Dahlquist N R, Perrault J, Callaway C W, Jones J D
Mayo Clin Proc. 1984 Mar;59(3):141-5. doi: 10.1016/s0025-6196(12)60764-2.
Two patients with recurring attacks of encephalopathy after jejunoileostomy for morbid obesity had elevated D-lactate concentrations in blood and urine. The syndrome and the biochemical abnormalities were reproduced by ingestion of a high carbohydrate diet. In the second case, fasting and intravenous supplementation with amino acids and glucose resulted in the disappearance of D-lactate from the urine and blood and amelioration of the symptoms. Stool cultures from the second patient were shown to be capable of producing D-lactate, and concentrations of D-lactate in saline and peptone yeast broth filtrates of the stool paralleled the changes in urinary excretion of the D-lactate during fasting and overfeeding. Thus, we have demonstrated a temporal relationship between the neurologic symptoms and the elevated concentrations of D-lactate in blood, urine, and stool. Whether D-lactate accounts for part or all of the encephalopathic changes remains to be determined.
两名病态肥胖患者在空肠回肠造口术后反复出现脑病发作,其血液和尿液中的D-乳酸浓度升高。高碳水化合物饮食可重现该综合征及生化异常。在第二个病例中,禁食并静脉补充氨基酸和葡萄糖后,尿液和血液中的D-乳酸消失,症状改善。第二个患者的粪便培养物显示能够产生D-乳酸,粪便生理盐水和蛋白胨酵母肉汤滤液中的D-乳酸浓度与禁食和过量喂养期间尿液中D-乳酸排泄的变化平行。因此,我们证明了神经症状与血液、尿液和粪便中D-乳酸浓度升高之间的时间关系。D-乳酸是否导致了部分或全部脑病变化仍有待确定。