Abstract
AUTOIMMUNE BASIS OF HYPERTHYROIDISM AND ITS LABORATORY DIAGNOSIS: AN OVERVIEW
Erhunmwunse R. U., Chukwuemeka C. P., *Ehiaghe F. A. and 3Ogbodo E. C.
ABSTRACT
This review explores hyperthyroidism, an endocrine disorder marked by excessive secretion of thyroid hormones, using Graves’ disease as a case study, the most common autoimmune cause. While hyperthyroidism can arise from several etiologies, Graves’ disease is distinguished by its autoimmune nature, where the body produces thyroid – stimulating immunoglobulin (TSI) that bind to and activate thyroid – stimulating hormone receptors (TSHR) on the thyroid gland. This abnormal immune response result in unregulated stimulation of thyroid hormone production and release, leading to the clinical manifestation of hyperthyroidism. Graves’ disease exemplifies a Type V hypersensitivity reaction, a subclass of hypersensitivity defined by stimulatory autoantibodies that mimic physiological ligands rather than destroy cells or tissues. This mechanism sets it apart from the known Type II hypersensitivity reactions, which involves cytotoxic antibody – mediated destruction. The Type V classification is critical to understanding the disease mechanism in Graves’ disease, as it explains the persistent hormonal overstimulation seen in affected individuals. This review details the immunopathological basis of Graves’ disease, beginning with the loss of immune tolerance, the role of antigen – presenting cells, T – helper cell differentiation, B – cell activation, and subsequent autoantibody production. It explores the molecular and cellular events that underpin this autoimmune activation and how they contribute to the thyroid gland. Special emphasis is placed on the role of TSHR autoantibodies, cytokine imbalances, and the involvement of genetic and environmental triggers that contribute to disease onset and progression. In addition, this work presents a comprehensive overview of laboratory diagnosis of hyperthyroidism and Graves’ disease, including thyroid function tests (T3, T4 TSH level), thyroid autoantibody assays (TRAb, TSI), imaging techniques like ultrasonography and other confirmatory investigations.
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