Although many individuals colonised with H. pylori remain asymptomatic, some develop stomach or duodenal ulcers or stomach cancer. Once an almost universal human pathogen, advances in sanitation and use of antibiotics have significantly reduced the prevalence of the bacterium, especially in Western counties. The decline in H. Pylori colonisation has been accompanied by a decline in the incidence of gastric cancer. In contrast, the number of cases of oesophageal adenocarcinoma (EAC) has increased sharply over a similar timescale. Worldwide, most cases of oesophageal cancer are oesophageal squamous cell carcinoma (ESCC), especially in high risk areas such as China and Iraq. In some Western countries such as the United States and the United Kingdom, however, approximately half of all cases of oesophageal cancer are EAC.
A new meta-analysis has examined the association between H. Pylori and oesophageal cancer. The results suggest that the risk of EAC, but not ESCC, is reduced in individuals colonised by the predominant CagA-positive strain of H. Pylori. The low rates of EAC in developing countries, where H. pylori is still common, are consistent with the hypothesis that decreased prevalence is contributing to the observed increase in incidence of EAC.
H. pylori may protect against EAC by reducing acid reflux to the oesophagus, and by reducing production of the hormone ghrelin which in turn may lead to lower incidence of obesity, an important risk factor for EAC. The protective association of H. pylori with EAC may also be part of a wider beneficial effect of H. pylori colonisation that has developed over many years of co-existence. Other important risk factors for EAC are gastroesophageal reflux, obesity, and smoking.