How does vitamin D supplementation affect thyroid function in hypothyroid patients. What are the potential benefits of vitamin D for thyroid health. Can vitamin D deficiency contribute to thyroid disorders. Is there a link between vitamin D levels and autoimmune thyroid diseases.

The Relationship Between Vitamin D and Thyroid Function

Vitamin D plays a crucial role in various bodily functions, including the regulation of the thyroid gland. Recent studies have shed light on the intricate connection between vitamin D levels and thyroid health, particularly in patients with hypothyroidism. This complex relationship involves several mechanisms that influence thyroid hormone production, autoimmune responses, and overall thyroid function.

Research has shown that vitamin D receptors are present in thyroid tissue, suggesting a direct impact of this nutrient on thyroid physiology. Additionally, vitamin D has been found to modulate the immune system, which is particularly relevant in autoimmune thyroid conditions such as Hashimoto’s thyroiditis.

How does vitamin D influence thyroid hormone production?

Vitamin D affects thyroid hormone production through several pathways:

• Regulating the expression of genes involved in thyroid hormone synthesis
• Influencing the activity of enzymes responsible for converting T4 to the more active T3 hormone
• Modulating the sensitivity of thyroid hormone receptors

These mechanisms highlight the potential benefits of maintaining optimal vitamin D levels for thyroid health.

Prevalence of Vitamin D Deficiency in Hypothyroid Patients

Multiple studies have reported a high prevalence of vitamin D deficiency among patients with hypothyroidism. This association raises questions about whether low vitamin D levels contribute to the development of thyroid disorders or if thyroid dysfunction leads to impaired vitamin D metabolism.

A study by Mackawy et al. (2013) found that 61% of hypothyroid patients had vitamin D deficiency, compared to 36% in the control group. Similar findings have been reported in various populations worldwide, emphasizing the global nature of this issue.

Are certain populations at higher risk of vitamin D deficiency and thyroid disorders?

Several factors can increase the risk of both vitamin D deficiency and thyroid disorders:

1. Geographic location (higher latitudes with less sunlight exposure)
2. Age (older adults are more prone to vitamin D deficiency)
3. Skin pigmentation (darker skin reduces vitamin D synthesis)
4. Obesity (vitamin D can be sequestered in adipose tissue)
5. Certain medical conditions and medications

Understanding these risk factors can help healthcare providers identify individuals who may benefit from closer monitoring and potential supplementation.

The Impact of Vitamin D Supplementation on Thyroid Function

The effects of vitamin D supplementation on thyroid function have been the subject of several clinical trials. While results have been mixed, some studies have shown promising outcomes for hypothyroid patients.

A randomized, double-blind, placebo-controlled trial conducted by Chaudhary et al. (2016) found that vitamin D supplementation significantly reduced thyroid peroxidase antibody levels in patients with autoimmune thyroid disease. This suggests that vitamin D may help modulate the autoimmune response in conditions like Hashimoto’s thyroiditis.

What dosage of vitamin D is effective for improving thyroid function?

The optimal dosage of vitamin D supplementation for thyroid health remains a topic of ongoing research. However, most studies have used doses ranging from 2000 to 4000 IU daily. It’s important to note that individual requirements may vary, and supplementation should be guided by a healthcare professional based on serum vitamin D levels and overall health status.

Vitamin D and Autoimmune Thyroid Diseases

Autoimmune thyroid diseases, such as Hashimoto’s thyroiditis and Graves’ disease, have been linked to vitamin D deficiency. The immunomodulatory properties of vitamin D play a crucial role in this relationship.

A meta-analysis by Wang et al. (2015) found a significant association between vitamin D deficiency and an increased risk of autoimmune thyroid diseases. The study suggested that individuals with low vitamin D levels were more susceptible to developing these conditions.

How does vitamin D influence the immune system in thyroid autoimmunity?

Vitamin D affects the immune system in several ways that may impact thyroid autoimmunity:

• Modulating T-cell responses and reducing inflammatory cytokine production
• Enhancing the function of regulatory T-cells, which help maintain immune tolerance
• Influencing B-cell activity and antibody production
• Regulating the expression of genes involved in immune function

These mechanisms suggest that maintaining adequate vitamin D levels could potentially help prevent or manage autoimmune thyroid diseases.

Genetic Factors Linking Vitamin D and Thyroid Function

Genetic variations in vitamin D metabolism and signaling pathways may influence the relationship between vitamin D and thyroid function. Polymorphisms in the vitamin D receptor (VDR) gene have been associated with an increased risk of autoimmune thyroid diseases.

A meta-analysis by Feng et al. (2013) found that certain VDR gene polymorphisms were significantly associated with the risk of Graves’ disease and Hashimoto’s thyroiditis. These findings suggest that genetic factors may play a role in determining an individual’s susceptibility to thyroid disorders and their response to vitamin D.

Can genetic testing help identify individuals at risk of vitamin D-related thyroid issues?

While genetic testing for VDR polymorphisms is not routinely performed in clinical practice, it may offer insights into an individual’s risk profile in the future. As our understanding of the genetic factors influencing vitamin D metabolism and thyroid function grows, personalized approaches to prevention and treatment may become more feasible.

Vitamin D and Thyroid Cancer

The potential role of vitamin D in thyroid cancer has garnered increasing attention in recent years. Some studies have suggested that vitamin D may have protective effects against thyroid cancer development and progression.

Research by Roskies et al. (2012) found that vitamin D receptor expression was significantly lower in thyroid cancer tissue compared to normal thyroid tissue. This observation hints at a possible link between vitamin D signaling and thyroid cancer pathogenesis.

Does vitamin D supplementation reduce the risk of thyroid cancer?

While some observational studies have suggested a potential protective effect of vitamin D against thyroid cancer, definitive evidence from large-scale clinical trials is lacking. Further research is needed to determine whether vitamin D supplementation can effectively reduce thyroid cancer risk or improve outcomes in patients with thyroid malignancies.

Practical Implications for Patient Care

The growing body of evidence linking vitamin D to thyroid function has important implications for patient care. Healthcare providers should consider the following approaches:

• Routine screening of vitamin D levels in patients with thyroid disorders
• Addressing vitamin D deficiency through supplementation and lifestyle modifications
• Monitoring thyroid function in patients receiving high-dose vitamin D supplementation
• Educating patients about the potential benefits of maintaining optimal vitamin D levels for thyroid health

Should all hypothyroid patients receive vitamin D supplementation?

While vitamin D supplementation may benefit many hypothyroid patients, a one-size-fits-all approach is not recommended. Treatment decisions should be based on individual serum vitamin D levels, thyroid function tests, and overall health status. Patients should work closely with their healthcare providers to determine the most appropriate management strategy.

In conclusion, the relationship between vitamin D and thyroid function is complex and multifaceted. While current evidence suggests potential benefits of vitamin D supplementation for hypothyroid patients, particularly those with autoimmune thyroid diseases, more research is needed to fully elucidate the mechanisms involved and establish optimal treatment protocols. As our understanding of this intricate relationship continues to evolve, it may pave the way for more targeted and effective approaches to managing thyroid disorders.

The Effects of Vitamin D Supplementation on Thyroid Function in Hypothyroid Patients: A Randomized, Double-blind, Placebo-controlled Trial

1. Lee SM, Meyer MB, Benkusky NA, O’Brien CA, Pike JW. Mechanisms of Enhancer-mediated Hormonal Control of Vitamin D Receptor Gene Expression in Target Cells. J Biol Chem. 2015;290:30573–86. [PMC free article] [PubMed] [Google Scholar]

2. Agmon-Levin N, Theodor E, Segal RM, Shoenfeld Y. Vitamin D in systemic and organ-specific autoimmune diseases. Clin Rev Allergy Immunol. 2013;45:256–66. [PubMed] [Google Scholar]

3. Mangin M, Sinha R, Fincher K. Inflammation and vitamin D: The infection connection. Inflamm Res. 2014;63:803–19. [PMC free article] [PubMed] [Google Scholar]

4. Gouni-Berthold I, Krone W, Berthold HK. Vitamin D and cardiovascular disease. Curr Vasc Pharmacol. 2009;7:414–22. [PubMed] [Google Scholar]

5. Naeem Z. Vitamin d deficiency- an ignored epidemic. Int J Health Sci (Qassim) 2010;4:V–VI. [PMC free article] [PubMed] [Google Scholar]

6. Saki F, Dabbaghmanesh MH, Omrani GR, Bakhshayeshkaram M. Vitamin D deficiency and its associated risk factors in children and adolescents in southern Iran. Public Health Nutr. 2017;20:1851–6. [PubMed] [Google Scholar]

7. Holick MF, Chen TC. Vitamin D deficiency: A worldwide problem with health consequences. Am J Clin Nutr. 2008;87:1080S–6S. [PubMed] [Google Scholar]

8. Mackawy AM, Al-Ayed BM, Al-Rashidi BM. Vitamin d deficiency and its association with thyroid disease. Int J Health Sci (Qassim) 2013;7:267–75. [PMC free article] [PubMed] [Google Scholar]

9. Aljohani NJ, Al-Daghri NM, Al-Attas OS, Alokail MS, Alkhrafy KM, Al-Othman A, et al. Differences and associations of metabolic and vitamin D status among patients with and without sub-clinical hypothyroid dysfunction. BMC Endocr Disord. 2013;13:31. [PMC free article] [PubMed] [Google Scholar]

10. Yasuda T, Okamoto Y, Hamada N, Miyashita K, Takahara M, Sakamoto F, et al. Serum vitamin D levels are decreased and associated with thyroid volume in female patients with newly onset Graves’ disease. Endocrine. 2012;42:739–41. [PMC free article] [PubMed] [Google Scholar]

11. Li X, Wang G, Lu Z, Chen M, Tan J, Fang X. Serum 25-hydroxyvitamin D predict prognosis in radioiodine therapy of Graves’ disease. J Endocrinol Invest. 2015;38:753–9. [PubMed] [Google Scholar]

12. Chaudhary S, Dutta D, Kumar M, Saha S, Mondal SA, Kumar A, et al. Vitamin D supplementation reduces thyroid peroxidase antibody levels in patients with autoimmune thyroid disease: An open-labeled randomized controlled trial. Indian J Endocrinol Metab. 2016;20:391–8. [PMC free article] [PubMed] [Google Scholar]

13. Alrefaie Z, Awad H. Effect of vitamin D3 on thyroid function and de-iodinase 2 expression in diabetic rats. Arch Physiol Biochem. 2015;121:206–9. [PubMed] [Google Scholar]

14. Vilarrasa N, Vendrell J, Maravall J, Elio I, Solano E, San Jose P, et al. Is plasma 25(OH) D related to adipokines, inflammatory cytokines and insulin resistance in both a healthy and morbidly obese population? Endocrine. 2010;38:235–42. [PubMed] [Google Scholar]

15. Robien K, Butler LM, Wang R, Beckman KB, Walek D, Koh WP, et al. Genetic and environmental predictors of serum 25-hydroxyvitamin D concentrations among middle-aged and elderly Chinese in Singapore. Br J Nutr. 2013;109:493–502. [PMC free article] [PubMed] [Google Scholar]

16. G R, Gupta A. Vitamin D deficiency in India: Prevalence, causalities and interventions. Nutrients. 2014;6:729–75. [PMC free article] [PubMed] [Google Scholar]

17. Yamashita H, Noguchi S, Takatsu K, Koike E, Murakami T, Watanabe S, et al. High prevalence of vitamin D deficiency in Japanese female patients with Graves’ disease. Endocr J. 2001;48:63–9. [PubMed] [Google Scholar]

18. Wang J, Lv S, Chen G, Gao C, He J, Zhong H, et al. Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients. 2015;7:2485–98. [PMC free article] [PubMed] [Google Scholar]

19. Tamer G, Arik S, Tamer I, Coksert D. Relative vitamin D insufficiency in Hashimoto’s thyroiditis. Thyroid. 2011;21:891–6. [PubMed] [Google Scholar]

20. Feng M, Li H, Chen SF, Li WF, Zhang FB. Polymorphisms in the vitamin D receptor gene and risk of autoimmune thyroid diseases: A meta-analysis. Endocrine. 2013;43:318–26. [PubMed] [Google Scholar]

21. Meng S, He ST, Jiang WJ, Xiao L, Li DF, Xu J, et al. Genetic susceptibility to autoimmune thyroid diseases in a Chinese Han population: Role of vitamin D receptor gene polymorphisms. Ann Endocrinol (Paris) 2015;76:684–9. [PubMed] [Google Scholar]

22. Sar M, Stumpf WE, DeLuca HF. Thyrotropes in the pituitary are target cells for 1,25 dihydroxy vitamin D3. Cell Tissue Res. 1980;209:161–6. [PubMed] [Google Scholar]

23. Smith MA, McHenry C, Oslapas R, Hofmann C, Hessel P, Paloyan E. Altered TSH levels associated with increased serum 1,25-dihydroxyvitamin D3: A possible link between thyroid and parathyroid disease. Surgery. 1989;106:987–91. [PubMed] [Google Scholar]

24. Gross HA, Appleman MD, Jr, Nicoloff JT. Effect of biologically active steroids on thyroid function in man. J Clin Endocrinol Metab. 1971;33:242–8. [PubMed] [Google Scholar]

25. Kinuta K, Tanaka H, Moriwake T, Aya K, Kato S, Seino Y. Vitamin D is an important factor in estrogen biosynthesis of both female and male gonads. Endocrinology. 2000;141:1317–24. [PubMed] [Google Scholar]

Supplements and Thyroid Health: What to Know

Thyroid conditions, including hypothyroidism, hyperthyroidism, and thyroid cancer, are common. For example, up to 7% of the U.S. population has hypothyroidism, a condition in which your thyroid doesn’t produce enough thyroid hormones (1).

Depending on the type of disease, thyroid conditions are typically treated with medications like thyroid hormone replacement, surgery, and other procedures, such as radiation therapy for thyroid cancer.

In addition to conventional treatments for thyroid conditions, research shows that dietary interventions, including supplements, may help treat certain thyroid diseases.

However, certain supplements may do more harm than good when it comes to thyroid health.

This article explains how supplements may help certain people with thyroid-related health conditions.

If you walk down the supplement aisle of your favorite health food store, you’ll likely see a section dedicated to thyroid health.

Due to the prevalence of thyroid conditions, many supplement companies have started making supplements that are designed to “support thyroid health.”

Although some of these products are harmless, certain thyroid supplements may lead to negative side effects and can even harm your thyroid.

Before addressing why thyroid-specific supplements may not be the best choice for everyone, it’s important to explain what nutrients the thyroid needs for optimal functioning. Here are some of the most important nutrients for thyroid health:

• Selenium. Selenium, a mineral needed for thyroid hormone production, helps protect the thyroid from damage caused by oxidative stress. The thyroid contains high amounts of selenium, and a deficiency can lead to thyroid dysfunction (2).
• Iodine. Iodine is critical for thyroid function. In fact, currently, the only known role of iodine is to support thyroid hormone production. Triiodothyronine (T3) and thyroxine (T4) are thyroid hormones that contain iodine. Iodine deficiency causes thyroid disease (3, 4).
• Zinc. The mineral zinc is required for thyroid hormone production. An optimal concentration of zinc is needed for healthy levels of T3, T4, and thyroid-stimulating hormone (TSH) (5).
• Iron. The thyroid needs iron to convert T4 into T3, the active form of thyroid hormone. Iron deficiency is associated with thyroid dysfunction (6).

Other nutrients, including B vitamins and vitamins A and E, are also needed for optimal thyroid function. Being deficient in one or more nutrients can negatively affect thyroid health and increase your risk of thyroid disease (7, 8, 9, 10).

For most people, following a nutrient-dense diet rich in whole foods is enough to maintain optimal thyroid function.

However, certain populations may need to supplement their diet with vitamins, minerals, and other nutrients to maintain overall health, including the health of the thyroid.

These populations include people on restrictive diets, people who are pregnant or breastfeeding, and those who have a thyroid condition or other health issues.

Should you take thyroid-specific supplements?

There’s no doubt that a nutritious diet that provides optimal nutrient levels is important for maintaining thyroid health, nor that nutrient deficiencies can lead to thyroid issues.

Still, for people who don’t have thyroid issues and follow a well-balanced, nutrient-dense diet, there’s typically no need to take thyroid-specific supplements.

In fact, certain supplements marketed toward those looking to promote thyroid health may be dangerous to take.

For example, many thyroid supplements contain high amounts of iodine and may contain thyroid hormones. Taking these supplements can lead to dangerous side effects and create thyroid issues in people with healthy thyroid function (11).

One study that analyzed 10 thyroid supplements found that the majority of them contained detectable amounts of T3 and T4. Some of the products tested contained more T3 and T4 than healthcare providers typically prescribe to people with hypothyroidism (11).

Taking these supplements may lead to elevated thyroid hormone levels in the blood and cause symptoms of hyperthyroidism, which can lead to dangerous complications (12, 13, 14).

What’s more, excessive iodine intake from supplements may cause hypothyroidism in susceptible individuals (12, 13, 14).

Thyroid supplements may be unsafe for people who have thyroid conditions, too.

This is because people with thyroid issues have specific needs, and taking supplements marketed to enhance thyroid health may negatively affect thyroid function, causing their health and symptoms to worsen.

As such, people with and without thyroid conditions should avoid taking supplements marketed to promote thyroid health. Instead, work with a practitioner to come up with a healthy and safe plan that’s based on your specific needs and health status.

Summary

It’s a smart idea to stay away from dietary supplements marketed to improve thyroid health. These products can cause health issues in people with and without thyroid disease.

Hashimoto’s disease is the most common cause of hypothyroidism in the United States. It’s an autoimmune disease in which the immune system produces antibodies that attack the thyroid, causing fibrosis or scarring of the thyroid tissue (15).

Hashimoto’s disease is associated with a variety of symptoms, including weight gain, fatigue, hair loss, anemia, constipation, cold intolerance, joint pain, dry skin, mood changes, difficulty concentrating, and more (15).

In addition to medication, diet and lifestyle modification can help reduce thyroid damage and improve symptoms and overall quality of life in people with Hashimoto’s.

Plus, people with Hashimoto’s disease are more likely to be deficient in certain nutrients, which can worsen Hashimoto’s-related symptoms.

Studies show that the following supplements can be beneficial for those with Hashimoto’s disease:

• Selenium. Studies have shown that supplementing with 200 mcg of selenium per day may help decrease thyroid antibodies and improve mood in people with Hashimoto’s (16, 17).
• Myo-Inositol. Inositol is a type of sugar that plays an important role in thyroid function. Some evidence suggests that daily treatment with 600 mg of Myo-Inositol and 83 mcg of selenium may help improve thyroid function in people with Hashimoto’s (18, 19).
• Zinc. Zinc is needed for thyroid hormone production, and a deficiency can result in hypothyroidism. When used alone or in combination with selenium, 30 mg of zinc per day may help enhance thyroid function in people with Hashimoto’s disease (20, 21).
• Vitamin B12. Vitamin B12 deficiency is common in people with Hashimoto’s disease. Taking a B12 or B complex supplement can help prevent and treat deficiency, as well as maintain optimal B12 levels (22, 23).
• Magnesium. A magnesium deficiency may increase your risk of developing Hashimoto’s disease and is associated with elevated thyroid antibody levels. Correcting magnesium deficiency may improve Hashimoto’s symptoms (24, 25).
• Iron. Many women with Hashimoto’s disease have low iron levels or iron deficiency anemia. Anemia negatively affects thyroid function. An iron supplement may be necessary to restore iron to optimal levels (26).
• Vitamin D. People with Hashimoto’s disease are more likely to be deficient in vitamin D than the general population, and vitamin D deficiency can have an adverse effect on thyroid function (22, 27).
• Curcumin. Curcumin may help protect your thyroid against oxidative damage. Plus, taking curcumin alongside other anti-inflammatory compounds may help reduce the size of thyroid nodules, which are common in Hashimoto’s disease (28, 29).
• Vitamin C. Research suggests that taking a vitamin C supplement may help reduce thyroid antibodies in people with Hashimoto’s disease (30).

Other supplements may help people with Hashimoto’s as well. However, the supplements above have the most research to support their use in the management of Hashimoto’s disease.

Summary

Research suggests that certain supplements, including selenium, zinc, iron, and vitamins D and B12, may be beneficial for people with Hashimoto’s disease.

Graves’ disease is the most common cause of hyperthyroidism in the United States. Like Hashimoto’s disease, it’s considered an autoimmune condition.

In Graves’ disease, the immune system attacks your thyroid, causing it to overproduce thyroid hormones. Graves’ disease can also lead to thyromegaly or an enlarged thyroid (31).

Symptoms associated with Graves’ disease include weight loss, heart palpitations, shortness of breath, diarrhea, eye pain and irritation, fatigue, weakness, menstrual irregularities, insomnia, nervousness, and more (32).

Current treatment of Graves’ disease includes surgery, medication, and radioactive iodine therapy (RAI) (32).

Like Hashimoto’s disease, some research shows that dietary modifications may help improve symptoms and quality of life in people with Graves’ disease (33).

The following supplements may help people with Graves’ disease:

• Selenium. Selenium deficiency can raise your risk of Graves’ disease. A review found selenium supplements in daily dosages of 100–300 mcg led to improved thyroid function at 6 months in people with Graves’ disease, but this effect was lost at 9 months (34).
• Vitamin D. Research shows that people with Graves’ disease are more likely to be deficient in vitamin D than the general population. Correcting deficiency by taking a supplement may improve thyroid function (35, 36, 37).
• L-carnitine. Research has found that hyperthyroidism depletes your body’s stores of carnitine, which plays a critical role in energy production. Taking L-carnitine may help reduce symptoms and improve quality of life in people with hyperthyroidism (38, 39).
• Vitamin B12. People with Graves’ disease are at a greater risk of developing a vitamin B12 deficiency. Taking a high quality B12 or B complex supplement can help maintain healthy B12 levels (40, 41, 42).

Other supplements may help people with Graves’ disease. Work with a knowledgeable healthcare practitioner to develop a supplement regimen that’s right for you.

Summary

According to research, vitamin D, selenium, L-carnitine, and vitamin B12 may help people with Graves’ disease.

Thyroid cancer is considered a rare type of cancer, accounting for just 1–4% of all cancers in the United States. Cancers that stem from follicular cells in the thyroid account for up to 95% of all thyroid cancers (43).

Treatment for thyroid cancer includes surgical resection, radiation therapy, thyroid-stimulating hormone (TSH) suppression, radioactive iodine (RAI) therapy, total thyroidectomy, and palliative care management for untreatable thyroid cancer.

In addition to traditional treatment, diet, supplements, and lifestyle modifications may enhance treatment outcomes and improve quality of life in people with thyroid cancer.

Some animal and test-tube research suggests that omega-3 fats, curcumin, L-carnitine, quercetin, melatonin, resveratrol, selenium, inositol, zinc, and vitamins C, E, A, and D may benefit those with thyroid cancer (44, 45, 46).

Additionally, low iodine intake is linked to an increased risk of thyroid cancer, and research suggests that correcting iodine deficiency can help protect against the development of more aggressive forms of thyroid cancer (47).

However, although many of these nutrients, including vitamin D and selenium, are known to have anticancer effects, there’s currently a lack of human studies investigating the effects of these dietary supplements in people with thyroid cancer (47, 48).

Therefore, more studies are needed before these supplements can be routinely recommended for people with thyroid cancer (47, 49).

The best way to determine the best supplement regimen for your specific needs is to consult your healthcare provider.

Oftentimes, either your healthcare provider or a registered dietitian that specializes in oncology nutrition will recommend supplements depending on your diet, overall health, and what treatments you’re currently undergoing for thyroid cancer.

Summary

Although research suggests that some supplements may benefit people with thyroid cancer, human research is lacking. To ensure your safety, it’s best to check with your medical provider before taking any supplements.

As mentioned above, it’s best to avoid thyroid-specific supplement blends unless they’re specifically recommended by your healthcare provider.

Taking these supplements can harm your thyroid and lead to a thyroid condition (11, 12, 13, 14).

Still, there are many vitamins, minerals, and other dietary supplements that have been shown to improve thyroid function, reduce disease symptoms, and improve overall quality of life in people with thyroid disease.

For people who have Hashimoto’s disease, Graves’ disease, thyroid cancer, or other condition that affects the thyroid gland, it’s best to work with a qualified healthcare provider who specializes in thyroid conditions.

This is especially important if you’re currently taking medications. Many supplements, especially herbal products, have the potential to interact with commonly prescribed medications and may lead to dangerous side effects.

Lastly, it’s important to always purchase supplements from trusted brands that independently test their products for quality and purity using organizations like USP and NSF International.

Summary

If you’re interested in taking supplements to treat a thyroid condition, it’s important to work with a qualified healthcare provider. They can help you choose supplements based on your specific needs and health status.

Research shows that some vitamins, minerals, and other nutrients may benefit people with certain thyroid conditions.

However, it’s important to develop a supplement regimen based on your specific needs and health issues.

If you’re interested in treating a thyroid condition with supplements, it’s important to work with a qualified healthcare provider to ensure safety and effectiveness.

Useful supplement shopping guides

Check out these two articles to help make supplement shopping a breeze:

• How to Choose High Quality Vitamins and Supplements
• How to Read Supplement Labels Like a Pro

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Hypothyroid coma – modern approaches to diagnosis and treatment | Petunina N.A.

Hypothyroid coma (HC) is an urgent, extremely severe complication of long-term uncompensated hypothyroidism, in which mortality reaches 50–80%. Doctors of various specialties are often not ready for timely diagnosis and adequate treatment of GC. Hypothyroid coma is a complication of any form of hypothyroidism, but is much more common in primary hypothyroidism. Data on the frequency and prevalence of GC are scarce. Thus, a survey of 800 medical centers in Germany over a two-year period revealed 24 cases of HC, while the average age of patients was 73 years. Myxedema coma was first described in 1879.d. It was not until 60 years later that a second case of her was reported in the literature. Approximately 300 deaths from coma have been described in the literature to date; thus, although this complication is currently quite rare, it is important to be able to recognize it due to its high mortality. The vast majority of patients had undiagnosed primary hypothyroidism, and only one had secondary hypothyroidism.

Reasons for the development of
Since hypothyroidism is 8 times more common in women than in men, the majority of patients with HC are women in the last decade of life. Acute decompensation of long-term hypothyroidism usually develops under the influence of provoking factors that exacerbate severe thyroid insufficiency. The most common provoking factors of GC are hypothermia, intoxication, trauma, anesthesia, surgical interventions, anesthesia, bleeding, as well as infectious diseases, hypoxic conditions, alcohol consumption and stressful situations. Other causes of GC are inadequate treatment of hypothyroidism, a sharp reduction in the daily dose, or discontinuation of thyroid hormone (TG). The development of GC is provoked by such severe concomitant diseases as myocardial infarction and cerebral stroke. In the elderly, pneumonia and sepsis are common causes of HC. Pneumonia can be primary, or develop against the background of stroke or aspiration. In some cases, especially in elderly patients, its development is facilitated by long-term use of drugs that depress the central nervous system (phenothiazines, tranquilizers, barbiturates, antihistamines), as well as amiodarone, lithium preparations, diuretics and b-blockers. More detailed provoking factors are presented in table 1.
Reasons for late diagnosis
In most cases, HC is difficult and late to diagnose, since long-term hypothyroidism often does not have clear clinical manifestations and proceeds under the guise of other diseases. Late diagnosis of hypothyroidism is mainly due to the gradual development of clinical symptoms, each of which is not specific in itself. Separate dominant symptoms of hypothyroidism with minimal severity or absence of characteristic manifestations are evaluated by practitioners as signs of another independent disease. Since GC is more common in female and elderly patients, mainly in the cold season, the clinical symptoms of the disease are perceived as natural age-related changes in the body. In addition, the paucity of subjective data, indistinct manifestations of hypothyroidism, and polymorbidity, characteristic of elderly patients, also do not allow a correct diagnosis to be established in a timely manner. It is extremely difficult to diagnose GC even in the absence of anamnestic information about hypothyroidism. It is also problematic to diagnose cases of HC with an atypical course. One of the variants of the atypical clinical picture of decompensated hypothyroidism is myxedematous delirium, the so-called insane myxedema, which manifests itself as acute psychosis against the background of severe memory and thinking disorders. The literature describes a clinical case when GC proceeded under the guise of a stem stroke. A rare variant of the course of GC is a condition resembling neurogenic, roto-pharyngeal dysphagia.
Clinical picture
The development of GC is preceded by a pre-coma, when all the symptoms of hypothyroidism are sharply aggravated. The severity of clinical manifestations, as a rule, occurs gradually over several weeks or months. The main manifestations of severe hypothyroidism are present: dry skin, sparse hair, hoarse voice, periorbital edema and dense swelling of the extremities, macroglossia and slowing of deep tendon reflexes, hypothermia. In addition to hyponatremia and hypoglycemia, clinical and biochemical blood tests may show anemia, hypercholesterolemia, high serum LDH and creatine kinase concentrations.
If it is possible to obtain information about the patient’s previous treatment, we will find indications of a previous thyroid disease, radioiodine therapy, thyroidectomy, or thyroid hormone therapy that was unreasonably interrupted.
Thus, a physical examination will show us a postoperative scar on the neck from a thyroidectomy, a non-palpable thyroid gland, or the presence of a goiter. Much less often (in about 5% of cases) the cause of GC is pituitary or hypothalamic origin. In one of the observations, a combination of two causes of HC was noted – primary thyroid and pituitary insufficiency due to Sheehan’s syndrome. Of the 24 patients seen in Germany, 23 had primary hypothyroidism and one had central hypothyroidism. Patients were observed: hypoxia in 80%, hypercapnia in 54% and hypothermia with t°<35°C in 88%. 6 patients (25%) died despite thyroid hormone treatment.
GC is characterized by increasing depression of the central nervous system from lethargy and disorientation to coma. Specific clinical symptoms of HC are impaired tolerance to cold, hypothermia (rectal temperature less than 36°C), although with concomitant pathology, subfebrile temperature, severe mucinous edema of the face and extremities, and characteristic hypothyroid changes in the skin may occur. Hypothermia is present in almost all patients and can be really deep (less than 26°C). In many case histories presented, hypothermia was the key (first clinical) symptom in the diagnosis of HC. The main criterion for the effectiveness of therapy and the prognosis of survival was body temperature. The worst prognosis was in patients with rectal t° less than 33°C.
Other symptoms are increasing drowsiness, lack of verbal contact, and hyporeflexia. Severe cardiovascular insufficiency is characterized by progressive bradycardia and arterial hypotension. Typical cardiovascular signs of HC, like hypothyroidism, include nonspecific ECG changes, cardiomegaly, bradycardia, and reduced cardiac contractility. Decreases in stroke and cardiac output are associated with decreased cardiac contractility, but overt heart failure was uncommon. Cardiac enlargement may be due to ventricular dilatation or pericardial effusion. Hypotension may be present due to a decrease in blood volume and may be refractory to treatment with vasopressors if thyroid hormones are not given.
Changes in the respiratory organs are manifested by a decrease in respiration, alveolar hypoventilation with hypercapnia, which, together with a deterioration in cerebral blood flow, aggravate cerebral hypoxia. Impaired respiratory muscle function and obesity can further exacerbate hypoventilation. Inhibition of respiratory function leads to alveolar hypoventilation and progression of hypoxemia, and, as an extreme manifestation, to hypercapnic anesthesia and coma. Although there is a multifactoriality in the development of coma, depression of the respiratory center, supported by hypercapnia, seems to be the principal factor. Most patients require mechanical ventilation, regardless of the cause of hypoventilation. Respiratory function can also be impaired due to pleural effusion or ascites, decreased lung volume, macroglossia, and edema (myxedema) of the nasopharynx and pharynx, which reduce the efficiency of airway conduction. Even after the start of thyroid hormone therapy, mechanical ventilation should continue.
A characteristic sign of HC is hypothyroid polyserositis with accumulation of fluid in the pleural, pericardial and abdominal cavities. Often there is acute urinary retention and rapid dynamic or mechanical intestinal obstruction, gastrointestinal bleeding is not uncommon. The course of GC may be complicated by severe hypoglycemia. Without adequate treatment, there is a further drop in body temperature and blood pressure, a decrease in respiration and heart rate, hypercapnia and hypoxia increase, a decrease in myocardial contractility and oliguria progress. Patients may experience bladder atony with acute urinary retention. Hypoxia of the brain is accompanied by dysfunction of the vital centers of the central nervous system, seizures may develop. The immediate cause of death is usually progressive cardiovascular and respiratory failure.
In rare cases, long-term undiagnosed severe hypothyroidism may present with mental disorders, including thought disorders, personality changes, neurosis, and psychosis. Often such patients are first observed by psychiatrists. Among patients in psychiatric clinics, the frequency of hypothyroidism reaches 3%.
Decompensation of severe hypothyroidism is accompanied by various cognitive impairments, including attention, concentration, memory, orientation, and perception, progressing against the background of an increasing deficiency of thyroid hormones. In the future, against the background of severe drowsiness, confusion develops. Rarely, there are acute psychoses that do not have specific features that can mimic paranoid or affective psychosis. In these cases, patients with HC are often misdiagnosed with mental illness. At the same time, a combination of myxedematous coma and mental illness is possible.
Diagnostics
Diagnosis and treatment of emergency conditions should be carried out at an earlier stage of CNS dysfunction, when their inhibition has not yet reached the limit. GC causes profound changes in electrolyte metabolism, which is one of the specific diagnostic features. In all cases of coma with hyponatremia, GC should be excluded. Laboratory diagnostic signs of GC include: hyponatremia, hypochloremia, hypoglycemia, increased levels of creatinine, creatinine phosphokinase, transaminases and lipids, hypoxia, hypercapnia, anemia and leukopenia. An ECG study reveals sinus bradycardia, low wave voltage, T-wave depression and inversion, and ST-segment depression. The presence of reasonable suspicion is the basis for the immediate initiation of thyroid hormone therapy, without waiting for the results of the analysis of serum TSH and free thyroxine (T4). Even in the presence of the previously mentioned disorders characteristic of GC, such as hypothermia, hypoventilation and hyponatremia in debilitated, somnolent or comatose patients, the diagnosis must be justified, appropriate tests must be taken and sent to the laboratory, after which therapy is initiated. Although in most patients, the clinical manifestations may be so obvious that serum TSH and T4 tests are only necessary to confirm the diagnosis.
Today, in most clinics, both hormones can be determined within an hour or, if necessary, on an emergency basis. Although a significant increase in serum TSH may be expected, patients with severe non-thyroidal systemic disease may exhibit a phenomenon similar to the “euthyroid pathology” syndrome, which may mimic the hypothyroid syndrome. Under these circumstances, TSH secretion is reduced and blood levels may not be as high as expected. As noted earlier, approximately 5% of cases of HC developed on the basis of central hypothyroidism and could be accompanied by normal or reduced serum TSH levels. Regardless of whether there is primary or secondary thyroid insufficiency, all patients with GC have low serum levels of total and free T4 and triiodothyronine (T3). In patients with euthyroid pathology syndrome, serum T3 levels may be unusually low (25 ng / ml).
Treatment
Therapy with thyroid hormones alone without correcting all other metabolic disorders, which was previously prescribed, is inadequate for recovery. Due to the potentially high mortality in the absence of vigorous complex therapy, all patients should be placed in an intensive care unit (ICU), where careful monitoring of pulmonary and cardiac status, CVP and pulmonary artery pressure should be carried out.
Significant difficulties in the treatment of GC are primarily due to the critical severity of the patient’s condition. Treatment of GC is carried out taking into account the state of the cardiovascular system due to the high sensitivity of the myocardium to TG, and concomitant diseases. Oxygen therapy is carried out, if necessary, tracheal intubation and artificial ventilation of the lungs, which contributes to the elimination of respiratory acidosis.
Urgent therapeutic measures for GC include the appointment of TG and glucocorticoids. Treatment is carried out under the control of body temperature (preferably rectal), respiratory rate, pulse, blood pressure, mental status. The introduction of glucocorticoids precedes or is carried out simultaneously with TG. Intravenous and oral routes of TG administration are possible. The intravenous route of administration is accompanied by a rapid increase in TG levels (on average after 3-4 hours) to subnormal levels, followed by a slow increase over 5-7 days. In domestic practice, there are no preparations of thyroid hormones for intravenous administration. Oral use of levothyroxine, despite a slow increase in TG levels with a long-term maintenance of them at the hypothyroid level, causes a clinical response after 24-72 hours. Absorption of L-T4 when administered orally is variable, but the clinical response develops quickly, even with myxedematous ileus. Intensive intravenous L-T4 therapy in the first hours (100-500 mcg, for 1 hour) dramatically reduces mortality. During the first day, L-T4 is administered intravenously, at a dose of 300-1000 mcg / day, then maintenance doses are used – 75-100 mcg / day. With the improvement of the patient’s well-being with the possibility of self-administration of the drug, a transition to its oral administration is carried out. Euthyrox is a levothyroxine preparation with a wide range of dosages: 25, 50, 75, 100, 125 and 150 mcg. Euthyrox therapy improves the quality of treatment: to ensure accurate dose selection and, accordingly, better compensation for hypothyroidism.
The convenience of taking the drug, the absence of the need to divide the tablets increases the adherence of patients to treatment, which is especially important when taking the drug for life, improves the quality of life and creates convenience for patients.
Normalization of metabolic processes during replacement therapy with Euthyrox compensates for the deficiency of thyroid hormones, normalizes elevated TSH levels, restores physical and mental activity, and prevents the adverse effects of a decrease in thyroid hormones on human health. The presence of a wide range of different dosages of the drug not only increases the accuracy of the dosage of levothyroxine and improves the degree of compensation for the disease, but also creates convenience for patients and improves their quality of life.
In the absence of L-T4 solutions for parenteral administration, which makes emergency therapy difficult, the drug is administered through a gastric tube. Due to the delayed clinical effects of L-T4, during the first day it is possible to administer L-triiodothyronine (L-T3) in small doses (20-40 mcg) intravenously or through a gastric tube (100 mcg initially, then 25-50 mcg every 12 hours), given the faster metabolic and CNS effects. In addition, there is an opinion that GC is accompanied by a pronounced violation of the peripheral conversion of thyroxine into metabolically active triiodothyronine. However, intravenous administration of the drug is dangerous due to the significant risk of severe cardiovascular complications, which led to the withdrawal of T3 preparations for intravenous administration. It should be emphasized that the more severe the patient’s condition, the lower initial doses of triglycerides should be used. The presence of coronary artery disease in a patient is a contraindication for the use of L-T3, and in this situation, small doses of L-T4 (50-100 mcg / day) are prescribed.
Intravenous drip is administered 200-400 mg / day. water-soluble hydrocortisone (fractionally, every 6 hours). After 2-4 days, depending on the dynamics of clinical symptoms, the dose of glucocorticoids is gradually reduced. Particular attention is paid to anti-shock measures, plasma substitutes, 5% glucose solution are introduced. The introduction of fluid is carried out in a volume of not more than 1 liter per day in order to avoid overloading the myocardium and increasing hyponatremia. Hyponatremia is eliminated as the concentration of triglycerides increases. With hypoglycemia, 20-30 ml of a 40% glucose solution is administered.
Rapid warming of the patient is contraindicated due to the deterioration of hemodynamics due to rapid peripheral vasodilation with the development of collapse and arrhythmias. Passive warming is recommended (increasing the room temperature by 1 degree per hour, wrapping in blankets). The appointment of sedatives should be avoided even when the patient is agitated, which is stopped by TH replacement therapy. In the future, infectious and other concomitant diseases that caused decompensation of hypothyroidism are treated. With concomitant infection, antibiotic therapy is carried out. The course of GC and its therapy can be complicated by the development of arrhythmias, myocardial infarction and severe heart failure.
Conclusions
Hypothyroid coma is the most severe manifestation of decompensated hypothyroidism and is often fatal despite treatment. Decompensation of hypothyroidism to coma can be triggered by various drugs, systemic diseases, and other causes. It usually develops in older women during the winter season and is combined with manifestations of hypothyroidism, such as hypothermia, hyponatremia, hypercapnia and hypoxia. Treatment should begin urgently in the intensive care unit or intensive care unit. Although thyroid hormone therapy is life-threatening, it is clearly necessary and is done with T4, T3, or a combination. Additional measures, such as mechanical ventilation, rewarming, fluid therapy, antibiotics, vasopressors, and corticosteroids, may be very important for the success of treatment.

Literature
1. Benfar G, de Vincentiis M. Postoperative airway obstruction: a complication of a previously undiagnosed hypothyroidism. Otolaryngol Head Neck Surg 2005;132:343–4.
2. Chernow B, Burman KD, Johnson DL, et al. T3 may be a better agent than T4 in the critically ill hypothyroid patient: evaluation of transport across the blood–brain barrier in a primate model. Crit Care Med 1983;11:99–104.
3. Cullen MJ, Mayne PD, Sliney I. Myxoedema coma. Ir J Med Sci 1979;148:201-6.
4. Fliers E, Wiersinga WM. Myxedema coma. Rev Endocr Metabol Disord 2003;4:137–41.
5. Hylander B, Rosenqvist U. Treatment of myxoedema coma: factors associated with fatal outcome. Acta Endocrinol (Copenh) 1985;108:65–71.
6. MacKerrowSD, Osborn LA, Levy H, et al. Myxedema–associated cardiogenic shock is treated with intravenous triiodothyronine. Ann Intern Med 1992;117:1014–5.
7. Mathes D.D. Treatment of myxedema coma for emergency surgery. Anesth Analg 1997;85: 30–6.
8. Nicoloff JT, LoPresti JS. Myxedema coma: a form of decompensated hypothyroidism. Endocrinol Metab Clin North Am 1993;22:279–90.
9. Reinhardt W, Mann K. Incidence, clinical picture, and treatment of hypothyroid coma: results of a survey. MedKlin 1997;92:521–4.
10. Ringel MD. Management of hypothyroidism and hyperthyroidism in the intensive care unit. Crit Care Clin 2001;17:59–74.
11. Rodriguez I, Fluiters E, Perez-Mendez LF, et al. Factors associated with mortality of patients with myxoedema coma: prospective study in 11 cases treated in a single institution. J Endocrinol 2004;180:347–50.
12. Turhan NO, Kockar MC, Inegol I. Myxedematous coma in a laboring woman suggested a pre-eclamptic coma: a case report. Acta Obstet Gynecol Scand 2004;83:1089–91.
13. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Phys 2000;62:2485–90.
14. Wartofsky L. Myxedema Coma. A Department of Medicine, Washington Hospital Center, Washington, DC 20010–2975, USA, 2005
15. Yamamoto T, Fukuyama J, Fujiyoshi A. Factors associated with mortality of myxedema coma: report of eight cases and literature survey. thyroid 1999;9:1167–74.
16. Yamamoto T. Delayed respiratory failure during the treatment of myxedema coma. Endocrinol Jpn 1984;31:769–75.
17. Zwillich CW, Pierson DJ, Hofeldt FD, et al. Ventilatory control in myxedema and hypothyroidism. N Engl J Med 1975;292:662–5.

Neurovitan in complex treatment and rehabilitation of patients with hypothyroidism

Hypothyroidism is one of the most common diseases of the endocrine system. According to various authors, the prevalence of overt hypothyroidism in the general population ranges from 3 to 8%, and taking into account subclinical forms, from 10 to 12%, and in recent years there has been a steady increase in this pathology in young and middle-aged people [1–4] . According to the Institute of Endocrinology. V.P. Komissarenko of the Academy of Medical Sciences of Ukraine, the prevalence of hypothyroidism in recent years continues to grow in 2009amounted to 174. 6 per 100 thousand population, an increase of 8.4% compared to 2000.

The medical and social significance of hypothyroidism is determined not only by its high prevalence and a tendency to a further increase in the number of patients, but also by the fact that thyroid hypofunction leads to various organ and neuropsychic disorders, a decrease in the intellectual potential of the population and impaired reproductive function in women [5 ]. Neurological symptoms in most cases constitute the core of the clinical picture of hypothyroidism [6]. The gradual increase in the symptoms of this disease, which accompanies the deterioration of the general condition of patients, leads to a decrease in their ability to work and causes early disability. Thus, our analysis [7] of medical expert documentation of 1160 patients and disabled people showed an increase in the rates of primary and acquired disability due to hypothyroidism, especially postoperative.

Changes in the central and peripheral nervous system have become the main disabling factors in these patients. It is known that thyroid hormones are essential for the development and maturation of the CNS, their deficiency is accompanied by a delay in physical and mental development and severe neurological defects [5]. Neuropathic symptoms also develop, which are detected in most patients and clinically occur in the form of distal paresthesia, painful dysesthesia, mono-, polyneuropathy and neuropathy of individual cranial nerves.

The pathogenesis of neurological disorders in patients with hypothyroidism is based on a deficiency of thyroid hormones. The latter leads to disruption of the synthesis of neurotransmitters, an increase in the level of blood lipids, a decrease in the energy potential of cells, activation of oxidative processes, a decrease in the synthesis of nitric oxide, and endothelial dysfunction [6]. Restoration of disturbed metabolic processes in hypothyroidism should first of all be carried out against the background of adequate hormone replacement therapy. But, as studies have shown, even with complete compensation of hypothyroidism with thyroxine, it is not possible to achieve complete recovery of certain neurological changes [8, 9]. That is why, over the past years, alpha-lipoic acid derivatives and B vitamins have been widely used in the treatment of polyneuropathies of various origins. Among the latter, Neurovitan should be singled out. It has proven itself in the complex treatment of polyneuropathies in diabetes mellitus [8, 10], subacute inflammatory demyelinating polyneuropathies [11], in obstetric and gynecological practice, dermatology, psychiatry, and neurological diseases. The uniqueness of Neurovitan lies in the fact that one tablet of this drug contains octothiamine (vitamin B1 + lipoic acid) – 25 mg, vitamin B2 (riboflavin) – 2.5 mg, vitamin B6 (pyridoxine) – 40 mg, vitamin B12 (cyanocobalamin) – 250 mcg. Due to the special form (the vitamins are in microgranules), the vitamins included in the preparation do not interact with each other and are well absorbed in the intestines. The pharmacodynamic effect of these vitamins is ensured by the fact that they participate as coenzymes in most metabolic processes, including energy-forming ones.

Thus, thiamine in the nervous system is involved in the synaptic transmission of nerve impulses, affecting the release of acetylcholine from nerve cells, and has anticholinesterase activity. This mechanism causes an increase in neuromuscular conduction. Thiamine also has the ability to reduce the toxicity of elevated glucose levels in diabetes mellitus. It is based on a decrease in the formation of glycosylation products of proteins, lipids, nucleic acids, activation of the pentose cycle of tricarboxylic acids, which inhibits the development of microangiopathy and neuropathy in diabetes mellitus.

Octothiamin is a combined substance that includes thiamine and thioctic acid. Thiamine and lipoic acid are formed from octothiamine during metabolism in the body. The latter regulates carbohydrate and fat metabolism, cholesterol metabolism, improves the detoxification function of the liver in various intoxications. The presence of SH-groups in lipoic acid determines the antioxidant effect of this drug, leads to a decrease in the level of pyruvic acid.

Riboflavin takes part in the redox processes of the nervous system, regulates the metabolism of carbohydrates, proteins, fats, is necessary for the activation of pyridoxine and tryptophan, and ensures the safety of red blood cells.

Pyridoxine is directly involved in protein metabolism, amino acid synthesis and transport, lipid metabolism, energy production in the body. It stimulates the synthesis of hemoglobin in erythrocytes, participates in the synthesis of neurotransmitters of the central and peripheral nervous system, as well as in the biosynthesis of the myelin sheath of nerves.

Cyanocobalamin suppresses abnormal changes in degenerative atrophy of nerve cells and thus restores their functions. In addition, it has a hematopoietic, erythropoietic, antianemic, metabolic effect. Vitamin B12 is involved in carbohydrate, lipid, protein metabolism; increases tissue regeneration, normalizes the hematopoietic function of the liver, the functioning of the nervous system, reduces the content of cholesterol and homocysteine ​​in the blood.

Given the pathogenesis of the development of hypothyroid polyneuropathies and the role of B vitamins in the normal functioning of the nervous system, Neurovitan attracted our attention.

The purpose of this work was to study the clinical efficacy of Neurovitan in the complex treatment of hypothyroid polyneuropathies.

Materials and methods of research

48 patients with hypothyroidism (38 women and 10 men) aged 32–64 years were examined. The duration of the disease ranged from 2 to 12 years. Verification of the diagnosis of hypothyroid polyneuropathy was carried out on the basis of clinical symptoms and additional research methods:

– vibration sensitivity;

– tactile sensitivity;

— temperature sensitivity;

– pain sensitivity;

— reflexometry;

– electroneuromyography.

Electroneuromyography was performed using a Neurosoft device (Russia) using a stimulating surface plate electrode (cathode – distally, anode – proximally, lead – with a standard set of monopolar plate electrodes). The motor processes of the peroneal nerves were studied with the determination of the amplitude, latency and area of ​​the M-response, and the speed of wave propagation.

The patients were divided into two groups. The first group included 28 people who, on the background of hormone replacement therapy, were prescribed Neurovitan, 1 tab. 3 times a day. The second group consisted of 20 patients who took only hormone replacement therapy – thyroxine or euthyroxine. The complex of the above research methods was carried out before the start of therapy with Neurovitan and one month after the treatment.

Research results and discussion

Prior to Neurovitan therapy, both groups of patients had clinical signs of distal polyneuropathy of the arms and legs in the form of distal paresthesia, painful dysesthesia, mono- and polyneuropathy. Clinical data were also confirmed by additional instrumental research methods. So, on the electroneuromyogram, there was a lengthening of the terminal latency, a decrease in the amplitude and area of ​​the M-response, a significant decrease in the rate of propagation of electrical excitation along the peroneal nerve (Fig. 1).

These studies were also confirmed by reflexometry, the indicator of which was 420.0 ± 35.6 m/s. In our opinion, the changes that we have identified that characterize hypothyroid polyneuropathy are primarily associated with the decompensation of the disease. The blood TSH level in 73.5% of cases exceeded 4 mIU/l, which indicates an insufficient adequate dose of thyroxin. This is confirmed by the results of a large population-based study conducted in the United States (13,344 people). In this population, the average TSH level was 1.5 mIU/l (quoted by V.V. Fadeev, 2005). Therefore, both in the treatment and in the rehabilitation of patients with hypothyroidism, the correct dose of thyroxin should be in the first place. And we fully agree with the authors, who rightly point out that the quality of life of patients with hypothyroidism, constantly receiving replacement therapy with adequate doses of L-thyroxine or euthyrox, differs slightly from that of patients without hypothyroidism [1, 12]. But, on the other hand, taking into account those metabolic disorders that develop with a deficiency of thyroid hormones and ultimately lead to damage to the central and peripheral nervous system, it is necessary to prescribe additional medications that normalize these changes. This position is confirmed by our comparative studies of the above two groups of patients. It should be noted that a month after treatment, positive results were obtained in both groups of patients. At the same time, a more significant improvement was observed in the first group of patients who were additionally prescribed Neurovitan in the complex of therapy. Most patients noted the restoration of strength in the legs, a significant reduction in sensitivity disorders. Achilles reflexes began to be called. So, if in patients of the second group who took only thyroxin, the reflexotherapy index was 420.0 ± 35.6 m/s, after a month of treatment – 340.0 ± 27.7 m/s, then in patients in the 1st group who took Neurovitan in complex treatment, this indicator decreased from 436. 8 ± 38.5 m/s to 290.0 ± 18.2 m/s (p < 0.01), that is, almost to normal values. These data were also confirmed by repeated electroneuromyography. After complex treatment with the inclusion of Neurovitan, there was a significant increase in the amplitude and area of ​​the M-response, a significant increase in the rate of propagation of electrical excitation along the peroneal nerve (Fig. 2).

Thus, treatment and rehabilitation of patients with hypothyroidism should be carried out against the background of hormone replacement therapy in doses that ensure the achievement and maintenance of euthyroidism. For a faster recovery of impaired functions, it is pathogenetically justified to prescribe drugs with neurotrophic effects, in particular Neurovitan. We [13] developed a method for the treatment of hypothyroid polyneuropathy with Neurovitan (patent No. 53982). For the treatment of hypothyroid polyneuropathy Neurovitan is recommended to prescribe 3-4 tablets per day for 1-2 months, 2 courses per year. To prevent the development of hypothyroid polyneuropathy, 2-3 tablets per day are prescribed for 1-2 months, 2-3 courses per year.

Our clinical studies indicate the positive effect of Neurovitan in the complex treatment of hypothyroidism and its neurological complications, which allows us to recommend it for widespread use in clinical practice.

References

1. Fadeev V.V. Professional view on the problem of hypothyroidism // The attending physician. – 2005. – No. 3. – S. 26-29.

2. Mitnik Z.M., Zhdanova M.G. Krushinska Z.G. that in. The endocrinological service of Ukraine in 2007 and prospects for the development of medical care for ailments with endocrine pathology // International Journal of Endocrinology. – 2008. – No. 3 (15). — P. 8-15.

3. Pankiv V.I. Extent of pathology of the thyroid gland in iodine-deficient regions of Western Ukraine // Endocrinology. – 2006. – T. 11. – S. 134-137.

4. Olijnik V.A. Pathology of the thyroid gland in Ukraine (epidemiology and regional peculiarities) // Journal of a practical doctor. – 2001. – No. 2. – S. 5-7.

5. Balabolkin M.N., Klebanova E.M., Kreminskaya V.M. Fundamental and clinical thyroidology: Proc. allowance. – M .: OJSC “Publishing house” Medicine “, 2007. – 816 p.

6. Tovazhnyanskaya E.L. Damage to the nervous system in endocrine pathology // Health of Ukraine. – 2009. – No. 11/1. – S. 1-3.

7. Vernigorodsky V.S., Yavorenko O.B., Fetisova N.M. that in. Problems of disability and rehabilitation of patients with hypothyroidism // International Journal of Endocrinology. — 2009. – No. 3 (21). – S. 36-40.

8. Kravchun M.O., Zemlyanitsina O.V., Kozakov O.V. Choice of Neurovitan for the treatment of polyneuropathy in endocrine diseases: a method. recommendations. – Kyiv; Kharkiv, 2004. – 16 p.

9. Zelinska N.B. Clinical manifestation of damage to the cardiovascular system in patients with hypothyroidism // Clinical endocrinology and endocrine surgery. – 2008. – No. 2 (23). – S. 22-31.

10. Lukash N.V., Kryuchkova O.