Antithyroid Therapy

Graves disease is an autoimmune cause of hyperthyroidism. Thyroid-stimulating immunoglobulins bind to and activate TSH receptors on thyroid cells. The gland behaves as though it is receiving a persistent TSH signal, producing and releasing excessive thyroxine (T4) and triiodothyronine (T3). Excess thyroid hormone accelerates metabolic activity and sensitizes tissues to catecholamines. The clinical pattern is therefore both metabolic and adrenergic: heat intolerance, sweating, weight loss despite appetite, tremor, anxiety, diarrhoea, palpitations, tachycardia, and exercise intolerance. Older adults may present less dramatically, with new atrial fibrillation, heart failure, weakness, confusion, or unexplained weight loss rather than obvious tremor and agitation. Thyrotoxicosis is not always Graves disease. Thyroiditis can release thyroid hormone already stored in damaged follicles, but the gland is not actively synthesizing excess hormone. Thionamides inhibit new hormone synthesis, so they are useful in Graves disease but do not correct hormone leakage from thyroiditis.