Endocrine Abstracts

A 32-year-old gentleman, of South-Asian origin was admitted with a 4-week history of abdominal pain, nausea and vomiting. He also had history of polyuria, polydipsia and weight loss over 6 weeks. Just prior to these symptoms he had been started on colecalciferol 20 000 units weekly by his GP for Vitamin D deficiency (25(OH) Vitamin D – 10.3 nmol/l (48–145)). On admission he had adjusted calcium of 4.52 mmol/l and acute kidney injury with his eGFR being 38 ml/min per 1.73 m². His bone profile and renal functions were normal earlier, before starting Dekristol. His PTH was suppressed at 0.53 pmol/l (1.1–5.5) and 25(OH) Vitamin D was still low at 37.1 nmol/l. Intravenous fluids and pamidronate resulted in only mild improvement. His chest X-ray showed bihilar lymphadenopathy which prompted us to start him on Prednisolone 30 mg daily. The serum calcium started to improve within 24 hours and the renal functions also improved gradually. His serum ACE level was 229 U/l (8–52) and 1,25(OH)₂ Vitamin D was increased at >250 pmol/l (20–120). CT chest confirmed chest X-ray findings and showed multiple cervical lymph nodes. A subsequent lymph node biopsy showed well formed non-caseating granulomata with multinucleated macrophages, confirming the diagnosis of sarcoidosis.

Discussion: The incidence of hypercalcaemia in sarcoidosis is 10–20%. Increased intestinal calcium absorption induced by high serum calcitriol concentrations is the primary abnormality, although a calcitriol-induced increase in bone resorption may also contribute. In sarcoidosis, conversion from calcidiol to calcitriol becomes independent of PTH and occurs in activated mononuclear cells (particularly macrophages). Parathyroid-hormone-related protein may also contribute to the hypercalcaemia in some patients with sarcoidosis. This case illustrates that replacement of oral colecalciferol to treat vitamin D deficiency can precipitate a dangerous elevation in serum calcium levels in previously un-recognised sarcoidosis.