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乳糖不耐受儿童的呼吸甲烷排泄

Respiratory methane excretion in children with lactose intolerance.

作者信息

Medow M S, Glassman M S, Schwarz S M, Newman L J

机构信息

Department of Pediatrics, New York Medical College, Valhalla 10595.

出版信息

Dig Dis Sci. 1993 Feb;38(2):328-32. doi: 10.1007/BF01307552.

Abstract

To evaluate the relationship between colonic methane production and carbohydrate malabsorption, we measured end-expiratory methane levels in 70 normal and 40 lactose-intolerant children. Time-dependent excretion of hydrogen and methane was determined every 30 min for 120 min following a fasting oral lactose challenge (2 g/kg). Mean breath hydrogen levels in normals (lactose-tolerant) equaled 3.7 parts per million (ppm) throughout the study, but increased to > 10 ppm by 60 min and remained elevated in lactose-intolerant subjects. Breath methane in normal children averaged 1.6 ppm from 0 to 120 min. In contrast, CH4 excretion by lactose-intolerant children averaged 5.1 ppm at 90 min; and, by 120 min levels increased significantly compared with control. Breath methane levels in lactose-intolerant subjects following a lactose load continued to increase, however, despite the coingestion of exogenous lactase in amounts calculated to result in complete hydrolysis of the disaccharide. These data demonstrate that lactase-deficient children manifest significant increases in breath methane excretion following lactose ingestion and that enhanced methane production may be a consequence of several factors, including altered fecal pH and increased methanogenic substrates provided by colonic lactose fermentation. Further studies are required to determine the clinical significance of elevated methane production in lactose intolerance.

摘要

为了评估结肠甲烷产生与碳水化合物吸收不良之间的关系,我们测量了70名正常儿童和40名乳糖不耐受儿童的呼气末甲烷水平。在空腹口服乳糖激发试验(2 g/kg)后120分钟内,每隔30分钟测定一次氢气和甲烷随时间的排泄情况。在整个研究过程中,正常(乳糖耐受)儿童的平均呼气氢气水平等于百万分之3.7(ppm),但在60分钟时增加到>10 ppm,并在乳糖不耐受的受试者中保持升高。正常儿童在0至120分钟内的呼气甲烷平均为1.6 ppm。相比之下,乳糖不耐受儿童在90分钟时的CH4排泄平均为5.1 ppm;到120分钟时,与对照组相比水平显著升高。尽管同时摄入了经计算可导致二糖完全水解的外源性乳糖酶,但乳糖负荷后乳糖不耐受受试者的呼气甲烷水平仍持续升高。这些数据表明,乳糖酶缺乏的儿童在摄入乳糖后呼气甲烷排泄显著增加,甲烷产生增加可能是多种因素的结果,包括粪便pH值改变和结肠乳糖发酵提供的产甲烷底物增加。需要进一步研究以确定乳糖不耐受中甲烷产生增加的临床意义。

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