Fecal hydrogen sulfide production in ulcerative colitis
J Levine, CJ Ellis, JK Furne, J Springfield… - Official journal of the …, 1998 - journals.lww.com
J Levine, CJ Ellis, JK Furne, J Springfield, MD Levitt
Official journal of the American College of Gastroenterology| ACG, 1998•journals.lww.comObjective: 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 H 2 S form that moves rapidly from feces to
surrounding gas. Our aim was to quantify the fecal release of H 2 S and other volatiles (CO
2, H 2, CH 2, methanethiol, and dimethylsulfide). Methods: Fecal samples from 25 subjects …
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 H 2 S form that moves rapidly from feces to
surrounding gas. Our aim was to quantify the fecal release of H 2 S and other volatiles (CO
2, H 2, CH 2, methanethiol, and dimethylsulfide). Methods: Fecal samples from 25 subjects …
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 H 2 S form that moves rapidly from feces to surrounding gas. Our aim was to quantify the fecal release of H 2 S and other volatiles (CO 2, H 2, CH 2, 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:
H 2 S 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 CO 2 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 H 2 S production than did sulfate.
Conclusions:
Increased H 2 S release is a relatively localized metabolic aberration of ulcerative colitis feces. This increased H 2 S may reflect abnormalities of the fecal bacteria and/or substrate availability.
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