Specific evidence is presented of the release of prostaglandins from the colon in active ulcerative colitis. An increase in the levels of bioassayed prostaglandin-like activity in the stools and colo-rectal venous plasma from patients with active ulcerative colitis is described. Radioimmunoassay confirms the presence of prostaglandin E and prostaglandin F in the stools in colitis. Increased urinary levels of prostaglandin F metabolite occur in patients with active colitis and return to normal as the disease becomes quiescent. Sulphasalazine and its faecal metabolite, 5-aminosalicylic acid, were shown by an indirect method (reduction of the tone of the isolated rat fundus strip) to inhibit prostaglandin biosynthesis in vitro. In contrast, sulphasalazine was without effect on the urinary excretion of prostaglandin F metabolite in 7 healthy subjects. In 2 patients with colitis withdrawal of sulphasalazine was associated with increasing levels of stool prostaglandin-like activity and urinary prostaglandin F metabolite excretion. Indomethacin, given to 3 patients with chronically active ulcerative colitis, unresponsive to standard medical treatment, was associated with a decreased urinary excretion of prostaglandin F metabolite but was without clinical benefit. The possible mode of action of sulphasalazine as a prostaglandin inhibitor in colitis is discussed along with the potential use of other prostaglandin inhibitors.