Clinical Presentation

Disease affecting the parathyroid glands usually presents as a consequence of altered function. Hyperparathyroidism describes an altered metabolic state due to increased secretion of parathyroid hormone (parathormone). Rarely seen nowadays is the full spectrum of "bones, stones, groans and moans"; biochemical investigation of non-specific complaints such as profound tiredness, nausea or thirst is the usual method of diagnosis although a small proportion of cases are detected during investigation of patients with organ-specific complaints. Primary hyperparathyroidism is due to an increased secretion of parathormone from one or more of the parathyroid glands, usually caused by an adenoma. Secondary hyperparathyroidism is due to the physiological response of the four parathyroid glands to persistent hypocalcaemia, usually renal failure, malabsorption syndromes or Vitamin D deficiency. Tertiary hyperparathyroidism is a result of persistent autonomous hypersecretion of parathormone in long-standing secondary hyper-parathyroidism following correction of the hypocalcaemia.

Hypoparathyroidism is a result of reduced secretion of parathormone and is characterised by neuromuscular excitability. Rapid onset of hypoparathyroidism, e.g., following surgery to the neck, results in muscular tetany and paraesthesia while an insidious onset, such as with autoimmune disease, may induce mucocutaneous candidosis, cataracts and basal ganglia changes as well.

Pseudohypoparathyroidism refers to a rare inherited defect of parathyroid hormone receptor function in peripheral tissue characterised by insensitivity to circulating parathormone; the glands are hyperplastic.

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