Calcium metabolism in sarcoidosis and its clinical implications

Objective. To examine the clinical implications of disturbed calcium metabolism in sarcoidosis and how the pathophysiology affects management strategies. Methods. The literature concerning calcium metabolism in sarcoidosis was reviewed. Results. Dysregulated calcium metabolism is a well‐recognized complication of sarcoidosis, resulting in hypercalcaemia (prevalence 5–10%), hypercalcuria (40–62%) and reduced bone density (40–55%). Extrarenal synthesis of calcitriol [1,25(OH)2D3] is central to the pathogenesis of abnormal calcium homeostasis, but alterations in parathyroid hormone (PTH) activity and the expression of PTH‐related peptide have also been demonstrated. The immunosuppressive properties of calcitriol suggest that the raised levels seen in sarcoidosis could represent an adaptive response to the undefined antigen that causes sarcoidosis. Conclusions. The mechanisms of abnormal calcium metabolism in sarcoidosis need to be understood when treating hypercalcaemia, hypercalcuria and corticosteroid‐induced osteoporosis. Studies are required to determine if the currently available therapies for osteoporosis are safe and effective in sarcoidosis.