Graves’ disease

Graves’ disease: is an autoimmune disorder produced by autoantibodies to the TSH receptor, thyroglobulin, and thyroid hormones (T₃ & T₄). It is the most common cause of endogenous hyperthyroidism, and is characterized by:

• Hyperthyroidism resulting from hyperfunctional diffuse enlargement of the thyroid

• Infiltrative ophthalmopathy with resultant exophthalmoses, in most, but not all cases

• Localized, infiltrative dermopathy sometimes called peritibial myxoedema in a minority of patients

• Also sometimes finger clubbing (not seen in other thyrotoxicosis)

Pathogenic mechanisms:

Graves’ disease is autoimmune thyroid hyperplasia in which there is an (autoantibodyLong Acting Thyroid Stimulator – LATS) against the cell TSH receptor. This antibody has the same effect as TSH (from pituitary) in stimulating production of thyroid hormones; but in the absence of negative feedback control, results in excess production of thyroid hormones (T3 & T4).

Other immunoglobulins (e.g. TSH growth-stimulating Ig) implicated in the proliferation of thyroid follicular epithelium and stimulation of thyroid epithelial cell activity also contributes to this disease process.

Clinical features of hyperthyroidism: affects many organs…

• Goitre

• Tachycardia

• Weight loss with increased appetite

• Osteoporosis

Many more including: anxiety, menorrhagia, lid retraction/lag, palpitations, atrial fibrillation, diarrhoea, hair loss, warm moist palms, and tremors.

Laboratory findings:

•  In radioactive iodine uptake by the thyroid (hyperfunction)

•  Levels of T₃ and T₄   levels of TSH (primary thyrotoxicosis)

• Presence of LATS immunoglobulin serum (specific to Graves’ disease)

Category: Pathology Notes