Helicobacter pylori and the oesophagus

The relationship between H. pylori and gastroesophageal reflux disease (GER D) continues to remain an area of active research. Epidemiological studies do not support an important role of H. pylori in the pathogenesis of GERD. However, recent papers suggest that inflammation may sensitize the gastroes ophageal junction to acid in non-erosive GERD. Otherwise, the impact of H. pylori infection on intragastric pH depends primarily on the distribution ( antral versus pangastritis) and severity of gastritis. When GERD develops, corpus gastritis and gastric atrophy may reduce the severity of oesophagiti s. In contrast there is no evidence that H. pylori infection can influence the underlying motor pattern responsible for the occurrence of reflux episo des. Several studies have contributed to the clarification of the relations hips between H. pylori and the cardia. It is becoming more and more obvious that carditis has at least two aetiologies namely H. pylori and GERD. Card itis with unremarkable Z-line is more frequently associated with H. pylori while short or long segment of Barrett's oesophagus are more likely related to GERD. In the absence of Barrett's aspect there is no evidence that inte stinal metaplasia associated with H. pylori-related carditis is a premalign ant lesion which deserves endoscopic surveillance. While H. pylori infectio n can accelerate the healing of oesophagitis and the speed of symptom relie f in patients treated with PPI, there is no evidence that H. pylori influen ces the therapeutic needs in the long-term. Conflicting results have been p ublished regarding the effects of eradicating H. pylori on the development of GERD. Studies in duodenal ulcer (DU) patients or healthy volunteers may not be relevant to the situation of GERD. The central role of the patient's inflammatory response to H. pylori infection has been demonstrated by a st udy showing a polymorphism in interleukin 1 beta gene and an association be tween some alleles and the risk of hypochlorhydria and gastric cancer. A 3- year prospective randomized study did not confirm that patients receiving m aintenance with PPI progress more frequently to corpus inflammation, atroph y or intestinal metaplasia than controls treated surgically. Finally, it is our opinion that the diagnosis of GERD should not influence the decision w hether to eradicate H. pylori which is more related to the risk of gastric cancer. Curr Opin Gastroenterol 16 (suppl 1):S33-S38 (C) 2000 Lippincott Wi lliams & Wilkins.