist, who draw up an individual treatment and follow-up plan.

Symptoms of thyroid diseases

The most typical manifestations of thyroid diseases:

  • general and muscle weakness
  • uncontrolled weight loss with increased appetite or, conversely, poorly controlled weight gain
  • memory impairment, attention, apathy, depression
  • nervousness, anger, increased emotionality, tearfulness, decreased performance
  • low productivity, lack of “strength to work”
  • common edema (face, arms, legs, anterior abdominal wall, tongue)
  • stool disorder (constipation or diarrhea )
  • heart rhythm disturbance (especially in elderly patients)
  • anemia, difficult to treat
  • constant feeling of internal trembling, anxiety, hand tremors (up to a change in handwriting and the inability to perform small movements)
  • changes in the eyes (bulging, change in view lada, swelling of the eyelids, lacrimation, especially from bright light)
  • Finally, the patient may complain of an increase in the front of the neck in size, deformation of the neck contour.

Symptoms of thyroid disease are not always specific. It is not at all necessary that all these symptoms are observed at the same time. If you have at least one of the listed symptoms, you need to check your thyroid function. The endocrinologist will also pay attention to these complaints when talking and examining the patient.


Since the influence of thyroid hormones on the body is very significant and diverse, its diseases will undoubtedly affect the functions of all organs, therefore timely diagnosis is important.

The survey is simple and very affordable.

The first step is an appointment with an endocrinologist, which includes a conversation and examination. As a rule, when questioning the patient, you can identify some disturbing symptoms that make you think about a violation of the thyroid gland. These symptoms are mostly nonspecific and can be observed in many patients, and sometimes healthy people under stress and fatigue.

The second step, if there is a reasonable suspicion of a violation of the function or structure of the thyroid gland, is to refer the patient to a blood test to determine the content of thyroid hormones.

  • in the blood, the level of T4, T3 (thyroid hormones) and TSH (pituitary hormone) is determined
  • , the study is often supplemented by the determination of the level of various antibodies to thyroid gland in the blood

T3 is reduced, and the “boss hormone” (TSH) is increased. On the contrary, with increased production of thyroid hormones, the level of T4 and T3 is increased, but TSH is reduced.

The third step in diagnosis is to visualize the thyroid gland.

The simplest, most accessible and informative method is ultrasound examination of the thyroid gland, in which the size and structure of the organ tissue is determined.

At the same time, one study does not replace another study. Examination, laboratory and instrumental examinations are three key points in the diagnosis of thyroid diseases.

Doctors of the EXPERT Clinic have compiled a list of all necessary examinations required for a basic examination of the thyroid gland.

There are also more specialized, necessary only in some cases, studies:

Thyroid scintigraphy is a method used when there is a suspicion of actively functioning nodules in the thyroid gland.It can also be used for differential diagnosis in conditions of thyrotoxicosis to confirm / exclude destructive thyroiditis.

Other instrumental examination methods (MRI, CT, PET) are used much less frequently in routine clinical practice. Good reasons are needed to carry out these survey methods additionally.

Of particular importance is the assessment of the functional state of the thyroid gland in a pregnant woman due to the fact that the development of the child – especially his nervous system – depends on the level of thyroxine (the main form of thyroid hormones) in the expectant mother.

Treatment of thyroid diseases

Treatment depends on the specific pathology and thyroid dysfunction.

Treatment of all forms of hypothyroidism is the same – the appointment of the drug thyroxine. The treatment is well tolerated and completely compensates for the deficiency of hormones in the body.

Treatment of hyperthyroidism is more complex. A number of drugs are required: some reduce excess thyroid function, others normalize the work of the heart and intestines. Often, participation in the treatment is required not only of an endocrinologist, but also of other specialists (cardiologist, gastroenterologist).

In the absence of thyroid dysfunction, most often they are limited to monitoring the pathology.


Any thyroid disease can be treated. Most often, it is possible to achieve a good response to drug (pill) therapy with a decent chance of a complete cure. Treatment of some thyroid diseases allows them to be transferred into long-term remission (the disease does not manifest itself actively, does not progress and does not violate the patient’s quality of life, and, accordingly, does not require constant treatment).Thyroid diseases occurring with persistent hypothyroidism can also be successfully compensated for with medication, when you have to constantly (all your life) take pills to replenish the lost thyroid function. In this case, the treatment is absolutely safe, since when prescribed for the purpose of treating thyroid hormone drugs, there are no side effects from the treatment.

If the disease cannot be compensated (or cured) with tablet drugs (this mainly concerns pathologies occurring with thyrotoxicosis; with large sizes of the thyroid gland and nodes in it; thyroid cancer), then surgery on the thyroid gland allows in the overwhelming majority of cases to solve disease problem.

Competent and timely treatment of thyroid diseases will prevent complications of the disease from other systems in the body: cardiovascular, digestive, bone, etc.

Absence of treatment for a long time will eventually cause changes in vital organs. They can be irreversible – even when starting therapy!

Prevention and recommendations

As such, there is no prevention of thyroid diseases.Therefore, a high degree of importance is acquired by periodic preventive examination (examination by an endocrinologist, ultrasound of the thyroid gland, blood tests), especially for risk groups (they include in the presence of heredity factors, unfavorable ecology of the place of residence, occupational harm, frequent stress).

Maintaining a healthy lifestyle, a protective attitude towards one’s nervous system, physiological consumption of products containing iodine, etc. will act as the best prevention of the pathology of this endocrine organ.

Frequently asked questions

Close relatives diagnosed with thyroid disease, is there a risk of getting sick?

Thyroid diseases are not “contagious”, but there is a genetic predisposition to thyroid pathology. Often (but not at all 100%), in one family, several people have thyroid disease. The pathology of the thyroid gland does not have to be the same for everyone; it can be completely different variants of thyroid diseases.

The only serious thyroid disease – medullary cancer – must be specified in all close blood relatives of the patient with this pathology, i.e.because there are genetic variants of the disease that affect relatives with 100% probability.

Nothing worries, but laboratory examination revealed very high levels of antibodies to thyroid gland in the blood, what next?

Approximately 15-20% of healthy people have antibodies (ABs) in their blood to various structures of the thyroid gland (as a rule, these are antibodies to TPO and TG, less often to the TSH receptor). If the function of the thyroid gland is not impaired, then the fact of the presence of antibodies will not have clinical significance, let us call it an “individual feature”.Of course, the mere fact of the presence of antibodies will not be treated, whatever their level is recorded in the blood. If the thyroid function is impaired or if the thyroid gland is enlarged, the determination of the presence of antibodies (mainly antibodies to TPO) will inform about the cause of the disorders in the gland. The combination of impaired thyroid function and a high titer of antibodies to the thyroid gland makes it possible to establish the diagnosis of autoimmune thyroid disease. The presence of antibodies to the thyroid gland will dictate the need for a more frequent assessment of thyroid function in conditions of taking drugs with a large (non-physiological) amount of iodine and lithium preparations, as well as during pregnancy, since there may be peculiarities in the functioning of the thyroid gland against this background.Note that the presence of antibodies in the blood itself has no effect on well-being. In most cases, the patient is more afraid of the “number” of antibodies in the laboratory form, sometimes hundreds of times higher than the upper limit of the norm. There is no need to treat the “blood antibody level”.

What can be done to reduce the risk of illness?

We are not able to influence the genetic predisposition to the disease. It was given to us from birth. The starting point in the implementation of a pathological hereditary predisposition may be stress, severe infectious diseases, taking certain medications, etc.Therefore, the implementation of general recommendations for a healthy lifestyle will to some extent prevent the manifestation of the disease.

To exclude thyroid dysfunction, what test should be taken?

The first (and sometimes the only) test to be performed if thyroid dysfunction is suspected is thyroid stimulating hormone (TSH). If this indicator is normal, then not a single disorder in the patient’s well-being can be associated with the thyroid gland. In fairness, it must be said that there are very rare diseases of the endocrine system, in which TSH remains normal, but there is a violation of hormone production.Determining the indications for expanding the examination is the prerogative of the endocrinologist who examines the patient. Sometimes the patients themselves ask the doctor to issue a referral for the study of “all thyroid hormones”, explaining this desire by the “dislike” for taking blood for analysis, but this is not always justified. A detailed conversation, an explanation of when an in-depth examination of thyroid function may be required, will help the patient not to waste “unnecessary”, but also not to miss the “necessary”.

A blood test for thyroid hormones is performed in the first half of the day, on an empty stomach.In women, regardless of the day of the menstrual cycle.

Changes in TSH level were detected for the first time, should they be treated immediately?

Most often, a very moderate (up to 10 Med / l) increase in the TSH level is detected with normal T4 values. This situation first requires re-monitoring in 2-3 months. If this increase is persistent, i.e. there was no independent normalization of the level of hormones, then individually with the patient, with a thorough assessment of the concomitant pathology, the endocrinologist decides whether to prescribe treatment.It is possible that the situation will simply be “taken on a pencil”. The only category of our patients for whom an increase in TSH levels does not require additional rechecking is pregnant women. In this case, thyroxine therapy is prescribed immediately, because “No time” to recheck in a few months.

Diagnosed with autoimmune thyroiditis, what should I do?

When such a diagnosis is established and substitution therapy with thyroxine drugs is prescribed, the dose of the drug is selected under the control of the TSH level.At the onset of the disease, the decrease in the function of one’s own thyroid gland may not be total, i.e. to compensate for the lack of thyroxine, a small dose of the hormone is required. Over the course of the disease, all new thyroid cells are captured by the pathological process and to replenish the lost, a corresponding increase in the thyroxine dose is required, which eventually reaches the individual daily requirement. Patients often draw “their” conclusions from this fact: “Taking the drug has stopped the work of my thyroid gland, now I will be“ dependent on hormones ”.This narrow-minded view is absolutely not true. Not taking the drug, but the thyroid gland itself gradually decreased and finally stopped its work. This is a completely natural course of autoimmune thyroiditis, when the need for thyroxine increases over time.

How often should thyroid function be monitored?

There are more common and less common thyroid diseases.

With autoimmune thyroiditis and a selected dose of thyroxine, it is sufficient to control the TSH level once a year.An exception is pregnancy, when control is carried out once a month. The need for correction of therapy is discussed with the doctor after receiving the results.

In Graves disease, thyroid hormone control is much more frequent. At first monthly, and with a good response to treatment, then once every 2 months. A doctor’s examination is mandatory, because correction of therapy is possible.

In case of a nodular goiter with a confirmed benign structure of a node in the thyroid gland, thyroid hormones are monitored once a year.

Other, more rare diseases require an individual plan-dynamic examination and observation by an endocrinologist.

What parameters, besides thyroid hormones, should be monitored?

In some thyroid diseases, periodic monitoring requires thyroid ultrasound. To a greater extent, this applies to nodular non-toxic goiter, when the dimensions of the nodules in the thyroid gland are assessed in dynamics. Also, dynamic thyroid ultrasound is performed with a diffuse increase in the thyroid gland, when it is necessary to assess the dynamics of thyroid size with or without treatment.Ultrasound of the bed of the removed thyroid gland and lymph nodes is necessary after radical treatment of thyroid cancer.

As a rule, there is no need for dynamic performance of ultrasound of the thyroid gland when observing a patient with autoimmune thyroiditis.

Other special methods of dynamic examination (scintigraphy, computed tomography, MRI of the neck) are rarely prescribed, only if there are special indications for that.

The material was prepared using data from the “Clinical guidelines of the Russian Association of Endocrinologists for the diagnosis and treatment of autoimmune thyroiditis in adults”; “Clinical recommendations of the Russian Association of Endocrinologists for the diagnosis and treatment of nodular goiter”

Treatment histories

Nodular goiter

Patient V., 45 years. I turned to the EXPERT Clinic with the data of an ultrasound of the thyroid gland. There were no complaints about the state of health. I went to be examined “for the company” with a friend. The patient’s family has no relatives suffering from thyroid pathology. The first ultrasound revealed multiple very small changes in the gland tissue 3-6 mm in diameter, described by the ultrasound specialist as “multiple nodes”. The patient performed a blood test for thyroid hormones, there were no abnormalities in the laboratory examination data.The patient was offered dynamic observation (ultrasound control) every six months, which the patient did. She came to the appointment with five ultrasound reports, in which there were no changes in the size of the lesions in the thyroid gland. However, dynamic examination was recommended by the ultrasound specialist.

Important! The “nodes” in the thyroid gland revealed in this patient, which do not have negative dynamics, do not require any treatment and monitoring in dynamics at all. These are accidental findings that have no clinical significance.

Patient I., 32 years old. She did not complain about her health. Sent to an endocrinologist after a dispensary examination, during which the therapist suspected a node in the thyroid gland. Examination of the nodular goiter was confirmed – a 12 mm diameter node with indistinct contours and increased blood flow inside. The hormonal function of the gland was not disturbed. A biopsy of the node was performed, which revealed a suspicion of thyroid cancer. The patient was operated on (the gland and partly the lymph nodes in the neck were removed).Subsequent histological examination confirmed the diagnosis of cancer, additionally revealed metastases to the lymph nodes. The patient required further treatment – radioiodine therapy. Currently, the patient is receiving treatment and is under the dynamic control of an endocrinologist and oncologist. There are no data on the progression and return of the disease after 2 years.

Subsequently (after 3 years), after making sure that the disease has not returned, the patient plans a pregnancy.

Important! Timely diagnosis and treatment allow to adequately treat the patient, giving him a good chance of recovery.


Patient M., 20 years old. Over the course of 3 years, it gradually and steadily gains weight. He notes swelling on the face, hands, legs, and abdomen. During all this time, persistent constipation is troubling. The skin became pale, with a yellowish tinge. The patient is studying at the institute in the third year. I began to study worse, tk. attention and ability to remember worsened, it became difficult to assimilate a large amount of information, although earlier learning was easy. I tried to study more.All the described complaints – in particular, weight change, swelling and constipation – were associated with the fact that she leads a predominantly sedentary lifestyle. I tried to use “different diets” for weight loss. They did not bring a significant effect. To normalize the stool, I used laxatives, enemas. I went to the student clinic. The examination revealed a reduced level of hemoglobin. Prescribed iron supplements, vitamin preparations, but there was no significant effect of the treatment.

Turned to the EXPERT Clinic.The examination revealed hypothyroidism against the background of autoimmune thyroiditis. The patient was prescribed treatment, all symptoms of the disease disappeared within 3 months.

Important! Hypothyroidism in adults, which most often occurs against the background of an autoimmune thyroid gland, is a common disease. It is easy to diagnose and easy to treat. The main thing is to diagnose in time and choose the right treatment. The patient’s quality of life will depend on this.

Diffuse toxic goiter

Patient N., 32 years. I went to the EXPERT Clinic with complaints of tearfulness, instability of mood, increased irritability. She became conflicted in relation to household members and work colleagues. I was worried about increased sweating, trembling hands – both during nervous stress and at rest. I began to notice frequent loose stools; weight loss. All these changes occurred in 3-4 months. The patient herself indicated that her state of health was disturbed soon after a traumatic situation in the family.

With the above complaints, the patient turned to the therapist of the polyclinic, where a diagnosis of “disorder of the autonomic nervous system” and “irritable bowel syndrome” was established.

Turned to a gastroenterologist, then to a neurologist at the EXPERT Clinic. On examination, a possible pathology of the thyroid gland was immediately suspected. The examination revealed for the first time and confirmed hyperthyroidism (Graves’ disease).

On the background of timely treatment, the patient’s state of health completely returned to normal. Gastroenterological and neurological treatment was not even required. The patient is currently continuing treatment and feels well. It is under the supervision of an endocrinologist (curator) who is correcting the treatment.The patient is satisfied with the supervision, the opportunity to consult and receive advice in case of any alarming changes in the state of health, has full information about the treatment and prognosis of her disease.

Important! Timely diagnosis of thyroid disease makes it possible to prescribe treatment in the shortest possible time, without waiting for a pronounced effect on other body systems.

Do you often get tired and constantly chill? Is it time to get tested for hypothyroidism?

  • Dr. Michael Moseley
  • BBC

Photo author, BURGER / PHANIE

Photo caption,

Excess weight, increased fatigue or sensitivity to cold can be symptoms of hypothyroidism

937 One in 70 women and one in a thousand men in the UK experience symptoms of hypothyroidism.However, for all the prevalence of this ailment, it is still difficult to diagnose and treat it. How many cases of the disease pass by doctors, the leading medical programs of the BBC, Dr. Michael Moseley, sorted out.

I recently received an e-mail from the author asking me if I had ever thought about the fact that I might suffer from hypothyroidism, that is, from an underactive thyroid gland. The author decided to ask me about this, because he saw on TV and noticed that I have rare eyebrows, which may be one of the symptoms of the disease.

I have no other symptoms – excess weight, increased fatigue or sensitivity to cold, so I decided not to get tested.

But if you have these symptoms, and it seems to you that you may suffer from thyroid insufficiency – what to do?

For an answer, I went to Dr. Anthony Toft, former president of the British Thyroid Association.

Dr. Toft compares the thyroid gland to the gas pedal in a car.It releases hormones that regulate the body’s metabolic rate. If your thyroid is not active enough, your metabolism will slow down.

This means that you are more likely to gain weight. Other symptoms include sensitivity to cold or heat, loss of energy, constipation, low mood or “blurred” perception.

Photo caption,

Dr. Moseley’s almost invisible eyebrows could be a symptom of hypothyroidism

The main hormones that stimulate the gland are involved in this process, thyroid stimulating hormone (TSH), as well as the hormones triiodothyronine (T3) and thyroxine (T4).They are secreted by the pituitary gland and stimulate the activity of the thyroid gland.

If you develop symptoms of hypothyroidism, your doctors will do a blood test for elevated TSH levels and low T4 levels.

Elevated TSH levels suggest that the pituitary gland, located in the human brain, sends signals to the thyroid gland to increase the production of the hormone T4, but for some reason, it does not.

In this case, the pituitary gland increases the level of TSH, but the level of T4 remains low.

In other words, the human body requires more thyroid hormones, but the thyroid gland ignores these calls. The result is hypothyroidism.

In such cases, patients are prescribed to take levothyroxine sodium, which eliminates most of the symptoms of the disease and improves the quality of life of patients.

Photo author, Science Photo Library

Photo caption,

Thyroid problems can also be detected with a scan

But, if everything is so simple, why are Internet forums filled with comments from disgruntled patients?

One problem is the lack of universally recognized international reference ranges for blood tests for hypothyroidism.

From the point of view of Dr. Toft, British doctors interpret the accepted standards too literally and often do not react in any way to an increased level of TSH and T4, if it does not go beyond the range adopted in Britain.

In almost all cases, patients are prescribed a synthetic version of T4, but some patients remain symptomatic. This may be due to the fact that although the thyroid itself is functioning correctly, their bodies do not convert thyroxine in their cells to a biologically active form – triiodothyronine.

In such cases, the patient can take the T3 hormone in pill form. But then another problem arises.

“The price of T3 pills has risen sharply in recent years. The cost of a two-month course can be up to £ 300, although the production of these pills costs a penny,” says Dr. Toft.

Photo Credit, Science Photo Library

Photo Caption,

Levothyroxine Sodium Tablets

As a result, doctors often refuse to prescribe these drugs.Many patients then buy them overseas online.

This is not ideal as those taking T3 pills must be monitored as they can cause serious side effects.

Hormonal supplements obtained from the organs of internal secretion of cows and pigs, which contain both T4 and T3, are somewhat cheaper.

But these hormonal supplements are not well understood, and according to Dr. Toft, they are unlikely to be widely used in the foreseeable future.

And some patients may have to admit that there is no effective medication for them and that they need to change their lifestyle.


In recent decades, the functional state of the thyroid gland in patients of various profiles has been actively studied. It is known that thyroid hormones regulate the state of all organs and systems in the human body, primarily the processes of growth, maturation and differentiation of cells.The effects of thyroid hormones on the cardiovascular system have been well studied [1]. Thyroid hormones regulate the processes of systolic contraction and diastolic relaxation of the heart muscle, total peripheral vascular resistance (OPSR), and the synthesis of structural myocardial proteins. Thyroid hormones regulate the activity of the apoB receptor in hepatocytes in a genomic and non-genomic way, mediating the catabolism of atherogenic low-density lipoproteins. In conditions of hypothyroidism, as a rule, atherogenic dyslipidemia is detected.Hypothyroidism is characterized by hyperhomocystinemia and peripheral insulin resistance. Thus, a decrease in the functional activity of the thyroid gland, the so-called hypothyroidism, is currently considered a factor of cardiovascular risk. It is known that patients with CKD also often have a violation of the functional state of the thyroid gland, especially hypothyroidism of varying severity. The contribution of hypothyroidism to the pathogenetic mechanisms of the formation of chronic kidney disease is being actively studied.At the same time, the issues of detecting thyroid diseases in patients with CKD have not been developed. There are no clear recommendations on therapeutic tactics in patients with CKD with impaired thyroid function [2].

The prevalence of hypothyroidism, especially subclinical hypothyroidism (SG), is quite high and can reach 10-20% among patients of the older age group. It should be noted that the clinical symptoms of hypothyroidism are usually nonspecific, especially in elderly patients, and the absence of any symptoms does not exclude the presence of hypothyroidism according to laboratory data [3].Therefore, in accordance with the existing clinical guidelines, it is necessary to carry out a screening determination of the TSH level in all patients with atherogenic dyslipidemia, overweight and obesity, type 1 and type 2 diabetes mellitus, ischemic heart disease and arterial hypertension. At the same time, the issues of screening determination of the functional state of the thyroid gland remain insufficiently worked out [3], especially in patients with CKD. Most experts consider it necessary to screen for the level of thyroid-stimulating hormone (TSH) for all patients who seek help.In the domestic literature, no large cohort studies on the functional state of the thyroid gland in patients with CKD are presented. The study of the prevalence of thyroid dysfunction in patients with CKD and the formation of recommendations for the treatment of thyroid dysfunction in patients with CKD seem to be extremely important [4, 5].

The prevalence of hypothyroidism, both overt and subclinical, is being actively studied in CKD. In a prospective study on the risk of atherosclerosis in the United States [6], 15 792 people from four US states were examined.The level of TSH, free T3 and T4, antibodies to TPO and glomerular filtration rate (GFR) were determined initially and over time. The follow-up period was 19.6 years. According to the survey results, 82% of the population was in a state of euthyroidism. Hypothyroidism was detected in 6.5% of the surveyed, hyperthyroidism – in 4.9% of the surveyed, anti-TPO antibodies were positive in 13.7% of the surveyed. The mean GFR was 96.4 ml / min, and 2% of those examined had a decrease in renal function (GFR <60 ml / min). A decrease in GFR was associated with an increase in TSH levels (RR 1.87, 95% CI 1.25-2.81; p = 0.002) Similar results were obtained in the NHANES III and the HUNT study [7.8].

According to the results of a database study of a large hospital in India [9], it was shown that the prevalence of FH and overt hypothyroidism among non-dialysis patients with CKD for the period 2013-2015. amounted to 10.84%. The average age of patients was 55.88 ± 12.85 and 55.16 ± 14.25 years for FH and overt hypothyroidism, respectively. It is known that the incidence of hypothyroidism and CKD correlates with age and is more often detected in elderly patients. However, the presented study showed that the relationship between a decrease in the functional activity of the thyroid gland and a decrease in GFR did not depend on the sex and age of the patients.The identification of hypothyroidism in a population is usually associated with female sex and older age, since the main cause of hypothyroidism in an iodine-rich population is the outcome of autoimmune thyroiditis. In conditions of CKD and decreased GFR, the mechanisms of hypothyroidism formation are most often different (the Wolf-Chaikov effect, systemic acidosis, impaired peripheral conversion of T4 to T3). The incidence of hypothyroidism increased as CKD progressed. Thus, in the group of patients with GFR ≥30 ml / min, the incidence of hypothyroidism was 32.68%, and in the group of patients with GFR <30 ml / min - 66.32%.

In a study by J.C. Lo et al. [10] also showed a high prevalence of subclinical hypothyroidism (23.1%) in CKD patients with GFR <30 ml / min. In a study by M. Chonchol et al. [11] The prevalence of hypothyroidism in CKD patients not on dialysis was 18–20%.

A study of elderly patients (85 years and older) revealed a relationship between an increase in TSH levels and a decrease in GFR among residents of the city of Leiden (Netherlands) [12]. In patients with overt hypothyroidism (7.2% of the examined) and FH (6.3% of the examined), GFR was 53.7 and 55.7 ml / min, respectively.In the state of euthyroidism, GFR was 59.7 ml / min (p = 0.02). Further prospective observation over 5 years did not confirm the initial patterns.

Prospective observation data are rather contradictory. Thus, the well-known Rotterdam study did not reveal a relationship between hypothyroidism and the progression of CKD [13]. Initially, 5103 patients were examined (mean age 63.6 years). An increase in TSH levels was associated with a decrease in GFR and was an independent risk factor for CKD. The follow-up period was 8.1 years.According to the results of prospective observation, it was shown that a decrease in the functional activity of the thyroid gland did not worsen the course of CKD.

US scientists presented a study to study the functional state of the thyroid gland and mortality in patients with the national center of peritoneal dialysis [14]. At baseline, among 1484 examined patients, the incidence of hyperthyroidism and hypothyroidism was 7 and 18%, respectively. The follow-up period was 5 years. Both low TSH (TSH <0.1 mIU / L) and high TSH (TSH> 5 mIU / L) were associated with increased mortality in patients with CKD on peritoneal dialysis.

Another large cohort study on the functional state of the thyroid gland was presented by US scientists [15]. 461,607 veterans with various stages of CKD (from 3 to 5) were examined. All study participants were measured serum creatinine and TSH at specific time intervals from October 2004 to September 2006. Renal function was determined by calculating GFR according to the CKD-EPI formula. Hypothyroidism was defined as an increase in TSH> 5.0 mIU / L and / or thyroid hormone replacement therapy.The association between GFR and serum TSH was calculated using linear regression. According to the results of the study, initially 68.9, 25.5, 25.3 and 0.3% of patients had CKD stages 3A, 3B, 4 and 5, respectively. For every 10 ml / min / 1.73 m 2 decrease in GFR, the risk of hypothyroidism increased by 18% (RR 1.18, 95% CI 1.17-1.20; p <0.001). It was shown that a decrease in GFR by 10 ml / min / 1.73 m 2 was associated with an increase in TSH by 0.11 mIU / L (95% CI 0.10-0.11, p <0.001). Thus, in a large cohort study in the United States, it was shown that patients with varying degrees of CKD have an inverse relationship between GFR and the risk of hypothyroidism.

A retrospective cohort study of thyroid dysfunction in patients with CKD was undertaken by Japanese scientists based on the results of an analysis of the database of the Department of Health (Taipei) [16]. The study included 41,454 patients over 65 years of age. The TSH level was ranked as follows: hyperthyroidism – TSH <0.1 mIU / L, euthyroidism - TSH 0.1-5.0 mIU / L, hypothyroidism was considered an increase in TSH above 5.0 mIU / L. The follow-up period was 5 years. High TSH levels have been associated with the subsequent development of CKD.Patients with subclinical hypothyroidism and overt hypothyroidism had an increased risk of developing CKD in the subsequent: (RR = 1.15, 95% CI 1.05-1.26) and (RR = 1.27, 95% CI 1.04-1, 55), respectively. Further, a retrospective cohort study was conducted to study the relationship between TSH levels and mortality from all causes in patients with CKD [17]. The study included 23 786 patients with CKD over 65 years old in Taipei (Japan). A retrospective analysis of the database of medical institutions in Taipei was carried out from 2005 to 2010.The TSH level was ranked as follows:

  • low-normal TSH level 0.341.074 mIU / L;
  • average normal level of TSH 1.074-2.46 mIU / l;
  • high-normal level TSH 2.465.2 mIU / l;
  • increased TSH level I 5.2-10.0 mIU / l;
  • Elevated II level TSH TSH> 10 mIU / L.

The mortality risk was calculated using the Cox regression model, taking into account gender, age, diabetes, hypertension, stage of CKD. The risk of death from all causes was increased in the group with increased TSH I (RR 1.21; 95% CI 1.021.45) and in the group with increased TSH II (RR 1.30; 95% CI 1.00-1.69 ) compared with the reference group (average TSH level).A highly significant association was found between an increase in TSH levels and mortality from all causes in patients of the older age group with CKD. However, the authors believe that the benefits of treating subclinical hypothyroidism in elderly patients with CKD need to be clarified in well-designed randomized, controlled trials.

Scientists in Korea have studied the effect of the annual dynamics of TSH level changes on the incidence of CKD. The results of observation of 24 184 patients of the Seoul hospital from 2006 to 2012 are presented.[eighteen]. The final statistical analysis included 17,067 Korean adults with normal thyroid function and no history of thyroid disease. A decrease in GFR <60 ml / min / 1.73 m 2 was regarded as CKD. During the follow-up period (the follow-up period was 5.2 years), 561 cases of CKD were registered. The risk of CKD was significantly higher in individuals with a rapid increase (quantile 5) or decrease (quantile 1) TSH compared with the reference group (quantile 3).The risk of CKD was 3.15 (95% CI 2.34-4.24; p <0.001) and 3.37 (95% CI 2.52-4.51; p <0.001) in patients with low and high TSH values. respectively. The risk of CKD in the patients observed in the study increased as the TSH level changed from baseline.

Violations of hemodynamics and renal function in patients with hypothyroidism

Violations of hemodynamics in patients with hypothyroidism have been well studied. It is known that hypothyroidism is associated with severe impaired cardiac contractility and a decrease in cardiac output, impaired diastolic relaxation of the myocardium, a decrease in myocardial oxygen saturation, and vascular resistance.This is mediated by abnormalities in the transcription of genes that control myocardial contractile function [19-21]. It has been shown that in hypothyroidism, the synthesis of endothelial factors of vasodilation is impaired, which leads to an increase in the rigidity of the vascular wall, an increase in systemic vascular resistance and diastolic hypertension [22-26]. Hypothyroidism is associated with decreased sensitivity to β-adrenergic stimuli, decreased expression of the renin gene and renin secretion [27], and decreased activity of the renin-angiotensin-aldosterone system.This leads to impaired renal autoregulation [28, 29]. Other hemodynamic disorders in hypothyroidism include a decrease in the level of atrial natriuretic peptide, a decrease in the production of erythropoietin, which, in turn, decreases the volume of circulating blood (BCC) [27, 30].

Experimental animal models have shown that under hypothyroidism conditions, the activity of Na + / K + -ATPase and Na + -H + -transporter is reduced [31]. It has been shown that under conditions of hypothyroidism there is a violation of sodium and water reabsorption in the proximal tubule.This leads to an increase in filtrate volume and volume overload of the tubular apparatus. In turn, the volume overload of the tubular system leads to stimulation of the macula densa and adaptive vasoconstriction of the afferent arteriole. These factors ultimately lead to a decrease in GFR [32]. Disruption of the activity of chloride channels (ClC-2) activates tubuloglomerular feedback, which also leads to a decrease in GFR [30]. Intrarenal vasoconstriction can reduce renal blood flow and predispose to prerenal kidney injury [19, 33].In patients with hypothyroidism, a decrease in the expression of renal vasodilators, vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1) has been shown [34]. A decrease in the matrix of Gla-protein, a potential inhibitor of vascular calcification, has also been shown [35]. An increase in glomerular capillary permeability leads to an increase in albumin excretion [36].

Increased urinary loss of Na and bicarbonate leads to impaired urine acidification (acidification of urine).A decrease in osmotic pressure in the medulla of the kidney reduces the ability of the kidney to concentrate urine [37]. The sensitivity of the collecting ducts to the action of antidiuretic hormone (ADH) increases, which leads to an increase in fluid reabsorption [38].

Thus, typical complications of hypothyroidism are hyponatremia and impaired excretion of free water. This is accompanied by a decrease in GFR, sodium reabsorption, a relative increase in vasopressin secretion and renal sensitivity to the action of ADH [39].

Features of the thyroid gland-hypophysis-hypothalamus system in patients with CKD

Synthesis and secretion of thyroid hormones are well studied. The starting substance for the synthesis of thyroid hormones is iodine. Inorganic iodine (I ) enters the human body as salts – NaI and KI. Follicular cells of the thyroid epithelium capture inorganic iodine (I ). Further, the oxidation (organization) of iodine occurs with the help of the key hormone enzyme – thyroid peroxidase.The formed organic iodine (I 0 ) participates in the process of iodination of the thyroglobulin molecule, mono- and diiodothyronines (T1 and T2) are formed. Subsequently, a condensation reaction occurs, and thyroid hormones (T3 and T4), ready for secretion, are synthesized, which are stored in the colloid of the thyroid follicle. Subsequently, with the help of a receptor (megalin), thyroglobulin is captured, and thyroglobulin enters the follicular cell. After cleavage by lysosomal enzymes, T3 and T4 are secreted into the blood (Fig.one).

Excretion of iodine from the body in people with normal renal function occurs mainly in the urine (up to 90%). In patients with normal renal function, 56% of 10 mg of iodine load is excreted within 24 hours compared to 11% excretion in patients with CKD (creatinine clearance <44 ml / min) [40]. Serum inorganic iodine concentration in individuals with ESRD is increased 4–9 times compared with individuals with normal renal function due to renal iodine excretion (<5 ml / min) [41]. After dietary restrictions on iodine intake for 2-15 weeks of observation, in patients with creatinine clearance of 5-44 ml / min, the serum iodine level was 3.5 times higher than normal.Although inorganic iodine is removed with all types of dialysis, serum iodine concentration was increased in 84% of patients on continuous hemodialysis and in 92% of patients on peritoneal dialysis. If the excretion of inorganic iodine is impaired in patients with CKD, a large depot of iodine is formed in the body. It is known that iodine accumulates in adipose tissue, gastric mucosa, salivary glands, and mammary glands. Under physiological conditions, it is possible that these are certain mechanisms of adaptation of the body to iodine deficiency.However, in conditions of disease, in particular in CKD, this can have negative consequences and support the pathological process.

In patients with ESRD, the circadian rhythm of TSH, its peaks in the late evening and early morning hours, and pulsatory release may be disturbed. In 10 patients with ESRD secretion, the TSH frequency was shorter, the pulse amplitude was less and the evening increase in TSH level was reduced or absent. TSH clearance (elimination) was reduced by 57% from the norm in patients with CKD [43], which may reflect a decrease in renal clearance, erosion of TSH variation, and a decrease in the TSH pulse amplitude in patients with ESRD.

Nocturnal increase in TSH level was also absent in 90% of euthyroid patients with ESRD, while basal morning TSH concentration was normal [44] (Fig. 2). However, these mechanisms of central TSH dysregulation do not reduce the production and secretion of free T4 by the thyroid gland. Glycosylation of the TSH molecule is also impaired in patients with severe non-thyroid diseases, including ESRD. Glycosylation of the TSH molecule can alter the plasma half-life of the TSH molecule. It was shown that the α-subunit of the TSH molecule was 14 times higher in euthyroid patients with ESRD than in healthy euthyroid individuals.At the same time, the response of TSH and the α-subunit of TSH to exogenous administration of thyroliberin is either normal or impaired [45]. Low T4 St. in serum in patients with ESRD is mainly associated with impaired binding of T4 to plasma proteins. Free fractions of T4 in dialysis patients are usually normal or increased [46-48]. Thyroxine-binding globulin is normal or elevated. The concentration of transthyretin is usually normal, and the concentration of serum albumin is reduced.

Fig.1. Synthesis and secretion of thyroid hormones [42].

Figure 1. Synthesis and secretion of thyroid hormones [42].

Fig. 2. The level of thyroid-stimulating hormone of the pituitary gland at night and in the morning and the peak of thyroid-stimulating hormone after administration of thyroliberin in patients with renal insufficiency and in healthy individuals (adapted from Bartalena L. et al. [44]).

Figure 2. The level of the thyroid-stimulating hormone at night and in the morning and the peak of the thyroid-stimulating hormone after administration of thyroliberine in patients with renal failure and in healthy individuals (adapted from Bartalena L.et al. [44]).

The concentration of total and free T3 in patients with ESRD is often reduced, as in the case of other non-thyroid diseases. Of the 287 euthyroid patients with ESRD, 76% had a total T3 below 100 ng / dL and 66% of patients had a free T3 index below 100 [49]. A low level of T3 is associated with impaired peripheral conversion of T4 to T3 in severe patients, while the synthesis and secretion of T3 by the thyroid gland are not impaired [50, 51].

Patients with ESRD have normal serum T3 reversal, while in most other non-thyroid diseases there is an increase in T3 reversal.In ESRD patients, normal serum total reversible T3 is associated with an increase in the concentration of free reversible T3 due to a decrease in the rate of elimination (clearance) of free reversible T3. There is a certain shift of the reverse T3 from the vessels to the extravascular spaces. There is an increase in the binding of reverse T3 in the tissues.

Thyroid disease in patients with CKD and kidney transplantation

Patients with CKD may have a higher incidence of goiter, nodules, hypothyroidism, and thyroid carcinoma than in the general population.Primary hypothyroidism develops in 9.5% of patients with ESRD compared with 0.6-1.1% in the general population. In a study (Los Angeles), 2.6% of 306 patients with ESRD had primary hypothyroidism, which was characterized by an increase in TSH> 20 mIU / L, a decrease in T4 sv. and the T4 index of St. Among hypothyroid patients, 88% were women over 50 years old, 50% of them had an increase in antimicrosomal antibodies, 50% – goiter, 50% – diabetes. The incidence of hyperthyroidism in ESRD patients was the same as in the general population, but only 10 cases have been reported in the literature.All patients were female, 5 people over 60 years old, 5 people under 40 years old. Hyperthyroidism was associated with Graves’ disease in 8 patients, and multinodular toxic goiter was identified in 2 patients [52].

An increase in the intrathyroid iodine concentration to a certain extent contributes to the induction and maintenance of autoimmune thyroid diseases, including Graves’ disease, and also provokes the formation of thyroid nodules.

The incidence of thyroid dysfunction in CKD may increase in older patients with diabetes and iodine load.In 1991, 45% of patients with CKD were over 65 years of age, and 33% of ESRD was due to diabetes [53]. The incidence of goiter in patients with ESRD can range from 0% in the UK to 50% in the United States, suggesting certain geographic differences [49]. The method of determining goiter matters: for example, in Denmark, goiter was not detected by palpation, and up to 60% of patients had goiter according to ultrasound.

In Los Angeles, 43% of ESRD patients had palpable goiter compared with 6.5% of hospitalized patients matched for gender, age, and race [49] without any renal disease.Goiter was more common (50%) in dialysis patients than in patients without chronic hemodialysis (39%). The incidence of goiter in patients with ESRD did not depend on age, race, diabetes mellitus, TSH or thyroliberin levels, or antithyroid antibodies. The formation of goiter in patients with CKD is associated with an increase in inorganic iodine in the plasma, since a high concentration of intrathyroid iodine can suppress the processes of organification of iodine in the thyroid gland and, accordingly, the synthesis of thyroid hormones. The previous pathology of the thyroid gland is important – Hashimoto’s thyrotoxicosis, history of treatment of Graves’ disease, hemithyroidectomy, as well as in patients with a relatively normal thyroid gland [54, 55].The volume of the thyroid gland and the functional state of the thyroid gland to a certain extent depend on the load with iodine. Thus, in normal individuals without kidney disease, against the background of the 4th week of iodine load (27 mg daily), there was an increase in the thyroid gland volume by 16% from 16.5 to 19.1 g. The study was carried out using ultrasound equipment with high resolution … These study participants had a transient decrease in T4 light, an increase in TSH and serum thyroglobulin. These changes reflect a transient inhibition of the synthesis and release of thyroid hormones associated with a high intrathyroid iodine concentration and suppression of the organification of iodine in the thyroid gland.According to ultrasound, nodules were detected in 55% of 60 women receiving hemodialysis. At the same time, in women of comparable age without kidney disease, nodular formations of the thyroid gland, according to ultrasound, were detected in 21%.

The risk of malignant neoplasms of the thyroid gland in patients on chronic hemodialysis was studied in the USA in 28,049 patients of the chronic hemodialysis unit. The relative risk of malignant neoplasms of the thyroid gland was increased 2.9 times in women, but not in men (1.2 times) [56].No additional risk factors for thyroid cancer were identified. In 913 kidney transplant patients in the United States, 5.3% had thyroid carcinoma compared with 1.2% in the general population [57.58]. Of these malignant neoplasms, 64% had papillary carcinomas, 18% had follicular cancer, 2.6% had medullary cancer, 15% had incidental findings during parathyroidectomy, and 7.7% had a relapse of tumor growth that ended in the death of one patient. According to the United Kingdom (EDTA-ERA registries), the incidence of thyroid cancer was 4.8 times higher among young women on dialysis (15-44 years old) and 2 times higher in older patients compared to the general population [59] …

Therapeutic tactics in the combination of CKD with hypothyroidism

At present, the treatment of subclinical hypothyroidism in patients with CKD is insufficiently developed. No large randomized, controlled prospective studies have been published. As a rule, the literature provides studies involving a small number of patients with CKD and hypothyroidism, and the follow-up period is 2-3 years.

In the study by D.H. Shin et al. [60] included 309 patients. The treatment group consisted of 180 (58.3%) patients receiving levothyroxine therapy.The control group consisted of 129 (41.7%) patients not receiving treatment. The observation period was 34.8 ± 24.3 months. According to the results of the study, the dynamics of GFR decline was significantly greater in the control group compared to the treatment group (-5.93 ± 1.65 versus -2.11 ± 1.12 ml / min / year / 1.73 m 2 ). Based on the Kaplan-Meier analysis, it was shown that survival in patients without renal events was significantly lower in the control group (p <0.01). Cox regression analysis showed that levothyroxine replacement therapy was an independent predictor of improved renal outcomes in the examined patients (RR 0.28, 95% CI 0.12-0.68; p = 0.01).

In a study by J.D. den Hollander et al. [61], which included 37 patients with hypothyroidism due to AIT and 14 patients with thyrotoxicosis (Graves’ disease), showed a significant improvement in renal function during treatment of hypothyroidism and its decrease during treatment of thyrotoxicosis. There was also a strong positive correlation between thyroid function (log 10 (T4 f. After treatment / T4 f. Before treatment) and changes in renal function during therapy with levothyroxine (serum creatinine r 2 = 0.81, p <0.0001; GFR r 2 = 0.69, p <0.0001).Thus, treatment of hypothyroidism in patients with CKD improved renal parameters (creatinine, GFR).

Based on a study by J. Montenegro et al. [39] also showed a positive effect of levothyroxine therapy on renal function. Patients with hypothyroidism (n = 41) showed a significant decrease in creatinine levels after 2 months of levothyroxine therapy (creatinine up to 1.16 ± 0.04 mg / dl, creatinine after 0.87 ± 0.02 mg / dl, p < 0.05).

In a retrospective analysis of Japanese scientists Y.Hataya et al. [62] included 51 patients with primary hypothyroidism and CKD. Kidney function was studied before and after hypothyroidism treatment. GFR increased rapidly in the first 6 months in all patients with CKD. A correlation was found between GFR and the severity of hypothyroidism regardless of age. A more significant improvement in GFR was in patients with a lower GFR value initially and increased by approximately 30% (47.5 ± 7.7 versus 62.1 ± 9.5 ml / min / 1.73 m 2 , p <0.01). The authors believe that all patients with CKD need screening for TSH levels, and thyroid hormone replacement therapy should be prescribed if hypothyroidism is detected.

Thus, according to the available literature data, therapy with levothyroxine in patients with CKD and hypothyroidism improves renal function indicators. However, to formulate clear recommendations for the treatment of patients with CKD and hypothyroidism, additional prospective observations are required.

1. Duntas LH, Biondi B. New insights into subclinical hypothyroidism and cardiovascular risk.Semin Thromb Hemost 2011; 37: 27-34. doi: 10.1055 / s-0030-1270068

2. Smirnov AV, Shilov EM, Dobronravov VA et al. National recommendations. Chronic kidney disease: basic principles of screening, diagnosis, prevention and treatment approaches. Clinical Nephrology 2012: 4–26. [Smirnov AV, Shilov EM, Dobronravov VA i dr. National recommendations. Chronic kidney disease: the basic principles of screening, diagnosis, prevention and treatment approaches.Clinicheskaia nefrologiia 2012: 4–26]

3. Fadeev VV. Based on the American Association of Clinical Endocrinologists and American Thyroid Association guidelines for the diagnosis and treatment of hypothyroidism in adults. Clinical and Experimental Thyroidology 2012; 8: 9-16. doi: 10.4158 / EP12280. GL [Fadeev VV. Based on the clinical recommendations of the American Association of Clinical Endocrinologists and the American Thyroid Association for Diagnosis and Treatment of Hypothyroidism in Adults.Clinicheskaia i e`ksperimental`naia tireoidologiia 2012; 8: 9-16. doi: 10.4158 / EP12280.GL]

4. Sazonova EG, Mohort TV. Thyroid function in diabetes mellitus complicated by chronic kidney disease. International Journal of Endocrinology 2013; 50: 62–67. [Sazonova EG, Mohort TV. Thyroid function in diabetes mellitus complicated by chronic kidney disease. Mezhdunarodny`i` e`ndokrinologicheskii` zhurnal 2013; 50: 62–67]

5.Orlova MM, Rodionova TI. Renal function status in hypothyroid patients (review). Medical almanac 2013: 112–114. [Orlova MM, Rodionova TI. Kidney function in patients with hypothyroidism (review). Meditcinskii` al`manakh 2013: 112-114]

6. Schultheiss UT, Daya N, Grams ME et al. Thyroid function, reduced kidney function and incident chronic kidney disease in a community-based population: the Atherosclerosis Risk in Communities study.Nephrol Dial Transplant 2017; 32: 1874-1881. doi: 10.1093 / ndt / gfw301

7. Åsvold BO, Bjøro T, Vatten LJ. Association of thyroid function with estimated glomerular filtration rate in a population-based study: The HUNT study. Eur J Endocrinol 2011; 164: 101– 105. doi: 10.1530 / EJE-10-0705

8. Inoue K, Tsujimoto T, Saito J et al.Association Between Serum Thyrotropin Levels and Mortality Among Euthyroid Adults in the United States. Thyroid 2016; 26: thy.2016.0156. doi: 10.1089 / thy.2016.0156

9. Meuwese CL, Gussekloo J, de Craen AJ et al. Thyroid status and renal function in older persons in the general population. J Clin Endocrinol Metab 2014; 99: 2689-2696. doi: 10.1210 / jc.2013-3778

10.Lo JC, Chertow GM, Go AS et al. Increased prevalence of subclinical and clinical hypothyroidism in persons with chronic kidney disease. Kidney Int 2005; 67: 1047-1052. doi: 10.1111 / j.1523-1755.2005.00169.x

11. Chonchol M, Lippi G, Salvagno G et al. Prevalence of subclinical hypothyroidism in patients with chronic kidney disease. Clin J Am Soc Nephrol 2008; 3: 1296-1300. doi: 10.2215 / CJN.00800208

12.Chandra A. Prevalence of hypothyroidism in patients with chronic kidney disease: a cross-sectional study from North India. Kidney Res Clin Pract 2016; 35: 165-168. doi: 10.1016 / j.krcp.2016.06.003

13. Chaker L, Sedaghat S, Hoorn EJ et al. The association of thyroid function and the risk of kidney function decline: a population-based cohort study. Eur J Endocrinol 2016; 175: 653-660. doi: 10.1530 / EJE-16-0537

14.Rhee CM, Ravel VA, Streja E et al. Thyroid Functional Disease and Mortality in a National Peritoneal Dialysis Cohort. J Clin Endocrinol Metab 2016; 101: 4054-4061. doi: 10.1210 / jc.2016-1691

15. Rhee CM, Kalantar-Zadeh K, Streja E et al. The relationship between thyroid function and estimated glomerular filtration rate in patients with chronic kidney disease. Nephrol Dial Transplant 2015; 30: 282-287. doi: 10.1093 / ndt / gfu303

16. Chuang M-H, Liao K-M, Hung Y-M et al. Abnormal Thyroid-Stimulating Hormone and Chronic Kidney Disease in Elderly Adults in Taipei City. J Am Geriatr Soc 2016; 64: 1267-1273. doi: 10.1111 / jgs.14102

17. Chuang M-H, Liao K-M, Hung Y-M et al. Association of TSH Elevation with All-Cause Mortality in Elderly Patients with Chronic Kidney Disease.PLoS One 2017; 12: e0168611. doi: 10.1371 / journal.pone.0168611

18. Lee DY, Jee JH, Jun JE et al. The effect of TSH change per year on the risk of incident chronic kidney disease in euthyroid subjects. Endocrine 2017; 55: 503-512. doi: 10.1007 / s12020-016-1138-8

19. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system.N Engl J Med 2001; 344: 501-509. doi: 10.1056 / NEJM200102153440707

20. Klein I, Danzi S. Thyroid Disease and the Heart. Curr Probl Cardiol 2016; 41: 65-92. doi: 10.1016 / j.cpcardiol.2015.04.002

21. Cini G, Carpi A, Mechanick J et al. Thyroid hormones and the cardiovascular system: pathophysiology and interventions.Biomed Pharmacother 2009; 63: 742-753. doi: 10.1016 / j.biopha.2009.08.003

22. Klein I, Danzi S. Thyroid disease and the heart. Circulation 2007; 116: 1725-1735. doi: 10.1161 / CIRCULATIONAHA.106.678326

23. Koch CA, Chrousos GP. Overview of Endocrine Hypertension. In: De Groot LJ, Chrousos G, Dungan K et al. Endotext.South Dartmouth (MA): 2000

24. Danzi S, Klein I. Thyroid hormone and blood pressure regulation. Curr Hypertens Rep 2003; 5: 513-520

25. Kotsis V, Alevizaki M, Stabouli S et al. Hypertension and hypothyroidism: results from an ambulatory blood pressure monitoring study. J Hypertens 2007; 25: 993-999. doi: 10.1097 / HJH.0b013e328082e2ff

26. Stabouli S, Papakatsika S, Kotsis V. Hypothyroidism and hypertension. Expert Rev Cardiovasc Ther 2010; 8: 1559-1565. doi: 10.1586 / erc.10.141

27. Vargas F, Moreno JM, Rodriguez-Gomez I et al. Vascular and renal function in experimental thyroid disorders. Eur J Endocrinol 2006; 154: 197-212. doi: 10.1530 / eje.1.02093

28. Ichihara A, Kobori H, Miyashita Y et al. Differential effects of thyroid hormone on renin secretion, content, and mRNA in juxtaglomerular cells. Am J Physiol 1998; 274: E224-31

29. Vargas F, Rodriguez-Gomez I, Vargas-Tendero P et al. The renin-angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations.J Endocrinol 2012; 213: 25-36. doi: 10.1530 / JOE-11-0349

30. van Hoek I, Daminet S. Interactions between thyroid and kidney function in pathological conditions of these organ systems: a review. Gen Comp Endocrinol 2009; 160: 205-215. doi: 10.1016 / j.ygcen.2008.12.008

31. Barlet C, Doucet A. Lack of stimulation of kidney Na-KATPase by thyroid hormones in long-term thyroidectomized rabbits.Pflugers Arch 1986; 407: 428-431

32. Zimmerman RS, Ryan J, Edwards BS et al. Cardiorenal endocrine dynamics during volume expansion in hypothyroid dogs. Am J Physiol 1988; 255: R61-6. doi: 10.1152 / ajpregu.1988.255.1.R61

33. Singer MA. Of mice and men and elephants: metabolic rate sets glomerular filtration rate.Am J Kidney Dis 2001; 37: 164-178

34. Schmid C, Brandle M, Zwimpfer C et al. Effect of thyroxine replacement on creatinine, insulin-like growth factor 1, acidlabile subunit, and vascular endothelial growth factor. Clin Chem 2004; 50: 228-231. doi: 10.1373 / clinchem.2003.021022

35. Sato Y, Nakamura R, Satoh M et al.Thyroid hormone targets matrix Gla protein gene associated with vascular smooth muscle calcification. Circ Res 2005; 97: 550–557. doi: 10.1161 / 01.RES.0000181431.04290.bd

36. Suher M, Koc E, Ata N et al. Relation of thyroid disfunction, thyroid autoantibodies, and renal function. Ren Fail 2005; 27: 739-742

37.Michael UF, Barenberg RL, Chavez R et al. Renal handling of sodium and water in the hypothyroid rat. Clearance and micropuncture studies. J Clin Invest 1972; 51: 1405-1412. doi: 10.1172 / JCI106936

38. Hanna FW, Scanlon MF. Hyponatraemia, hypothyroidism, and role of arginine- vasopressin. Lancet (London, England) 1997; 350: 755-756. doi: 10.1016 / S0140-6736 (05) 62563-9

39.Montenegro J, Gonzalez O, Saracho R et al. Changes in renal function in primary hypothyroidism. Am J Kidney Dis 1996; 27: 195-198

40. Sato K, Okamura K, Yoshinari M et al. Reversible primary hypothyroidism and elevated serum iodine level in patients with renal dysfunction. Acta Endocrinol (Copenh) 1992; 126: 253–259

41.Gardner DF, Mars DR, Thomas RG et al. Iodine retention and thyroid dysfunction in patients on hemodialysis and continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1986; 7: 471–476

42. Cattail VM, Arches RA. Pathophysiology of the endocrine system. BINOM Publishers 2001. 81. [Kettai’l VM, Arki RA. Patofiziologiia e`ndokrinnoi` sistemy`. BINOM Publishers 2001. 81.]

43.Beckers C, Machiels J, Soyez C et al. Metabolic clearance rate and production rate of thyroid-stimulating hormone in man. Horm Metab 1971; 3: 34-36. doi: 10.1055 / s-0028- 1095044

44. Bartalena L, Pacchiarotti A, Palla R et al. Lack of nocturnal serum thyrotropin (TSH) surge in patients with chronic renal failure undergoing regular maintenance hemofiltration: a case of central hypothyroidism. Clin Nephrol 1990; 34: 30–34

45.Medri G, Carella C, Padmanabhan V et al. Pituitary glycoprotein hormones in chronic renal failure: evidence for an uncontrolled alpha-subunit release. J Endocrinol Invest 1993; 16: 169-174. doi: 10.1007 / BF03344939

46. Kaptein EM, Feinstein EI, Nicoloff JT et al. Serum reverse triiodothyronine and thyroxine kinetics in patients with chronic renal failure. J Clin Endocrinol Metab 1983; 57: 181-189. doi: 10.1210 / jcem-57-1-181

47. Hershman JM, Krugman LG, Kopple JD et al. Thyroid function in patients undergoing maintenance hemodialysis: unexplained low serum thyroxine concentration. Metabolism 1978; 27: 755-759

48. Faber J, Heaf J, Kirkegaard C et al. Simultaneous turnover studies of thyroxine, 3,5,3 ‘and 3,3′, 5′-triiodothyronine, 3,5-, 3,3’-, and 3 ‘, 5′-diiodothyronine, and 3’-monoiodothyronine in chronic renal failure.J Clin Endocrinol Metab 1983; 56: 211-217. doi: 10.1210 / jcem-56-2-211

49. Kaptein EM, Quion-Verde H, Chooljian CJ, et al. The thyroid in end-stage renal disease. Medicine (Baltimore) 1988; 67: 187-197

50. Lim VS, Fang VS, Katz AI et al. Thyroid dysfunction in chronic renal failure. A study of the pituitary-thyroid axis and peripheral turnover kinetics of thyroxine and triiodothyronine.J Clin Invest 1977; 60: 522-534. doi: 10.1172 / JCI108804

51. Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the ‘euthyroid sick syndrome’. Endocr Rev 1982; 3: 164-217. doi: 10.1210 / edrv-3-2-164

52. Kaptein EM. Thyroid hormone metabolism and thyroid diseases in chronic renal failure.Endocr Rev 1996; 17: 45-63. doi: 10.1210 / edrv-17-1-45

53. US Renal Data System 1994 annual data report, the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney diseases, Bethesda, MD. Am J kidney Dis 1994; 24 (suppl .: S12-94).

54. Namba H, Yamashita S, Kimura H et al. Evidence of thyroid volume increase in normal subjects receiving excess iodide.J Clin Endocrinol Metab 1993; 76: 605-608. doi: 10.1210 / jcem.76.3.8445017

55. Konno N, Makita H, Yuri K et al. Association between dietary iodine intake and prevalence of subclinical hypothyroidism in the coastal regions of Japan. J Clin Endocrinol Metab 1994; 78: 393-397. doi: 10.1210 / jcem.78.2.8106628

56.Kantor AF, Hoover RN, Kinlen LJ et al. Cancer in patients receiving long-term dialysis treatment. Am J Epidemiol 1987; 126: 370-376

57. Penn I. The effect of immunosuppression on pre-existing cancers. Transplantation 1993; 55: 742-747

58. Schneider AB. Carcinoma of follicular epithelium. In: Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text.1991.1121–1129

59. Brunner FP, Landais P, Selwood NH. Malignancies after renal transplantation: the EDTA- ERA registry experience. European Dialysis and Transplantation Association-European Renal Association. Nephrol Dial Transplant 1995; 10 Suppl 1: 74-80

60. Shin DH, Lee MJ, Kim SJ et al. Preservation of renal function by thyroid hormone replacement therapy in chronic kidney disease patients with subclinical hypothyroidism.J Clin Endocrinol Metab 2012; 97: 2732-2740. doi: 10.1210 / jc.2012-1663

61. den Hollander JG, Wulkan RW, Mantel MJ et al. Correlation between severity of thyroid dysfunction and renal function. Clin Endocrinol (Oxf) 2005; 62: 423-427. doi: 10.1111 / j.1365-2265.2005.02236.x

62. Hataya Y, Igarashi S, Yamashita T et al.Thyroid hormone replacement therapy for primary hypothyroidism leads to significant improvement of renal function in chronic kidney disease patients. Clin Exp Nephrol 2013; 17: 525-531. doi: 10.1007 / s10157-012-0727-y

Thyroid stimulating hormone


The information in this section cannot be used for self-diagnosis and self-medication. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests.For a diagnosis and correct prescription of treatment, you should contact your doctor.

We remind you that independent interpretation of the results is unacceptable and the information below is for reference only.

TSH (thyroid stimulating hormone, thyrotropin, Thyroid StimulatingHormone, TSH): indications for the appointment, the rules for preparing for the test, decoding the results and indicators of the norm.

Thyroid stimulating hormone is synthesized in the anterior lobe of the pituitary gland (gland in the brain) and stimulates the function of the thyroid gland according to the principle of “feedback”.

With a shortage of thyroid hormones (thyroid hormones) in the blood, the production of thyroid-stimulating hormone increases, and vice versa, with an increase in the level of thyroid hormones in the blood, the synthesis of TSH decreases.

In what cases is an analysis necessary TSH Determination of the level of thyroid-stimulating hormone is used as a basic test to assess the function of the thyroid gland both in hypothyroidism and in hyperthyroidism.

Hypothyroidism (a decrease in the production of thyroid hormones), characterized by a slowdown in the basic functions of the body: the patient usually complains of weakness, depression, fatigue, low blood pressure, hair loss, etc. A severe form of hypothyroidism is called myxedema and can lead to heart failure, convulsive syndrome and coma.

Hyperthyroidism (excessive production of thyroid hormones) is characterized by an acceleration of body functions: patients, on the contrary, complain of rapid heartbeat, anxiety, anxiety, insomnia, weight loss.The most severe form of hyperthyroidism is a thyrotoxic crisis, a life-threatening condition.

A change in the synthesis of TSH is caused by

  • Brain trauma, massive blood loss and hypothalamic-pituitary diseases, primarily tumors in the hypothalamic-pituitary zone.
  • Tumors of the pituitary gland (mainly adenomas of the anterior or glandular lobe) cause an increase in the production of pituitary hormones.They, in turn, affect the activity of other endocrine glands (thyroid, ovaries, adrenal glands, etc.) and contribute to the development of hypothyroidism, diabetes mellitus and diabetes insipidus, hypothalamic-pituitary insufficiency and endocrine infertility.
  • Diseases of other endocrine glands , in particular tumors or adrenal insufficiency, can also suppress or stimulate TSH production.
  • Hypothalamic-pituitary insufficiency , arising in the defeat of the pituitary gland and hypothalamic nuclei due to the infectious process, toxic effects, autoimmune (in which the immune system attacks the tissues of the body) and vascular diseases, as well as the removal of the pituitary gland, is accompanied by a change in the control of the TSH level and requires its control.
  • Hemorrhage (hemorrhagic stroke) in the pituitary gland causes a sharp drop in the TSH level, however, with this pathology, the symptoms of cerebral bleeding come to the fore (impaired consciousness, a sharp headache of a diffuse nature, photophobia, nausea, repeated vomiting).
  • In women, the TSH level changes with complicated childbirth or abortions , as well as during pregnancy .An analysis for TSH is mandatory for screening pregnant women in the first trimester.

Preparation for the procedure

The TSH level can be influenced by a change in the circadian rhythm: there is a decrease in TSH with sleep disturbance or work at night. The highest hormone level is recorded from 2 am to 6-8 am, while in the evening it decreases.

The TSH test must be taken in the morning, after a full sleep.

Three days before the study, it is necessary to stop taking alcohol, fatty and spicy foods.Taking biomaterial (blood) for analysis is carried out on an empty stomach (acceptable 4 hours after a light snack), at the same time during a dynamic study of TSH (for example, to monitor the effectiveness of treatment).


The research result can be obtained within one working day (excluding the day of taking the material).

What can affect the results of the TSH analysis

  • Circadian rhythms
  • Stress and prolonged nervous tension
  • Pregnancy
  • Age (the highest TSH levels in newborns, with age, the level of the hormone decreases significantly)
  • Medicines

For research, venous blood serum is used.

The concentration of TSH in serum is determined using immunochemiluminescent analysis on microparticles. The analysis consists in studying the specific reaction of antigens (TSH receptors) and antibodies to them and is highly sensitive – up to 90%.

Thyroid stimulating hormone: normal values ​​

Normally, the average TSH levels in the blood differ depending on age, especially during the first months of a child’s life.

Age Concentration of TSH, honey / l
4 days – 6 months 0.73-4.77
6 months – 14 years 0.7-4.17
14-19 years old 0.47-3.41
> 19 years old 0.4-4.0

During pregnancy, the level of TSH in the blood decreases and the reference values ​​look like this:

Trimester of pregnancy Concentration of TSH, honey / l
I trimester 0.1-2.5
II trimester 0.2-3.0
III trimester 0.3-3.0

Explanation of indicators:

What do elevated TSH readings mean?

  • An increase in TSH concentration can occur due to primary hypothyroidism, even in asymptomatic cases.However, with a more detailed survey, the patient may notice physical weakness and fatigue, unstable mood with a predominance of apathy, memory impairment, hair loss, dry skin.
  • An increase in TSH concentration may be a consequence of subacute thyroiditis, an inflammatory disease of the thyroid gland (de Quervain’s thyroiditis, granulomatous thyroiditis). In these cases, the tissue of the thyroid gland is damaged due to an infectious disease of the upper respiratory tract. At the same time, there is pain and an increase in the lobules of the thyroid gland from one or both sides, as well as muscle pain, weakness and fatigue.
  • An increase in the concentration of TSH in the blood is noted in the case of abnormal synthesis of this hormone by tumor tissue in lung or breast cancer, with pituitary adenoma and thyroid cancer.
  • High TSH levels are found in many severe diseases in the convalescent phase and in thyroid hormone resistance syndrome.
  • Taking certain medications can cause an increase in TSH levels (beta-blockers (atenolol, metoprolol, propranolol), antipsychotics (phenothiazine derivatives, aminoglutethimide), prokinetics (motilium, metoclopramide), anticonvulsants (phenytoin, carbodamazepine), and iodide-containing drugs furosemide, lithium salts, etc.etc.)

What do the lowered TSH values ​​mean?

  • Diseases of the thyroid gland: primary hyperthyroidism (diffuse toxic goiter, toxic multinodular goiter, toxic adenoma, autonomously functioning thyroid nodes), subclinical hyperthyroidism, etc.
  • Itsenko-Cushing’s syndrome, which occurs when the adrenal cortex increases secretion of the hormone cortisol, is also accompanied by a decrease in TSH levels.
  • Extensive brain injury.
  • Stroke in the hypothalamic-pituitary region.

A decrease in TSH concentration below the reference values ​​does not necessarily indicate a disease. The level of TSH in the blood decreases during pregnancy and during stress or hunger.

A decrease in TSH in the blood can provoke the intake of certain medications. These include corticosteroids, dopamine, thyroxine, triiodothyronine, amiodarone, cytostatics, beta-adrenomimetics (dobutamine, dopexamine), somatostatin, octreotide, nifedipine, drugs for the treatment of hyperprolactinemia (methergoline, peribedil, bromocriptine drugs) ).

Additional examinations

As a rule, the TSH test is complemented by a study of the level of triiodothyronine and thyroxine (T3 and T4), which are produced by the thyroid gland, and their level allows you to more accurately identify the cause of the disease.

If the indicator deviates from the norm, the following studies are additionally carried out:

  • total triiodothyronine (T3 total, Total Triiodthyronine, TT3);
  • free triiodothyronine (free T3, FreeTriiodthyronine, FT3);
  • total thyroxine (total T4, total tetraiodothyronine, Total Thyroxine, TT4);
  • free thyroxine (free T4, FreeThyroxine, FT4);
  • antibodies to thyroglobulin (AT-TG, anti-thyroglobulinautoantibodies);
  • antibodies to thyroid peroxidase (AT-TPO, microsomal antibodies, anti-thyroid);
  • AT to rTTG (antibodies to TSH receptors, TSH receptorautoantibodies).