Fecal Hydrogen Sulfide Production in Ulcerative Colitis

粪便 溃疡性结肠炎 结肠炎 微生物学 人类粪便 硫酸盐还原菌 医学 细菌 硫化氢 胃肠病学 食品科学 化学 内科学 硫黄 生物 疾病 有机化学 遗传学
作者
Jimmy Levine,Carol Ellis,Julie Furne,John Springfield,Michael D. Levitt
出处
期刊:The American Journal of Gastroenterology [Lippincott Williams & Wilkins]
卷期号:93 (1): 83-87 被引量:198
标识
DOI:10.1111/j.1572-0241.1998.083_c.x
摘要

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.
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