There is no controversy that H. Pylori (HP) causes gastritis. However, to date, there is no direct evidence that HP causes any ulcers. There is good statistical correlation between ulcer diseases and HP yet statistical correlation does not imply causality. HP induced gastritis is associated with hypochlorohydria and increased bicarbonate secretion seen with gastric ulcer (GU). Low acid and high bicarbonate secretion associated with HP has been found to be protective against the development of reflux oesophagitis (GORD). This is believed to be the reason why GORD develops for the first time after eradication of HP for duodenal ulcers (DU)(1).Despite greater than 90% correlation of HP and DU, paradoxically acid secretion is increased and bicarbonate secretion is decreased in DU. Yet HP eradication reduces relapse of DU although not to the extent it was believed in the past. Recent meta-analysis of randomized trials indicate a relapse rate of 20% of DU 6 months after HP eradication(2).So what shall we do? The following are my suggestions:

Five year survival of oesophageal cancers is approximately 10% globally. Early cancers are operable. Of the two types of oesophageal cancers we see, incidence of squamous cell carcinomas (SCC) is declining while there is progressive rise of the incidence of the adenocarcinoma (AC) of the oesophagus. This article focuses on the identification of at risk individuals.