Potential impact of Helicobacter pylori-related metabolic syndrome on upper and lower gastrointestinal tract oncogenesis.

Both Helicobacter pylori infection and metabolic syndrome present significant global public health burdens. Metabolic syndrome is closely related to insulin resistance, the major underlying mechanism responsible for metabolic abnormalities, and Helicobacter pylori infection has been proposed to be a contributing factor. There is growing evidence for a potential association between Helicobacter pylori infection and insulin resistance, metabolic syndrome and related morbidity, including abdominal obesity, type 2 diabetes mellitus, dyslipidemia, hypertension, all of which increase mortality related to cardio-cerebrovascular disease, neurodegenerative disorders, nonalcoholic fatty liver disease and malignancies. More specifically, insulin resistance, metabolic syndrome and hyperinsulinemia have been associated with upper and lower gastrointestinal tract oncogenesis. Apart from cardio-cerebrovascular, degenerative diseases and nonalcoholic fatty liver disease, a number of studies claim that Helicobacter pylori infection is implicated in metabolic syndrome-related Barrett's esophagus and esophageal adenocarcinoma development, gastric and duodenal ulcers and gastric oncogenesis as well as lower gastrointestinal tract oncogenesis. This review summarizes evidence on the potential impact of Helicobacter pylori-related metabolic syndrome on gastroesophageal reflux disease-Barrett's esophagus-esophageal adenocarcinoma, gastric atrophy-intestinal metaplasia-dysplasia-gastric cancer and colorectal adenoma-dysplasia-colorectal cancer sequences. Helicobacter pylori eradication might inhibit these oncogenic processes, and thus further studies are warranted.

Helicobacter pylori infection and esophageal adenocarcinoma: a review and a personal view.

Esophageal adenocarcinoma (EAC) is etiologically associated with gastroesophageal reflux disease (GERD). There is evidence to support the sequence GERD, Barrett's esophagus (BE), dysplasia, and finally EAC, with Helicobacter pylori (H. pylori) being implicated in each step to EAC. On the other side of this relation stands the hypothesis of the protective role of H. pylori against EAC. Based on this controversy, our aim was to review the literature, specifically original clinical studies and meta-analyses linking H. pylori infection with EAC, but also to provide our personal and others' relative views on this topic. From a total of 827 articles retrieved, 10 original clinical studies and 6 meta-analyses met the inclusion criteria. Original studies provided inconclusive data on an inverse or a neutral association between H. pylori infection and EAC, whereas meta-analyses of observational studies favor an inverse association. Despite these data, we consider that the positive association between H. pylori infection and GERD or BE, but not EAC, is seemingly a paradox. Likewise, the oncogenic effect of H. pylori infection on gastric and colon cancer, but not on EAC, also seems to be a paradox. In this regard, well-designed prospective cohort studies with a powered sample size are required, in which potential confounders should be taken into consideration since their design.