Low S-adenosylmethionine concentrations found in patients with severe inflammatory bowel disease

Anne Schmedes1, Jens Nederby Nielsen, Henrik Hey

  • 1Department of Clinical Biochemistry, Vejle County Hospital, Vejle, Denmark. asch@vs.vejleamt.dk

Abstract

Insights

S-adenosylmethionine (SAMe) levels are significantly lower in patients with severe inflammatory bowel disease (IBD). This finding suggests SAMe may be a marker for IBD activity and potential sulfur toxicity.

Area of Science:

  • Biochemistry
  • Gastroenterology
  • Clinical Medicine

Background:

  • S-adenosylmethionine (SAMe) is a crucial methyl donor involved in detoxification processes, including the removal of hydrogen sulfide in the colon.
  • Impaired hydrogen sulfide detoxification is hypothesized to contribute to inflammatory bowel disease (IBD) pathogenesis.
  • This study investigates whether SAMe concentrations are reduced in IBD patients.

Purpose of the Study:

  • To compare S-adenosylmethionine concentrations in the whole blood of patients with severe and moderate IBD against healthy controls.
  • To explore the relationship between SAMe levels and IBD disease activity.

Main Methods:

  • Whole blood S-adenosylmethionine concentrations were quantified using high-pressure liquid chromatography.
  • The study included patients with Crohn's disease (n=21) and ulcerative colitis (n=7), along with healthy age-matched controls (n=17).

Main Results:

  • Patients with severe IBD exhibited significantly lower S-adenosylmethionine concentrations (mean 1.10 mg/l) compared to those with moderate IBD (mean 1.83 mg/l) and healthy controls (mean 1.84 mg/l).
  • Inverse correlations were observed between S-adenosylmethionine levels and both general activity index (p<0.01, R2=0.86) and Crohn's disease activity index (p<0.01, R2=0.50) scores.

Conclusions:

  • Low S-adenosylmethionine concentrations are associated with severe inflammatory bowel disease.
  • Further research is warranted to determine if S-adenosylmethionine can serve as a biomarker for disease activity and to investigate the role of sulfur toxicity in IBD etiology.

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