Harmelin D L, Martin F I, Wark J D
Royal Melbourne Hospital, Vic., Australia.
Aust N Z J Med. 1990 Dec;20(6):803-5. doi: 10.1111/j.1445-5994.1990.tb00427.x.
A 29-year-old insulin-dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma, 1,25-dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. We propose that phosphate depletion secondary to antacid abuse caused 1 alpha-hydroxylase activation and elevation of the plasma 1,25-dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid-induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease.
一名29岁的胰岛素依赖型糖尿病女性因滥用抗酸剂出现了磷酸盐缺乏、肾结石和双侧输尿管梗阻。与以往关于慢性磷酸盐缺乏的描述不同,该患者没有肌痛、无力和骨痛。生化特征包括低磷血症、高钙尿症、低磷尿症、血浆1,25-二羟维生素D升高和血浆完整甲状旁腺激素降低。当减少抗酸剂摄入并补充磷酸盐摄入时,这些异常情况得到纠正。我们认为,抗酸剂滥用继发的磷酸盐缺乏导致1α-羟化酶激活和血浆1,25-二羟维生素D水平升高,从而导致明显的高钙尿症。一旦确诊,抗酸剂滥用是高钙尿症和肾结石的一个易于逆转的病因。此外,抗酸剂引起的磷酸盐缺乏可能在没有肌肉骨骼症状的情况下表现为肾结石。本报告旨在引起对这种肾结石疾病重要病因的关注。