DOI: 10.5281/zenodo.15412246
title: Title :- "Steroids and Thyroid Hormones: Unraveling the connection in rheumatoid arthritis patients". Author - Abjamilova Jazgul Students - 1). Akshay Kadam                     2). Dhiraj Kor                     3). Ishwari Bhagwat                    4). Insha Shaikh Abstract Rheumatoid Arthritis (RA) is a chronic autoimmune condition with persistent inflammation of the synovial joints. Glucocorticoids, or steroids as they are otherwise called, remain a cornerstone of treatment for acute inflammation in RA. The chronic effect of steroids on the system, however, extends beyond immunosuppression. One of these lesser-explored but clinically significant arenas is their impact on the endocrine system, the thyroid gland in particular. There has been recent evidence in favor of a bidirectional interaction between the alterations of thyroid hormone and the use of corticosteroids in patients with RA. The current article investigates mechanistic knowledge, clinical implication, and proposals for integrating monitoring of the thyroid in RA therapy. Introduction Rheumatoid Arthritis affects approximately 0.5%–1% of the global population, causing pain, disability, and systemic complications. RA, apart from joints, impacts various organ systems due to systemic inflammation and immune dysregulation. While DMARDs and biologics are commonly employed, corticosteroids are also used for rapid symptom control. At the same time, thyroid dysfunction, particularly hypothyroidism, is more and more frequently reported in RA patients. This association is not fortuitous. Both RA and thyroid disease (particularly autoimmune thyroiditis) are rooted in immune dysregulation, and glucocorticoid use can worsen or obscure underlying thyroid disease. Awareness of this relationship can result in more integrated care for RA patients Rheumatoid Arthritis and Its Management RA is marked by chronic synovitis leading to joint destruction. Key pathological features include: Pro-inflammatory cytokines (TNF-α, IL-1, IL-6) Autoantibodies like rheumatoid factor (RF) and anti-CCP Systemic manifestations, such as fatigue, weight loss, and organ involvement Management strategies: NSAIDs for symptom control DMARDs like methotrexate Biologic agents targeting specific immune pathways Corticosteroids, used for flares or as bridging therapy Thyroid Function and Immune Regulation The thyroid gland synthesizes T3 (triiodothyronine) and T4 (thyroxine), regulated by TSH of the pituitary gland. These are essential for development, metabolism, and immune responses. Thyroid autoimmunity, e.g., Hashimoto's thyroiditis and Graves' disease, often coexists with other autoimmune disorders such as RA. Thyroid hormones also affect: Lymphocyte maturation Cytokine production MHC expression This bidirectional relationship suggests that not only does thyroid dysfunction impact RA, but immune dysregulation in RA may predispose patients to thyroid disease. How Steroids Affect Thyroid Function Corticosteroids affect the hypothalamic-pituitary-thyroid (HPT) axis and peripheral thyroid hormone metabolism: 4.1 Central effects: Suppress secretion of TRH and TSH Suppress pituitary response to hypothalamic stimulation 4.2 Peripheral effects: Suppress conversion of T4 to T3 by inhibiting deiodinase activity Accumulate reverse T3 (rT3), an inactive metabolite These changes can lead to "functional hypothyroidism" or non-thyroidal illness syndrome (NTIS), especially with high or prolonged use of steroids. Thyroid Dysfunction in RA: Coincidence or Connection? Research has shown: RA patients can have up to 15–20% thyroid dysfunction Most frequent is subclinical hypothyroidism Female RA patients are more common Steroid therapy can mask hypothyroidism by suppressing TSH, and diagnosis is therefore delayed This is suggestive of both autoimmune clustering and therapy-induced changes having a role in thyroid dysfunction in RA patients. Clinical Implications 6.1 Diagnosis challenges: TSH suppression by steroids may lead to false negatives Symptoms of hypothyroidism (fatigue, depression, cold intolerance) overlap with RA 6.2 Disease progression: Hypothyroidism may worsen fatigue and joint stiffness Uncontrolled thyroid dysfunction can affect the metabolism of DMARDs and biologics 6.3 Steroid tapering and thyroid axis: Sudden steroid withdrawal can unmask adrenal or thyroid insufficiency Recommendations for Clinical Practice In RA patients, especially on long-term steroids: Baseline thyroid screening (TSH, Free T4) at diagnosis Annual or bi-annual thyroid function tests In symptomatic patients, rT3 and T3 levels should be measured to diagnose NTIS Refer to endocrinologists in complex cases Steroid therapy should be carefully titrated, and any thyroid abnormality addressed early to prevent compounded systemic effects Future Directions Possible areas of future research are: Longitudinal observations of thyroid profiles in RA patients receiving different steroid regimens Biologics and their role in modulating thyroid autoimmunity Development of clinical recommendations for endocrine screening in RA Conclusion The interaction of steroids with thyroid hormone kinetics in RA patients is an essential yet neglected aspect of autoimmune disease management. While corticosteroids provide rapid symptom relief, they can mask or worsen thyroid disease. With shared symptoms and similar autoimmune processes, regular assessment of the thyroid should be an integral part of RA management—especially in patients on long-term steroid therapy. Multidisciplinary care, with the inclusion of rheumatologists and endocrinologists, will yield safer and better outcomes for patients who have this complex autoimmune disease References Boelaert K. "Thyroid dysfunction in patients with rheumatoid arthritis." Nat Clin Pract Rheumatol. 2008. Weetman AP. "Autoimmune thyroid disease." Autoimmunity. 2004. Cutolo M. "Glucocorticoids and chronotherapy in rheumatoid arthritis." RMD Open. 2016. Duntas LH. "Glucocorticoid-induced thyroid dysfunction." Endocrine. 2015.

description: Rheumatoid Arthritis (RA) is a chronic autoimmune condition with persistent inflammation of the synovial joints. Glucocorticoids, or steroids as they are otherwise called, remain a cornerstone of treatment for acute inflammation in RA. The chronic effect of steroids on the system, however, extends beyond immunosuppression. One of these lesser-explored but clinically significant arenas is their impact on the endocrine system, the thyroid gland in particular. There has been recent evidence in favor of a bidirectional interaction between the alterations of thyroid hormone and the use of corticosteroids in patients with RA. The current article investigates mechanistic knowledge, clinical implication, and proposals for integrating monitoring of the thyroid in RA therapy.