To investigate whether enough evidence exists to support H pylori eradication at the population level, we examined the randomised controlled clinical trials (RCTs) referenced in the consensus. The RCT conducted by Wong et al2 was one of the studies used to support the recommendation. This cohort had the longest follow-up period (7.5 years), but the...]]> 2013-04-30T00:24:21-07:00 info:doi/10.1136/gutjnl-2012-303472 hwp:master-id:gutjnl;gutjnl-2012-303472 BMJ Publishing Group 2013-06-01 PostScript 62 6 950 950 http://gut.bmj.com/cgi/content/short/62/6/950-a?rss=1 Dr Zhu Wang and coauthors write a critical note1 regarding the important issue of Helicobacter pylori eradication aiming at the prevention of gastric cancer and challenge the statement made in the Maastricht IV–Florence Consensus Report.

The statement in the Maastricht IV–Florence Consensus Report intends to drive actions against gastric cancer by using H. pylori eradication as there are few beneficial alternative strategies.

Gastric cancer is detected in most cases in advanced and non-curable stages. Screening strategies based on radiography, upper gastrointestinal endoscopy and serum pepsinogens for detection of early gastric cancer with the chance for cure have successfully been adopted so far only in Japan and Korea.2–4

There are several arguments for adopting a screen-and-treat strategy with its potential to prevent gastric cancer.

H. pylori is the key trigger in the multifactorial complexity of gastric cancer based on direct and indirect...]]> 2013-04-30T00:24:21-07:00 info:doi/10.1136/gutjnl-2012-303564 hwp:master-id:gutjnl;gutjnl-2012-303564 BMJ Publishing Group 2013-06-01 PostScript 62 6 950 951 http://gut.bmj.com/cgi/content/short/62/6/951?rss=1 We read with great interest, the recent article titled ‘Metformin decreases hepatocellular carcinoma risk in a dose-dependent manner: population-based and in vitro studies’ by Chen and colleagues published online in July in Gut.1 In this large, population-based, case-control study using the Taiwanese National Health Insurance Research Database, they reported that in patients with diabetes mellitus (DM), metformin use is associated with a decrease in the risk of hepatocellular cancer (HCC) in a dose- and duration-dependent manner. Metformin users had a 21% lower risk of HCC on multivariate stratified analysis, after adjusting for potential confounders (age, gender, hepatitis B, hepatitis C, liver cirrhosis, DM duration and antidiabetic therapy). This effect was not significant in a subset of diabetic patients with hepatitis B or hepatitis C, and in patients on thiazolidinediones, which had an independent protective effect against HCC. They appropriately acknowledged unmeasured confounders (smoking status, body mass index)...]]> 2013-04-30T00:24:21-07:00 info:doi/10.1136/gutjnl-2012-304232 hwp:master-id:gutjnl;gutjnl-2012-304232 BMJ Publishing Group 2013-06-01 PostScript 62 6 951 952 http://gut.bmj.com/cgi/content/short/62/6/952?rss=1 We read with interest the paper by Rehman et al1 reporting the contribution of Nod2 genotype to the composition of gut microbiota in mice and Crohn's disease (CD) patients. This was followed by a similar description for another CD-predisposing gene, FUT2.2 To date, 163 CD- and ulcerative colitis-risk loci have been identified, and while most of the known causative genes are involved in immune functions and response to infections, their effects on the composition of the gut microbiota are mostly unknown. Studies like those mentioned above are therefore very important, since the relative abundance of specific enteric bacteria has been clearly shown to be of pathogenetic relevance in mouse models of colitis.3 By studying genotype–microbiota correlations in healthy individuals, key information could also be sought for devoid of potentially confounding effects from disease status and therapeutic treatment.

We studied the impact of 30...]]> 2013-04-30T00:24:21-07:00 info:doi/10.1136/gutjnl-2012-304214 hwp:master-id:gutjnl;gutjnl-2012-304214 BMJ Publishing Group 2013-06-01 PostScript 62 6 952 954 http://gut.bmj.com/cgi/content/short/62/6/952-a?rss=1

We thank Singh et al1 for their letter2 commenting on our recent paper.3 The authors briefly summarised current evidence regarding the chemopreventive effects of statins on hepatocellular carcinoma (HCC) and noted the lack of analyses on the role of statins in HCC in our study.

We agree that the use of statins was found to be associated with a reduced risk of HCC according to previous studies.3 However, not only statins but also non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, thiazolidinediones, antiviral agents, etc, were all reported to be associated with a lower risk of HCC. Sahasrabuddhe et al analysed the National Institutes of Health-AARP Diet and Health Study cohort and reported that aspirin users had significantly reduced risks of HCC (relative risk (RR)=0.59, 95% CI 0.45 to 0.77) and mortality (RR=0.55, 95% CI 0.45 to 0.67) due to chronic liver disease. 2013-04-30T00:24:21-07:00 info:doi/10.1136/gutjnl-2012-304319 hwp:master-id:gutjnl;gutjnl-2012-304319 BMJ Publishing Group 2013-06-01 PostScript 62 6 952 952