ABSTRACT
Graves’ disease (GD) is an organ-specific autoimmune thyroid disorder characterized clinically by hyperthyroidism, various degrees of diffuse goiter, ophthalmopathy, and, less commonly, pretibial myxedema (1). The hyperthyroidism is due to the presence of autoantibodies that bind to and activate the thyrotropin receptor, thus simulating the action of thyrotropin (2). Although GD is one of the most common thyroid disorders its cause is still incompletely understood. According to current thinking (3-5), GD is considered as a member of the group of diseases referred to as ‘‘complex diseases,’’ which include insulin-dependent diabetes mellitus, rheumatoid arthritis, osteoporosis, and hypertension, among others. These conditions are common, show familial clustering but no Mendelian mode of transmission, and vary in their prevalence and severity. They are thus multifactorial, with the clinical phenotype representing the net effect of all the contributing environmental, endogenous, and genetic factors (Fig. 1). In these complex conditions, GD being no exception, it has been difficult to separate environmental influences from genetic susceptibility (6,7).
