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后天性单糖不耐受婴儿体内潴留氢离子的饮食来源。

Dietary origin of retained H+ in infants with acquired monosaccharide intolerance.

作者信息

Carrazza F R, Carrazza M Z, Nichols V N, Nichols B L

机构信息

USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030.

出版信息

J Pediatr Gastroenterol Nutr. 1989 Feb;8(2):181-8. doi: 10.1097/00005176-198902000-00010.

DOI:10.1097/00005176-198902000-00010
PMID:2709249
Abstract

Net external acid balance was studied in 12 malnourished infants with chronic diarrhea (some of whom had acquired monosaccharide intolerance). When the infants achieved an adequate energy intake from a formula that contained either glucose or glucose polymers, seven developed metabolic acidosis and five remained free of acidosis. During the study, the acidotic infants produced a significant excess of acid (3.7 +/- 2 vs. 0.5 +/- 2 mEq/kg/day, p less than 0.005). The amount they excreted in urine (2.9 +/- 2 mEq/kg/day), however, was similar to that excreted by nonacidotic infants (2.7 +/- 2 mEq/kg/day) and indicated renal inability to reduce the excess acid load. The net effect was hydrogen ion (H+) retention (+0.8 +/- 0.8 vs. -2.2 +/- 0.8 mEq/kg/day, p less than 0.001). Good correlation existed between the net acid balance and the acid-base measurement in the blood. We speculate that (a) the increased acid load was a consequence of colonic bacterial production of volatile fatty acids from carbohydrate malabsorbed from the small bowel and (b) the renal incapacity to excrete H+ probably was secondary to potassium and phosphate depletion.

摘要

对12名患有慢性腹泻的营养不良婴儿(其中一些婴儿患有获得性单糖不耐受症)的净外部酸平衡进行了研究。当这些婴儿从含有葡萄糖或葡萄糖聚合物的配方奶中获得足够的能量摄入时,7名婴儿出现了代谢性酸中毒,5名婴儿未出现酸中毒。在研究过程中,酸中毒婴儿产生的酸显著过量(3.7±2 vs. 0.5±2 mEq/kg/天,p<0.005)。然而,他们的尿液排泄量(2.9±2 mEq/kg/天)与非酸中毒婴儿的排泄量(2.7±2 mEq/kg/天)相似,表明肾脏无法减少过量的酸负荷。净效应是氢离子(H+)潴留(+0.8±0.8 vs. -2.2±0.8 mEq/kg/天,p<0.001)。净酸平衡与血液中的酸碱测量值之间存在良好的相关性。我们推测:(a)酸负荷增加是结肠细菌从小肠吸收不良的碳水化合物中产生挥发性脂肪酸的结果;(b)肾脏排泄H+的能力不足可能继发于钾和磷酸盐缺乏。

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