Levine J, Ellis C J, Furne J K, Springfield J, Levitt M D
Department of Medicine, Minneapolis VA Medical Center and University of Minnesota Medical School, 55417, USA.
Am J Gastroenterol. 1998 Jan;93(1):83-7. doi: 10.1111/j.1572-0241.1998.083_c.x.
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, CH4, methanethiol, and dimethylsulfide).
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.
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.
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.
硫化物是硫酸盐还原菌的产物，有人提出它在溃疡性结肠炎的病因学中起作用。溃疡性结肠炎患者的粪便中硫酸盐还原菌的数量和活性增加，但硫化物仅适度增加。然而，粪便中的硫化物主要以挥发性、剧毒的H2S形式存在，它会迅速从粪便转移到周围气体中。我们的目的是量化粪便中H2S和其他挥发性物质（CO2、H2、CH4、甲硫醇和二甲基硫醚）的释放量。
将25名溃疡性结肠炎患者和17名对照者的粪便样本置于4升容器中培养，并在24小时内定期评估气体释放情况。
与正常粪便相比，溃疡性结肠炎粪便在每个测量点的H2S释放量均升高了3至4倍（24小时时p < 0.003）。唯一的其他显著差异是溃疡性结肠炎粪便在1小时时的CO2释放量增加。用含硫底物补充粪便匀浆表明，有机化合物（粘蛋白、半胱氨酸、牛磺胆酸盐）比硫酸盐为H2S产生提供了更易利用的底物。
H2S释放增加是溃疡性结肠炎粪便相对局部的代谢异常。这种增加的H2S可能反映了粪便细菌和/或底物可用性的异常。
