Jonas A, Avigad S, Diver-Haber A, Katznelson D
J Pediatr. 1979 Sep;95(3):366-72. doi: 10.1016/s0022-3476(79)80508-9.
Fat absorption was studied in 10 patients recovering from an episode of acute infectious gastroenteritis who failed to gain weight despite adequate caloric intake. Three patients restudied after clinical improvement and three other infants with failure to thrive, unrelated to gastrointestinal problems, served as control subjects. Fat balance studies during the ingestion of a formula containing long-chain fatty acids demonstrated significant degrees of steatorrhea in patients (mean CFA 70.6 +/- 10.7 compared to 90.3 +/- 2.4 in control subjects). The administration of a test meal demonstrated a marked deficiency of duodenal bile acid concentration and of fat incorporation into the micellar phase in patients. Fecal bile acid excretion was significantly increased in patients (mean 33.9 +/- 11.6 microM/kg/day) as compared to control subjects (mean 13.5 +/- 3.1 microM/kg/day). Bacterial overgrowth and abnormalities of the small intestinal mucosa were not constant. Ileal dysfunction and associated bile acid loss are possible causes of disturbed fat assimilation following acute intestinal infection in children.
对10例急性感染性胃肠炎发作后康复但尽管摄入足够热量仍未增重的患者进行了脂肪吸收研究。3例临床症状改善后再次接受研究的患者以及另外3例与胃肠道问题无关的发育不良婴儿作为对照对象。在摄入含长链脂肪酸的配方奶期间进行的脂肪平衡研究表明,患者存在明显程度的脂肪泻(患者平均CFA为70.6±10.7,而对照对象为90.3±2.4)。给予试验餐显示患者十二指肠胆汁酸浓度明显不足,且脂肪进入微胶粒相存在缺陷。与对照对象(平均13.5±3.1微摩尔/千克/天)相比,患者粪便胆汁酸排泄显著增加(平均33.9±11.6微摩尔/千克/天)。细菌过度生长和小肠黏膜异常并不持续存在。回肠功能障碍及相关胆汁酸丢失可能是儿童急性肠道感染后脂肪同化紊乱的原因。