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Contributed by Mr David Scott-Coombes, consultant endocrine surgeon at the University Hospital of Wales, Cardiff.
Section 1 Epidemiology and pathology
On the surface of every parathyroid cell is a calcium-sensing receptor (set to 2.20-2.60mmol/l). A fall in serum calcium or a rise in serum phosphate triggers the secretion of parathyroid hormone (PTH). PTH has effects on the intestines, bones and kidneys, which all result in an increase in serum calcium until the normal physiological concentration has been restored. A chronic excess secretion of PTH is termed hyperparathyroidism (HPT).
Classification of HPT
Primary hyperparathyroidism (1HPT) results from an inappropriate autonomous excess secretion of PTH. This may be due to a solitary adenoma (>85 per cent), four-gland hyperplasia (10 per cent), double adenoma (2 per cent) or, rarely, carcinoma (<1 per cent).1 The vast majority of cases of 1HPT are sporadic, but rarely it can be associated with multiple endocrine neoplasia type 1.
Secondary hyperparathyroidism (2HPT) results from an appropriate excess secretion of PTH in response to prolonged reduction in serum calcium The patient has a high PTH with normal calcium. Vitamin D deficiency is the most common underlying cause, which may be either dietary or secondary to renal failure. Vitamin D replacement will rectify the former cause of 2HPT.
Tertiary hyperparathyroidism (3HPT) occurs in patients who, after a period of dialysis, undergo successful renal transplantation.
The previously appropriate excess secretion of PTH (2HPT) becomes inappropriate and results in hypercalcaemia. In an attempt to avoid confusion, …