The normal colon absorbs water, sodium and chloride and secretes potassium and bicarbonate. In ulcerative colitis (UC), modifications occur in the absorption of water, sodium and chloride, whereas the secretion of potassium remains unchanged. There appear to be no data in the literature on bicarbonate secretion. Since some 25% of chloride absorption is coupled with bicarbonate secretion by an anion exchange mechanism, the impairment in chloride absorption should be accompanied by modifications in bicarbonate secretion. Faecal bicarbonate was therefore measured in 20 patients with active UC and 15 normal control subjects. Faecal pH, pCO2 and electrolytes (Na+, K+, Cl-, HCO3-), blood acid-base balance, urinary pH and bicarbonate were determined on the same day in all patients. Faecal pH and bicarbonate were significantly reduced in UC versus controls: pH 6.06 +/- 0.39 versus 6.52 +/- 0.43; HCO3- 8.4 +/- 5.2 versus 34.6 +/- 12.3 mEq/l (mean +/- SD), whereas sodium and chloride were increased. Faecal potassium concentration was normal, but potassium output was increased. Metabolic alkalosis was observed in 8 patients and a normal acid-base balance in the remaining 12. Urinary pH was acid and urinary bicarbonate negligible in all patients. No correlation was observed between plasma, faecal and urinary bicarbonate. Data emerging from this study show that the faecal excretion of bicarbonate is reduced in patients with active UC. A possible explanation for this finding may be impairment of the colonic anion exchange mechanism induced by inflammation of the mucosa. The role of organic anions is also hypothesized. The acid-base balance does not seem to be directly affected by the decrease in faecal bicarbonate loss.