The contribution of sulphate reducing bacteria and 5-aminosalicylic acid to faecal sulphide in patients with ulcerative colitis

Citation
Mcl. Pitcher et al., The contribution of sulphate reducing bacteria and 5-aminosalicylic acid to faecal sulphide in patients with ulcerative colitis, GUT, 46(1), 2000, pp. 64-72
Citations number
77
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
GUT
ISSN journal
00175749 → ACNP
Volume
46
Issue
1
Year of publication
2000
Pages
64 - 72
Database
ISI
SICI code
0017-5749(200001)46:1<64:TCOSRB>2.0.ZU;2-5
Abstract
Background-Butyrate oxidation within the colonocyte is selectively inhibite d by hydrogen sulphide, reproducing the metabolic lesion observed in active ulcerative colitis. Aims-To study generation of hydrogen sulphide by sulphate reducing bacteria (SRB) and the effects of 5-aminosalicylic acid (5-ASA) in patients with ul cerative colitis in order to identify a role of this noxious agent in patho genesis. Patients-Fresh faeces were obtained from 37 patients with ulcerative coliti s (23 with active disease) and 16 healthy controls. Methods-SRB were enumerated from fresh faecal slurries and measurements mad e of sulphate reducing activity, and sulphate and hydrogen sulphide concent rations. The effect of 5-ASA on hydrogen sulphide production was studied in vitro. Results-All controls and patients with active ulcerative colitis carried SR B and total viable counts were significantly related to the clinical severi ty grade. SRB were of two distinct types: rapidly growing strains (desulfov ibrios) which showed high sulphate reduction rates, present in 30% of patie nts with ulcerative colitis and 44% of controls; and slow growing strains w hich had little activity, In vitro, 5-ASA inhibited sulphide production in a dose dependent manner; in patients with ulcerative colitis not on these d rugs faecal sulphide was significantly higher than in controls (0.55 versus 0.25 mM, p=0.027). Conclusions-Counts and carriage: rates of SRB in faeces of patients with ul cerative colitis are not significantly different from those in controls. SR B metabolism is not uniform between strains and alternative sources of hydr ogen sulphide production exist in the colonic lumen which may be similarly inhibited by 5-ASA. The evidence for hydrogen sulphide as a metabolic toxin in ulcerative colitis remains circumstantial.