[Drug-induced hypercalcemia].
Drug-induced hypercalcemia is caused by increased bone resorption (vitamin D and vitamin A intoxication), increased calcium absorption in the gastrointestinal tract (vitamin D intoxication, excessive intake of calcium) or increased calcium reabsorption in the renal tubules (thiazide diuretics). When vitamin D (D(2) or D(3)) intoxication develops, the hypercalcemia persists for more than several months. Therefore, short-acting active vitamin D (1alpha-OHD(3), 1,25- (OH) (2)D(3)) are clinically used. Recently, various analogs of 1,25- (OH) (2)D(3) with potent differentiation stimulating activity on keratinocytes but insufficient calcium-movilizing activity have been developed (tacalcitol, calcipotriol, 22-oxacalcitriol). However, severe hypercalcemia may develop when these ointments were abundantly applied to patients with psoriasis since the agents can be easily absorbed through the skin lesions.
Sato
Kanji
K
Field of Thyroid and Parathyroid Disease, Division of Internal Medicine, Graduate School of Medicine, Tokyo Women's Medical University.
D001862:Bone Resorption / Q000150:complications*; D004872:Ergocalciferols / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D006934:Hypercalcemia / Q000139:chemically induced*; D011565:Psoriasis / Q000188:drug therapy; D013250:Steroid Hydroxylases / Q000009:adverse effects / Q000627:therapeutic use; D014807:Vitamin D / Q000506:poisoning*
D004872:Ergocalciferols; D014807:Vitamin D; D013250:Steroid Hydroxylases; C406322:vitamin D 1-alpha hydroxylase