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The molecular mechanisms of parathyroid gland function and primary hyperparathyroidism (PHPT) are progressively being elucidated. The cloning of the extracellular calcium sensing receptor has increased our understanding of the regulation of parathyroid hormone (PTH) production. Molecular biology techniques are also unravelling the defects in parathyroid cell growth and differentiation, which result in adenoma formation and PHPT. Our understanding of the nature of PHPT has also radically altered in recent years with the introduction of routine automated calcium measurements in the 1970s leading to earlier detection of hypercalcaemia due to PHPT. Consequently the classical phenotype of PHPT has shifted from a condition characterised by marked hypercalcaemia, symptomatic renal and bone complications to a mild, asymptomatic condition, where a slight elevation in plasma calcium may be the only presenting feature. Mild PHPT appears usually to be a non-progressive condition with little change in plasma calcium, renal function or bone mineral density. Parathyroidectomy is the treatment of choice for symptomatic disease; however there is debate as patients with mild PHPT may be managed conservatively. Within the last decade there has been an expansion in the treatment options for PHPT. Improvements in parathyroid imaging techniques have led to the development of minimally invasive surgery. Several randomised controlled trials show that conventional anti-resorptive therapies such as hormone replacement therapy and bisphosphonates are useful for managing PHPT in patients not suitable for surgery. Insights into the parathyroid calcium sensing receptor have facilitated the development of calcimimetic agents able to suppress parathyroid hormone production and provide a non-surgical way of altering the disease pathogenesis.


Journal article


CPD Bulletin Clinical Biochemistry

Publication Date





71 - 73