Intervention Review

S-adenosyl-L-methionine for alcoholic liver diseases

  1. Andrea Rambaldi*,
  2. Christian Gluud

Editorial Group: Cochrane Hepato-Biliary Group

Published Online: 19 APR 2006

Assessed as up-to-date: 20 FEB 2006

DOI: 10.1002/14651858.CD002235.pub2


How to Cite

Rambaldi A, Gluud C. S-adenosyl-L-methionine for alcoholic liver diseases. Cochrane Database of Systematic Reviews 2006, Issue 2. Art. No.: CD002235. DOI: 10.1002/14651858.CD002235.pub2.

Author Information

  1. Copenhagen Trial Unit, Centre for Clinical Intervention Research, Department 3344, Rigshospitalet, Copenhagen University Hospital, Cochrane Hepato-Biliary Group, Copenhagen, Denmark

*Andrea Rambaldi, Cochrane Hepato-Biliary Group, Copenhagen Trial Unit, Centre for Clinical Intervention Research, Department 3344, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, Copenhagen, DK-2100, Denmark. arambaldi@hotmail.com. rambaldi.andrea@libero.it.

Publication History

  1. Publication Status: Edited (no change to conclusions)
  2. Published Online: 19 APR 2006

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Abstract

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

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

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

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.

 

摘要

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

背景

以SadenosylLmethionine治療酒精性肝病

酒精是引起肝病的主要原因之一,其破壞methionine和氧化平衡。腺?蛋氨酸(SadenosylLmethionine (SAMe))作為甲基化反應的甲基供給體,參與glutathione的合成,是一種主要的細胞抗氧化劑。隨機臨床試驗已提出是否SAMe 對治療酒精性肝病的病人有效的問題。

目標

評估SAMe 對治療酒精性肝病的病人的利弊。

搜尋策略

我們搜尋The Cochrane HepatoBiliary Group Controlled Trials Register (2005年5月), Cochrane Library(2005年第2期)的The Cochrane Central Register of Controlled Trials ,MEDLINE (1950 年−2005年5月)、EMBASE (1980年 2005年5月)和Science Citation Index Expanded (2005年5月)。

選擇標準

我們收入所有研究酒精性肝病病人的隨機臨床試驗。以口服或非口服任意劑量的SAMe干預治療對照安慰劑或無干預法。

資料收集與分析

我們利用Cochrane Collaboration提供的RevMan分析軟體根據治療意向進行所有分析。我們藉助品質成分評估隨機臨床試驗的研究方法品質。

主要結論

我們找出9個隨機臨床試驗,包括共434位酒精性肝病病人的異質性樣本。以隨機化來說,研究方法品質較低,但是9個試驗有8個試驗是安慰劑對照試驗。只有一個包括123位酒精性肝硬化病人的試驗採用適當的方法,清楚記錄全因死亡率和肝移植。我們發現,在全因死亡率 (relative risks (RR) 0.62, 95% 信賴區間 (CI) 0.30 – 1.26)、和肝臟相關死亡率 (RR 0.68, 95% CI 0.31 1.48)、全因死亡率、肝移植 (RR 0.55; 95% CI 0.27 – 1.09),併發症 (RR 1.35, 95% CI 0.84 – 2.16)等方面,SAMe沒有明顯作用,但是分析結果主要是依據唯一一個試驗得出的。 SAMe 和非嚴重不良事件(RR 4.92; 95% CI 0.59 – 40.89)沒有顯著關聯,沒有記錄有嚴重的不良事件。

作者結論

我們沒有發現有證據支持或反對SAMe 治療酒精性肝病病人。我們需要更多長期、高品質的隨機試驗,以研究 SAMe對酒精性肝病病人的療效,然後才能在臨床實踐中推薦使用SAMe。

翻譯人

此翻譯計畫由臺灣國家衛生研究院(National Health Research Institutes, Taiwan)統籌。

總結

沒有證據支持或反對SAMe治療酒精性肝病病人。 酒精是引起肝病的主因。酒精性肝臟損害降低了glutathioneSAMe(SAMe)的合成。作為甲基化反應的甲基供給體,SAMe參與glutathione的合成,是一種主要的細胞抗氧化劑。隨機臨床試驗把酒精性肝病使用的SAMe和安慰劑進行比較,但是試驗包括的病人具有多樣性。本次文獻回顧不能指出SAMe 對治療肝病明顯存在臨床療效。我們需要進一步研究,然後才能向酒精性肝病病人推薦SAMe。