7. Diseases of the parathyroid gland: diagnosis and treatment

ANATOMY AND PHYSIOLOGY

• Usually four parathyroid glands lie on the posterior thyroid surface, with variable ectopic positions including the thymus and mediastinum.
• Chief cells secrete parathyroid hormone (PTH), which maintains extracellular calcium by increasing renal calcium reabsorption, increasing phosphate excretion, stimulating renal activation of vitamin D and indirectly increasing intestinal calcium absorption.
• PTH also increases bone resorption when chronically elevated.
• Calcium, phosphate, magnesium, vitamin D and renal function are central to interpretation.

CLASSIFICATION

• Hyperparathyroidism may be primary (autonomous gland secretion, commonly adenoma; also hyperplasia or carcinoma), secondary (compensatory PTH elevation due to chronic kidney disease, vitamin D deficiency or malabsorption) or tertiary (autonomous secretion after longstanding secondary disease).
• Hypoparathyroidism is usually postoperative, autoimmune or related to congenital/genetic disorders.
• Parathyroid carcinoma is rare and often causes severe hypercalcaemia.

PATHOPHYSIOLOGY AND FEATURES

• Primary hyperparathyroidism causes hypercalcaemia with low phosphate, increased bone turnover and renal calcium load.
• It may be asymptomatic or cause renal stones, polyuria, constipation, abdominal discomfort, weakness, depression, bone pain and fragility fractures.
• Secondary hyperparathyroidism is driven by phosphate retention, reduced calcitriol and hypocalcaemia in chronic kidney disease.
• Hypoparathyroidism causes hypocalcaemia and hyperphosphataemia, producing perioral tingling, paraesthesia, cramps, tetany, seizures and prolonged QT interval.
• Severe hypocalcaemia can cause laryngospasm or arrhythmia.