Bustos D, Pons S, Pernas J C, Gonzalez H, Caldarini M I, Ogawa K, De Paula J A
Instituto de Gastroenterologia Dr. Jorge Perez Companc, Buenos Aires, Argentina.
Dig Dis Sci. 1994 Nov;39(11):2315-9. doi: 10.1007/BF02087644.
In patients with short bowel syndrome (SBS), the carbohydrate overload to the colon may disturb the normal pattern of colonic fermentation with production of D-lactic acid and subsequent development of a metabolic D-lactic acidosis. We measured D-lactic acid in blood, urine, and feces, as well as the composition of fecal water and fecal reducing substances from 11 patients with SBS, comparing the results with those from normal subjects. The fecal water from patients with SBS was characterized by low pH, potassium, and volatile fatty acids, high osmotic gap, and high concentration of L- and D-lactic acid. Five of 11 had abnormal amounts of fecal reducing substances. Fecal D-lactic acid was increased in nine of 11 patients. However, none of these patients showed D-lactic acid in urine, and only one had a very low concentration in plasma. These results show that D-lactic acid was overproduced in the colon of most of the patients with SBS. However, other factors such as absorption or impaired D-lactic acid metabolism may be necessary for a plasmatic increase of D-lactic acid.
在短肠综合征(SBS)患者中,结肠碳水化合物负荷过重可能会扰乱结肠正常发酵模式,导致D-乳酸生成,并随后引发代谢性D-乳酸酸中毒。我们检测了11例SBS患者血液、尿液和粪便中的D-乳酸,以及粪便水和粪便还原物质的成分,并将结果与正常受试者的结果进行比较。SBS患者的粪便水具有低pH值、低钾、低挥发性脂肪酸、高渗透间隙以及高浓度L-和D-乳酸的特点。11例患者中有5例粪便还原物质含量异常。11例患者中有9例粪便D-乳酸增加。然而,这些患者中没有一人尿液中出现D-乳酸,只有一人血浆中D-乳酸浓度极低。这些结果表明,大多数SBS患者的结肠中D-乳酸产生过多。然而,D-乳酸血浆水平升高可能还需要其他因素,如吸收或D-乳酸代谢受损。