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Fecal hydrogen sulfide production in ulcerative colitis
J Levine1, C J Ellis, J K Furne
1Department of Medicine, Minneapolis VA Medical Center and University of Minnesota Medical School, 55417, USA.
The American Journal of Gastroenterology
|February 3, 1998
Summary
Feces from ulcerative colitis patients release significantly more hydrogen sulfide (H2S) gas. This localized metabolic issue may stem from altered gut bacteria or available substrates in the gut.
Area of Science:
- Gastroenterology
- Microbiology
- Biochemistry
Background:
- Sulfide, produced by sulfate-reducing bacteria, is implicated in ulcerative colitis etiology.
- Ulcerative colitis (UC) feces show increased sulfate-reducing bacteria but only modestly increased sulfide.
- Fecal sulfide, particularly hydrogen sulfide (H2S), is volatile and toxic, rapidly transferring to gas.
Purpose of the Study:
- To quantify the release of hydrogen sulfide (H2S) and other volatile gases from ulcerative colitis (UC) feces.
- To compare gas release between UC patients and healthy controls.
- To investigate the role of different substrates in H2S production.
Main Methods:
- Fecal samples from 25 UC patients and 17 controls were incubated in 4-L containers.
- Gas release (H2S, CO2, H2, CH4, methanethiol, dimethylsulfide) was measured over 24 hours.
- Fecal homogenates were supplemented with sulfur-containing substrates (sulfate, mucin, cysteine, taurocholate) to assess H2S production.
Main Results:
- H2S release was 3-4 fold higher in UC feces compared to controls at all time points (p < 0.003 at 24h).
- Increased carbon dioxide (CO2) release was observed in UC feces at 1 hour.
- Organic compounds (mucin, cysteine, taurocholate) were better substrates for H2S production than sulfate.
Conclusions:
- Elevated H2S release is a localized metabolic abnormality in ulcerative colitis feces.
- This increased H2S production may be linked to abnormalities in fecal bacteria or substrate availability in UC.
- Further research is needed to elucidate the precise mechanisms and implications of increased H2S in UC.