Our review demonstrated over 30 conditions with suspected calcitriol-mediated hypercalcemia, including infections, foreign body exposures, autoimmune diseases, and neoplasms ( Table 1 ). In several cases of calcitriol-mediated hypercalcemia, a distinct disease entity was not found despite extensive investigations ( 14 , 15 ). At the heart of these associations appears to be overexpression of 1α-hydroxylase by tissue macrophages, identified in non-Hodgkin’s lymphoma ( 16 ), dysgerminoma ( 17 ), and granulomatous slack skin disease ( 18 ), and the case of GCP presented here. In addition to sarcoidosis ( 19 ), calcitriol-mediated hypercalcemia has been described in association with Crohn’s disease, where serum calcium and 1,25(OH) 2 D levels parallel disease activity ( 2 , 3 ), as well as Wegener’s granulomatosis ( 20 – 22 ), Langerhans cell granulomatosis ( 23 ), liver granulomas in chronic dialysis patients ( 24 ), and subcutaneous fat necrosis of the newborn ( 25 ). Rheumatoid arthritis ( 26 ) and severe osteoarthritis ( 27 ) may have a similar mechanism, supported by observations that synovial fluid macrophages in inflammatory arthritides may produce 1,25(OH) 2 D ( 28 ).