Gilman R H, Partanen R, Brown K H, Spira W M, Khanam S, Greenberg B, Bloom S R, Ali A
Johns Hopkins University, School of Hygiene and Public Health, Department of International Health, Baltimore, Maryland.
Gastroenterology. 1988 Jun;94(6):1308-14. doi: 10.1016/0016-5085(88)90668-3.
To assess the effect of malnutrition on gastric acidity and gastric bacterial colonization, we studied 35 severely malnourished Bangladeshi children before (0 wk) and after (3 wk) they received nutritional rehabilitation for 3 wk. These results were compared with those obtained from a similarly examined group of 20 better-nourished Bangladeshi children. Gastric acid output, both basal and after betazole stimulation, was significantly lower in the malnourished group at 0 wk compared with the better-nourished children (p less than 0.01): basal 0.22 vs. 0.52 mEq HCl/h and stimulated 0.90 vs. 2.5 mEq HCl/h. Both the concentration of acid and the rate at which gastric juice was secreted were decreased in the malnourished group but serum gastrin levels were not significantly different. After 3 wk, the malnourished children had improved from 61% (+/- 9.0%; SD) to 81% (+/- 8.1%) of expected weight-for-height and were not significantly different than the better-nourished group (86% +/- 11%). Nevertheless, gastric acid concentration remained depressed in the 3-wk group, although the rate of gastric juice secretion equaled levels observed in the better-nourished group. None of the better-nourished children had detectable gram-negative bacterial colonization of their gastric juice. In contrast, 26 of 32 (81%) malnourished children at 0 wk were colonized--even after betazole stimulation, 11 of 33 (33%) gastric juice samples yielded viable organisms--suggesting that the decrease in gastric acid output greatly reduced the gastric acid barrier. Interestingly, only 9 of 20 (45%) better-nourished children had gastric juice with basal pH values below 4.0, suggesting that the gastric acid barrier may be an intermittent defense factor in Bangladeshi children.
为评估营养不良对胃酸度和胃细菌定植的影响,我们对35名严重营养不良的孟加拉儿童在接受3周营养康复治疗前(0周)和治疗后(3周)进行了研究。这些结果与20名营养状况较好的孟加拉儿童组成的类似检查组的结果进行了比较。与营养状况较好的儿童相比,营养不良组在0周时基础胃酸分泌量和倍他唑刺激后的胃酸分泌量均显著降低(p小于0.01):基础胃酸分泌量分别为0.22 mEq HCl/h和0.52 mEq HCl/h,刺激后胃酸分泌量分别为0.90 mEq HCl/h和2.5 mEq HCl/h。营养不良组胃酸浓度和胃液分泌速率均降低,但血清胃泌素水平无显著差异。3周后,营养不良儿童的身高别体重从预期的61%(±9.0%;标准差)提高到81%(±8.1%),与营养状况较好的组(86%±11%)无显著差异。然而,3周组的胃酸浓度仍然较低,尽管胃液分泌速率与营养状况较好的组相当。营养状况较好的儿童胃液中均未检测到革兰氏阴性菌定植。相比之下,32名营养不良儿童中有26名(81%)在0周时存在细菌定植——即使在倍他唑刺激后,33份胃液样本中有11份(33%)培养出活菌——这表明胃酸分泌量的减少大大降低了胃酸屏障。有趣的是,20名营养状况较好的儿童中只有9名(45%)的基础胃液pH值低于4.0,这表明胃酸屏障可能是孟加拉儿童的一种间歇性防御因素。