FECAL DL-LACTATE CONCENTRATION IN 100 GASTROINTESTINAL PATIENTS
FECAL DL-LACTATE CONCENTRATION IN 100 GASTROINTESTINAL PATIENTS
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DOI：
10.3109/00365529409090473
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发表时间：
1994-03-01
影响因子：
1.9
通讯作者：
MORTENSEN, PB
中科院分区：
文献类型：
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作者：
HOVE, H;NORDGAARDANDERSEN, I;MORTENSEN, PB
粪便乳酸乳酸与肠道炎症或吸收不良之间的关系被评估100非选择住院患者在转诊中心胃肠道疾病。21人（21%）的dl -乳酸浓度（范围8-95 mmol/l）超过健康个体95%的限值（6.1 mmol/l）。15例患者中有11例（73%）伴有活动性直肠炎的炎症性肠病患者（平均32 mmol/l，范围8-95 mmol/l）和1例伴有袋炎的患者（8 mmol/l）的粪便乳酸浓度升高与l -乳酸浓度升高相关，而8例伴有活动性炎症性肠病且无直肠炎的患者中只有1例（13%）出现l -乳酸浓度升高（25 mmol/l）。在26例吸收不良和静止或非炎症性肠病患者中，17例保留结肠功能的患者中有3例（18%），9例空肠造口患者中有3例（33%）的粪便乳酸增加。50例既没有活动性炎症性肠病也没有吸收不良的患者中只有2例（4%）出现粪便乳酸dl升高。在体外细菌发酵大多数饲料多糖不引起乳酸积累，对应于粪便碳水化合物排泄和乳酸积累之间缺乏相关性。13例炎症性肠病患者中有6例观察到单独的粪便l -乳酸增加，而d -乳酸没有同时增加l -乳酸异构体。综上所述，在炎症性肠病和直肠炎患者中，粪便乳酸浓度经常升高，在严重吸收不良患者中偶尔升高，而在静止性炎症性肠病或局限性克罗恩回肠炎患者中，粪便乳酸浓度通常正常。炎性肠病患者中l -乳酸的分离产生表明，乳酸是由这些患者发炎的结肠粘膜产生的。
The relation between faecal DL-lactate and intestinal inflammation or malabsorption was evaluated in 100 nonselected inpatients at a referral center for gastrointestinal disorders. Twenty-one (21%) had DL-lactate concentrations (range, 8-95 mmol/l) above the 95% limit (6.1 mmol/l) in healthy individuals. Inflammatory bowel disease with active proctitis was associated with increased faecal DL-lactate in 11 of 15 patients (73%) (mean, 32 mmol/l; range, 8-95 mmol/l) and in the 1 patient with pouchitis (8 mmol/l), whereas only 1 of 8 patients (13%) with active inflammatory bowel disease without proctitis had L-lactate elevation (25 mmol/l). Among 26 patients with malabsorption and quiescent or noninflammatory bowel disease, 3 of 17 (18%) with preserved colonic function and 3 of 9 (33%) with jejunostomy had increased faecal lactate. Only 2 of 50 (4%) patients with neither active inflammatory bowel disease nor malabsorption had faecal DL-lactate elevation. In vitro bacterial fermentation of most dietary polysaccharides did not cause accumulation of lactate, corresponding to a lack of correlation between faecal carbohydrate excretion and lactate accumulation. An isolated increase in faecal L-lactate was observed in 6 of 13 patients with inflammatory bowel disease, whereas D-lactate was not increased without a simultaneous increase of the L-lactate isomer. In conclusion, the faecal lactate concentration was frequently increased in patients with inflammatory bowel disease and proctitis, occasionally increased in patients with severe malabsorption, and often normal in patients with quiescent inflammatory bowel disease or localized Crohn's ileitis. The isolated production of L-lactate in patients with inflammatory bowel disease indicates that lactate is produced by the inflamed colonic mucosa in these patients.