ABSTRACT
BACKGROUND AND PURPOSE: Acute pancreatitis is the most frequent complication of endoscopic retrograde cholangiopancreatography (ERCP). We conducted a meta-analysis to evaluate the efficacy and safety of rectal nonsteroidal anti-inflammatory drugs (NSAIDs) for the prevention of post-ERCP pancreatitis (PEP). METHODS: PubMed and Embase databases were searched through April 2013. Results are reported as relative risk (RR) or weighted mean difference (WMD) with 95% confidence interval (95% CI). The primary outcome measure was the incidence of PEP. Secondary outcome measures included the severity of PEP and serum amylase level 2 h, 24 h after ERCP. RESULTS: Seven trials containing 1846 patients were eligible. Rectal NSAIDs significantly reduced the incidence of PEP (RR 0.45, 95% CI 0.34-0.61, P < 0.001). The results were maintained in subsequent subgroup analysis. Rectal NSAIDs also was associated with a reduction in the incidence of mild PEP (RR 0.54, 95% CI 0.35-0.83, P = 0.005), moderate to severe PEP (RR 0.39, 95% CI 0.22-0.70, P = 0.002), or serum amylase level 2 h after ERCP (WMD -91.09 IU/L, 95% CI -149.78 to -32.40, P = 0.002). CONCLUSIONS: Rectal NSAIDs reduced the incidence and severity of PEP, as well as serum amylase level 2 h after ERCP.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Cholangiopancreatography, Endoscopic Retrograde/adverse effects , Pancreatitis, Acute Necrotizing/prevention & control , Postoperative Complications/prevention & control , Administration, Rectal , Humans , Pancreatitis, Acute Necrotizing/etiology , Postoperative Complications/etiology , Randomized Controlled Trials as TopicABSTRACT
Glutathione S-transferases (GSTs) are a family of enzymes which are involved in the detoxification of potential carcinogens. Glutathione S-transferase M1 (GSTM1) null genotype can impair the enzyme activity of GSTs and is suspected to increase the susceptibility to gallbladder cancer. Previous studies investigating the association between GSTM1 null genotype and risk of gallbladder cancer reported inconsistent findings. To quantify the association between GSTM1 null genotype and risk of gallbladder cancer, we performed a meta-analysis of published studies. We searched PubMed, Embase, and Wanfang databases for all possible studies. We estimated the pooled odds ratio (OR) with its 95% confidence interval (95% CI) to assess the association. Meta-analysis of total included studies showed that GSTM1 null genotype was not associated with gallbladder cancer risk (OR = 1.13, 95% CI 0.88-1.46, P = 0.332). Subgroup analysis by ethnicity showed that there was no association between GSTM1 null genotype and risk of gallbladder cancer in both Caucasians and Asians. However, meta-analysis of studies with adjusted estimations showed that GSTM1 null genotype was associated with increased risk of gallbladder cancer (OR = 1.46, 95% CI 1.02-2.09, P = 0.038). Thus, this meta-analysis shows that GSTM1 null genotype is likely to be associated with risk of gallbladder cancer. More studies with well design and large sample size are needed to further validate the association between GSTM1 null genotype and gallbladder cancer.
Subject(s)
Gallbladder Neoplasms/genetics , Genetic Association Studies , Glutathione Transferase/genetics , Homozygote , Case-Control Studies , Genetic Predisposition to Disease , Humans , Odds Ratio , Publication Bias , RiskABSTRACT
Previous studies investigated the association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and hepatocellular carcinoma risk, but the impact of MTHFR C677T polymorphism on hepatocellular carcinoma was still unclear, owing to the obvious inconsistence from those studies. This study aimed to quantify the strength of the association between MTHFR C677T polymorphism and hepatocellular carcinoma risk by performing a meta-analysis. We searched the PubMed and Wanfang databases for studies on the association between MTHFR C677T polymorphism and hepatocellular carcinoma risk. We estimated the pooled odds ratios (ORs) with their 95% confidence intervals (95% CIs) to assess the association. Fifteen studies with 8,625 participants were finally included into the meta-analysis. Meta-analyses of total 15 studies suggested that MTHFR C677T polymorphism was significantly associated with an increased risk of hepatocellular carcinoma under two main genetic models (for TT versus CC, OR = 1.19, 95% CI 1.03-1.37, P = 0.016; for TT versus CT/CC, OR = 1.14, 95% CI 1.01-1.28, P = 0.032). Subgroup meta-analyses suggested that MTHFR C677T polymorphism was associated with an increased risk of hepatocellular carcinoma in Asians, but not in Caucasians. Thus, individuals with homozygote genotype TT of MTHFR C677T have obviously increased risk of hepatocellular carcinoma.
