Hypercalcaemia and hypocalcaemia
The most frequent cause of hypercalcaemia outside hospital is primary hyperparathyroidism (PHPT). This has to be separated from familial hypocalciuric (benign) hypercalcaemia (FHH) sharing the same biochemical characteristics but caused by a mutation in the Calcium Sensing Receptor (CaSR) gene (Nissen PH et al. 2007). PHPT is treated surgically whereas surgery is contraindicated in FHH. We have shown that this diagnostic separation can be achieved by a two step procedure where the calcium/creatinine clearance ratio (CCCR) is determined first followed by a CaSR-gene analysis if CCCR < 0.02 (Christensen SE et al. 2008).
PHPT is characterized by a reduced vitamin D status compared with healthy age, gender and season matched controls (Moosgaard B et al. 2005). In a recently published randomised controlled trial, we have shown that a six-month supplement with 70 microgram/day of vitamin D3 lowers PTH levels by 17% and increases BMD at the lumbar spin by 2.5% compared with placebo (Rolighed et al JCEM 2014). A replete vitamin D status should therefore be ensured in all patients with PHPT.
Congenital or acquired (postsurgical) hypoparathyroidism (HypoPT) is a common course of symptomatic hypocalcaemia. Until now it has been treated by a calcium supplementation in combination with 1alpha-hydroxylated vitamin D analogues However, this treatment is followed by low bone turnover, increased bone mass, hypercalciuria with risk of renal stones, reduced muscle strength and reduced quality of life. We have shown in a RCT that treatment with PTH (1-84) can maintain normocalcaemia, increase bone turnover and renew accumulated old bone (Sikjaer T et al. 2011).
Lars Rejnmark, Associate professor, MD, PhD, DMSci, firstname.lastname@example.org