Abstract

It has been well established that S-adenosyl-L-methionine (SAMe) is the principal methyl donor in methyltransferase reactions and that SAMe supplementation restores hepatic glutathione (GSH) deposits and attenuates liver injury. However, the effectiveness of SAMe therapy in chronic liver disease has not been adequately addressed. We searched globally recognized electronic databases, including PubMed, the Cochrane Database and EMBASE, to retrieve relevant randomized controlled trials (RCTs) of chronic liver disease published in the past 20 years. We then performed a systematic review and meta-analysis of the enrolled trials that met the inclusion criteria.The results showed that twelve RCTs from 11 studies, which examined 705 patients, were included in this research. For liver function, certain results obtained from data synthesis and independent comparisons demonstrated significant differences between the levels of total bilirubin (TBIL) and aspartate transaminase (AST). However, no studies identified significant differences regarding alanine transaminase (ALT) levels. An analysis of the adverse events and long-term prognosis also indicated no significant differences between the SAMe and the placebo groups. In a subgroup analysis of gravidas and children, several of the included data indicated that there was a significant difference in the pruritus score. Furthermore, the results regarding ursodeoxycholic acid (UDCA) and stronger neo-minophagen C (SNMC) indicated that both treatments were more effective than SAMe was in certain chronic liver diseases. These findings suggest that SAMe could be used as the basis of a medication regimen for liver function improvement because of its safety. However, SAMe also demonstrated limited clinical value in the treatment of certain chronic liver diseases.

Highlights

  • S-adenosyl-L-methionine (SAMe) is a pleiotropic molecule that is involved in multiple cellular reactions

  • A flow chart of the selection of the included trials is given in Fig. 1 and S1 Fig. 11 studies [22,23,24,25,26,27,28,29,30,31,32] that included randomized controlled trials (RCTs) were identified in the present analysis

  • Drug-induced liver disease, post-hepatectomy patients, nonalcoholic fatty liver disease and cholestatic hepatitis were described by Zhu Shishu, Su Zhaoran, V

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Summary

Introduction

S-adenosyl-L-methionine (SAMe) is a pleiotropic molecule that is involved in multiple cellular reactions. This molecule participates in the following three types of reactions: PLOS ONE | DOI:10.1371/journal.pone.0122124. S-Adenosyl-L-Methionine for the Treatment of Liver Disease transmethylation, transsulfuration and aminopropylation [1, 2]. It has been well established that SAMe is the principal methyl donor in methyltransferase reactions [3] and that SAMe supplementation restores hepatic glutathione (GSH) deposits and attenuates liver injury [4, 5]. SAMe biosynthesis is depressed in patients with chronic liver disease [9]. Preclinical studies indicate that this depression might exacerbate liver injury; supplementation might represent a useful therapy [10]

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