What is the connection between hypothyroidism and rheumatoid arthritis. How do these conditions affect each other. What are the shared symptoms and risks of hypothyroidism and RA. How can patients manage both conditions effectively.

The Thyroid Gland: Function and Impact on Overall Health

The thyroid gland, a small butterfly-shaped organ located in the neck, plays a crucial role in regulating various bodily functions. Its primary responsibility is to produce and store hormones that control metabolism, the rate at which cells perform their duties. These hormones influence heart rate, calorie burning, body temperature, and the proper functioning of the brain, muscles, and other organs.

When the thyroid gland doesn’t produce enough hormones, a condition known as hypothyroidism occurs. This underactivity slows down bodily processes, leading to a range of symptoms that can significantly impact a person’s quality of life.

Key Functions of the Thyroid Gland:

• Regulating metabolism
• Controlling heart rate
• Managing body temperature
• Supporting brain function
• Maintaining muscle and organ health

The Surprising Connection Between Rheumatoid Arthritis and Thyroid Disorders

Research has revealed an intriguing link between rheumatoid arthritis (RA) and thyroid conditions, particularly hypothyroidism. Studies indicate that individuals with RA are more likely to develop thyroid disorders compared to the general population. Dr. Eric Matteson, a rheumatologist and professor of medicine at Mayo Clinic, notes that between 15% and 25% of RA patients may develop thyroid disease during their lifetime, compared to 10% to 12% of adults in the general population.

Interestingly, this connection appears to be bidirectional. People with autoimmune thyroid diseases, such as Hashimoto’s thyroiditis, also face an increased risk of developing rheumatoid arthritis. A study published in the American Journal of Medicine found that approximately 14% of individuals with Hashimoto’s thyroiditis had another autoimmune disorder, with RA being the most common.

Why do these conditions often coexist?

The exact mechanisms behind the coexistence of RA and thyroid disorders are not fully understood. However, experts have identified several factors that may contribute to this relationship:

1. Autoimmune predisposition: Having one autoimmune disease increases the likelihood of developing another.
2. Systemic immune response: The abnormal immune system activity in RA can affect multiple organ systems, including the thyroid.
3. Shared genetic factors: There may be common genetic predispositions for both RA and autoimmune thyroid diseases.

Hypothyroidism: Symptoms and Causes

Hypothyroidism occurs when the thyroid gland is underactive and unable to produce sufficient thyroid hormone to maintain normal bodily functions. The symptoms of hypothyroidism tend to develop gradually over several years and can vary in severity depending on the extent of hormone deficiency.

Common symptoms of hypothyroidism include:

• Fatigue
• Increased sensitivity to cold
• Weight gain
• Dry skin and hair
• Constipation
• Puffy face
• Muscle aches
• Forgetfulness
• Depression
• Enlarged thyroid gland (goiter)

The most common cause of hypothyroidism is Hashimoto’s thyroiditis, an autoimmune disorder in which the immune system mistakenly attacks the thyroid gland. Other potential causes include thyroid surgery, radiation therapy for cancer treatment, thyroiditis (inflammation of the thyroid gland), and certain medications.

Joint Pain: A Shared Symptom of Hypothyroidism and Rheumatoid Arthritis

Both hypothyroidism and rheumatoid arthritis can cause joint pain, leading to potential confusion in diagnosis. However, there are some key differences in how these conditions affect the joints.

In hypothyroidism, joint pain and stiffness may occur, along with muscle aches and tenderness, particularly in the shoulders and hips. The condition can also cause swelling of the soft tissue in the hands, arms, legs, and feet, as well as facial puffiness in some cases.

Rheumatoid arthritis, on the other hand, is characterized by swelling in the affected joints themselves. This distinction can be crucial for accurate diagnosis and appropriate treatment.

It’s worth noting that both conditions can lead to carpal tunnel syndrome, causing numbness, tingling, and other symptoms in the hand and arm.

Cardiovascular Risks Associated with Rheumatoid Arthritis and Hypothyroidism

Individuals with rheumatoid arthritis already face an elevated risk of heart disease, with studies suggesting their heart attack risk is up to 68% higher than that of the general population. When hypothyroidism is present alongside RA, the cardiovascular risk may be further amplified.

An underactive thyroid can contribute to heart disease risk through various mechanisms:

• Slowing heart rate
• Increasing cholesterol levels
• Causing fluid accumulation around the heart
• Potentially leading to heart failure

Research indicates that the combination of inflammatory arthritis and hypothyroidism may significantly increase cardiovascular risk. A Dutch study found that women with both conditions had more than three times the risk of cardiovascular disease compared to individuals without either condition.

Diagnosis and Treatment of Hypothyroidism in Patients with Rheumatoid Arthritis

Given the increased prevalence of thyroid disorders in individuals with rheumatoid arthritis, regular screening for thyroid function is crucial. Diagnosis typically involves blood tests to measure levels of thyroid-stimulating hormone (TSH) and thyroxine (T4).

Treatment for hypothyroidism usually involves thyroid hormone replacement therapy, most commonly with synthetic thyroxine (levothyroxine). The medication is taken orally and aims to restore normal thyroid hormone levels, alleviating symptoms and reducing associated health risks.

Challenges in managing both conditions:

• Symptom overlap can complicate diagnosis
• Medication interactions may require careful monitoring
• Thyroid function can affect RA disease activity and treatment response

Healthcare providers must take a comprehensive approach when managing patients with both RA and hypothyroidism, considering the potential interactions between the two conditions and their treatments.

Lifestyle Modifications for Managing Hypothyroidism and Rheumatoid Arthritis

While medical treatment is essential for both hypothyroidism and rheumatoid arthritis, lifestyle modifications can play a significant role in managing symptoms and improving overall well-being. Here are some strategies that may benefit individuals dealing with both conditions:

1. Maintain a balanced diet: Focus on nutrient-rich foods that support thyroid function and reduce inflammation.
2. Regular exercise: Engage in low-impact activities to improve joint flexibility and cardiovascular health.
3. Stress management: Practice relaxation techniques such as meditation or yoga to reduce stress, which can exacerbate both conditions.
4. Adequate sleep: Prioritize getting sufficient, quality sleep to support immune function and overall health.
5. Avoid environmental triggers: Identify and minimize exposure to factors that may worsen symptoms of either condition.

It’s important to work closely with healthcare providers to develop a comprehensive management plan that addresses both hypothyroidism and rheumatoid arthritis. Regular monitoring and adjustments to treatment strategies may be necessary to achieve optimal results.

Future Research and Emerging Treatments

As our understanding of the relationship between rheumatoid arthritis and thyroid disorders continues to evolve, researchers are exploring new avenues for treatment and management. Some areas of ongoing investigation include:

• Identifying shared genetic markers for RA and autoimmune thyroid diseases
• Developing targeted therapies that address both conditions simultaneously
• Exploring the potential of precision medicine approaches to tailor treatments to individual patients
• Investigating the role of the gut microbiome in autoimmune disorders and thyroid function

These research efforts hold promise for improving outcomes for individuals living with both rheumatoid arthritis and hypothyroidism. As new discoveries are made, treatment strategies may become more refined and effective, potentially leading to better quality of life for patients.

Potential future developments:

1. Novel biomarkers for early detection of thyroid dysfunction in RA patients
2. Immunomodulatory therapies targeting shared pathways in RA and autoimmune thyroid diseases
3. Advanced imaging techniques for monitoring thyroid health in individuals with autoimmune disorders
4. Personalized treatment algorithms based on genetic and environmental factors

As research progresses, it is crucial for patients and healthcare providers to stay informed about the latest developments in the field. This knowledge can help guide treatment decisions and improve long-term outcomes for those living with both rheumatoid arthritis and hypothyroidism.

In conclusion, the link between hypothyroidism and rheumatoid arthritis represents a complex interplay of autoimmune processes, shared risk factors, and overlapping symptoms. By understanding this relationship, healthcare providers can offer more comprehensive care, addressing both conditions effectively. Patients, in turn, can benefit from improved management strategies, potentially reducing the impact of these chronic conditions on their daily lives and long-term health.

Hypothyroidism and Arthritis: Understanding the Link

Your thyroid is a butterfly-shaped gland located in your neck, just under your Adam’s apple. Its job: to produce and store hormones that help regulate your metabolism (or the rate at which cells perform their duties). Thyroid hormone helps control how fast your heart beats, how quickly you burn calories, and your body temperature. It also helps keep your brain, muscles, and other organs working as they should. Too little hormone production (called hypothyroidism) slows your body down; too much (or hyperthyroidism) sends it into overdrive.

What does a joint condition like arthritis have to do with this tiny gland? Research has shown people with rheumatoid arthritis (RA) are more likely to develop a thyroid condition such as hypothyroidism. “Estimates suggest between 15 percent and 25 percent of patients with RA will develop thyroid disease sometime during their lifetime,” says Eric Matteson, MD, rheumatologist and professor of medicine at Mayo Clinic in Rochester, Minnesota. In comparison, about 10 percent to 12 percent of adults in the general population develop thyroid disease.

The connection appears to go both ways: People living with autoimmune thyroid disease are also at higher risk for developing rheumatoid arthritis. One study published in the American Journal of Medicine found that about 14 percent of people with Hashimoto’s thyroiditis — a condition in which your immune system attacks your thyroid and often leads to hypothyroidism — had another autoimmune disorder, most commonly RA.

What Exactly Is Hypothyroidism?

This condition occurs when your thyroid gland is underactive, which means that it can’t make enough thyroid hormone to keep your body running normally. You have hypothyroidism if you have little thyroid hormone in your blood. When cells can’t get enough of this hormone, the body’s processes slow down.

“Thyroid hormone is a necessary hormone, thus a dysregulation for thyroid hormone changes the whole body,” says Alexa Simon Meara, MD, assistant professor in the division of immunology and rheumatology at The Ohio State University Wexner Medical Center. Signs of hypothyroidism vary, depending on the severity of the hormone deficiency. Symptoms tend to develop slowly, often over several years, and may include:

• Fatigue
• Increased sensitivity or intolerance to cold
• Weight gain
• Dry skin and hair
• Constipation
• Puffy face
• Muscle aches
• Forgetfulness
• Depression
• Enlarged thyroid gland (goiter)

What Causes Hypothyroidism?

The most common cause of hypothyroidism is the autoimmune disease Hashimoto’s thyroiditis. In this disorder, the immune system mistakenly targets and damages the thyroid, causing inflammation and leading to an underactive thyroid.

Other causes of hypothyroidism include thyroid surgery, radiation therapy to treat certain cancers, thyroiditis (or inflammation of the thyroid gland), and certain medications.

Why Do Rheumatoid Arthritis and Hypothyroidism Often Coexist?

While the link between the two conditions isn’t fully understood, experts do know that having one autoimmune disease raises your risk of developing another. “Patients with rheumatoid arthritis are more likely to develop any number of other autoimmune conditions, including autoimmune thyroid dysfunction,” says Dr. Matteson. “The link relates to the systemic abnormal response of the immune system leading to involvement of other organ systems.”

Another potential connection: There may be shared genetic predispositions to both RA and autoimmune thyroid disease, adds Dr. Matteson.

Does Hypothyroidism Cause Joint Pain?

It can, according to the Mayo Clinic. Hypothyroidism may lead to joint pain and stiffness, as well as muscle aches and tenderness particularly in the shoulders and hips. In RA, however, swelling occurs in affected joints, while hypothyroidism can cause swelling of the soft tissue in the hands, arms, legs and feet, and even puffiness in the face in some people, explains Dr. Matteson.

Both RA and hypothyroidism can also cause carpel tunnel syndrome, a condition that causes numbness, tingling, and other symptoms in the hand and arm.

Increased Cardiovascular Risk for Rheumatoid Arthritis and Hypothyroidism

Just having RA means your heart attack risk is as much as 68 percent higher than it is for someone without RA. An underactive thyroid can further contribute to heart disease risk because it may cause a slow heart rate, a rise in cholesterol, an increase in fluid around the heart, and heart failure.

Research suggests having the two conditions together may drive up cardiovascular risk. According to Dutch research, women with inflammatory arthritis and hypothyroidism had more than three times the risk for cardiovascular disease, compared to people who didn’t have either condition.

How Is Hypothyroidism Diagnosed?

With well-controlled RA, your doctor may suspect thyroid disease if you have unusual swelling in your hands, arms, legs and feet, or even unusual fatigue and weight gain, says Dr. Matteson. “Thyroid tests will help to sort this out,” he says.

Hypothyroidism is diagnosed with a physical exam for symptoms and results from a blood test that measures the levels of thyroid-stimulating hormone (TSH). An abnormally high TSH means hypothyroidism. It indicates the thyroid gland is being asked to make more of the hormone thyroxine (T4) because there isn’t enough T4 in the blood.

Sometimes doctors may run another blood test to measure T4 levels, if needed.

How Is Hypothyroidism Treated if You Have RA?

Hypothyroidism is treated the same whether or not you have RA, explains Dr. Meara. The goal is to get thyroid hormone back to normal levels. It’s also important to continue to manage your RA and keep it under good control to help manage symptoms and for your overall health.

Hypothyroidism can’t be cured, but in most cases, it can be completely controlled. Standard treatment involves a daily dose of the synthetic thyroid hormone levothyroxine (Levo-T, Synthroid). It comes in pill form, works just like your own body’s thyroid hormone, and helps bring hormones back to normal levels, thus reversing hypothyroid symptoms.

“Medications used to replace thyroid hormone do not interfere with RA medications,” adds Dr. Matteson. Your doctor will determine the best dose initially and over time.

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Antibodies to thyroid hormones in rheumatoid arthritis | Gontar

Metabolic and degenerative changes in connective tissue largely determine the pathogenesis and clinical picture of various diseases. A significant proportion of the pathology of the joints, musculoskeletal system, connective tissue are rheumatic diseases, the most common of which is rheumatoid arthritis (RA). It affects 0.5-1% of the world’s population, which is about 63 million patients. In the Russian Federation, RA accounts for 38.2% of the total number of people with disabilities due to diseases of the musculoskeletal system [17].

At present, RA is considered as a chronic systemic inflammatory disease that leads to damage not only to the joints and periarticular tissues, but also to the autonomic and central nervous systems, the endocrine system, with a possible violation of their relationship, which leads to an additional complication of the course of the underlying disease [10 ].

Clinicians are aware of frequent manifestations of endocrine gland function pathology in patients with RA in the form of goiter, hypothyroidism, chronic adrenal insufficiency, etc. Thyroid hormones (thyroid gland) increase the activity of metabolic processes, stimulate lipogenesis, increase the absorption of glucose by adipose and muscle tissue, activate gluconeogenesis and glycogenolysis [19]. Thyroid hormones (triiodothyronine – T ₃ , thyroxine – T ₄ ) enhance both resorption and synthesis of bone tissue, the production of glycosaminoglycans and proteoglycans in the connective tissue. An increase in their amount in the body leads to an acceleration of bone tissue metabolism due to an increase in the number and activity of osteoclasts, and also stimulates osteoblastic function, which is expressed in an increase in bone formation markers in the blood [1, 11, 20]. With a lack of thyroid hormones, the activity of adenylate cyclase in the synovial membranes increases, which increases the production of hyaluronic acid by fibroblasts, leading to the accumulation of synovial fluid in the joints, and causes clinical manifestations of synovitis [20, 22].

Enzyme-linked immunosorbent assay (ELISA), used to determine the level of antibodies to the thyroid gland, is a fast, fairly sensitive and quite reliable method for diagnosing its autoimmune lesion. In clinical practice, it is customary to investigate antibodies directly to the thyroid tissue, the TSH receptor, and antibodies to thyroperoxidase [25, 26].

Autoantibodies to thyroid hormones (THAAA) directed specifically against T ₃ and T ₄ are less common. They have been known since 1956, when J. Robbins et al. [27] first described the presence of γ-binding y-globulin in the case of papillary adenocarcinoma of the thyroid gland, which was treated with iodine. S. Sakata, M. Matsuda, T. Ogava et al. [2, 9, 21, 28] also studied antibodies to thyroid hormones, and concluded that the prevalence of autoantibodies (anti-T ₃ and anti-T ₄ ) in the majority of the population is not typical, but their presence may increase in patients with hy- on-, hyperfunction of the thyroid gland and in autoimmune diseases not associated with the pathology of the thyroid gland. According to the conclusions of D. Thomas et al. [29, 32], even in the absence of any clinical or biochemical changes in the thyroid gland, the presence of these antibodies nevertheless reflects the early stages of the pathological process.

In the available literature, there is little information about the processes of antibody formation to thyroid hormones in rheumatic diseases. Therefore, assuming that the determination of antibodies directly to thyroid hormones can be a test for the diagnosis of autoimmune thyroid disease, it became necessary to study the possibility of their determination, as well as their role and effect on thyroid function in patients with RA.

The purpose of this work is to study the functional activity of the thyroid gland in RA and to identify the features of antibody genesis to T ₃ and T ₄ in patients with RA, depending on the activity and systemic manifestations of the underlying disease.

Materials and methods

We examined 75 patients with RA (61 (81.4%) women and 14 (18.6%) men) aged 25—78 years who were hospitalized at Clinical Hospital No. 25 of Volgograd. Of these, 35 (46.6%) women and 11 (14.6%) men belonged to the socially active population, i. e., were in the age groups up to 55 and 60 years, respectively. Thus, a significant (45 (60%)) part of patients with RA) belonged to working age. The mean age of the patients was 54.1 ± 11.6 years. The average duration of the disease is 9.47 ± 8.83 years.

The control group consisted of 30 practically healthy donors of the regional blood transfusion station aged 24 to 56 years (22 women and 11 men) who underwent a preliminary medical examination.

Diagnosis of RA was made on the basis of a thorough clinical, laboratory and instrumental examination of patients in accordance with the working classification and nomenclature of rheumatic diseases recommended by the III All-Union Congress of Rheumatologists, and according to the system of diagnostic criteria of the American Rheumatological Association (1987). The activity of the rheumatic process was assessed on the basis of clinical data, immunobiochemical parameters and the DAS 28 index (Disease Activity Score).

During the follow-up, the following was carried out: collection of complaints and anamnesis, examination, physical examination and a set of general laboratory tests, immunological tests were performed. The amount of TSH, free T ₄ (st. T ₄ ), total T ₃ (Alcor-Bio, St. Petersburg) and free T _{3 9 was determined by ELISA.0008 (St. T 3 ) (ZAO NVO Immunotech, Moscow), antibodies to TPO and TG (OOO “CHEMA-MEDICA”, Moscow). According to the indications, instrumental studies were performed: ECG, X-ray of the chest and joints, ultrasound of the heart, abdominal organs and thyroid gland. The study was carried out in accordance with the principles of the Declaration of Helsinki of the International Medical Association and recommendations on the ethics of biomedical research [31].}

The articular form of RA was noted in 45 (60%) people, and 23 (51%) of them had a polyarticular form of the disease. Systemic manifestations of RA were observed in 30 (40%) patients. Among patients with RA, signs of thyroid pathology were found in 11 (14.6%) cases. Of these, diffuse toxic goiter (DTG) with thyrotoxicosis was observed in 4 patients, primary hypothyroidism (increased TSH level) – in 2 patients, and an increase in the level of antibodies to TPO and TG – in 5 patients.

When determining the content of antibodies to T ₃ (anti-T ₃ ) and T ₄ (anti-T ₄ ) in blood serum by the method of solid-phase ELISA, immobilized granular antigenic preparations with magnetic properties were used in the modification T.P. Gontarya et al. [5, 6] with obtaining soluble forms of hormones T ₃ and T ₄ (from commercial preparations “Berlin-Chemie”, Germany). The results were expressed in units of optical density (opt. square units) and were considered positive if the extinction values ​​of the control group were exceeded by more than 2 hundred.

The obtained data were analyzed using the statistical program “Statistica 6.0” (StatSoft, USA). The data are presented as mean (M) and standard deviation (st), the calculation of the median (Me) and 25% and 75% percentiles were also used if the distribution of the indicator was different from normal. Statistical analysis was performed using the test x ² For qualitative data, Student’s /-test and Mann-Whitney test. Spearman’s correlation coefficient was used to assess the relationship between quantitative traits. The critical level of significance of differences was taken equal to 0.05.

Fig. 1. The number of antibodies to triiodothyronine (ordinate axis) in RA patients and healthy individuals (abscissa axis).

Results and discussion

According to the data obtained for determining the amount of antibodies to thyroid hormones T ₃ and T ₄ , it was found that the majority of patients with RA compared with the control group had an increased titer: anti-T ₃ — 0.143 ± 0.03 units opt. pl (in healthy individuals 0.028 ± 0.008 u opt. pl.) (Fig. 1) and anti-T ₄ – 0.146 ± 0.05 units opt. sq. (in healthy individuals 0.034 ± 0.008 units of opt. area) (Fig. 2). A rather high detection rate of anti-T ₃ (39%) and anti-T ₄ (45%) in patients with RA prompted us to study in detail the processes of autoantibody formation to thyroid hormones depending on the activity and form of RA.

The activity of the pathological process in RA was assessed on the basis of clinical data, immunobiochemical parameters, as well as the combined activity index Disease Activity Score — DAS 28, recommended by the American Rheumatology Association for use in research and clinical trials in patients with RA (1987). The values ​​of the DAS 28 index, which are 3.2 or less, corresponding to the I degree of RA activity, were detected in 20 (26.7%)

2. The number of antibodies to thyroxin (y-axis) in patients with RA and healthy individuals (abscissa).

people, DAS 28 over 3.2 to 5.1 (II degree of activity) – in 42 (41.3%) and DAS 28 over 5.1 (III degree) – in 23 (32%) patients.

With an increase in the activity of the pathological process, an increase in St. T ₄ and decrease in St. T ₃ in the blood serum of patients with RA, i.e., a pattern of thyroid hormone imbalance was observed. We have found a significant correlation between the level of St. T ₄ and RA activity (r, = 0.26, p = 0.029) and inverse correlation between the amount of St. T ₃ and the activity of the pathological process in rheumatoid arthritis and amounted to (r, – 0.25, p = 0.03). The content of anti-T ₄ and anti-T ₃ in patients with RA was significantly higher than in the group of healthy individuals (p < 0.001), and progressed with an increase in the degree of disease activity: correlation coefficient of anti-T levels ₄ with the activity of the pathological process r _s was 0.32 (p = 0.023), and for anti-T ₃ and RA activity r _s = 0.24 (p = 0.049) (Table 1).

At high RA activity, free thyroxine concentrations were higher than those at minimal and moderate disease activity, while free triiodothyronine concentrations were lower. At the maximum activity of RA, a correlation was found between the concentration of free thyroxine and the level of antibodies to it (r, = 0. 6, p < 0.05) and the concentration of free triiodothyronine and the level of antibodies to it (r, = 0.3, p < 0.05).

To identify the relationship between the form of the disease, the amount of thyroid hormones and antibodies to them in RA patients, 3 groups were formed:

Table 1

Group 1 — healthy individuals, group 2 — patients with articular RA, and group 3 — patients with systemic RA (Table 2). Patients with systemic RA and impaired thyroid function (n = 6) were not included in the analysis. Maximum indicators of St. T ₄ , antibodies to T ₃ and T ₄ and the minimum level of St. T ₃ were observed in the 3rd group of RA patients, especially in the case of high activity of the pathological process.

The euthyroid state noted by us in RA patients without concomitant thyroid pathology differs qualitatively from that in healthy individuals, since this pathology develops a syndrome of low T ₃ (low T ₃ ) against the background of euthyroidism [15]. It is believed that Low T ₃ arises as a general response of the body as a compensatory reaction and reflects adaptive metabolic reactions and energy savings in a chronic inflammatory process. In addition, we noted a shift in the ratio of the levels of St. T ₃ and St. T ₄ in RA, which is possibly associated with changes in the metabolism of thyroid hormones in peripheral tissues, a decrease in the sensitivity of receptors to them in cells and target tissues, as well as a decrease in the activity of T ₄ -deiodase [3, 13, 14], which leads to a decrease in the level of T ₃ in serum, an increase in the content of reverse T ₃ and is often combined with an increase in the amount of T ₄ . With an increase in RA activity, there is an increase in protein breakdown, which leads to a more rapid accumulation of free forms of hormones in the blood [7, 17], and, possibly, a more intensive formation of autoantibodies to them already at the early stages of the disease. According to the literature, thyroid hormones are involved in the processes of immunogenesis and antibody formation, so thyroid pathology can be a factor contributing to the chronic course of RA [15].

When the thyroid gland is involved during RA, the pathological process intensifies, its course becomes more severe. An excess of thyroid hormones leads to a disruption in the formation of a general adaptation syndrome, patients become torpid to any therapy. The condition improves with a gradual decrease in the functional activity of the thyroid gland during treatment [18]. On the other hand, this can be explained by the fact that in addition to autoimmune mechanisms, an important role in thyroid damage is played by the direct influence of anti-inflammatory cytokines, which can enhance immune responses and additionally stimulate the production of thyroid hormones [8, 23, 24, 30]. The thyroid gland expresses interleukins when exposed to circulating immune complexes (which are produced in excess in RA), and cytokines, in turn, stimulate fibroblast proliferation, excess production of collagen and glycosaminoglycans, leading to narrowing of the joint space, the formation of bone outgrowths and a decrease in the functional activity of the joint [4, 12].

Conclusions

1. In the blood serum of a significant proportion of patients with RA, antibodies to thyroid hormones were found (in 45% – anti-T ₄ and in 39% – anti-T ₃ ), the content of which depends on the activity of the pathological process.
2. Revealed a significant decrease in the level of T ₃ and a tendency to increase T ₄ are proportional to the increase in RA activity, which should be considered as a syndrome of “low T ₃ ” in this disease.
3. Thyroid hormone antibodies can be used as an additional test to characterize RA activity along with traditional clinical and laboratory parameters.

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