Fecal Hydrogen Sulfide Production in Ulcerative Colitis : Official journal of the American College of Gastroenterology | ACG (original) (raw)

ORIGINAL CONTRIBUTIONS: PDF Only

Levine, Jimmy MD1,*; Ellis, Carol J1; Furne, Julie K BS1; Springfield, John MA1; Levitt, Michael D MD1

1Research Service and Department of Medicine. Minneapolis VA Medical Center and University of Minnesota Medical School, Minneapolis, Minnesota

*% Michael D. Levitt, M.D., Minneapolis VA Medical Center (151), 1 Veterans Drive, Minneapolis, MN 55417

Abstract

Objective:

Sulfide, a product of sulfate-reducing bacteria, has been proposed to play an etiologic role in ulcerative colitis. Ulcerative colitis feces have increased numbers and activity of sulfate-reducing bacteria, but only modestly increased sulfide. However, fecal sulfide exists largely in the volatile, highly toxic H2S form that moves rapidly from feces to surrounding gas. Our aim was to quantify the fecal release of H2S and other volatiles (CO2, H2, CH2, methanethiol, and dimethylsulfide).

Methods:

Fecal samples from 25 subjects with ulcerative colitis and 17 controls were incubated in 4-L containers, and gas release was assessed at intervals over 24 h.

Results:

H2S release by ulcerative colitis feces was elevated 3–4-fold at every measurement point compared with normal feces (p < 0.003 at 24 h). The only other significant difference was increased CO2 release by ulcerative colitis feces at 1 h. Supplementation of fecal homogenates with sulfur-containing substrates showed that organic compounds (mucin, cysteine, taurocholate) provided more readily utilizable substrate for H2S production than did sulfate.

Conclusions:

Increased H2S release is a relatively localized metabolic aberration of ulcerative colitis feces. This increased H2S may reflect abnormalities of the fecal bacteria and/or substrate availability.