S‐adenosyl‐L‐methionine for alcoholic liver diseases
Abstract
Background
Alcohol is a major cause of liver disease and disrupts methionine and oxidative balances. S‐adenosyl‐L‐methionine (SAMe) acts as a methyl donor for methylation reactions and participates in the synthesis of glutathione, the main cellular antioxidant. Randomised clinical trials have addressed the question whether SAMe may benefit patients with alcoholic liver diseases.
Objectives
To evaluate the beneficial and harmful effects of SAMe for patients with alcoholic liver diseases.
Search methods
We searched The Cochrane Hepato‐Biliary Group Controlled Trials Register (May 2005), The Cochrane Central Register of Controlled Trials in The Cochrane Library (Issue 2, 2005), MEDLINE (1950 to May 2005), EMBASE (1980 to May 2005), and Science Citation Index Expanded (searched May 2005).
Selection criteria
We included randomised clinical trials studying patients with alcoholic liver diseases. Interventions encompassed per oral or parenteral administration of SAMe at any dose versus placebo or no intervention.
Data collection and analysis
We performed all analyses according to the intention‐to‐treat method using RevMan Analyses provided by the Cochrane Collaboration. We evaluated the methodological quality of the randomised clinical trials by quality components.
Main results
We identified nine randomised clinical trials including a heterogeneous sample of 434 patients with alcoholic liver diseases. The methodological quality regarding randomisation was generally low, but 8 out of 9 trials were placebo controlled. Only one trial including 123 patients with alcoholic cirrhosis used adequate methodology and reported clearly on all‐cause mortality and liver transplantation. We found no significant effects of SAMe on all‐cause mortality (relative risks (RR) 0.62, 95% confidence interval (CI) 0.30 to 1.26), liver‐related mortality (RR 0.68, 95% CI 0.31 to 1.48), all‐cause mortality or liver transplantation (RR 0.55; 95% CI 0.27 to 1.09), or complications (RR 1.35, 95% CI 0.84 to 2.16), but the analysis is based mostly on one trial only. SAMe was not significantly associated with non‐serious adverse events (RR 4.92; 95% CI 0.59 to 40.89) and no serious adverse events were reported.
Authors' conclusions
We could not find evidence supporting or refuting the use of SAMe for patients with alcoholic liver diseases. We need more long‐term, high‐quality randomised trials on SAMe for these patients before SAMe may be recommended for clinical practice.
Plain language summary
No evidence to support or refute S‐adenosyl‐L‐methionine for alcoholic liver diseases
Alcohol is a major cause for liver diseases. Alcoholic liver injury reduces s‐adenosyl‐L‐methionine (SAMe) synthesis. SAMe acts as a methyl donor and participates in the synthesis of glutathione, the main cellular antioxidant. Randomised clinical trials have compared SAMe versus placebo for alcoholic liver diseases, but the included patients are heterogeneous. The review could not demonstrate significant clinical effects of SAMe on the course of the liver diseases. We need more research before SAMe may be recommended for patients with alcoholic liver diseases.
