Abstract
Autoimmune diseases are characterized by the persistent activation of immunologic effector mechanisms that alter the function and integrity of individual cells and organs. This process of abnormal self-reactivity may be initiated by environmental agents, and it probably becomes sustained because of some abnormality causing persistent T-lymphocyte activation that overrides normal tolerance of self-antigens.1 The clinical manifestations of the resulting disease may reflect tissue abnormalities due to antibody-mediated or cell-mediated immunity, or both.The clinical spectrum of autoimmune thyroid disease is very broad. Affected persons may have hyperthyroidism or hypothyroidism or may be euthyroid, with or without ophthalmopathy or goiter. The . . .