Endocrine Abstracts

The sustained over-secretion of PTH is a common clinical problem with particular consequences for the skeleton. Hyperparathyroidism (HPT) increases the bone surface undergoing remodelling, amplifies the negative balance at the bone multicellular unit and increases activation frequency, eroded surface and formation, without increased trabecular perforation. Cortical bone is particularly susceptible to the effects of hyperparathyroidism and bone mineral density (BMD) measurements should include the radius or total body, The presence and severity of bone loss has important therapeutic implications.

Primary hyperparathyroidism is now usually asymptomatic but the classic renal, musculoskeletal, abdominal and neuropsychiatric symptoms together with severe life-threatening hypercalcaemia may still occur. Recent studies have shown an increase in fracture risk in HPT: vertebrae, approximately 3-fold; forearm, approximately 2–fold; hip, approximately 1.5 fold; and all fractures approximately 1.5-fold. The recent recommendation is that management of bone disease should assume the same relationship between BMD and fracture risk as exists in normocalcaemic individuals and as a consequence intervention is indicated at a T score below −2.5. Since both men and women lose bone as they age the T score will invariably be low merely as a consequence of aging. In the elderly with other co-morbidity it may still be appropriate to base management decisions on the Z score (age-matched BMD) which will reflect the age-independent effect of hyperparathyroidism. Parathyroidectomy seemed to have a beneficial effect but the increase in vertebral fracture risk seen in the untreated condition is difficult to reconcile with the lack of an excess of trabecular perforation in PHPT.