Levy Y, Bansal M, Zackson D A, Lane J, Shike M
Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.
JPEN J Parenter Enteral Nutr. 1988 May-Jun;12(3):313-7. doi: 10.1177/0148607188012003313.
A 44-yr-old woman with a 16-yr history of heavy antacid ingestion was evaluated for severe weight loss, weakness, bone pain, and multiple fractures. Laboratory investigation revealed severe hypophosphatemia with undetectable phosphate in the urine. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels were normal. Transiliac bone biopsy revealed evidence of mineralization defect compatible with hypophosphatemic osteomalacia. Bone densitometry documented decreased bone density with a low mineral content. Management included withdrawal of antacids and provision of phosphate-supplemented enteral nutrition, which resulted in prompt weight gain and resolution of the clinical and biochemical abnormalities. The pathogenesis, diagnosis and histological features of hypophosphatemic osteomalacia are discussed.
一名有16年大量服用抗酸剂病史的44岁女性,因严重体重减轻、乏力、骨痛和多处骨折接受评估。实验室检查发现严重低磷血症,尿液中无法检测到磷酸盐。血清甲状旁腺激素(PTH)、25-羟维生素D和1,25-二羟维生素D水平正常。经髂骨活检显示有与低磷性骨软化症相符的矿化缺陷证据。骨密度测定显示骨密度降低,矿物质含量低。治疗措施包括停用抗酸剂并提供补充磷酸盐的肠内营养,这导致体重迅速增加,临床和生化异常得到缓解。本文讨论了低磷性骨软化症的发病机制、诊断和组织学特征。