Hypercalcemia is seen in all except-
biologic action of the vitamin, perhaps the consequence of increased levels of 25(OH)D rather than merely increased levels of the active metabolite 1,25(OH) 2 D (the latter may not be elevated in vitamin D intoxication). 25(OH)D has definite, if low, biologic activity in the intestine and bone. The production of 25(OH)D is less tightly regulated than is the production of 1,25(OH) 2 D. Hence concentrations of 25(OH)D are elevated severalfold in patients with excess vitamin D intake.Lithium, used in the management of bipolar depression and other psychiatric disorders, causes hypercalcemia in ~10% of treated patients. The hypercalcemia is dependent on continued lithium treatment, remitting and recurring when lithium is stopped and restaed. The parathyroid adenomas repoed in some hypercal- cemic patients with lithium therapy may reflect the presence of an independently occurring parathyroid tumor; a permanent effect of lithium on parathyroid gland growth need not be implicated as most patients have complete reversal of hypercalcemia when lithium is stopped. (Harrison 17 pg 2385)
Lithium
Multiple myeloma
Loop diuretics
HypervitaminosisD
Endocrinology