Functional hypoparathyroidism: causes, pathogenesis, clinical significance in Bone tissue pathology

Abstract

Parathyroid hormone (PTH) regulates the maintenance of serum calcium concentration in strict limits through direct effects on bones and kidneys and indirectly due to the effect on the gastrointestinal tract. PTH also regulates phosphorus metabolism. Secondary hyperparathyroidism develops in response to a decreased serum calcium and vitamin D levels, leading to an increased bone resorption. However, the increase in parathyroid hormone above the reference values is not observed in all cases of vitamin D deficiency or hypocalcemia. Supressed or inadequately normal PTH in these conditions is referred to as functional hypoparathyroidism. Various theories have been suggested to explain the functional hypoparathyroidism: magnesium deficiency, intestinal calcistat, lower reference values for plasma PTH compared to current cut off interval, biological variations of vitamin D-binding protein. However, at present none of these theories are generally accepted. The clinical significance of functional hypoparathyroidism may be that vitamin D deficiency, hypocalcemia, and hypomagnesemia are associated with a risk of fracture, regardless PTH level.

Keywords

• functional hypoparathyroidism
• vitamin d deficiency
• hypocalcemia
• hypomagnesemia
• fracture risk