Systematic Review with Meta-analysis: Association of Helicobacter pylori Infection with Esophageal Cancer

Abstract

Background Helicobacter pylori is an important carcinogenic factor in gastric cancer. Studies have shown that Helicobacter pylori infection is inversely associated with certain diseases such as esophageal cancer and whose infection appears to have a “protective effect.” At present, the relationship between Helicobacter pylori infection and esophageal cancer remains controversial. This study was designed to investigate the relationship between Helicobacter pylori infection and the risk of esophageal cancer in different regions and ethnicities. Methods Systematic search of the articles on the relationship between Helicobacter pylori infection and esophageal cancer from the database with the duration time up to December 2018. This systematic review was performed under the MOOSE guidelines. Results This meta-analysis included 35 studies with 345,886 patients enrolled. There was no significant correlation between Helicobacter pylori infection and esophageal squamous cell carcinoma in the general population (OR: 0.84; 95% CI: 0.64-1.09/OR: 0.74; 95% CI: 0.54-0.97). However, a significant correlation was found in the Middle East (OR: 0.34; 95% CI: 0.22-0.52/95% CI: 0.26-0.44). There was no significant difference in the prevalence of Helicobacter pylori between the case group and the control group in esophageal adenocarcinoma (8.87% vs. 9.67%). The pooled OR was 0.55 (95% CI: 0.43-0.70) or 0.23 (95% CI: 0.15-0.36). When grouped by match or not, the pooled OR of the nonmatching group and the matching group was 0.48/0.21 (95% CI: 0.36-0.65/95% CI: 0.13-0.36) and 0.73/0.71 (95% CI: 0.57-0.92/95% CI: 0.60-0.84), respectively. Conclusion In the general populations, no significant association was found between Helicobacter pylori infection and the risk of esophageal squamous cell carcinoma. However, lower risk was found in the Middle East. Helicobacter pylori infection may reduce the risk of esophageal adenocarcinoma, but such “protection effect” may be overestimated.

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

“…A meta-analysis of 72 studies (84,717 patients with BO and 390,749 controls) found that HPI reduces the risk of BO by 32% (OR 0.68, 95% CI 0.58–0.79) [ 237 ]. Six meta-analyses on association of HPI and esophageal adenocarcinoma indicated an inverse relationship [ 238 ], whereas a recent meta-analysis (35 studies including 345,886 patients) did not find such association, except the Middle East data [ 239 ]. Other researchers concluded that presence of HPI might aggravate GERD [ 240 ], or, at least, is not “protective” against GERD, as the incidence of GERD and its sequelae in patients with HPI is higher than that after eradication of the infection [ 241 , 242 ], HPI eradication improves GERD symptoms and esophagitis [ 243 , 244 , 245 , 246 , 247 ] and does not increase the risk of BO [ 248 , 249 , 250 ].…”

“…The other topic which deserves more attention is HPI-associated dysregulation of gut microbiota [ 239 , 606 , 653 , 654 , 655 , 656 , 657 , 658 , 659 , 660 , 661 , 662 , 663 , 664 , 665 , 666 , 667 ], a phenomenon described also in animal models (infected Mongolian gerbils [ 668 ]) and thought to be due mainly to gut immunopathological/inflammatory responses and suppressed gastric acid secretion following chronic/atrophic gastritis or use of acid-suppressive drugs. Gut dysbiosis by affecting various biological processes contributes to the pathogenesis of OP [ 669 , 670 , 671 , 672 , 673 , 674 , 675 , 676 , 677 , 678 , 679 , 680 , 681 , 682 , 683 , 684 , 685 , 686 , 687 , 688 , 689 , 690 , 691 , 692 , 693 , 694 , 695 , 696 , 697 , 698 , 699 ] as well as to numerous other extra-digestive system diseases associated with OFs [ 700 , 701 , 702 ,…”

Influence of microbiota on immunity and immunotherapy for gastric and esophageal cancers

“…Higher pH can alleviate GERD, the leading cause of premalignant BE; thus, it is believed that H. pylori eventually can result in a reduction in EAC. However, the relationship between H. pylori infection and EC remains controversial [ 59 , 60 ]. An earlier meta-analysis including 19 studies showed that H. pylori has a ‘beneficial’ effect on EAC with the summary odds ratio (OR) (95% confidence interval (CI)) as 0.56 (0.46–0.68) [ 59 ].…”

“…They further revealed that colonization with cytotoxin-associated gene A (CagA)-positive strains but not CagA-negative strains was inversely associated with EAC risk. Recently, Gao et al [ 60 ] also performed meta-analysis including 35 studies with 345,886 patients enrolled. This analysis showed no significant correlation between H. pylori infection and ESCC in the general population.…”

Letter:Helicobacter pyloriinfection and its role in oesophageal adenocarcinoma

“…4 Epidemiological data, as summarised in meta-analyses, favour a negative association between H pylori and OAC. 7 However, this may have been overestimated, since many included studies had not recruited matched cases and controls, and did not consider residual confounding factors including smoking and alcohol consumption. 6 Nevertheless, some epidemiological studies do not favour an inverse association between H pylori and GERD, BO or OAC.…”