Kassem M, Eriksen E F, Melsen F, Mosekilde L
Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Denmark.
J Intern Med. 1991 Mar;229(3):275-9. doi: 10.1111/j.1365-2796.1991.tb00344.x.
The case of a 75-year-old woman with severe osteomalacia secondary to ingestion of large amounts of an aluminum-containing antacid is reported. Biochemical analysis revealed signs of phosphate malabsorption and increased levels of bone markers (S-alkaline phosphatase and U-hydroxyproline). A 99mTc-bone scan revealed multiple areas of increased uptake. The patient was normocalcaemic, with normal serum levels of intact parathyroid hormone and 25-hydroxyvitamin D. Serum 1,25-dihydroxyvitamin D was high normal. A transiliac bone biopsy from the patient showed severe osteomalacia. Symptoms, biochemical parameters, bone scan and bone morphology were all normalized 1 year after stoppage of antacid ingestion and treatment with vitamin D2. calcium phosphate and sodium fluoride because of severe osteopeni. The characteristics of this condition and the role of phosphate depletion and aluminum in the pathogenesis of bone lesions are discussed.
报告了一例75岁女性因大量摄入含铝抗酸剂继发严重骨软化症的病例。生化分析显示有磷酸盐吸收不良的迹象以及骨标志物（血清碱性磷酸酶和尿羟脯氨酸）水平升高。锝-99m骨扫描显示多个摄取增加区域。患者血钙正常，血清完整甲状旁腺激素和25-羟维生素D水平正常。血清1,25-二羟维生素D处于正常高值。患者的髂骨活检显示严重骨软化症。在停止摄入抗酸剂并用维生素D2、磷酸钙和氟化钠治疗后，由于严重骨质减少，症状、生化参数、骨扫描和骨形态在1年后均恢复正常。讨论了这种情况的特征以及磷酸盐缺乏和铝在骨病变发病机制中的作用。
