Published online Apr 21, 2020. doi: 10.3748/wjg.v26.i15.1820
Peer-review started: December 16, 2019
First decision: January 7, 2020
Revised: March 15, 2020
Accepted: April 1, 2020
Article in press: April 1, 2020
Published online: April 21, 2020
Helicobacter pylori (H. pylori) infection is a risk factor for gastric cancer (GC), especially in East Asian populations. Most East Asian populations infected with H. pylori are at higher risk for GC than H. pylori-positive European and United States populations. H. pylori eradication therapy reduces GC risk in patients after endoscopic and operative resection for GC, as well as in patients with atrophic gastritis. However, it remains unclear whether eradication therapy exerts the same chemopreventive effect on GC among different groups, e.g., those of different nationalities, those with a history of gastritis alone, those with a prior history of GC resection, etc., with different risk levels for GC development.
We hope to up-date evidences for preventive effect on development of GC after eradication therapy in East Asian populations.
To clarify the preventive effects of H. pylori eradication therapy for development of GC in an East Asian population with a high incidence of GC.
PubMed and the Cochrane Library were searched for randomized control trials (RCTs) and cohort studies published in English up to March 2019 using the terms “H. pylori,” “GC,” and “eradication therapy”. Subgroup analyses were conducted with regard to study designs (i.e., RCTs or cohort studies), country where the study was conducted (i.e., Japan, China, and South Korea), and observation periods (i.e., ≤ 5 years and > 5 years). The heterogeneity and publication bias were also measured.
For patients with atrophic gastritis alone and patients after resection for GC, 4 and 4 RCTs and 12 and 18 cohort studies were included, respectively. In RCTs, the median incidence of GC for the untreated control groups and the treatment groups in cases of gastritis alone was 272.7 (180.4–322.4) and 162.3 (72.5–588.2) per 100000 person-years. In RCTs, the median incidence of metachronous GC for the untreated control groups and the treatment groups was 1790.7 (406.5–2941.2) and 1126.2 (678.7–1223.1) per 100000 person-years. Compared with non-treated H. pylori-positive controls, the eradication groups had a significantly reduced risk of GC, with a relative risk of 0.67 [95% confidence interval: 0.47–0.96] for patients with atrophic gastritis alone and 0.51 (0.36–0.73) for patients after resection for GC in the RCTs and 0.39 (0.30–0.51) and 0.54 (0.44–0.67) in cohort studies.
The current meta-analysis showed that in the East Asian population with high incidence rates of GC, H. pylori eradication effectively reduced the risk of GC, irrespective of past history of previous cancer. The surveillance interval in patients after endoscopic and operative resection and patients with atrophic gastritis alone is important after eradication therapy.
The results of the current meta-analysis may offer gastroenterologists and endoscopists more reliable evidence in efficacy of H. pylori eradication therapy and importance of surveillance after eradication therapy.