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[药物性高钙血症]

[Drug-induced hypercalcemia].

作者信息

Sato Kanji

机构信息

Field of Thyroid and Parathyroid Disease, Division of Internal Medicine, Graduate School of Medicine, Tokyo Women's Medical University.

出版信息

Clin Calcium. 2006 Jan;16(1):67-72.

Abstract

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.

摘要

药物性高钙血症是由骨吸收增加(维生素D和维生素A中毒)、胃肠道钙吸收增加(维生素D中毒、钙摄入过多)或肾小管钙重吸收增加(噻嗪类利尿剂)引起的。当发生维生素D(D₂或D₃)中毒时,高钙血症会持续数月以上。因此,临床上使用短效活性维生素D(1α-OHD₃、1,25-(OH)₂D₃)。最近,已开发出各种对角质形成细胞具有强分化刺激活性但钙动员活性不足的1,25-(OH)₂D₃类似物(他卡西醇、卡泊三醇、22-氧阿法骨化醇)。然而,由于这些药物可通过皮肤病变轻易吸收,当将这些药膏大量应用于银屑病患者时,可能会发生严重高钙血症。

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