Arola H, Koivula T, Karvonen A L, Jokela H, Ahola T, Isokoski M
Tampere Occupational Health Center, Dept of Clinical Chemistry, University Hospital of Tampere, Finland.
Scand J Gastroenterol. 1999 Sep;34(9):898-903. doi: 10.1080/003655299750025372.
The purpose of the study was to evaluate whether maldigestion of trehalose causes abdominal symptoms and which available diagnostic method best distinguishes intolerant from tolerant subjects.
A 25-g oral trehalose load test was performed in 64 subjects. The 19 experiencing clear symptoms constituted the trehalose-intolerant subjects. Changes from base-line levels of blood glucose, breath hydrogen, and methane and symptoms were recorded after the test. Trehalase activity was determined in serum and on a duodenal biopsy specimen obtained by endoscopy.
Intolerant subjects were best differentiated from tolerant subjects by changes in breath gases (hydrogen and methane) and duodenal trehalase to sucrase ratio. The change in breath gases correlated inversely with duodenal trehalase activity, duodenal trehalase to sucrase ratio, and plasma trehalase activity. The correlation between serum and duodenal trehalase activities was on the order of 0.6. Two subjects were found to have trehalase deficiency.
It is obvious that trehalose maldigestion can cause symptoms similar to those of lactose maldigestion and intolerance. Three factors control the genesis of symptoms: 1) the activity of small-bowel trehalase: if it is low, trehalose is maldigested and more trehalose is passed into the colon; 2) the maldigested trehalose, which causes osmotic water flow into the colon, resulting in loose stools and diarrhea; and 3) most importantly, the microflora of the colon, from which symptoms will arise if there are bacteria capable of producing gases from maldigested trehalose. If colonic bacteria cannot produce gases, then distention of the abdomen and intestinal gas expulsion as eructations and flatus will not occur.
本研究旨在评估海藻糖消化不良是否会引起腹部症状，以及哪种现有诊断方法能最佳区分不耐受者和耐受者。
对64名受试者进行了25克口服海藻糖负荷试验。19名出现明显症状的受试者构成海藻糖不耐受组。试验后记录血糖、呼气氢气和甲烷水平以及症状相对于基线水平的变化。在内镜检查获取的血清和十二指肠活检标本中测定海藻糖酶活性。
通过呼气气体（氢气和甲烷）变化以及十二指肠海藻糖酶与蔗糖酶比值，不耐受组受试者与耐受组受试者能得到最佳区分。呼气气体变化与十二指肠海藻糖酶活性、十二指肠海藻糖酶与蔗糖酶比值以及血浆海藻糖酶活性呈负相关。血清和十二指肠海藻糖酶活性之间的相关性约为0.6。发现两名受试者存在海藻糖酶缺乏。
显然，海藻糖消化不良可引起与乳糖消化不良和不耐受类似的症状。有三个因素控制症状的发生：1）小肠海藻糖酶的活性：如果其活性低，海藻糖消化不良，更多海藻糖进入结肠；2）消化不良的海藻糖，其导致渗透性水流进入结肠，引起稀便和腹泻；3）最重要的是结肠微生物群，如果存在能够从消化不良的海藻糖产生气体的细菌，就会出现症状。如果结肠细菌不能产生气体，那么腹部膨胀以及以嗳气和放屁形式排出肠道气体的情况就不会发生。
