Vogelsang H, Ferenci P, Frotz S, Meryn S, Gangl A
1st Department of Gastroenterology and Hepatology, University of Vienna, Austria.
Gut. 1988 Jan;29(1):21-6. doi: 10.1136/gut.29.1.21.
About 5% of normal subjects fail to produce increased hydrogen breath concentration after ingestion of the non-digestible carbohydrate lactulose (low hydrogen producers). The existence of low hydrogen producers limits the diagnostic use of hydrogen (H2) breath tests. We studied the effects of lactulose and of magnesium sulphate (MgSO4) pretreatment on stool-pH and on hydrogen exhalation after oral loading with lactulose or lactose in 17 hydrogen producers and 12 low hydrogen producers. In seven hydrogen producers acidification of stool pH by lactulose pretreatment (20 g tid) decreased hydrogen exhalation and three of seven (43%) became low hydrogen producers. In contrast, after pretreatment of eight low hydrogen producers with magnesium sulphate (5 g twice daily) all eight produced hydrogen after a lactulose load. Similarly four lactose intolerant low hydrogen producers had abnormal lactose hydrogen breath tests after MgSO4 pretreatment. MgSO4 pretreatment neither resulted in false positive lactose hydrogen breath tests in five lactose tolerant hydrogen producers, nor increased the hydrogen exhalation in five additional hydrogen producing controls after ingestion of lactulose. The results of these studies confirm that hydrogen production from lactulose decreases when the colonic pH is lower (lactulose pretreatment), and increases when colonic pH is higher (MgSO4 pretreatment). In low hydrogen producers the lacking increase of H2 exhalation after ingestion of non-digestible carbohydrates can be overcome by MgSO4 pretreatment, thus increasing the sensitivity of the test by avoiding false negative hydrogen breath tests in low hydrogen producers with disaccharide malabsorption or maldigestion. The underlying mechanism of this remarkable effect of MgSO4 pretreatment warrants further investigation.
约5%的正常受试者在摄入不可消化的碳水化合物乳果糖后,呼出氢气浓度未升高(低氢气产生者)。低氢气产生者的存在限制了氢气(H2)呼气试验的诊断应用。我们研究了乳果糖和硫酸镁(MgSO4)预处理对17名氢气产生者和12名低氢气产生者口服乳果糖或乳糖后粪便pH值及氢气呼出量的影响。在7名氢气产生者中,乳果糖预处理(20克,每日三次)使粪便pH值酸化,降低了氢气呼出量,7人中有3人(43%)变为低氢气产生者。相比之下,8名低氢气产生者用硫酸镁(5克,每日两次)预处理后,所有8人在摄入乳果糖后都产生了氢气。同样,4名乳糖不耐受的低氢气产生者在MgSO4预处理后乳糖氢气呼气试验异常。MgSO4预处理在5名乳糖耐受的氢气产生者中既未导致乳糖氢气呼气试验出现假阳性,在另外5名摄入乳果糖后的氢气产生对照者中也未增加氢气呼出量。这些研究结果证实,当结肠pH值较低时(乳果糖预处理),乳果糖产生的氢气减少,而当结肠pH值较高时(MgSO4预处理),氢气产生增加。在低氢气产生者中,硫酸镁预处理可克服摄入不可消化碳水化合物后氢气呼出量缺乏增加的情况,从而通过避免低氢气产生者因二糖吸收不良或消化不全导致的氢气呼气试验假阴性来提高检测的敏感性。MgSO4预处理这种显著效果的潜在机制值得进一步研究。