What are the common symptoms of hypothyroidism. How is hypothyroidism diagnosed. What causes hypothyroidism. How is hypothyroidism treated. What is Hashimoto’s thyroiditis. What is the role of T4 in thyroid function. How does hypothyroidism affect pregnancy.

What is Hypothyroidism and How Does it Affect the Body?

Hypothyroidism is a condition where the thyroid gland, an important organ responsible for regulating metabolism, fails to produce sufficient thyroid hormones. The thyroid gland typically produces two forms of these hormones: thyroxine (T4) and triiodothyronine (T3). When the production of these hormones is inadequate, it can lead to a variety of symptoms affecting the entire body.

The impact of hypothyroidism on the body is significant, as thyroid hormones play a crucial role in numerous bodily functions. When thyroid hormone levels are low, the body’s normal rate of functioning slows down, resulting in both mental and physical sluggishness. This can manifest in various ways, with symptoms ranging from mild to severe.

How does hypothyroidism affect metabolism?

Hypothyroidism significantly impacts metabolism by slowing it down. This occurs because thyroid hormones are essential for regulating the body’s energy production and consumption. When thyroid hormone levels are low, the body’s cells become less efficient at converting nutrients into energy, leading to a decrease in overall metabolic rate.

Recognizing the Signs and Symptoms of Hypothyroidism

Identifying hypothyroidism can be challenging, as its symptoms often develop gradually and may be mistaken for other conditions, such as depression. However, being aware of the common signs and symptoms can help in early detection and treatment.

• Fatigue and lack of energy
• Sensitivity to cold temperatures
• Weight gain
• Constipation
• Dry skin and hair
• Muscle weakness and joint pain
• Depression and mood changes
• Slowed heart rate
• Impaired memory and concentration
• Hoarse voice and slowed speech

Can hypothyroidism symptoms vary among individuals?

Indeed, the manifestation of hypothyroidism symptoms can vary significantly from person to person. Some individuals may experience a wide range of severe symptoms, while others might have only a few mild ones. Factors such as the severity of the hormone deficiency, the duration of the condition, and individual physiology can all contribute to this variation.

Diagnosing Hypothyroidism: Tests and Procedures

Accurate diagnosis of hypothyroidism is crucial for effective treatment. At specialized centers like the UCLA Endocrine Center, patients undergo a comprehensive evaluation process that includes:

1. A detailed medical history review
2. A thorough physical examination
3. Blood tests to assess thyroid function

The primary blood tests used to diagnose hypothyroidism include:

• Thyroid-stimulating hormone (TSH) test
• Free T4 test
• Free T3 test (in some cases)
• Thyroid antibody tests (to check for autoimmune thyroid disorders)

Why is the TSH test considered the most sensitive for diagnosing hypothyroidism?

The TSH test is considered the most sensitive indicator of thyroid function because it can detect even subtle changes in thyroid hormone levels. When thyroid hormone levels drop, the pituitary gland responds by producing more TSH to stimulate the thyroid gland. As a result, TSH levels often rise before T4 and T3 levels fall below the normal range, making TSH an early marker of thyroid dysfunction.

Understanding the Causes of Hypothyroidism

Several factors can lead to the development of hypothyroidism. The most common cause is an autoimmune disorder called Hashimoto’s thyroiditis. Other potential causes include:

• Thyroid surgery or radioactive iodine treatment
• Certain medications
• Iodine deficiency or excess
• Congenital thyroid disorders
• Pituitary gland disorders (secondary hypothyroidism)
• Pregnancy-related thyroid dysfunction

How does Hashimoto’s thyroiditis lead to hypothyroidism?

Hashimoto’s thyroiditis is an autoimmune condition where the body’s immune system mistakenly attacks the thyroid gland. This chronic inflammation leads to gradual destruction of thyroid tissue, impairing its ability to produce thyroid hormones. Over time, this results in a decrease in thyroid hormone production, ultimately leading to hypothyroidism.

Treatment Options for Hypothyroidism

The primary goal of hypothyroidism treatment is to restore thyroid hormone levels to their normal range. This is typically achieved through thyroid hormone replacement therapy. The most common treatment approach involves:

• Oral administration of synthetic thyroid hormone (levothyroxine)
• Regular monitoring of thyroid hormone levels through blood tests
• Dose adjustments as needed to maintain optimal hormone levels

In most cases, individuals with hypothyroidism will need to take thyroid hormone replacement medication for life. However, with proper management, most people with hypothyroidism can lead normal, healthy lives.

How long does it take for thyroid hormone replacement therapy to take effect?

The effects of thyroid hormone replacement therapy are not immediate. It typically takes several weeks to a few months for thyroid hormone levels to stabilize and for symptoms to improve. During this time, patients may require dose adjustments based on their blood test results and symptom progression. Full symptom relief may take up to six months in some cases.

Hashimoto’s Thyroiditis: The Leading Cause of Hypothyroidism

Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis, is the most common cause of hypothyroidism in the United States. This autoimmune disorder occurs when the immune system produces antibodies that attack and damage the thyroid gland, leading to inflammation and impaired thyroid function.

Key features of Hashimoto’s thyroiditis include:

• Gradual onset of hypothyroidism symptoms
• Presence of thyroid antibodies in blood tests
• Enlarged thyroid gland (goiter) in some cases
• Fluctuations in thyroid function over time

Can individuals with Hashimoto’s thyroiditis have normal thyroid function?

Yes, some individuals with Hashimoto’s thyroiditis may maintain normal thyroid function for extended periods. This is known as euthyroid Hashimoto’s thyroiditis. However, these individuals are at an increased risk of developing hypothyroidism in the future and should be monitored regularly for changes in thyroid function.

The Role of T4 in Thyroid Function and Diagnosis

T4, or thyroxine, is one of the primary hormones produced by the thyroid gland. It plays a crucial role in regulating metabolism and energy production throughout the body. Understanding T4 levels is essential for diagnosing and managing thyroid disorders, including hypothyroidism.

The T4 test measures the amount of thyroxine in the blood and is often used in conjunction with other thyroid function tests, such as TSH, to provide a comprehensive picture of thyroid health. There are two main types of T4 tests:

• Total T4: Measures both protein-bound and free T4
• Free T4: Measures only the unbound, biologically active form of T4

Why is the free T4 test often preferred over total T4?

The free T4 test is generally considered more accurate and reliable than the total T4 test for assessing thyroid function. This is because free T4 represents the biologically active hormone that is available for use by the body’s cells. Total T4 levels can be affected by changes in protein levels in the blood, which may not necessarily reflect true thyroid function.

Hypothyroidism and Pregnancy: Special Considerations

Hypothyroidism can have significant implications for both maternal and fetal health during pregnancy. Proper management of thyroid function is crucial for ensuring a healthy pregnancy and optimal fetal development. Special considerations for women with hypothyroidism who are pregnant or planning to become pregnant include:

• Increased monitoring of thyroid function throughout pregnancy
• Adjustment of thyroid hormone replacement dosage as needed
• Early detection and treatment of thyroid dysfunction
• Careful planning for women requiring thyroid surgery or radioactive iodine treatment

Untreated or poorly managed hypothyroidism during pregnancy can lead to complications such as:

• Increased risk of miscarriage
• Preeclampsia
• Anemia
• Postpartum hemorrhage
• Impaired fetal growth and development
• Cognitive and developmental issues in the child

How often should thyroid function be monitored during pregnancy?

For women with known hypothyroidism, thyroid function should be monitored closely throughout pregnancy. Typically, TSH and free T4 levels are checked every 4-6 weeks during the first half of pregnancy and at least once between 26 and 32 weeks gestation. More frequent monitoring may be necessary if dose adjustments are required or if thyroid function is unstable.

In conclusion, understanding hypothyroidism, its symptoms, causes, and treatment options is crucial for effective management of this common endocrine disorder. Regular monitoring, proper medication, and lifestyle adjustments can help individuals with hypothyroidism lead healthy, productive lives. For those with thyroid concerns or symptoms, consulting with an endocrinologist or healthcare provider specializing in thyroid disorders is recommended for accurate diagnosis and personalized treatment plans.

Hypothyroidism: What is Hypothyroidism? Hypothyroidism Symptoms, Treatment, Diagnosis

Hypothyroidism (underactive thyroid)

What is Hypothyroidism?

The thyroid gland is an important organ that regulates metabolism. The thyroid gland makes two forms of thyroid hormone – thyroxine (T4) and triiodothyronine (T3). Hypothyroidism is when the thyroid gland is not producing enough of these hormones. Primary hypothyroidism affects the whole body and may cause a variety of symptoms.

Having too little thyroid hormone can affect the whole body. The body’s normal rate of functioning slows, causing mental and physical sluggishness. Symptoms may vary from mild to severe.

What Are Signs and Symptoms Hypothyroidism?

Symptoms are different for each person. They are usually hard to notice and start slowly. They may be mistaken for symptoms of depression.

Here are the most common symptoms and signs:

• Dull facial expressions
• Tiredness and lack of energy (fatigue)
• Not being able to handle cold
• Hoarse voice
• Slow speech
• Droopy eyelids
• Puffy and swollen face
• Weight gain
• Constipation

• Sparse, coarse, and dry hair
• Coarse, dry, and thickened skin
• Hand tingling or pain (carpal tunnel syndrome)
• Slow pulse
• Muscle cramps
• Joint pain
• Sides of eyebrows thin or fall out
• Confusion
• Increased or irregular menstrual flow in women

How is Hypothyroidism Diagnosed?

At the UCLA Endocrine Center, you will meet with an endocrinologist who will ask about your past health and perform a comprehensive physical exam.

Blood tests can help diagnose hypothyroidism. Laboratory tests to determine thyroid function include:

What Causes Hypothyroidism?

The most common cause of hypothyroidism is an autoimmune disorder called Hashimoto’s Thyroiditis. This means your immune system starts to attack itself. It makes antibodies against the thyroid gland. The normal thyroid cells are overrun by white blood cells and scar tissue. Sometimes hypothyroidism occurs after treatment for an overactive thyroid gland. That may include radioactive iodine therapy or surgery. Hypothyroidism may also develop shortly after pregnancy.

A condition called secondary hypothyroidism can also sometimes happen. It’s when your pituitary gland stops working. The pituitary gland then no longer tells the thyroid gland to make thyroid hormones.

There are special considerations for women who have had thyroid disease in the past or currently, and who might be considering pregnancy or are already pregnant. Increased monitoring and adjustment of thyroid-related medications is recommended during this period for the health of both the mother and her baby. Special planning might also be necessary for women with a condition in which thyroid surgery and/or radioactive iodine are required.

Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis is a type of inflammation of the thyroid gland that results from an autoimmune process.  It is the most common cause of Hashimoto’s hypothyroidism in the U.S.  However, some individuals with Hashimoto’s thyroiditis may never develop hypothyroidism and thus never have any symptoms.

How is Hypothyroidism Treated?

Treatment will depend on your symptoms, age, and general health. It will also depend on how severe the condition is.

The goal of treatment is to return your level of thyroid hormone back to normal. You may need to take medicine that gives you a dose of thyroid hormones. This dose may need to be changed over time. You will likely need to take this medicine for the rest of your life. You will need follow-up blood tests to make sure you are taking the correct dose of thyroid hormone replacement.

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T4: What is a T4 Test? T4 Thyroxine Test

What is a T4 (thyroxine) Test?

Definition

A T4 test measures the amount of the T4 hormone in the blood. T4 is produced by the thyroid gland. T4 levels are important, because T4 increases numerous enzymes that produce energy for the body. Alternative Name: Thyroxine test.

How the test is performed:

Blood is drawn from a vein on the inside of the elbow or the back of the hand. The puncture site is cleaned with antiseptic, and an elastic band is placed around the upper arm to apply pressure and restrict blood flow through the vein. This causes veins below the band to swell with blood.

A needle is inserted into the vein, and the blood is collected in an air-tight vial or a syringe. During the procedure, the band is removed to restore circulation. Once the blood has been collected, the needle is removed, and the puncture site is covered to stop any bleeding. For an infant or young child, the area is cleansed with antiseptic and punctured with a sharp needle or a lancet. The blood may be collected in a pipette (small glass tube), on a slide, onto a test strip, or into a small container. Cotton or a bandage may be applied to the puncture site if there is any continued bleeding.

How to prepare for the test:

The health care provider may advise you to stop taking drugs that may affect the test (see “special considerations”). For infants and children: The preparation you can provide for this test depends on your child’s age and experience. For specific information regarding how you can prepare your child, see the following topics:

• infant test or procedure preparation (birth to 1 year)
• toddler test or procedure preparation (1 to 3 years)
• preschooler test or procedure preparation (3 to 6 years)
• schoolage test or procedure preparation (6 to 12 years)
• adolescent test or procedure preparation (12 to 18 years)

How the test will feel:

When the needle is inserted to draw blood, some people feel moderate pain, while others feel only a prick or stinging sensation. Afterward, there may be some throbbing.

Why the test is performed:

This test may be performed as part of an evaluation of thyroid function. Thyroid function is complex and depends on the action of many different hormones:

1. Thyroid-stimulating hormone (TSH) is a secreted by the pituitary gland.
2. TSH causes the thyroid gland to produce two more hormones, T4 (thyroxine) and T3 (triiodothyronine).
3. Finally, TSH itself is stimulated by another hormone, thyroid-releasing hormone (TRH), which is made by the hypothalamus.

In people with normal thyroid function, having enough T3 and T4 inhibits both TSH and TRH, which prevents the body from making too much T3 and T4. Most T3 and T4 is transported by a protein called TBG (thyroxine binding globulin), but smaller amounts are found on prealbumin and albumin. When not bound to proteins, they are called “free” T3 or T4.

Normal Values:

Normal values vary among different laboratories. A typical normal range is: 4.5 to 11.2 mcg/dL (micrograms per deciliter).

What abnormal results mean:

Greater-than-normal levels of T4 along with low levels of TSH may indicate hyperthyroid conditions, such as:

• Graves’ disease
• toxic multinodular goiter
• subacute or chronic thyroiditis
• early Hashimoto’s disease
• iodine-induced hyperthyroidism
• germ cell tumors
• trophoblastic disease

Lower-than-normal levels of T4 may indicate:

• hypothyroidism (including Hashimoto’s disease, cretinism, myxedema, goitrous diseases, scleroderma, amyloid goiter, or hemochromatosis following neck irradiation for head and neck cancer)
• malnutrition or fasting
• illness throughout the body
• use of certain prescribed medication, including dexamethasone, propranolol, lithium, iodine, methimazole, propylthiouracil, interferon alfa, interleukin-2, and amiodarone

Additional conditions under which the test may be performed:

• hypopituitarism
• hypothyroidism – primary
• hypothyroidism – secondary
• thyrotoxic periodic paralysis

Risks:

Risks associated with having blood drawn are slight:

• excessive bleeding
• fainting or feeling lightheaded
• hematoma (blood accumulating under the skin)
• infection (a slight risk any time the skin is broken)
• multiple punctures to locate veins

Considerations:

Drugs that can increase T4 measurements include clofibrate, estrogens, methadone, amiodarone, and birth control pills. Drugs that can decrease T4 measurements include anabolic steroids, androgens, antithyroid drugs (for example, propylthiouracil and methimazole), lithium, phenytoin, propranolol, amiodarone, interferon alpha, and interleukin-2. Veins and arteries vary in size from one patient to another and from one side of the body to the other. Obtaining a blood sample from some people may be more difficult than from others.

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Hyperthyroidism: What is Hyperthyroidism? Hyperthyroidism Symptoms, Treatment, Diagnosis

Hyperthyroidism (overactive thyroid)

What is Hyperthyroidism?

Hyperthyroidism is a condition describing the overproduction of thyroid hormone from the thyroid gland.

What Are Signs and Symptoms Hyperthyroidism?

Symptoms are different for each person. Here are the most common ones:

• Nervousness
• Irritability
• Sweating more than normal
• Thinning of the skin
• Fine, brittle hair
• Weak muscles, especially in the upper arms and thighs
• Shaky hands
• Fast heartbeat (palpitations)
• High blood pressure
• More bowel movements than normal, diarrhea

• Weight loss
• Trouble dealing with the heat
• Problems sleeping
• Prominent eyes
• Sensitivity to bright light
• Confusion
• Irregular menstrual cycle in women
• Tiredness and lack of energy (fatigue)
• Larger than normal thyroid gland (goiter)

How is Hyperthyroidism Diagnosed?

At the UCLA Endocrine Center, you will meet with an endocrinologist who will ask about your past health, including your medications and diet, and perform a comprehensive physical exam.

Blood tests can help diagnose hyperthyroidism. Laboratory tests to determine thyroid function include:

• Thyroid Stimulating Hormone (aka TSH) helps indicate whether the thyroid is working correctly
• Measurements of the two forms of thyroid hormone, T4 and T3
• If indicated, measurements of specific antibodies targeted to the thyroid and its receptors

The workup may also include neck ultrasound to assess for thyroid nodules that could be overproducing thyroid hormone.

What Causes Hyperthyroidism?

Hyperthyroidism has several causes. These may include:

Graves’ Disease

This is an autoimmune disorder. It is the most common cause of hyperthyroidism. It happens when an antibody overstimulates the thyroid. This condition is most often found in young to middle-aged women. It also tends to run in families.

Toxic nodular goiter

This condition happens when one or more lumps (nodules) of the thyroid gland become too active. Health experts don’t know what causes this to happen. In most cases, the nodules are not cancer (benign). But in rare cases the overactive thyroid tissue is cancer.

Thyroiditis

This is a general term that refers to inflammation of the thyroid. Depending on the severity, thyroiditis may or may not produce any symptoms or need to be treated. The inflammation releases an excessive amount of thyroid hormone, leading to temporary hyperthyroidism. As the thyroid “burns out,” the thyroid then often becomes underactive.

Less common causes of hyperthyroidism include:

• Taking too much thyroid hormone medicine to treat an underactive thyroid
• Having too much iodine in your diet or in medicines, such as amiodarone
• Having a noncancer tumor in the pituitary gland that makes your thyroid overactive

What are Causes of Thyroiditis?

Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)

Hashimoto’s thyroiditis is a type of inflammation of the thyroid gland that results from an autoimmune process.  It is the most common cause of Hashimoto’s hypothyroidism (in which the inflammation results in an underactive thyroid gland) in the U.S.  However, some individuals with Hashimoto’s thyroiditis may never develop hypothyroidism and thus never have any symptoms.

Infectious thyroiditis

Infectious thyroiditis is inflammation of the thyroid gland resulting from an infection in the thyroid.  Patients with this will usually have neck pain, enlargement of the thyroid gland, and symptoms of an infection, such as fever and generalized body aches.

Painless thyroiditis

Painless thyroiditis is an inflammation of the thyroid gland in which there is a short period of both hyperthyroidism and hypothyroidism.  The thyroid gland is not painful.  Both usually resolve without treatment.  Painess postpartum thyroiditis refers to this disorder when it occurs in women who were recently pregnant.

Drug-induced or radiation thyroiditis

Inflammation of the thyroid gland may also occur in individuals who are taking certain medications, including amiodarone, lithium, and interferon.  Radiation of the neck can also result in thyroiditis.  The hyperthyroid and hypothyroid phases of thyroid inflammation can be managed usually with medications alone.

Fibrous thyroiditis (Riedel’s thyroiditis)

Fibrous thyroiditis is an extremely rare condition in which the thyroid becomes hardened from a significant inflammatory process in the thyroid that extends locally in the neck.  Surgery may be required to treat this condition.

How is Hyperthyroidism Treated?

Treatment will depend on your symptoms, age, and general health. It will also depend on how severe the condition is.

Treatment may include:

• Medicine. It can help lower the level of thyroid hormones in the blood.
• Radioactive iodine. It comes in the form of a pill or liquid. It slowly destroys the cells of the thyroid gland so that less thyroid hormone is made.
• Surgery. You may need to have all or part of your thyroid removed.
• Beta blockers. These medicines block the action of the thyroid hormone on the body. That helps with rapid heart rate and palpitations.

Frequently Asked Questions

What are possible complications of hyperthyroidism?

If your hyperthyroidism is not treated, these complications may happen:

• Thyroid crisis, when symptoms get worse because of stress or illness
• Heart problems, such as an abnormal rhythm or heart failure
• Weak, brittle bones (osteoporosis)
• Pregnancy problems, such as miscarriage, early delivery, and preeclampsia or high blood pressure

Contact us for more information or to request an appointment.

Tips to help you prepare for your visit:

• Know the reason for your visit and what you want to happen.
• Before your visit, write down questions you want answered.
• Bring someone with you to help you ask questions and remember what your provider tells you.
• At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
• Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
• Ask if your condition can be treated in other ways.
• Know why a test or procedure is recommended and what the results could mean.
• Know what to expect if you do not take the medicine or have the test or procedure.
• If you have a follow-up appointment, write down the date, time, and purpose for that visit.
• Know how you can contact your provider if you have questions.

Endocrine Specialists: Located in Westwood, Encino, Torrance, Westlake Village, Thousand Oaks

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Q and A: TSH (thyroid stimulating hormone)

Home » Patients Portal » Thyroid Q&A » Q and A: TSH (thyroid stimulating hormone)

Q: Is the TSH (thyroid stimulating hormone) a good way to titrate my thyroid hormone therapy?

A: Yes, absolutely! Once you have been diagnosed with hypothyroidism and started on thyroid hormone therapy, the TSH blood test is the best way to monitor your thyroid hormone replacement. TSH is made in the pituitary and the blood levels reflect how your own body is responding to the amount of thyroxine in your blood. When thyroid hormone levels are low, the pituitary gland increases secretion of TSH and indicates that your thyroxine dose should be increased. If your TSH level is low, your thyroid hormone dose is excessive and should be reduced. In most patients on thyroxine replacement, the goal TSH level is between 0.5 to 2.5 mU/L. Patients who have had thyroid cancer are usually on higher doses of thyroxine and their target TSH level is lower than normal. A TSH blood test should be obtained at least every 6-12 months while you are on a stable thyroxine dose, and more often if your dose is changed. Your doctor will usually wait 6-8 weeks after a thyroxine dose adjustment to measure your TSH, when the levels of thyroxine have reached a steady state. If you are on thyroxine and planning a pregnancy, or are currently pregnant, you will need more frequent TSH monitoring and should contact your physician. Although TSH is the best test for most patients on thyroxine replacement, those who have pituitary disease or previous pituitary surgery or radiation, are usually followed with measurement of free thyroxine, rather than a TSH.

Take a look at our Patient Web Brochure Hypothyroidism to learn more about hypothyroidism and how it is treated.

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Mild hypothyroidism: Who should be treated?

What to do about mild hypothyroidism is a subject that has been studied and debated for years. Mild hypothyroidism is also called subclinical hypothyroidism. It doesn’t meet the standard definition of overt hypothyroidism. You may have no symptoms, and your thyroid function blood tests show a mixed picture.

Your free T4 level is normal, meaning your body is getting enough thyroid hormone. It is your TSH (thyroid stimulating hormone) level that is above the normal range, which indicates your thyroid gland has to work harder to pump out that thyroid hormone.

One worry about mild hypothyroidism is the potential link between untreated subclinical hypothyroidism and coronary artery disease. Results of research on whether subclinical thyroid disease causes heart problems have been conflicting. However, the condition has been associated with heart and blood vessel abnormalities, and some studies suggest that treating mild hypothyroidism can improve various markers of heart structure and function.

However, there are potential downsides to treating subclinical hypothyroidism. There is the risk of overtreatment, which might cause symptoms, such as feeling jittery and insomnia. Also, long-term overtreatment can lead to loss of bone density.

If your TSH level is elevated to between 4.5 and 10 mIU/L and your T4 is normal, you should be considered for treatment with thyroid medication, especially if you have symptoms of hypothyroidism, or you have a positive test for thyroid antibodies, a history of heart disease, or risk factors for atherosclerosis. If you aren’t treated, your doctor should continue to monitor your thyroid function with blood tests every six to 12 months to check for progression.

If your TSH level is higher than 10 mIU/L, you should start treatment, because you will develop symptoms of an underactive thyroid, even if you don’t have them now.

For information on thyroid function in older adults, buy Thyroid Disease: Understanding hypothyroidism and hyperthyroidism, a Special Health Report from Harvard Medical School.

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should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

Underactive thyroid: Deciding whether or not to treat subclinical hypothyroidism – InformedHealth.org

Subclinical (latent) hypothyroidism means that the thyroid gland is still producing enough thyroid hormones. But some blood values may suggest the early stages of a hormone deficiency. Experts don’t agree on whether subclinical hypothyroidism should be treated. It’s not clear in which cases treatment would have advantages.

If you already have noticeable (“overt” or “manifest”) hypothyroidism, the thyroid is no longer producing enough thyroid hormones. Thyroxine is the most important of the thyroid hormones. It helps regulate many of the body’s functions to balance your metabolism. Too little thyroxine can cause a number of different health problems. The symptoms range from cold hands to physical weakness, difficulty concentrating and depression. Hypothyroidism can be treated easily by taking a tablet containing the thyroid hormone once a day. These tablets act to replace the thyroxine that is not being produced. This usually makes the symptoms disappear completely.

Because it doesn’t cause any symptoms, subclinical hypothyroidism isn’t noticeable. The TSH (thyroid-stimulating hormone) value is too high, but the thyroid is still producing enough hormones. This hormone is produced in the pituitary gland and acts as a trigger for the thyroid to start producing the thyroid hormones. TSH levels that are just a little too high may be the first sign of the early stages of hypothyroidism: The pituitary gland responds to lower levels of thyroid hormones by increasing TSH production to activate the thyroid.

It is estimated that about 5 out of 100 people have subclinical hypothyroidism. Slightly elevated TSH levels are usually detected by accident during a routine examination. But taken on their own they don’t pose any health risk. It’s also possible that TSH levels are high only temporarily, for example after intense physical activity. Experts don’t fully agree on how to decide when subclinical hypothyroidism should be treated.

How is subclinical hypothyroidism diagnosed?

Thyroid values like TSH are measured in blood tests. Because a single test can be misleading, a second test is usually done 2 or 3 months later. In both tests, the blood is taken at the same time of day because TSH levels can fluctuate over the course of 24 hours. Subclinical hypothyroidism is diagnosed when both TSH readings are high but the thyroid hormone thyroxine is still within the normal range.

Experts don’t agree on which TSH levels should be considered too high. Some suggest that TSH levels of over 2.5 milliunits per liter (mU/L) are abnormal, while others consider levels of TSH to be too high only after they have reached 4 to 5 mU/L.

Both children and teenagers as well as older people have somewhat higher TSH levels than middle-aged people. Because of this, thyroid specialists have been debating whether a higher threshold should be used for these age groups. Being severely overweight and certain medications can also increase TSH. TSH levels are likely to fluctuate more during pregnancy.

How does subclinical hypothyroidism develop?

The way that subclinical hypothyroidism develops depends on a number of different factors – including the TSH level: Slightly elevated TSH levels (between 5 and 10 mU/L) often return to normal on their own. But people who have highly elevated levels (over 15 mU/L) often develop symptomatic overt hypothyroidism within several months or years.

One study followed people with high levels of TSH over a period of two to three years. The participants didn’t have any symptoms or diagnosed thyroid disorders. They were divided into three groups depending on how high their TSH levels were. The study produced the following results:

• Slightly elevated TSH levels (between 5 and 10 mU/L): Each year, 2% of the participants in this group developed overt hypothyroidism.

• Moderately elevated TSH levels (between 10 and 15 mU/L): Each year, 20% of the participants in this group developed hypothyroidism with symptoms.

• Highly elevated TSH levels (over 15 mU/L): Each year, 73% of the participants in this group developed overt hypothyroidism.

TSH levels that are slightly or only moderately elevated don’t necessarily need to be treated. Some people who have high TSH levels never even develop symptoms. It is also very common for TSH levels to return to normal in children and teenagers.

The probability that overt hypothyroidism develops from subclinical hypothyroidism is greater if the thyorid is enlarged and thyroid antibodies are detectable in the blood. And women generally have a higher risk than men.

Thyroid antibodies are usually a sign of a condition called Hashimoto’s thyroiditis. This autoimmune disease is the most common cause of hypothyroidism. But detecting thyroid antibodies in your blood is not a sure sign that you have an underactive thyroid.

Does thyroxine treatment have any benefits if your TSH levels are high?

Some doctors will advise you to start treatment immediately if you have subclinical hypothyroidism. This is because there is some evidence suggesting that your risk of cardiovascular disease might slightly increase over the long term if TSH levels are higher than 10 mU/L. This link has not been observed for slightly elevated TSH levels lower than 10 mU/L.

Only a few good-quality studies have looked into what advantages and disadvantages thyroxine treatment may have for subclinical hypothyroidism. The largest and best quality study done yet involved nearly 800 people over the age of 65. It wasn’t large enough to answer the question of whether thyroxine treatment lowers the risk of complications, though. There was also no evidence that treatment offered other benefits: People who didn’t use thyroxine developed symptoms of hypothyroidism just as rarely as people who took thyroxine.

There are no studies showing any advantages of treating subclinical hypothyroidism in children and teenagers. Sometimes young people have higher TSH levels because they are overweight, so treatment with medication is usually not a good idea.

Does thyroxine treatment have side effects?

No good-quality research is available on the side effects of treating subclinical hypothyroidism with thyroxine, but it’s generally considered to be a well-tolerated drug. Because the body usually produces this hormone on its own, there are no problems if the dose is correct. If it’s too high though, side effects can’t be ruled out. Possible side effects include heart problems like atrial fibrillation or a racing heartbeat.

Does treatment make sense during pregnancy

Sometimes subclinical hypothyroidism in pregnant women is treated. For this purpose, they are occasionally offered a diagnostic screening test. In Germany this is provided as a “individual health care service” (IGeL Leistung).

Some evidence suggests that subclinical hypothyroidism during pregnancy can increase the risk of miscarriage or premature birth. But there is no proof that treatment with thyroxine can lower this risk in women who have high levels of TSH or thyroid antibodies. The largest study yet doesn’t show any advantage of treatment with thyroxine in pregnancy, neither for the risk of a premature birth or miscarriage, nor for the child’s development.

Treatment: Yes or no?

People who have no symptoms and only slightly elevated TSH levels usually don’t need treatment. Many doctors don’t recommend treatment unless the TSH levels are very high (over 10 mU/L). Other factors may also play a role in the decision, such as how high your overall risk of cardiovascular disease is.

Treatment is sometimes recommended already starting at TSH levels of over 6 mU/L in people with high levels of thyorid antibodies (Hashimoto’s thyroiditis). That is done to prevent subclinical hypothyroidism from becoming overt hypothyroidism. There is hardly any research on whether treatment can achieve that goal.

Deciding whether to have treatment or not very much comes down to personal preference since so many questions are still unanswered. You might prefer to not take any hormones unless it is absolutely necessary – even though thyroxine treatment is considered to be quite safe when taken at the correct dose. Especially if you have no symptoms or just very mild symptoms and hardly notice any effect from the medication, it can be a challenge to keep taking the tablets on a daily basis.

Some people may believe things like exhaustion or constipation are symptoms of their subclinical hypothyroidism and because of this try out treatment – even though it’s not the thyroid causing their problems. Instead, their symptoms may have a number of other causes.

If they don’t go away with treatment, they are probably not being caused by an underactive thyroid. Then you could stop taking the medication after talking it over with your doctor.

Sources

• IQWiG health information is written with the aim of helping
  people understand the advantages and disadvantages of the main treatment options and health
  care services.

  Because IQWiG is a German institute, some of the information provided here is specific to the
  German health care system. The suitability of any of the described options in an individual
  case can be determined by talking to a doctor. We do not offer individual consultations.

  Our information is based on the results of good-quality studies. It is written by a
  team of
  health care professionals, scientists and editors, and reviewed by external experts. You can
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  our methods.

Subclinical Hypothyroidism: Deciding When to Treat

1. Sawin CT,
Chopra D,
Azizi F,
Mannix JE,
Bacharach P.
The aging thyroid. Increased prevalence of elevated serum thyrotropin levels in the elderly. JAMA.
1979;242:247–50….

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

3. Helfand M,
Crapo LM.
Screening for thyroid disease. Ann Intern Med.
1990;112:840–9.

4. Danese MD,
Powe NR,
Sawin CT,
Ladenson PW.
Screening for mild thyroid failure at the periodic health examination: a decision and cost-effectiveness analysis. JAMA.
1996;276:285–92.

5. Dayan CM,
Daniels GH.
Chronic autoimmune thyroiditis. N Engl J Med.
1996;335:99–107.

6. Franklyn JA,
Daykin J,
Drolc Z,
Farmer M,
Sheppard MC.
Long-term follow-up of treatment of thyrotoxicosis by three different methods. Clin Endocrinol [Oxford].
1991;34:71–6.

7. Tamai H,
Kasagi K,
Takaichi Y,
Takamatsu J,
Komaki G,
Matsubayashi S,

et al.
Development of spontaneous hypothyroidism in patients with Graves’ disease treated with antithyroidal drugs: clinical, immunological, and histological findings in 26 patients. J Clin Endocrinol Metab.
1989;69:49–53.

8. Tunbridge WM,
Brewis M,
French JM,
Appleton D,
Bird T,
Clark F,

et al.
Natural history of autoimmune thyroiditis. Br Med J [Clin Res].
1981;282:258–62.

9. Rosenthal MJ,
Hunt WC,
Garry PJ,
Goodwin JS.
Thyroid failure in the elderly. Microsomal antibodies as discriminant for therapy. JAMA.
1987;258:209–13.

10. Cooper DS,
Halpern R,
Wood LC,
Levin AA,
Ridgway EC.
L-Thyroxine therapy in subclinical hypothyroidism. A double-blind, placebo-controlled trial. Ann Intern Med.
1984;101:18–24.

11. Staub JJ,
Althaus BU,
Engler H,
Ryff AS,
Trabucco P,
Marquardt K,

et al.
Spectrum of subclinical and overt hypothyroidism: effect on thyrotropin, prolactin, and thyroid reserve, and metabolic impact on peripheral target tissues. Am J Med.
1992;92:631–42.

12. Arem R,
Patsch W.
Lipoprotein and apolipoprotein levels in subclinical hypothyroidism. Effect of levothyroxine therapy. Arch Intern Med.
1990;150:2097–100.

13. Franklin JA,
Daykin J,
Betteridge J,
Hughes EA,
Holder R,
Jones SR,

et al.
Thyroxine replacement therapy and circulating lipid concentrations. Clin Endocrinol [Oxford].
1993;38:453–9.

14. Nystrom E,
Caidahl K,
Fager G,
Wikkelso C,
Lundberg PA,
Lindstedt G.
A double-blind cross-over 12-month study of L-thyroxine treatment of women with ‘subclinical’ hypothyroidism. Clin Endocrinol [Oxford].
1988;29:63–75.

15. Roti E,
Minelli R,
Gardini E,
Braverman LE.
The use and misuse of thyroid hormone. Endocr Rev.
1993;14:401–23.

16. Sawin CT,
Geller A,
Wolf PA,
Belanger AJ,
Baker E,
Bacharach P,

et al.
Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. N Engl J Med.
1994;331:1249–52.

17. Ross DS.
Hyperthyroidism, thyroid hormone therapy, and bone. Thyroid.
1994;4:319–26.

Standards for the level of thyrsotropic hormone in the blood: current state of the problem | Samsonova

One of the most controversial issues in modern thyroidology is the question of the norms for the level of TSH in the blood [4, 10]. The interest in this problem is understandable, since it is well known that the determination of the TSH concentration in the blood is currently considered a reference test in the laboratory assessment of the functional state of the thyroid gland, which allows timely detection of any violation of its function, including at the stage of asymptomatic hyper- and hypothyroxinemia.Thus, an increase in the TSH content in the blood serves as the earliest laboratory sign of not only obvious, but also threatened thyroid pathology, especially thyroid insufficiency. In this regard, it is quite obvious that the verification of thyroid insufficiency largely depends on the upper limit of the TSH level in the blood. At present, it is generally accepted that the concentration of TSH in the blood of more than 4-5 mU / l indicates a decrease in the function of the thyroid gland.

This article is a continuation of the discussion devoted to the norms of the upper limit of the norm for the level of TSH in the blood, opened on the pages of both foreign and domestic journals.

The reason for the discussion was the recent recommendations of the US National Academy of Clinical Biochemistry to reduce the upper limit of the norm for the level of TSH in the blood from 4 to 2.5 mU / L [8]. The basis for making such decisions was the results of the NHANES-111 epidemiological study, which showed that when examining 13 344 people receiving adequate iodine prophylaxis, the TSH level in the blood above 2.5 mU / l was determined in no more than 5% of cases [11] … At the same time, the study did not include those population groups that could potentially have abnormalities in the functional state of the thyroid gland [11].Similar results were obtained in the European SHIP-1 study [18]. Thus, as a result of a survey of 1488 adults in Pomerania, no more than 5% of the TSH level in the blood was higher than 2.12 mU / l [18].

It should be noted that not only after the publication of the recommendations of the US National Academy of Clinical Biochemistry, but also long before that, articles began to appear in foreign literature indicating that adult patients with a TSH level in the blood of 2-4 mU / L, for a number of clinical signs and laboratory tests differ from the population with a TSH level in the blood below 2 mU / L.So, back in 1992 J. Staub et al. showed that a group of adults with an average TSH content in the blood of 3.0 ± 0.3 mU / l demonstrates a hyperergic response of TSH to stimulation with thyroliberin, which is known to indicate a decrease in the functional reserve of the thyroid gland [16]. According to the data of the Wickham study, in the group of persons with a TSH level in the blood above 2 mU / L, subsequently, overt hypothyroidism is more often diagnosed [17]. Finally, in adults, this level of TSH is associated with an increased risk of hypercholesterolemia [7, 9, 14], endothelial dysfunction [12] and miscarriage [15].According to our data, such a concentration of TSH in the blood in women of reproductive age is associated with hypoestrogenism. Thus, every 8th (12.5%) woman of reproductive age, in whom the TSH level in the blood was determined from 2 to 4 mU / L when assessing the functional state of the thyroid gland, had a reduced level of estrogen in the blood (the median estradiol in this group of women was 167 pmol / l), while in all women with a TSH level in the blood below 2 mU / l, the estradiol content is within the normal range (median estradiol 235.25 pmol / l; /> = 0.01) [5] …

Moreover, in pregnant women (the most vulnerable part of the population in terms of the formation of pathological conditions associated with hypothyroxinemia), the TSH level in the first trimester of gestation more than 2 mU / L is currently a recognized factor of increased risk of developing gestational hypothyroxinemia. So, according to our data, gestational hypothyroxinemia occurs in almost every 2nd pregnant woman with diffuse endemic goiter, having a TSH level in the first trimester of gestation from 2 to 4 mU / l (/> = 0.05) [2].

Thus, a similar level of TSH in the blood in adults is associated with a known spectrum of pathological conditions, which are currently recognized as a consequence of chronic hypothyroxinemia.

At the same time, it should be emphasized that all the accumulated knowledge and ideas about the clinical and prognostic value of the TSH concentration in the blood of more than 2, but less than 4 mU / l were obtained on the basis of a survey of the adult population. The following data make it possible to form an opinion on the significance, competence and expediency of isolating this particular range of TSH levels in the blood and in pediatric practice.So, according to the results of the study by D.E.Shilin (2002), children and adolescents (n = 114) with a basal TSH level in the blood above 2 mU / l (on average 2.57 ± 0.06 mU / l) , differ from children and adolescents (n = 475) with a basal TSH level below 2 mU / l (on average, 1.19 ± 0.02 mU / l) [6].

In 94.1% of children (p <0.05) of this group, there is a hyperergic response of TSH to stimulation with thyroliberin, which indicates a reduced functional reserve of the thyroid gland [6]. According to the data of the same author, such children and adolescents have significantly (/> = 0.03) higher concentrations of atherogenic lipid fractions, and adolescent girls with a similar level of TSH in the blood show signs of age-related immaturity of the uterus and gonads (p = 0.01) [6].In addition, such girls have a tendency to polymenorrhea (menstruation on average lasts 5.5 ± 0.3 days versus 4.7 ± 0.1 days in the group of girls with a TSH level in the blood below 2 mU / l; p = 0.01) and a lower level of estradiol in the blood (the average content of estradiol is 162 ± 23 pmol / l versus 239 ± 22 pmol / l in the group of girls with a TSH concentration in the blood of less than 2 mU / l; p = 0.05 ) [6].

According to our data, it is adolescent girls with a TSH level in the blood above 2 but below 4 mU / l that are most vulnerable in terms of the formation of functional disorders from the reproductive system.So, according to the results of our research, every 2nd (54%) girl with a similar level of TSH in the blood has menstrual dysfunction of the type of opsomenorrhea (while only 28% of girls with a TSH level below 2 mU / l, P = 0.032 ) [1].

So, in our opinion, today there are enough arguments in favor of the fact that the level of TSH in the blood from 2 to 4 mU / l in children also reflects the earliest in terms of appearance and the mildest in severity of thyroid insufficiency.

It is obvious that thyroid insufficiency in iodine-deficient regions has its own evolution.In our opinion, the evolution of thyroid insufficiency can be represented as follows: 1) normal level of free thyroxine and TSH level from 2 to 4 mU / l, there are no clinical signs of hypothyroidism; 2) normal level of free thyroxine and TSH level above 4-5 mU / l, there are no clinical symptoms of hypothyroidism; 3) a reduced level of free thyroxine and a TSH level above 4-5 mU / l in combination with clinical signs of hypothyroidism. The last two stages of thyroid insufficiency are well known and are classified as subclinical and overt hypothyroidism, respectively.

At the same time, today there is no single generally accepted term characterizing the level of TSH from 2 to 4 mU / l. This is understandable, since terminology issues are always the most difficult. In the English-language literature, the TSH level within the traditionally normal limits, but above 2 mU / L, is denoted by the following terms: “high-normal TSH” [14], “very mild thyroid failure” [15], “a lessened thyroid reserve” [15], “mildest form of subclinical hypothyroidism” [16]. We propose to use the term “minimal thyroid insufficiency” to denote a condition, which is reflected in a TSH level from 2 to 4 mU / l.In our opinion, it is he who most accurately characterizes the earliest in terms of appearance and the mildest in severity thyroid insufficiency.

At the same time, at a given level of TSH, the functionality of the thyroid gland should be assessed depending on its size. Thus, in persons without goiter, a slight increase in the level of TSH (2-4 mU / l) only indicates that the thyroid gland at normal size is unable to provide adequate production of thyroid hormones.In this group of people, a similar level of TSH reflects the readiness to activate compensatory mechanisms leading to an increase in the size of the thyroid gland and to the normalization of the level of thyroid hormones. Thus, in persons with normal sizes of the thyroid gland, this condition cannot yet be classified as a pathology, but should be considered as a borderline state.

In patients with long-standing goiter, this level of TSH indicates that an increase in the size of the thyroid gland did not lead to the elimination of hypothyroxinemia and, therefore, the required level of thyroid hormones was not achieved.Most likely, in this case, there was a decrease in the compensatory and functional reserves of the thyroid gland due to a slight genetic defect in morpho- or hormonogenesis. Even with mild congenital failure of the thyroid gland in conditions of insufficient iodine intake, the formation of a goiter will not lead to the normalization of the thyroid status, that is, to the elimination of hypothyroxinemia and, consequently, the risk of iodine deficiency diseases.

We are deeply convinced that the use of the term “minimal thyroid insufficiency” in the context in which it is presented in the article will not only not mislead readers, but, on the contrary, will help to understand the essence of the problem and present the evolution of thyroid insufficiency in iodine-deficient regions.

It should be noted that another, no less, and perhaps more important question of this discussion is whether people with a TSH level in the blood need therapy from 2 to 4 mU / l. Foreign and domestic authors consider the danger of expanding indications for verification of hypothyroidism and treatment of such a patient with levothyroxine preparations as a serious argument against the recognition of new standards for THG in blood [4, 10].

In our opinion, the TSH level in the range from 2 to 4 mU / L indicates only that in the region of iodine deficiency, the thyroid gland is able to maintain an ideal euthyroid state only under the condition of an adequate intake of iodine.It is quite obvious that in the absence of adequate iodine prophylaxis in regions even with moderate and / or mild iodine deficiency (i.e., in most of the territory of Russia), it is this degree of thyroid insufficiency that will continue to occur frequently and determine the formation of medico-socially significant iodine deficiency states. … Hence the conclusion that the overwhelming majority of people living in these conditions and having a similar level of TSH in the blood only need adequate iodine prophylaxis.Adequate iodine prophylaxis in most of them is able to maintain an ideal euthyroid state for many years of life.

Exceptions are 2 groups of persons. These are primarily pregnant women with a TSH level in the first trimester of gestation above 2 mU / L, that is, having a risk factor for the development of gestational hypothyroxinemia [2]. Considering the exceptional role of the normal maternal thyroxine level for the formation and maturation of the central nervous system of the unborn child and the need for rapid and effective correction of gestational hypothyroxinemia, today no one doubts and objections that pregnant women with a similar TSH level need treatment with levothyroxine drugs.In addition, it is required to prescribe levothyroxine preparations to persons exposed to other (except for iodine deficiency) strumogenic factors of the external environment or having more pronounced genetically determined defects in the morpho- or hormonogenesis of the thyroid gland. It should be emphasized that we are talking about extremely rare cases.

When deciding on the TSH level standards, modern double standards used to assess the functional state of the thyroid gland in untreated individuals and in patients receiving replacement therapy with levothyroxine drugs are somewhat surprising [3, 13].In this regard, another weighty argument in favor of narrowing the normal range for the TSH level in the blood is that the overwhelming majority of researchers recognize and do not raise objections to the TSH level values ​​in the range from 0.5 to 2 mU / L as reflecting the euthyroid state of the thyroid gland. in patients receiving replacement therapy with levothyroxine drugs [3, 13].

So, the above data convince us that today there are more than enough arguments in favor of recognizing the fact that (in both adults and children) the TSH level from 2 to 4 mU / l reflects the earliest in terms of appearance and the mildest thyroid insufficiency in severity, namely, minimal thyroid insufficiency.

Narrowing the range of TSH levels in the blood from 0.5 to 2-2.5 mU / l and the early introduction of these standards into healthcare practice is a prerequisite for optimizing early diagnosis, prevention, treatment of hypothyroxinemia and, consequently, the elimination of iodine deficiency conditions in Russia …

1. Bukanova SV Thyroid status and functional state of the reproductive system in children and adolescents living in an industrial metropolis with moderately mild iodine deficiency: Authorsf.dis …. cand. honey. sciences. -M., 2004.

2. Ivakhnenko VN Thyrsoid, neuropsychiatric and somatic status of children born to mothers with goiter: Author’s abstract. dis …. cand. honey. sciences. – M., 2005.

3. Kasatkina E. P., Martynova M. I., Peterkova V. A. et al. // Klin. thyroidol. – 2003. – T. 1, No. 1. – S. 26-27.

4.Fadeev V.V., Klin. thyroidol. – 2004. – T. 2, No. 3. – S. 5-9.

5. Chubarova D. Yu. Reproductive health of women in the region of mild goiter endemic: Author’s abstract. dis …. cand. honey. sciences. – M., 2006.

6. Shilin D. Ye. // Laboratory. – 2002. – No. 3. – S. 22-26.

7.Bakker S. J. L., Ter Matten J. C, Popp-Sni / ders C. et al. // J. Clin. Endocrinol. Metab. – 2001. – Vol. 86. – P. 1206-1211.

8. Baloch Z, Carayon P., Conte-Devolx B. et al. // Thyroid. – 2003. Vol. 13.-P. 3-126.

9. Bindels A. J., Weslendorp R. C, Frolich M. et al. // J. Clin. Endocrinol. – 1999. – Vol. 50.- P. 217-220.

10. Brabant G., Beek-Peccoz P., Jarzab B. et al. // Eur. J. Endocrinol. – 2006. – Vol. 154. – P. 633-637.

11. Hollowell J. C, Siaehling N. W, Flanders W. D. et al. // J. Clin. Endocrinol. Metab. – 2002. – Vol. 87. – P. 489-499

12.Lekakis J, Paramlchael C, Alevizaki M. et al. // Thyroid. – 1997. – Vol. 7. – P. 411-414.

13. McDermott M. T., Ridgway C // i. Clin. Endocrinol. Metab. -2001. – Vol. 86. – P. 585-590.

14. Michalopoulou C, Alevizaki M, Piperingos C et al. // Eur. J. Endocrinol. – 199S. – Vol. 138. – P. 141-145.

15.Prummel M. F, Wienlnga W. M. // Eur. J. Endocrinol. – 2004. – Vol. 150. – P. 751-755.

16. Staub J. J., Althaus B. V., Engler H. et al. // Am. J. Med. – 1992. – Vol. 92, No. 6. – P. 632-642.

17. Vanderpump M. P., Tunbridge W. M. C, French J. M. et al. // J. Clin. Endocrinol. – 1995. – Vol. 43. – P. 55-68.

18.Volzke H., Ludemann J., Robinson D. M. et al. // Thyroid. – 2003. – Vol. 13. – P. 803-810.

Subclinical hypothyroidism and metabolic syndrome: reasons for drug intervention | Ruyatkina

1. Du F-M, Kuang H-Y, Duan B-H, et al. Associations Between Thyroid Hormones Within the Euthyroid Range and Indices of Obesity in Obese Chinese Women of Reproductive Age.Metab Syndr Relat Disord. 2019; 17 (8): 416-422. DOI: 10.1089 / met.2019.0036

2. Ruyatkina L.A., Ruyatkin D.S. Integral cardiovascular risk: metabolic syndrome and thyroid dysfunction. // Siberian Medical Review. – 2010. – No. 4. – S. 11-16. [Ruyatkina LA, Ruyatkin DS. Integral cardiovascular risk: metabolic syndrome and thyroid dysfunction. Siberian medical review. 2010; (4): 11-16. (In Russ.)]

3. Mohan V, Bodhini D. Mediators of insulin resistance & cardiometabolic risk: Newer insights. Indian J Med Res. 2018; 148 (2): 127. DOI: 10.4103 / ijmr.IJMR_969_18

4. Ruyatkina L.A., Ruyatkin D.S., Iskhakova I.S. Possibilities and options for surrogate assessment of insulin resistance. // Obesity and Metabolism. – 2019.- T. 16. – No. 1. – S. 27-32. [Ruyatkina LA, Ruyatkin DS, Iskhakova IS. Opportunities and options for surrogate assessment of insulin resistance. Obesity and metabolism. 2019; 16 (1): 27-32. (In Russ.)] DOI: 10.14341 / omet10082

5. Park SY, Park SE, Jung SW, et al. Free triiodothyronine / free thyroxine ratio rather than thyrotropin is more associated with metabolic parameters in healthy euthyroid adult subjects.Clin Endocrinol. 2017; 87 (1): 87-96. DOI: 10.1111 / cen. 13345

6. Yang L, Lv X, Yue F, et al. Subclinical hypothyroidism and the risk of metabolic syndrome: A meta-analysis of observational studies. Endocr Res. 2016; 41 (2): 158-165. DOI: 10.3109 / 07435800.2015.1108332

7. Eftekharzadeh A, Khamseh ME, Farshchi A, Malek M.The Association Between Subclinical Hypothyroidism and Metabolic Syndrome as Defined by the ATP III Criteria. Metab Syndr Relat Disord. 2016; 14 (3): 137-144. DOI: 10.1089 / met.2015.0065

8. Nakajima Y, Yamada M, Akuzawa M, et al. Subclinical Hypothyroidism and Indices for Metabolic Syndrome in Japanese Women: One-Year Follow-Up Study. J Clin Endocrinol Metab. 2013; 98 (8): 3280-3287. DOI: 10.1210 / jc.2013-1353

9.Amouzegar A, Mehran L, Takyar M, et al. Tehran Thyroid Study (TTS). Int J Endocrinol Metab. 2018; 16 (4 Suppl): e84727. DOI: 10.5812 / ijem.84727

10. Amouzegar A, Kazemian E, Abdi H, et al. Association Between Thyroid Function and Development of Different Obesity Phenotypes in Euthyroid Adults: A Nine-Year Follow-Up. Thyroid. 2018; 28 (4): 458-464. DOI: 10.1089 / thy.2017.0454

11.Iwen KA, Oelkrug R, Kalscheuer H, Brabant G. Metabolic Syndrome in Thyroid Disease. Front Horm Res. 2018; 49: 48-66. DOI: 10.1159 / 000485996

12. Razvi S, Jabbar A, Pingitore A, et al. Thyroid Hormones and Cardiovascular Function and Diseases. J Am Coll Cardiol. 2018; 71 (16): 1781-1796. DOI: 10.1016 / j.jacc.2018.02.045

13.Gyawali P, Takanche JS, Shrestha RK, et al. Pattern of thyroid dysfunction in patients with metabolic syndrome and its relationship with components of metabolic syndrome. Diabetes Metab J. 2015; 39 (1): 66-73. DOI: 10.4093 / dmj.2015.39.1.66

14. Duntas LH, Chiovato L. Cardiovascular Risk in Patients with Subclinical Hypothyroidism. Eur Endocrinol. 2014; 10 (2): 157-160. DOI: 10.17925 / EE.2014.10.02.157

15.Biondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev. 2008; 29 (1): 76-131. DOI: 10.1210 / er.2006-0043

16. Floriani C, Gencer B, Collet TH, Rodondi N. Subclinical thyroid dysfunction and cardiovascular diseases: 2016 update. Eur Heart J. 2018; 39 (7): 503-507. DOI: 10.1093 / eurheartj / ehx050

17.Mendes D, Alves C, Silverio N, Batel Marques F. Prevalence of Undiagnosed Hypothyroidism in Europe: A Systematic Review and Meta-Analysis. Eur Thyroid J. 2019; 8 (3): 130-143. DOI: 10.1159 / 000499751

18. Tekle HA, Bobe TM, Tufa EG, Solomon FB. Age-sex disparities and sub-clinical hypothyroidism among patients in Tikur Anbesa Specialized Hospital, Addis Ababa, Ethiopia. J Health Popul Nutr. 2018; 37 (1): 18. DOI: 10.1186 / s41043-018-0149-x

19. Surks MI, Ortiz E, Daniels GH, et al. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. JAMA. 2004; 291 (2): 228-238. DOI: 10.1001 / jama.291.2.228

20. Polikar R, Burger AG, Scherrer U, Nicod P. The thyroid and the heart. Circulation. 1993; 87 (5): 1435-1441.DOI: 10.1161 / 01.cir.87.5.1435

21. Kahaly GJ. Cardiovascular and atherogenic aspects of subclinical hypothyroidism. Thyroid. 2000; 10 (8): 665-679. DOI: 10.1089 / 10507250050137743

22. Tseng FY, Lin WY, Lin CC, et al. Subclinical hypothyroidism is associated with increased risk for all-cause and cardiovascular mortality in adults.J Am Coll Cardiol. 2012; 60 (8): 730-737. DOI: 10.1016 / j.jacc.2012.03.047

23. Nekrasova TA, Strongin LG, Morozova EP, et al. Modifying effect of subclinical hypothyroidism on the course of arterial hypertension: relationship with latent treatment ineffectiveness, daily blood pressure profile and the state of target organs. // Clinical and experimental thyroidology. – 2015. – T. 11. – No. 2.- S. 55-62. [Nekrasova TA, Strongin LG, Morozova EP, et al. Modifying influence of subclinical hypothyroidism on arterial hypertension: relationship to masked treatment failure, circadian blood pressure profile and target organs status. Clinical and experimental thyroidology. 2015; 11 (2): 55-62. (In Russ.)] DOI: 10.14341 / ket2015255-62

24. Owen PJ, Sabit R, Lazarus JH. Thyroid disease and vascular function.Thyroid. 2007; 17 (6): 519-524. DOI: 10.1089 / thy.2007.0051

25. Rodondi N, Bauer DC, Cappola AR, et al. Subclinical thyroid dysfunction, cardiac function, and the risk of heart failure. The Cardiovascular Health study. J Am Coll Cardiol. 2008; 52 (14): 1152-1159. DOI: 10.1016 / j.jacc.2008.07.009

26. Hak AE, Pols HA, Visser TJ, et al.Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Ann Intern Med. 2000; 132 (4): 270-278. DOI: 10.7326 / 0003-4819-132-4-200002150-00004

27. Bielecka-Dabrowa A, Godoy B, Suzuki T, et al. Subclinical hypothyroidism and the development of heart failure: an overview of risk and effects on cardiac function. Clin Res Cardiol.2019; 108 (3): 225-233. DOI: 10.1007 / s00392-018-1340-1

28. Dhital R, Poudel DR, Tachamo N, et al. Ischemic Stroke and Impact of Thyroid Profile at Presentation: A Systematic Review and Meta-analysis of Observational Studies. J Stroke Cerebrovasc Dis. 2017; 26 (12): 2926-2934. DOI: 10.1016 / j.jstrokecerebrovasdis.2017.07.015

29.Gong Y, Ma Y, Ye Z, et al. Thyroid stimulating hormone exhibits the impact on LDLR / LDL-c via up-regulating hepatic PCSK9 expression. Metabolism. 2017; 76: 32-41. DOI: 10.1016 / j.metabol.2017.07.006

30. Ebrahimpour A, Vaghari-Tabari M, Qujeq D, et al. Direct correlation between serum homocysteine ​​level and insulin resistance index in patients with subclinical hypothyroidism: Does subclinical hypothyroidism increase the risk of diabetes and cardio vascular disease together? Diabetes Metab Syndr.2018; 12 (6): 863-867. DOI: 10.1016 / j.dsx.2018.05.002

31. Sieminska L, Wojciechowska C, Walczak K, et al. Associations between metabolic syndrome, serum thyrotropin, and thyroid antibodies status in postmenopausal women, and the role of interleukin-6. Endokrynol Pol. 2015; 66 (5): 394-403. DOI: 10.5603 / EP.2015.0049

32.Altay S, Onat A, Can G, et al. High-normal thyroid-stimulating hormone in euthyroid subjects is associated with risk of mortality and composite disease endpoint only in women. Arch Med Sci. 2018; 14 (6): 1394-1403. DOI: 10.5114 / aoms.2016.63264

33. Gupta G, Sharma P, Kumar P, Itagappa M. Study on Subclinical Hypothyroidism and its Association with Various Inflammatory Markers. J Clin Diagn Res. 2015; 9 (11): BC04-06.DOI: 10.7860 / JCDR / 2015 / 14640.6806

34. Liu J, Duan Y, Fu J, Wang G. Association Between Thyroid Hormones, Thyroid Antibodies, and Cardiometabolic Factors in Non-Obese Individuals With Normal Thyroid Function. Front Endocrinol (Lausanne). 2018; 9: 130. DOI: 10.3389 / fendo.2018.00130

35. Chen Y, Zhu C, Chen Y, et al.Are Thyroid Autoimmune Diseases Associated with Cardiometabolic Risks in a Population with Normal Thyroid-Stimulating Hormone? Mediators Inflamm. 2018; 2018: 1856137. DOI: 10.1155 / 2018/1856137

36. Roifman I, Beck PL, Anderson TJ, et al. Chronic inflammatory diseases and cardiovascular risk: a systematic review. Can J Cardiol. 2011; 27 (2): 174-182. DOI: 10.1016 / j.cjca.2010.12.040

37.Xu C, Zhou L, Wu K, et al. Abnormal Glucose Metabolism and Insulin Resistance Are Induced via the IRE1alpha / XBP-1 Pathway in Subclinical Hypothyroidism. Front Endocrinol (Lausanne). 2019; 10: 303. DOI: 10.3389 / fendo.2019.00303

38. Brenta G, Caballero AS, Nunes MT. Case Finding for Hypothyroidism Should Include Type 2 Diabetes and Metabolic Syndrome Patients: A Latin American Thyroid Society (Lats) Position Statement.Endocr Pract. 2019; 25 (1): 101-105. DOI: 10.4158 / EP-2018-0317

39. Chang YC, Hua SC, Chang CH, et al. High TSH Level within Normal Range Is Associated with Obesity, Dyslipidemia, Hypertension, Inflammation, Hypercoagulability, and the Metabolic Syndrome: A Novel Cardiometabolic Marker. J Clin Med. 2019; 8 (6). Doi: 10.3390 / jcm8060817

40.Feller M, Snel M, Moutzouri E, et al. Association of Thyroid Hormone Therapy With Quality of Life and Thyroid-Related Symptoms in Patients With Subclinical Hypothyroidism: A Systematic Review and Meta-analysis. JAMA. 2018; 320 (13): 1349-1359. DOI: 10.1001 / jama.2018.13770

41. Andersen MN, Olsen AM, Madsen JC, et al. Levothyroxine Substitution in Patients with Subclinical Hypothyroidism and the Risk of Myocardial Infarction and Mortality.PLoS One. 2015; 10 (6): e0129793. Doi: 10.1371 / journal.pone.0129793

42. Andersen MN, Olsen AS, Madsen JC, et al. Long-Term Outcome in Levothyroxine Treated Patients With Subclinical Hypothyroidism and Concomitant Heart Disease. J Clin Endocrinol Metab. 2016; 101 (11): 4170-4177. DOI: 10.1210 / jc.2016-2226

43. Jasim S, Gharib H.Thyroid and Aging. Endocr Pract. 2018; 24 (4): 369-374. DOI: 10.4158 / EP171796.RA

44. Leng O, Razvi S. Hypothyroidism in the older population. Thyroid Res. 2019; 12: 2. DOI: 10.1186 / s13044-019-0063-3

45. Vigersky RA, Filmore-Nassar A, Glass AR. Thyrotropin suppression by metformin. J Clin Endocrinol Metab. 2006; 91 (1): 225-227.DOI: 10.1210 / jc.2005-1210

46. Lupoli R, Di Minno A, Tortora A, et al. Effects of treatment with metformin on TSH levels: a meta-analysis of literature studies. J Clin Endocrinol Metab. 2014; 99 (1): E143-148. DOI: 10.1210 / jc.2013-2965

47. Fournier JP, Yin H, Yu OH, Azoulay L. Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus.CMAJ. 2014; 186 (15): 1138-1145. Doi: 10.1503 / cmaj.140688

48 Distiller LA, Polakow ES, Joffe BI. Type 2 diabetes mellitus and hypothyroidism: the possible influence of metformin therapy. Diabet Med. 2014; 31 (2): 172-175. DOI: 10.1111 / dme. 12342

49. Nurcheshmeh Z, Aliasgarzadeh A, Bahrami A, Mobasseri M. The Effects of Metformin on Thyroid Function among Patients with Subclinical Hypothyroidism and Coexisting Metabolic Syndrome.Pharm Sci. 2018; 24 (2): 118-123. DOI: 10.15171 / ps.2018.18

50. Palui R, Sahoo J, Kamalanathan S, et al. Effect of metformin on thyroid function tests in patients with subclinical hypothyroidism: an open-label randomized controlled trial. J Endocrinol Invest. 2019; 42 (12): 1451-1458. Doi: 10.1007 / s40618-019-01059-w

51.Krysiak R, Szkrobka W, Okopien B. Sex-dependent effect of metformin on hypothalamic-pituitary-thyroid axis activity in patients with subclinical hypothyroidism. Pharmacol Rep. 2016; 68 (6): 1115-1119. DOI: 10.1016 / j.pharep.2016.07.002

52. Meng X, Xu S, Chen G, et al. Metformin and thyroid disease. J Endocrinol. 2017; 233 (1): R43-R51. DOI: 10.1530 / JOE-16-0450

53.Cetinkalp S, Simsir IY, Ertek S. Insulin resistance in brain and possible therapeutic approaches. Curr Vasc Pharmacol. 2014; 12 (4): 553-564. DOI: 10.2174 / 1570161112999140206130426

54. Wang B, Cheng KK. Hypothalamic AMPK as a Mediator of Hormonal Regulation of Energy Balance. Int J Mol Sci. 2018; 19 (11). DOI: 10.3390 / ijms19113552

55.Ruyatkina L.A., Ruyatkin D.S. The multifaceted effects of metformin in patients with type 2 diabetes. // Diabetes. – 2017. – T. 20. – No. 3. – S. 210-219. [Ruyatkina LA, Ruyatkin DS. Multidimensional effects of metformin in patients with type 2 diabetes. Diabetes mellitus. 2017; 20 (2): 210-219. (In Russ.)] DOI: 10.14341 / DM2003458-64

56. Cho K, Chung JY, Cho SK, et al. Antihyperglycemic mechanism of metformin occurs via the AMPK / LXRalpha / POMC pathway.Sci Rep. 2015; 5: 8145. DOI: 10.1038 / srep08145

57. Andrade BM, de Carvalho DP. Perspectives of the AMP-activated kinase (AMPK) signaling pathway in thyroid cancer. Biosci Rep. 2014; 34 (2). DOI: 10.1042 / BSR20130134

58. Piskovatska V, Stefanyshyn N, Storey KB, et al. Metformin as a geroprotector: experimental and clinical evidence.Biogerontology. 2019; 20 (1): 33-48. DOI: 10.1007 / s10522-018-9773-5

59. Dedov II, Shestakova MV, Mayorov A.Yu., et al. Algorithms of specialized medical care for patients with diabetes mellitus. / Ed. Dedova I.I., Shestakova M.V., Mayorova A.Yu. 9th edition. // Diabetes. – 2019. – T. 22. – No. S1. – S. 1-144. [Dedov II, Shestakova MV, Mayorov AY, et al. Dedov II, Shestakova MV, Mayorov AY, editors.Standards of specialized diabetes care. 9th ed. Diabetes mellitus. 2019; 22 (S1): 1-144. (In Russ.)] DOI: 10.14341 / DM221S1

60. Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over 15-year follow-up: the Diabetes Prevention Program Outcomes Study. Lancet Diabetes Endocrinol. 2015; 3 (11): 866-875. DOI: 10.1016 / s2213-8587 (15) 00291-0

61.Derosa G, D’Angelo A, Romano D, Maffioli P. Effects of metformin extended release compared to immediate release formula on glycemic control and glycemic variability in patients with type 2 diabetes. Drug Des Devel Ther. 2017; 11: 1481-1488. Doi: 10.2147 / dddt.s131670

62. rlsnet.ru [Internet]. Glucophage® long [accessed 25.04.2020]. Access by link: https://www.rlsnet.ru/tn_index_id_45613.htm. [Rlsnet.ru [Internet]. Glucophage® long [cited 2020 Apr 25]. Available from: https://www.rlsnet.ru/tn_index_id_45613.htm. (In Russ.)]

63. Mehran L, Amouzegar A, Azizi F. Thyroid disease and the metabolic syndrome. Current Opinion in Endocrinology & Diabetes and Obesity. 2019; 26 (5): 256-265. DOI: 10.1097 / med.0000000000000500

64.Chiovato L, Magri F, Carle A. Hypothyroidism in Context: Where We’ve Been and Where We’re Going. Adv Ther. 2019; 36 (Suppl 2): ​​47-58. DOI: 10.1007 / s12325-019-01080-8

65. Sui M, Yu Y, Zhang H, et al. Efficacy of Metformin for Benign Thyroid Nodules in Subjects With Insulin Resistance: A Systematic Review and Meta-Analysis. Front Endocrinol (Lausanne). 2018; 9: 494. DOI: 10.3389 / fendo.2018.00494

66.Yildirim Simsir I, Cetinkalp S, Kabalak T. Review of Factors Contributing to Nodular Goiter and Thyroid Carcinoma. Med Princ Pract. 2020; 29 (1): 1-5. DOI: 10.1159 / 000503575

Thyroid stimulating hormone (TSH, thyrotropin, Thyroid Stimulating Hormone, TSH)

Study material
Blood serum

Method of determination
Microparticle chemiluminescence immunoassay

A pituitary hormone that regulates the function of the thyroid gland.One of the most important tests in the laboratory diagnosis of thyroid diseases. …

TSH is a glycoprotein with a molecular weight of about 28 kDa. It is synthesized in the anterior pituitary gland. It activates the production and secretion of thyroid hormones (thyroid hormones), initiates cell growth and mitotic activity of thyroid cells. The synthesis and secretion of TSH is stimulated by the thyrotropin-releasing hormone of the hypothalamus in response to a decrease in the level of circulating thyroid hormones. The level of TSH is in inverse logarithmic dependence on the concentration of T4: with an increase in the level of T4, the production of TSH decreases, with a decrease in the level of T4, the production of TSH increases compensatory, which helps to maintain the concentration of thyroid hormones at the required height.TSH secretion is influenced by various neuronal mechanisms and changes during sleep, temperature drop, nonspecific stress. For TSH, daily fluctuations in concentration are characteristic: the highest values ​​of TSH in the blood reach by 2-4 a.m., a high level in the blood remains until 6-8 a.m., the minimum TSH values ​​are at 17-18 hours. The reference values ​​for TSH levels below are applicable for outpatients between 8 and 18 hours. The normal rhythm of thyrotropin secretion is disturbed when awake at night.

With clinically pronounced primary hypothyroidism (i.e., damage at the level of the thyroid gland, which leads to a decrease in its function), there is a significant increase in TSH levels against the background of low levels of thyroid hormones. In contrast, primary hyperthyroidism is associated with decreased or undetectable TSH levels and high thyroid hormone levels. Determination of the TSH level makes it possible to identify subclinical stages of thyroid diseases, when the concentration of thyroid hormones is still maintained by regulatory mechanisms within the framework of reference values.Usually, in a screening study of thyroid function, TSH is used as the only test or in combination with the determination of free T4.

Taking thyroxine preparations on the eve of blood sampling for research does not affect the TSH concentration. Normalization of the TSH level during replacement therapy of hypothyroidism with L-thyroxine drugs occurs slowly (over several weeks and months), since hyperplasia of thyrotrophs develops in chronic severe hypothyroidism.A paradoxical combination – a high level of TSH and a high level of free T4 – during this period is an artificially induced (iatrogenic) state. Repeated studies of the TSH level in order to control therapy should be carried out no earlier than 6 weeks after changing the dose or type of drug.

In secondary and tertiary hypothyroidism associated with pituitary dysfunction due to pathology of the pituitary gland and hypothalamus, significantly reduced levels of T3 and T4 are combined with a normal or slightly increased level of TSH, which in these cases has a reduced biological activity.Rare clinical cases of secondary hyperthyroidism may be due to TSH-secreting tumors.

Severe non-thyroid diseases can cause temporary changes in TSH concentration. The reason may be the use of drugs or the consequences of the disease itself. Usually there is a decrease in the level of TSH in the acute phase of the disease and a slight increase in the level during recovery. If necessary, in such cases, it is advisable to focus on the extended reference range of TSH (0.02-10 mU / L) and use the complex of TSH and T4 tests (or free T4).

Physiological changes in TSH concentration have been observed during pregnancy. High concentrations of chorionic gonadotropin, which has a certain structural similarity to TSH, are capable of stimulating the synthesis of thyroid hormones. In the first trimester of pregnancy, there is a temporary increase in the content of T4 and a decrease in the level of TSH. During the II and III trimesters, the TSH level returns to normal. An increased level of TSH in early pregnancy may indicate latent hypothyroidism in the mother, potentially dangerous for the development of the fetus.

Limits of determination: 0.0025 mU / l-100 mU / l

A pituitary hormone that regulates the function of the thyroid gland. One of the most important tests in the laboratory diagnosis of thyroid diseases.

90,000 Subclinical Hypothyroidism and Metabolic Syndrome: Basis for Drug Intervention | Ruyatkina

1. Du F-M, Kuang H-Y, Duan B-H, et al.Associations Between Thyroid Hormones Within the Euthyroid Range and Indices of Obesity in Obese Chinese Women of Reproductive Age. Metab Syndr Relat Disord. 2019; 17 (8): 416-422. DOI: 10.1089 / met.2019.0036

2. Ruyatkina L.A., Ruyatkin D.S. Integral cardiovascular risk: metabolic syndrome and thyroid dysfunction. // Siberian Medical Review. – 2010. – No. 4. – S. 11-16. [Ruyatkina LA, Ruyatkin DS.Integral cardiovascular risk: metabolic syndrome and thyroid dysfunction. Siberian medical review. 2010; (4): 11-16. (In Russ.)]

3. Mohan V, Bodhini D. Mediators of insulin resistance & cardiometabolic risk: Newer insights. Indian J Med Res. 2018; 148 (2): 127. DOI: 10.4103 / ijmr.IJMR_969_18

4. Ruyatkina L.A., Ruyatkin D.S., Iskhakova I.S. Possibilities and options for surrogate assessment of insulin resistance. // Obesity and Metabolism. – 2019. – T. 16. – No. 1. – S. 27-32. [Ruyatkina LA, Ruyatkin DS, Iskhakova IS. Opportunities and options for surrogate assessment of insulin resistance. Obesity and metabolism. 2019; 16 (1): 27-32. (In Russ.)] DOI: 10.14341 / omet10082

5. Park SY, Park SE, Jung SW, et al. Free triiodothyronine / free thyroxine ratio rather than thyrotropin is more associated with metabolic parameters in healthy euthyroid adult subjects.Clin Endocrinol. 2017; 87 (1): 87-96. DOI: 10.1111 / cen. 13345

6. Yang L, Lv X, Yue F, et al. Subclinical hypothyroidism and the risk of metabolic syndrome: A meta-analysis of observational studies. Endocr Res. 2016; 41 (2): 158-165. DOI: 10.3109 / 07435800.2015.1108332

7. Eftekharzadeh A, Khamseh ME, Farshchi A, Malek M.The Association Between Subclinical Hypothyroidism and Metabolic Syndrome as Defined by the ATP III Criteria. Metab Syndr Relat Disord. 2016; 14 (3): 137-144. DOI: 10.1089 / met.2015.0065

8. Nakajima Y, Yamada M, Akuzawa M, et al. Subclinical Hypothyroidism and Indices for Metabolic Syndrome in Japanese Women: One-Year Follow-Up Study. J Clin Endocrinol Metab. 2013; 98 (8): 3280-3287. DOI: 10.1210 / jc.2013-1353

9.Amouzegar A, Mehran L, Takyar M, et al. Tehran Thyroid Study (TTS). Int J Endocrinol Metab. 2018; 16 (4 Suppl): e84727. DOI: 10.5812 / ijem.84727

10. Amouzegar A, Kazemian E, Abdi H, et al. Association Between Thyroid Function and Development of Different Obesity Phenotypes in Euthyroid Adults: A Nine-Year Follow-Up. Thyroid. 2018; 28 (4): 458-464. DOI: 10.1089 / thy.2017.0454

11.Iwen KA, Oelkrug R, Kalscheuer H, Brabant G. Metabolic Syndrome in Thyroid Disease. Front Horm Res. 2018; 49: 48-66. DOI: 10.1159 / 000485996

12. Razvi S, Jabbar A, Pingitore A, et al. Thyroid Hormones and Cardiovascular Function and Diseases. J Am Coll Cardiol. 2018; 71 (16): 1781-1796. DOI: 10.1016 / j.jacc.2018.02.045

13.Gyawali P, Takanche JS, Shrestha RK, et al. Pattern of thyroid dysfunction in patients with metabolic syndrome and its relationship with components of metabolic syndrome. Diabetes Metab J. 2015; 39 (1): 66-73. DOI: 10.4093 / dmj.2015.39.1.66

14. Duntas LH, Chiovato L. Cardiovascular Risk in Patients with Subclinical Hypothyroidism. Eur Endocrinol. 2014; 10 (2): 157-160. DOI: 10.17925 / EE.2014.10.02.157

15.Biondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev. 2008; 29 (1): 76-131. DOI: 10.1210 / er.2006-0043

16. Floriani C, Gencer B, Collet TH, Rodondi N. Subclinical thyroid dysfunction and cardiovascular diseases: 2016 update. Eur Heart J. 2018; 39 (7): 503-507. DOI: 10.1093 / eurheartj / ehx050

17.Mendes D, Alves C, Silverio N, Batel Marques F. Prevalence of Undiagnosed Hypothyroidism in Europe: A Systematic Review and Meta-Analysis. Eur Thyroid J. 2019; 8 (3): 130-143. DOI: 10.1159 / 000499751

18. Tekle HA, Bobe TM, Tufa EG, Solomon FB. Age-sex disparities and sub-clinical hypothyroidism among patients in Tikur Anbesa Specialized Hospital, Addis Ababa, Ethiopia. J Health Popul Nutr. 2018; 37 (1): 18. DOI: 10.1186 / s41043-018-0149-x

19. Surks MI, Ortiz E, Daniels GH, et al. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. JAMA. 2004; 291 (2): 228-238. DOI: 10.1001 / jama.291.2.228

20. Polikar R, Burger AG, Scherrer U, Nicod P. The thyroid and the heart. Circulation. 1993; 87 (5): 1435-1441.DOI: 10.1161 / 01.cir.87.5.1435

21. Kahaly GJ. Cardiovascular and atherogenic aspects of subclinical hypothyroidism. Thyroid. 2000; 10 (8): 665-679. DOI: 10.1089 / 10507250050137743

22. Tseng FY, Lin WY, Lin CC, et al. Subclinical hypothyroidism is associated with increased risk for all-cause and cardiovascular mortality in adults.J Am Coll Cardiol. 2012; 60 (8): 730-737. DOI: 10.1016 / j.jacc.2012.03.047

23. Nekrasova TA, Strongin LG, Morozova EP, et al. Modifying effect of subclinical hypothyroidism on the course of arterial hypertension: relationship with latent treatment ineffectiveness, daily blood pressure profile and the state of target organs. // Clinical and experimental thyroidology. – 2015. – T. 11. – No. 2.- S. 55-62. [Nekrasova TA, Strongin LG, Morozova EP, et al. Modifying influence of subclinical hypothyroidism on arterial hypertension: relationship to masked treatment failure, circadian blood pressure profile and target organs status. Clinical and experimental thyroidology. 2015; 11 (2): 55-62. (In Russ.)] DOI: 10.14341 / ket2015255-62

24. Owen PJ, Sabit R, Lazarus JH. Thyroid disease and vascular function.Thyroid. 2007; 17 (6): 519-524. DOI: 10.1089 / thy.2007.0051

25. Rodondi N, Bauer DC, Cappola AR, et al. Subclinical thyroid dysfunction, cardiac function, and the risk of heart failure. The Cardiovascular Health study. J Am Coll Cardiol. 2008; 52 (14): 1152-1159. DOI: 10.1016 / j.jacc.2008.07.009

26. Hak AE, Pols HA, Visser TJ, et al.Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Ann Intern Med. 2000; 132 (4): 270-278. DOI: 10.7326 / 0003-4819-132-4-200002150-00004

27. Bielecka-Dabrowa A, Godoy B, Suzuki T, et al. Subclinical hypothyroidism and the development of heart failure: an overview of risk and effects on cardiac function. Clin Res Cardiol.2019; 108 (3): 225-233. DOI: 10.1007 / s00392-018-1340-1

28. Dhital R, Poudel DR, Tachamo N, et al. Ischemic Stroke and Impact of Thyroid Profile at Presentation: A Systematic Review and Meta-analysis of Observational Studies. J Stroke Cerebrovasc Dis. 2017; 26 (12): 2926-2934. DOI: 10.1016 / j.jstrokecerebrovasdis.2017.07.015

29.Gong Y, Ma Y, Ye Z, et al. Thyroid stimulating hormone exhibits the impact on LDLR / LDL-c via up-regulating hepatic PCSK9 expression. Metabolism. 2017; 76: 32-41. DOI: 10.1016 / j.metabol.2017.07.006

30. Ebrahimpour A, Vaghari-Tabari M, Qujeq D, et al. Direct correlation between serum homocysteine ​​level and insulin resistance index in patients with subclinical hypothyroidism: Does subclinical hypothyroidism increase the risk of diabetes and cardio vascular disease together? Diabetes Metab Syndr.2018; 12 (6): 863-867. DOI: 10.1016 / j.dsx.2018.05.002

31. Sieminska L, Wojciechowska C, Walczak K, et al. Associations between metabolic syndrome, serum thyrotropin, and thyroid antibodies status in postmenopausal women, and the role of interleukin-6. Endokrynol Pol. 2015; 66 (5): 394-403. DOI: 10.5603 / EP.2015.0049

32.Altay S, Onat A, Can G, et al. High-normal thyroid-stimulating hormone in euthyroid subjects is associated with risk of mortality and composite disease endpoint only in women. Arch Med Sci. 2018; 14 (6): 1394-1403. DOI: 10.5114 / aoms.2016.63264

33. Gupta G, Sharma P, Kumar P, Itagappa M. Study on Subclinical Hypothyroidism and its Association with Various Inflammatory Markers. J Clin Diagn Res. 2015; 9 (11): BC04-06.DOI: 10.7860 / JCDR / 2015 / 14640.6806

34. Liu J, Duan Y, Fu J, Wang G. Association Between Thyroid Hormones, Thyroid Antibodies, and Cardiometabolic Factors in Non-Obese Individuals With Normal Thyroid Function. Front Endocrinol (Lausanne). 2018; 9: 130. DOI: 10.3389 / fendo.2018.00130

35. Chen Y, Zhu C, Chen Y, et al.Are Thyroid Autoimmune Diseases Associated with Cardiometabolic Risks in a Population with Normal Thyroid-Stimulating Hormone? Mediators Inflamm. 2018; 2018: 1856137. DOI: 10.1155 / 2018/1856137

36. Roifman I, Beck PL, Anderson TJ, et al. Chronic inflammatory diseases and cardiovascular risk: a systematic review. Can J Cardiol. 2011; 27 (2): 174-182. DOI: 10.1016 / j.cjca.2010.12.040

37.Xu C, Zhou L, Wu K, et al. Abnormal Glucose Metabolism and Insulin Resistance Are Induced via the IRE1alpha / XBP-1 Pathway in Subclinical Hypothyroidism. Front Endocrinol (Lausanne). 2019; 10: 303. DOI: 10.3389 / fendo.2019.00303

38. Brenta G, Caballero AS, Nunes MT. Case Finding for Hypothyroidism Should Include Type 2 Diabetes and Metabolic Syndrome Patients: A Latin American Thyroid Society (Lats) Position Statement.Endocr Pract. 2019; 25 (1): 101-105. DOI: 10.4158 / EP-2018-0317

39. Chang YC, Hua SC, Chang CH, et al. High TSH Level within Normal Range Is Associated with Obesity, Dyslipidemia, Hypertension, Inflammation, Hypercoagulability, and the Metabolic Syndrome: A Novel Cardiometabolic Marker. J Clin Med. 2019; 8 (6). Doi: 10.3390 / jcm8060817

40.Feller M, Snel M, Moutzouri E, et al. Association of Thyroid Hormone Therapy With Quality of Life and Thyroid-Related Symptoms in Patients With Subclinical Hypothyroidism: A Systematic Review and Meta-analysis. JAMA. 2018; 320 (13): 1349-1359. DOI: 10.1001 / jama.2018.13770

41. Andersen MN, Olsen AM, Madsen JC, et al. Levothyroxine Substitution in Patients with Subclinical Hypothyroidism and the Risk of Myocardial Infarction and Mortality.PLoS One. 2015; 10 (6): e0129793. Doi: 10.1371 / journal.pone.0129793

42. Andersen MN, Olsen AS, Madsen JC, et al. Long-Term Outcome in Levothyroxine Treated Patients With Subclinical Hypothyroidism and Concomitant Heart Disease. J Clin Endocrinol Metab. 2016; 101 (11): 4170-4177. DOI: 10.1210 / jc.2016-2226

43. Jasim S, Gharib H.Thyroid and Aging. Endocr Pract. 2018; 24 (4): 369-374. DOI: 10.4158 / EP171796.RA

44. Leng O, Razvi S. Hypothyroidism in the older population. Thyroid Res. 2019; 12: 2. DOI: 10.1186 / s13044-019-0063-3

45. Vigersky RA, Filmore-Nassar A, Glass AR. Thyrotropin suppression by metformin. J Clin Endocrinol Metab. 2006; 91 (1): 225-227.DOI: 10.1210 / jc.2005-1210

46. Lupoli R, Di Minno A, Tortora A, et al. Effects of treatment with metformin on TSH levels: a meta-analysis of literature studies. J Clin Endocrinol Metab. 2014; 99 (1): E143-148. DOI: 10.1210 / jc.2013-2965

47. Fournier JP, Yin H, Yu OH, Azoulay L. Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus.CMAJ. 2014; 186 (15): 1138-1145. Doi: 10.1503 / cmaj.140688

48 Distiller LA, Polakow ES, Joffe BI. Type 2 diabetes mellitus and hypothyroidism: the possible influence of metformin therapy. Diabet Med. 2014; 31 (2): 172-175. DOI: 10.1111 / dme. 12342

49. Nurcheshmeh Z, Aliasgarzadeh A, Bahrami A, Mobasseri M. The Effects of Metformin on Thyroid Function among Patients with Subclinical Hypothyroidism and Coexisting Metabolic Syndrome.Pharm Sci. 2018; 24 (2): 118-123. DOI: 10.15171 / ps.2018.18

50. Palui R, Sahoo J, Kamalanathan S, et al. Effect of metformin on thyroid function tests in patients with subclinical hypothyroidism: an open-label randomized controlled trial. J Endocrinol Invest. 2019; 42 (12): 1451-1458. Doi: 10.1007 / s40618-019-01059-w

51.Krysiak R, Szkrobka W, Okopien B. Sex-dependent effect of metformin on hypothalamic-pituitary-thyroid axis activity in patients with subclinical hypothyroidism. Pharmacol Rep. 2016; 68 (6): 1115-1119. DOI: 10.1016 / j.pharep.2016.07.002

52. Meng X, Xu S, Chen G, et al. Metformin and thyroid disease. J Endocrinol. 2017; 233 (1): R43-R51. DOI: 10.1530 / JOE-16-0450

53.Cetinkalp S, Simsir IY, Ertek S. Insulin resistance in brain and possible therapeutic approaches. Curr Vasc Pharmacol. 2014; 12 (4): 553-564. DOI: 10.2174 / 1570161112999140206130426

54. Wang B, Cheng KK. Hypothalamic AMPK as a Mediator of Hormonal Regulation of Energy Balance. Int J Mol Sci. 2018; 19 (11). DOI: 10.3390 / ijms19113552

55.Ruyatkina L.A., Ruyatkin D.S. The multifaceted effects of metformin in patients with type 2 diabetes. // Diabetes. – 2017. – T. 20. – No. 3. – S. 210-219. [Ruyatkina LA, Ruyatkin DS. Multidimensional effects of metformin in patients with type 2 diabetes. Diabetes mellitus. 2017; 20 (2): 210-219. (In Russ.)] DOI: 10.14341 / DM2003458-64

56. Cho K, Chung JY, Cho SK, et al. Antihyperglycemic mechanism of metformin occurs via the AMPK / LXRalpha / POMC pathway.Sci Rep. 2015; 5: 8145. DOI: 10.1038 / srep08145

57. Andrade BM, de Carvalho DP. Perspectives of the AMP-activated kinase (AMPK) signaling pathway in thyroid cancer. Biosci Rep. 2014; 34 (2). DOI: 10.1042 / BSR20130134

58. Piskovatska V, Stefanyshyn N, Storey KB, et al. Metformin as a geroprotector: experimental and clinical evidence.Biogerontology. 2019; 20 (1): 33-48. DOI: 10.1007 / s10522-018-9773-5

59. Dedov II, Shestakova MV, Mayorov A.Yu., et al. Algorithms of specialized medical care for patients with diabetes mellitus. / Ed. Dedova I.I., Shestakova M.V., Mayorova A.Yu. 9th edition. // Diabetes. – 2019. – T. 22. – No. S1. – S. 1-144. [Dedov II, Shestakova MV, Mayorov AY, et al. Dedov II, Shestakova MV, Mayorov AY, editors.Standards of specialized diabetes care. 9th ed. Diabetes mellitus. 2019; 22 (S1): 1-144. (In Russ.)] DOI: 10.14341 / DM221S1

60. Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over 15-year follow-up: the Diabetes Prevention Program Outcomes Study. Lancet Diabetes Endocrinol. 2015; 3 (11): 866-875. DOI: 10.1016 / s2213-8587 (15) 00291-0

61.Derosa G, D’Angelo A, Romano D, Maffioli P. Effects of metformin extended release compared to immediate release formula on glycemic control and glycemic variability in patients with type 2 diabetes. Drug Des Devel Ther. 2017; 11: 1481-1488. Doi: 10.2147 / dddt.s131670

62. rlsnet.ru [Internet]. Glucophage® long [accessed 25.04.2020]. Access by link: https://www.rlsnet.ru/tn_index_id_45613.htm. [Rlsnet.ru [Internet]. Glucophage® long [cited 2020 Apr 25]. Available from: https://www.rlsnet.ru/tn_index_id_45613.htm. (In Russ.)]

63. Mehran L, Amouzegar A, Azizi F. Thyroid disease and the metabolic syndrome. Current Opinion in Endocrinology & Diabetes and Obesity. 2019; 26 (5): 256-265. DOI: 10.1097 / med.0000000000000500

64.Chiovato L, Magri F, Carle A. Hypothyroidism in Context: Where We’ve Been and Where We’re Going. Adv Ther. 2019; 36 (Suppl 2): ​​47-58. DOI: 10.1007 / s12325-019-01080-8

65. Sui M, Yu Y, Zhang H, et al. Efficacy of Metformin for Benign Thyroid Nodules in Subjects With Insulin Resistance: A Systematic Review and Meta-Analysis. Front Endocrinol (Lausanne). 2018; 9: 494. DOI: 10.3389 / fendo.2018.00494

66.Yildirim Simsir I, Cetinkalp S, Kabalak T. Review of Factors Contributing to Nodular Goiter and Thyroid Carcinoma. Med Princ Pract. 2020; 29 (1): 1-5. DOI: 10.1159 / 000503575

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 is diagnosed with 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 . Long-term use of thyroxine 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.

Feline hypothyroidism – symptoms, treatment

Feline hypothyroidism is a type of endocrine disorder caused by a thyroid disorder that results in a deficiency of thyroid hormones in the bloodstream. Hypothyroidism is a rare endocrine disorder in cats.

In cats, the thyroid gland is a key component of a number of bodily processes and produces a number of different hormones. The two most well-known thyroid hormones are liothyronine (T3) and levothyroxine (T4). Both liothyronine and levothyroxine play a role in the metabolic function of the body.

When a cat suffers from hypothyroidism, there is a marked decrease in the level of thyroid hormones in the blood. Since less thyroid hormones are produced and distributed throughout the body, the metabolism slows down significantly.Some cats may have other complications caused by less secretion of thyroid hormones throughout the body.

Causes of hypothyroidism in cats

Feline hypothyroidism occurs:

1. Congenital hypothyroidism,

2. Spontaneous acquired hypothyroidism,

3. Iatrogenic hypothyroidism.

Feline congenital hypothyroidism

Causes disproportionate dwarfism and may result from agenesis or dysgenesis of the thyroid glands or from dyshormonogenesis.Disruption in the activity of thyroid peroxidase, leading to impaired organofixation of iodine, was noted in domestic short-haired cats and cats of the Abyssinian breed. With this type of hypothyroidism, goiter can be expected. In addition, the condition of hypothyroidism due to the inability of the thyroid gland to respond to thyroid-stimulating hormone (thyroid-stimulating hormone, TSH) is described in the Japanese cat family. These disorders, which cause congenital hypothyroidism, are usually inherited as an autosomal recessive trait.

Rare cases of hypothyroidism due to iodine deficiency have been reported in cats fed exclusively meat.

Feline spontaneous acquired hypothyroidism

Has been described in adult cats and is associated with lymphocytic thyroiditis, which is extremely rare.

Iatrogenic feline hypothyroidism

Iatrogenic hypothyroidism usually results from treatment for hyperthyroidism, and spontaneous hypothyroidism is much more common in cats. Iatrogenic hypothyroidism can develop as a result of bilateral thyroid resection, treatment with radioactive iodine, or drugs that suppress thyroid function.

Symptoms of feline hypothyroidism

Clinical signs of hypothyroidism can be overt or mild, depending on the nature of the metabolic disorder, which, like in humans, can be partial or complete.

Many affected kittens die before hypothyroidism is suspected. Most kittens look healthy up to 4 weeks, but by 4-8 weeks their growth slows down, signs of disproportionate dwarfism are observed: an enlarged wide head, short limbs and a short rounded body.They show signs of lethargy, mental retardation, such cats are less active compared to their littermates. Teeth are often underdeveloped and replacement of deciduous teeth can be delayed up to 18 months or older. There are signs of delayed closure of long bone ossification centers. The coat of kittens is represented mainly by the undercoat with a small amount of guard hair.

In hypothyroid cats, signs of the disease are changes in the skin (dry seborrhea, felting, unkempt appearance) along with lethargy, depression, bradycardia and hypothermia.The coat can easily be pulled out, and in places where the coat is trimmed, its re-regrowth is delayed. Alopecia may develop, and in some cats, hair falls out in the area of ​​the auricle.

Diagnosis of feline hypothyroidism

Initially, tests are carried out for standard hematological and biochemical parameters.

The level of hormones is assessed: total T4 and TSH. Also, tests with stimulation of TSH and a test with thyrotropin-releasing hormone are used.

Basal serum T4 is the best initial screening method for hypothyroidism in symptomatic cats.Typically, in hypothyroid cats, basal T4 concentrations are below the low end of the normal range, and sometimes undetectable. The concentration of T4 in the normal range allows to exclude the diagnosis of “hypothyroidism”, however, a low concentration does not in itself confirm hypothyroidism, since other diseases and drugs can lead to a decrease in the concentration of T4 to a level characteristic of hypothyroidism. If the history and clinical signs are consistent with the disease, the lower the T4, the higher the likelihood of true hypothyroidism in a cat.If the degree of suspicion of hypothyroidism on the clinical picture is not high enough, but the concentration of T4 is low, other factors are much more likely, such as diseases not related to the thyroid gland.

The TSH test has been successfully tested for use in cats. Although the sensitivity of the method is less than optimal, a high TSH concentration in a cat with a concomitant decrease in total T4 is a highly specific indicator of hypothyroidism. Elevated TSH levels have been reported in cats with congenital hypothyroidism, spontaneous adult hypothyroidism, and iatrogenic hypothyroidism.

The TSH challenge test is similar in dogs and cats, with the exception of a lower dose of recombinant human thyrotropin. The results of studies of the stimulation test with TSH gave reason to believe that this test is suitable for the diagnosis of hypothyroidism in cats, but this test is rarely used in clinical practice due to the high cost of recombinant human TSH.

The thyrotropin-releasing hormone assay is also recommended for the diagnosis of hypothyroidism in cats, but is rarely used for this purpose and has not been evaluated as a method for diagnosing hypothyroidism in cats.But if the results of the test with TSH stimulation were normal, but the result of the test with thyrotropin-releasing hormone was not, then this indicates pituitary dysfunction.

Diagnosis of hypothyroidism in cats should be based on a combination of history, clinical signs, physical findings, low serum thyroxine and elevated TSH levels. To identify changes that indicate hypothyroidism, and to assess the presence of other diseases, it is necessary to do basic laboratory tests: a clinical blood test, a biochemical blood test and a urinalysis.This is important because other diseases can affect the concentration of thyroid hormones, as well as the use of drugs (such as glucocorticoids).

Treatment of hypothyroidism in cats

Feline hypothyroidism can be temporary, which means it may disappear over time. An example is cats that develop hypothyroidism as a result of radioactive iodine therapy or surgery. It takes a while for their bodies to readjust and begin to regulate their thyroid hormone levels.Because feline hypothyroidism can be temporary, it may not require intervention or treatment. In some cases, hypothyroidism does not go away on its own. In these cases, the cat requires treatment throughout its life cycle.

For the treatment of hypothyroidism, replacement therapy is used in the form of a synthetic form of hormones. It often takes time to adjust the dosage of drugs because thyroid hormone levels can fluctuate and change over time. The veterinarian decides to adjust the dose of the drug throughout the cat’s life cycle depending on the cat’s physical condition and changes in thyroid hormone levels when the drugs are prescribed.

In cats receiving synthetic hormone replacement therapy to regulate thyroid function, symptoms of hypothyroidism usually resolve within a few months after starting treatment. Cats requiring daily thyroid hormone replacement therapy should be regularly examined by a healthcare professional and donated regularly for thyroid hormone levels. If the attending physician detects a change in the level of thyroid hormones, then he adjusts the dosage of the drugs.

The treatment plan for hypothyroid cats can be very difficult and intimidating. If the cat is diagnosed with hypothyroidism, which is not temporary and requires the appointment of replacement therapy and control of thyroid hormone levels, then the owner will need to adapt to the cat’s health.