Colonic luminal hydrogen sulfide is not elevated in ulcerative colitis
Date
1998
Authors
Moore, J.
Babidge, W.
Millard, S.
Roediger, W.
Editors
Advisors
Journal Title
Journal ISSN
Volume Title
Type:
Journal article
Citation
Digestive Diseases and Sciences, 1998; 43(1):162-165
Statement of Responsibility
Moore, J. ; Babidge, W. ; Millard, S. ; Roediger, W.
Conference Name
Abstract
It has been proposed that the reduction in n-butyrate oxidation by colonic epithelial cells observed in ulcerative colitis may be related to exposure to reduced forms of sulfur derived from dissimilatory sulfate reduction by luminal microflora. This study aims to compare stool sulfide concentrations in control and colitic subjects. Control subjects had significant colorectal disease excluded by virtue of their selection. Patients with ulcerative colitis were stratified by disease extent and activity, and by salicylate drug use. Stool sulfide was measured using a direct spectrophotometric method on NaOH (free sulfide) and zinc acetate (total sulfide) stool slurries. Fifteen control and 19 colitic subjects were studied. There was no significant difference in stool sulfide between control and colitic patients (free sulfide, control = 0.52 (0.17), colitic = 0.45 (0.10), t = 0.36, P = 0.71, total sulfide, control = 1.33 (0.21), colitic = 0.96 (0.15), t = 1.44, P = 0.16). Disease extent or activity did not significantly influence stool sulfide. These results do not support a primary etiologic role for luminal sulfide in ulcerative colitis.