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0FEATURES OF COMORBID COURSE OF RHEUMATOID ARTHRITIS AND HYPOTHYROID DISEASES
1Sadullayeva Sh.M., 2Shonazarova N.X.
Samarkand State Medical University Scientific supervisor. https://doi.org/10.5281/zenodo.13144778
Abstract. According to data, frequent manifestations of goiter, hypothyroidism, chronic adrenal insufficiency and other endocrine gland pathologies were found in patients with RA. QB hormones increase the activity of metabolic processes, enhance lipogenesis, increase the absorption of glucose by fat and muscle tissue, activate gluconeogenesis and glycogenolysis. QB hormones (triiodothyronine - T3, thyroxine - T4) enhance both resorption and synthesis of bone tissue, activate the production ofglycosaminoglycans and proteoglycans in connective tissue. An increase in the number of hormones leads to an acceleration of bone metabolism due to an increase in the number and activity of osteoclasts, and an increase in bone formation markers in the blood indicates an increase in osteoblastic function. Lack of QB hormones increases the activity of adenyl cyclase in synovial membranes, increases the production of hyaluronic acid by fibroblasts, which leads to the accumulation of synovial fluid in the joints and causes the clinical appearance of synovitis.
Keywords: rheumatoid arthritis, thyroid gland, autoimmune thyroiditis, hypothyroidism.
The fact that RA is often accompanied by QB pathology indicates the similarity of their immunogenic genetic predisposition and mechanisms of immunopathogenesis [A.E. Dvorovkin 2016, F.V. Valeeva, T.A. Kiseleva, G.R. Akhunova 2011]. There is evidence of genetic similarity between autoimmune thyroid diseases and RA. In particular, one of the causes of RA and thyroid autoimmune diseases is smoking [L.V. Kondrateva, T.V. Popkova 2017].
Hypothyroidism is an absolute lack of thyroid hormones in the body. Depending on the level of injury, it can be primary, secondary, or tertiary. QB hormones (triiodothyronine - T3, thyroxine - T4) enhance both resorption and synthesis of bone tissue, activate the production of glycosaminoglycans and proteoglycans in connective tissue. An increase in the number of hormones leads to an acceleration of bone metabolism due to an increase in the number and activity of osteoclasts, and an increase in bone formation markers in the blood indicates an increase in osteoblastic function. [1,2] Deficiency of QB hormones increases the activity of adenylate cyclase in synovial membranes and increases the production of hyaluronic acid by fibroblasts, which leads to the accumulation of synovial fluid in the joints and causes the clinical manifestation of synovitis [7].
The most common primary hypothyroidism occurs, and one of the main causes is autoimmune thyroiditis. Its prevalence is 1-10% depending on gender and age. Diagnosis of hypothyroidism is based only on the amount of thyrotropin hormone and T4. Only an increase in thyrotropin in the blood is called subclinical hypothyroidism, an increase in thyrotropin and a decrease in T4 is called hypothyroidism. In hypothyroidism, replacement therapy is indicated. Replacement therapy is 1.6 pg/kg of levothyroxine depending on the patient's weight. In young adults, this dose is reduced to 1 pg/kg. In patients with obesity, the amount of levothyroxine is taken according to the ideal body weight. Replacement therapy is confirmed depending on the
thyrotropin hormone in the blood, the appropriate range of which is 0.4-4 mEd/L. In most cases, the clinic of hypothyroidism is dominated by the clinic of nonendocrine diseases, and doctors often confuse it with nonendocrine diseases on the side of the nervous system (drowsiness, depression, memory loss, impaired attention and intellect), on the side of the cardiovascular system (bradycardia, diastolic hypertension, accumulation of pericardial fluid), digestive system (constipation, gallbladder dyskinesia, hepatomegaly, loss of appetite), musculoskeletal system (adhesive capsulitis, paralysis of proximal muscles, Raynaud's phenomenon, synovitis and arthropathy). According to M. Cakir, 30.4% of patients with hypothyroidism had carpal syndrome, 8.7% of patients had fibromyalgia, 13% of patients - adhesive capsulitis, 21.7% of patients -Dupuytren's contracture. Arthropathy is common both in subclinical hypothyroidism and in overt hypothyroidism. Pain in the joint, swelling of soft tissues, accumulation of fluid in the joint, which is not characteristic of inflammation, are observed. Most often, the knee joint, elbow joint, proximal part of the paw the interphalangeal joint are damaged. Arthralgia is observed in 30% of patients with uncompensated hypothyroidism. According to the data, frequent manifestations of goiter, hypothyroidism, chronic adrenal insufficiency and other endocrine gland pathologies have been identified in patients with RA. Patients with RA are more prone to autoimmune diseases of the thyroid gland. In RA, the occurrence of QB diseases is 28%, and Hashimoto's thyroiditis is 413.5%. [27, 41]. The incidence of RA and thyroid autoimmune diseases ranges from 0.5% to 27% in different countries. As a result, there is a high incidence of autoimmune thyroiditis in RA, and attention should be paid to the condition of QB in patients with RA. E.I. Zenovko (1998) determined the amount of TTG, T3, T4 in blood and synovial fluid in patients with RA. As a result, the increase of TTG, T4, T3 was related to the increase in the activity level of the main disease. A decrease in the amount of T3 was observed in RA receiving glucocorticosteroids. According to sources, the syndrome of "low T3" related to the QB functional state is included in rheumatic diseases. This syndrome is considered a compensatory response of the body in severe RA disease and indicates a lack of tissue energy. According to Baimukhamedov, T3 decrease has long duration and high activity of RA. The syndrome of "low T3", swelling and pain of RA joints were often observed, and the disease had many complications.
In the literature, the addition of hypothyroidism in RA disease has a severe course of the disease, destructive changes that are clearly manifested in the joints. At the same time, the clinical condition of patients with rheumatoid arthritis with the addition of hypothyroidism is rapid. Improvement and reduction of arthropathy was observed.
The purpose of the study is to improve the early and differential diagnosis of the disease, as well as the method of treatment, as a result of the analysis of clinical and laboratory indicators in patients with RA and hypothyroidism.
Materials and methods of research: In order to carry out the investigation, 75 patients with RA who came to the rheumatologist's examination at the cardio rheumatology department of Samarkand City Medical Association were examined. The age of patients is 27-65, the average age is 42 years. Duration of disease with RA is 5-12 years. Patients were divided into two groups. The first group is patients with RA without changes in the thyroid gland, and the second group is patients with rheumatoid arthritis and hypothyroidism. In the examined patients, the following were performed for laboratory diagnostic purposes: clinical examination, general blood analysis, general urinalysis, rheumatism analysis, antibody against cyclic citrulline peptide (SSPQA), joint radiography, thyroid ultrasound examination (UTT), hormonal examination (TTG, T4(sv),)
antibody TPO, vitD, densitometry. The number of hormones in blood serum was checked by the immunoenzymatic method using the "Human" (Germany) test system.
The analysis of the obtained results showed that 29 out of 75 patients (39%) had changes in the structure of the thyroid gland during UTT examination. Among them, hyperplasia of the thyroid gland was observed in 55% (16 cases), nodular goiter - in 24% (7 cases), atrophy of the thyroid gland in 21% (6 cases). Serum TTG, free T3 and free T4 concentration, antibody TPO were determined in all patients. According to the changes, patients were divided into 2 groups. 64 (85%) patients with RA thyroid gland changes were included into 1 group, 11 (15%) patients with rheumatoid arthritis thyroid gland changes were included into 2 group. One of the main causes of hypothyroidism is autoimmune thyroiditis.
The results of our investigation showed that the second group of patients with rheumatoid arthritis with hypothyroidism had more SOE, swollen joints, and the course of the disease had higher clinical and laboratory activity compared to the group without thyroid pathology.
Conclusion
As a result of the examination, it was found that the level of hypothyroidism and the detection of antibodies to TPO in patients with RA is high. Patients with rheumatoid arthritis with hypothyroidism have more ECHT, swollen joints, and higher clinical and laboratory activity in the course of the disease compared to patients without thyroid pathology.
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