Graves' Disease I: Introduction

Graves' disease is an autoimmune condition and the leading cause of hyperthyroidism. It develops when the immune system produces thyroid-stimulating immunoglobulins, a type of autoantibody that abnormally activates the thyroid gland.

These antibodies bind to TSH receptors on the thyroid gland, leading to excessive production of thyroid hormones.

This increases the body’s metabolic rate and affects functions such as heart rate and temperature regulation.

Graves’ disease is linked to a genetic predisposition—particularly the HLA-DR3 and HLA-B8 variants—along with environmental triggers such as smoking and stress.

These specific HLA types can present thyroid proteins in an altered manner, increasing the likelihood of activating autoreactive T cells and, in turn, raising the risk of developing Graves’ disease.

Clinically, it presents with symptoms of hyperthyroidism, including weight loss, heat intolerance, palpitations, and menstrual irregularities.

A goiter, or an enlarged thyroid gland, is typically present. Ophthalmopathy, characterized by exophthalmos and periorbital edema, is a distinctive feature.