Karton M A, Rettmer R, Lipkin E W, Ott S M, Chait A
Department of Medicine, University of Washington, Seattle 98195.
JPEN J Parenter Enteral Nutr. 1989 Mar-Apr;13(2):132-5. doi: 10.1177/0148607189013002132.
D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
在一些吸收不良且持续口服碳水化合物的患者中,D-乳酸会蓄积,从而导致酸中毒和脑病的临床综合征。为了评估在接受长期肠外营养但仍保持口服摄入的吸收不良患者中,D-乳酸是否会导致酸中毒和/或代谢性骨病,我们对14名长期接受肠外营养的受试者(平均支持时间74个月)和27名对照受试者的血清和尿液中的D-乳酸水平进行了测量。仅在两名肠外营养受试者中发现血清和尿液中的D-乳酸显著升高。两名D-乳酸水平升高的受试者均有骨痛、骨折的X线证据以及骨软化症的活检证据。这些研究表明,D-乳酸蓄积可能是一种迄今未被认识到的代谢异常,与长期接受肠外营养支持的吸收不良患者的代谢性骨病和酸中毒有关。