Read N W, Al-Janabi M N, Bates T E, Holgate A M, Cann P A, Kinsman R I, McFarlane A, Brown C
Gut. 1985 Aug;26(8):834-42. doi: 10.1136/gut.26.8.834.
The extent to which monitoring breath hydrogen excretion provides information concerning the entry of the residues of a solid test meal into the colon was investigated in 89 normal subjects, and 11 patients with the irritable bowel syndrome. The profile of breath hydrogen concentration showed an early peak, that occurred soon after ingesting the test meal in 89% subjects. This was followed by a later more prolonged rise in breath hydrogen concentration. The early peak occurred well before a radioactive marker, incorporated in the test meal, reached the caecum and the data suggest it was predominantly caused by the emptying of the remnants of the previous meal from the ileum into the colon. This hypothesis was supported by direct measurements of the rate of delivery of ileostomy effluent in 12 subjects with terminal ileostomies. Fermentation of carbohydrate in the mouth may, however, contribute to the initial peak, but this contribution may be avoided by collecting gas samples from the nares. The secondary rise in breath hydrogen excretion was closely correlated with the arrival of the radioactive marker in the caecum (r = 0.91), p less than 0.001), though the time, at which the secondary peak of breath hydrogen excretion occurred was poorly correlated with the time that all the radioactive test meal had entered the colon. When lactulose was infused directly into the colon, as little as 0.5 g produced a discernible hydrogen response, which occurred within two minutes of the infusion. Increasing the rate of colonic infusion of a 50 ml solution of 10% lactulose from 0.02 to 0.15 g/min in five subjects significantly increased the breath hydrogen concentration. At infusion rates below 0.075 g lactulose/minute, the peak breath hydrogen response preceded the end ot the infusion, while at higher rates of infusion, the peak hydrogen response occurred after the end of the infusion. Although these results confirmed that monitoring breath hydrogen concentration usefully signalled the time taken for a meal containing unabsorbed carbohydrate to reach the colon, it did not reliably indicate the time when all of the meal had entered the colon. Finally, the use of the maximum increase in breath hydrogen concentration as an index of the degree of carbohydrate malabsorption assumes uniform rates of entry into the colon.
在89名正常受试者和11名肠易激综合征患者中，研究了监测呼气中氢气排泄量能在多大程度上提供有关固体试验餐残留物进入结肠的信息。呼气氢气浓度曲线显示出一个早期峰值，89%的受试者在摄入试验餐后不久就出现了这个峰值。随后呼气氢气浓度出现了更持久的后期上升。早期峰值在试验餐中加入的放射性标记物到达盲肠之前就出现了，数据表明它主要是由上一餐的残余物从回肠排空进入结肠引起的。对12名末端回肠造口术患者回肠造口流出物输送速率的直接测量支持了这一假设。然而，口腔中碳水化合物的发酵可能会导致初始峰值，但通过从鼻孔收集气体样本可以避免这种影响。呼气氢气排泄量的二次上升与放射性标记物到达盲肠密切相关（r = 0.91，p < 0.001），尽管呼气氢气排泄量二次峰值出现的时间与所有放射性试验餐进入结肠的时间相关性较差。当将乳果糖直接注入结肠时，低至0.5 g就能产生可察觉的氢气反应，该反应在注入后两分钟内出现。在5名受试者中，将50 ml 10%乳果糖溶液的结肠注入速率从0.02 g/min提高到0.15 g/min，显著增加了呼气氢气浓度。在低于0.075 g乳果糖/分钟的注入速率下，呼气氢气反应峰值在注入结束之前出现，而在较高的注入速率下，氢气反应峰值在注入结束之后出现。尽管这些结果证实了监测呼气氢气浓度能有效地表明含有未吸收碳水化合物的餐食到达结肠所需的时间，但它并不能可靠地指示餐食全部进入结肠的时间。最后，将呼气氢气浓度的最大增加量用作碳水化合物吸收不良程度的指标，假定进入结肠的速率是均匀的。
