It has been shown that feces of patients with ulcerative colitis uniformly contain sulfate reducing bacteria. Sulfide produced by these bacteria interferes with butyrate-dependent energy metabolism of cultured colonocytes and may be involved in the pathogenesis of ulcerative colitis. Mucosal biopsies from the sigmoid rectum of 10 patients (no caner, polyps, inflammatory bowel disease) were incubated with either NaCl, sodium hydrogen sulfide (1 mmol/L), a combination of both sodium hydrogen sulfide and butyrate (10 mmol/L), or butyrate. Mucosal proliferation was assessed by bromodeoxyuridine labeling of cells in S-phase. Compared to NaCl, sulfide increased the labeling of the entire crypt significantly, by 19% (p < 0.05).="" this="" effect="" was="" due="" to="" an="" expansion="" of="" the="" proliferative="" zone="" to="" the="" upper="" crypt="" (compartments="" 3–5),="" where="" the="" increase="" in="" proliferation="" was="" 54%.="" sulfide-induced="" hyperproliferation="" was="" reversed="" when="" samples="" were="" coincubated="" with="" sulfide="" and="" butyrate.="" the="" study="" shows="" that="" sodium="" hydrogen="" sulfide="" induces="" mucosal="" hyperproliferation.="" our="" data="" support="" a="" possible="" role="" of="" sulfide="" in="" the="" pathogenesis="" of="" uc="" and="" confirm="" the="" role="" of="" butyrate="" in="" the="" regulation="" of="" colonic="" proliferation="" and="" in="" the="" treatment="" of="">