FECAL DL-LACTATE CONCENTRATION IN 100 GASTROINTESTINAL PATIENTS

The relation between faecal DL-lactate and intestinal inflammation or malabsorption was evaluated in 100 nonselected inpatients at a referra l center for gastrointestinal disorders. Twenty-one (21%) had DL-lacta te concentrations (range, 8-95 mmol/l) above the 95% limit (6.1 mmol/l ) in healthy individuals. Inflammatory bowel disease with active proct itis was associated with increased faecal DL-lactate in 11 of 15 patie nts (73%) (mean, 32 mmol/l; range, 8-95 mmol/l) and in the 1 patient w ith pouchitis (8 mmol/l), whereas only 1 of 8 patients (13%) with acti ve inflammatory bowel disease without proctitis had L-lactate elevatio n (25 mmol/l). Among 26 patients with malabsorption and quiescent or n oninflammatory bowel disease, 3 of 17 (18%) with preserved colonic fun ction and 3 of 9 (33%) with jejunostomy had increased faecal lactate. Only 2 of 50 (4%) patients with neither active inflammatory bowel dise ase nor malabsorption had faecal DL-lactate elevation. In vitro bacter ial fermentation of most dietary polysaccharides did not cause accumul ation of lactate, corresponding to a lack of correlation between faeca l carbohydrate excretion and lactate accumulation. An isolated increas e in faecal L-lactate was observed in 6 of 13 patients with inflammato ry bowel disease, whereas D-lactate was not increased without a simult aneous increase of the L-lactate isomer. In conclusion, the faecal lac tate concentration was frequently increased in patients with inflammat ory bowel disease and proctitis, occasionally increased in patients wi th severe malabsorption, and often normal in patients with quiescent i nflammatory bowel disease or localized Crohn's ileitis. The isolated p roduction of L-lactate in patients with inflammatory bowel disease ind icates that lactate is produced by the inflamed colonic mucosa in thes e patients.