Graves’ Disease : Introduction

Graves’ disease (GD) is an autoimmune disorder predominantly affecting the thyroid gland, making it the most prevalent cause of hyperthyroidism. This condition can occur at any age but is particularly common in women of reproductive age. The pathogenesis of Graves’ disease involves the production of autoantibodies targeting the thyroid-stimulating hormone receptor (TSHR). These autoantibodies function as agonists, stimulating excessive thyroid hormone secretion and thus bypassing the regulatory control of the pituitary gland.

Apart from hyperthyroidism, TSHR autoantibodies are also implicated in extrathyroidal manifestations such as Graves’ orbitopathy (GO) and pretibial myxedema. In GO, there is a notable interaction between TSHR autoantibodies and insulin-like growth factor 1 receptor (IGF1R), leading to tissue expansion and inflammation around the eyes. Although the precise etiology of Graves’ disease is unknown, it is believed to arise from a combination of genetic predisposition and environmental factors in an immunologically susceptible individual.

Graves’ disease accounts for approximately 60% to 80% of all hyperthyroidism cases. It is significantly more common in women than in men, with lifetime risk estimates of about 3% for women and 0.5% for men​.