Endocrine Abstracts

Parathyroid hormone(PTH) is released by the parathyroid glands to regulate the concentration of ionised calcium in extracellular fluid.Any change in ionised calcium is followed by reciprocal changes in PTH secretion. PTH acts on the kidney to increase the renal tubular reabsorption of calcium and to increase the synthesis of the hormonal metabolite of vitamin D which enhances the intestinal absorption of calcium. Prolonged PTH secretion increases calcium release from bone as a result of an increase in osteoclastic bone resorption and can result in bone disease whereas pulsatile dosing with PTH is anabolic to bone and is used to treat osteoporosis.

Parathyroid overactivity results in an increase in bone turnover due to an increase in both osteoblastic and osteoclastic activity and any pre-existing remodelling imbalances are exacerbated by PTH excess.

The ravages of PTH excess on the skeleton are more pronounced in cortical as opposed to trabecular bone. The commonest consequence of PTH excess is to exacerbate the remodelling imbalances which affect the aging skeleton and this PTH excess may arise in Primary Hyperparathyroidism when ionised calcium is raised or in secondary hyperparathyroidism when in response to a reduction in ionised calcium a compensatory increase in PTH secretion is required to correct hypocalcaemia. Secondary hyperparathyroidism is seen in renal insufficiency, vitamin D deficiency and certain malabsorptive states.

Dramatic and prolonged increases in PTH secretion are seen in prolonged vitamin D deficiency and the rare but severe forms of Primary Hyperparathyroidism when bone cysts are sometimes seen as well as demineralisation of the skeleton, a condition called osteitis fibrosa cystica.

The effects of changes to parathyroid physiology and pathology on the skeleton will be discussed in the presentation.