Rambaldi A, Gluud C
Ospedale San Paolo, Divisione di Medicina Generale, Via Terracina, Napoli, Campania, Italy, 80100.
Cochrane Database Syst Rev. 2006 Apr 19(2):CD002235. doi: 10.1002/14651858.CD002235.pub2.
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.
To evaluate the beneficial and harmful effects of SAMe for patients with alcoholic liver diseases.
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).
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.
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.
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.
酒精是肝脏疾病的主要病因，会破坏蛋氨酸和氧化平衡。S-腺苷-L-蛋氨酸（SAMe）作为甲基化反应的甲基供体，参与细胞主要抗氧化剂谷胱甘肽的合成。随机临床试验探讨了SAMe是否对酒精性肝病患者有益的问题。
评估SAMe对酒精性肝病患者的有益和有害影响。
我们检索了Cochrane肝胆组对照试验注册库（2005年5月）、Cochrane图书馆中的Cochrane对照试验中央注册库（2005年第2期）、MEDLINE（1950年至2005年5月）、EMBASE（1980年至2005年5月）和科学引文索引扩展版（2005年5月检索）。
我们纳入了研究酒精性肝病患者的随机临床试验。干预措施包括口服或肠外给予任何剂量的SAMe与安慰剂或不干预。
我们使用Cochrane协作网提供的RevMan分析软件，根据意向性分析方法进行所有分析。我们通过质量成分评估随机临床试验的方法学质量。
我们确定了9项随机临床试验，包括434例酒精性肝病患者的异质性样本。随机化方面的方法学质量普遍较低，但9项试验中有8项采用了安慰剂对照。只有一项纳入123例酒精性肝硬化患者的试验采用了适当的方法，并明确报告了全因死亡率和肝移植情况。我们发现SAMe对全因死亡率（相对危险度（RR）0.62，95%置信区间（CI）0.30至1.26）、肝脏相关死亡率（RR 0.68，95%CI 0.31至1.48）、全因死亡率或肝移植（RR 0.55；95%CI 0.27至1.09）或并发症（RR 1.35，95%CI 0.84至2.16）均无显著影响，但该分析大多仅基于一项试验。SAMe与非严重不良事件无显著关联（RR 4.92；95%CI 0.59至40.89），且未报告严重不良事件。
我们找不到支持或反驳在酒精性肝病患者中使用SAMe的证据。在SAMe可被推荐用于临床实践之前，我们需要针对这些患者开展更多关于SAMe的长期、高质量随机试验。
