Autoimmune Mechanisms and Treatment Approaches in Graves' Disease-Induced Hyperthyroidism: A Comprehensive Review
نویسندگان
1 Department of Biochemistry, Faculty of Basic Medical Sciences, University of Lagos, Idi-Araba, Nigeria
2 Departments of Medicine, College of Medicine, University of Gullas, Cebu, Philippines
3 Department of Medicine and Surgery, College of Medicine, Kursk State Medical University, Kursk City, Russia
4 Department of Pharmacognosy, Faculty of Pharmacy, University of Lagos. Idia-Araba, Nigeria
5 Department of Internal Medicine and Surgery, Faculty of Clinical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
6 Department of Microbiology, Faculty of Biological Sciences, University of Nigeria Nsukka, Nsukka, Nigeria
7 Department of Biochemistry, Faculty of Biosciences, Federal University Wukari, Taraba State, Nigeria
8 Department of Biochemistry, Faculty of Biosciences, Federal University Wukari, Taraba State, Nigeria
9 Department of Medicine and Surgery, Faculty of Clinical sciences, University of Ibadan, Ibadan, Nigeria
10 Department of Internal Medicine, Internal Medicine and Public Health, Federal Medical Center, Ebute Metta, Lagos, Nigeria
11 Department of Internal Medicine and Surgery, Faculty of Clinical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
12 Department of Computer Science, Faculty of Science and Technology, Babcock University, Ilisan-Remo Ogun State, Nigeria
doi
10.48309/ijabbr.2026.2062050.1616چکیده
Graves' disease represents the predominant etiology of hyperthyroidism globally, affecting 60-80% of hyperthyroid cases worldwide. This autoimmune disorder results from thyroid-stimulating immunoglobulins (TSI) inappropriately activating thyroid-stimulating hormone receptors (TSHR), leading to excessive thyroid hormone production and subsequent metabolic dysfunction. The disease predominantly affects women of reproductive age, with a female-to-male ratio of 5-10:1, and exhibits significant geographical variation in prevalence and clinical presentation. This comprehensive review aims to provide an in-depth analysis of the complex autoimmune mechanisms underlying Graves' disease pathogenesis and critically evaluate current therapeutic modalities alongside emerging treatment strategies that target specific immunological pathways. A systematic literature review was conducted using PubMed, Scopus, and Web of Science databases, focusing on peer-reviewed articles published between 2010 and 2024. Search terms included "Graves' disease," "hyperthyroidism," "autoimmune thyroid," "TSH receptor antibodies," "immunomodulatory therapy," and "thyroid autoimmunity." Articles were screened for relevance and methodological quality. The pathophysiology involves complex molecular interactions between genetic predisposition (HLA-DR3, CTLA-4 polymorphisms), environmental triggers including iodine excess and stress, and immune system dysregulation. CD11c+ B cells have emerged as novel therapeutic targets, demonstrating strong correlation with serum TRAb levels and disease activity markers. Current treatment modalities include antithyroid drugs (methimazole, propylthiouracil), radioiodine therapy, and surgical thyroidectomy. Emerging therapeutic approaches focus on TRAb-targeting strategies, including novel TSHR antagonists (K1-70) and precision medicine strategies that incorporate detailed immunophenotyping profiles. Recent advances in understanding immune mechanisms have opened promising new therapeutic avenues. TRAb-targeted biologics and personalized precision medicine approaches show significant potential for individualized treatment strategies, potentially improving long-term remission rates and substantially reducing disease recurrence in comprehensive Graves' disease management.
