Helicobacter pylori: controversial and unsolved issues.

As part of the recent meeting "Current Perspectives in Acid Inhibitory Therapy" held at Yale University School of Medicine, a large group of experts met to discuss and debate a number of unsolved issues with regard to Helicobacterpylori infection in man. The discussion leaders were G.N.J. Tytgat and I.N. Marks, and the panelists were J. Calam, D. Cave, J. Freston, R.H. Hunt, G. Krejs, F. Megraud and M. Quina. J. Calam addressed the issue of the effect of H. pylori eradication on acid secretion in general, and in duodenal ulcer in particular. He stated that there were consistent falls in acid secretion in duodenal ulcer patients with regard to basal secretion and the response to GRP stimulation; the response to pentagastrin stimulation after H. pylori cure was variable. Functional dyspepsia patients, on the other hand, showed no fall in basal secretion, and he drew attention to a recently completed 24-hour pH study by Andre Blum's group in which gastric acidity increased significantly following H. pylori eradication. J. Calam speculated as to the cause of the seemingly different responses in duodenal ulcer and functional dyspepsia patients. According to McColl, stepped infusions of gastrin show a greater sensitivity of the parietal cell mass to gastrin in patients with duodenal ulcer disease than in functional dyspepsia. For some unexplained reason, H. pylori infection is affecting the gastric corpus in functional dyspepsia in a way that negates the effect of elevated gastrin, while this does not happen in duodenal ulcer patients. It would, therefore, be extremely important, to also look at the state of the mucosa both in antrum and corpus to see whether mucosal alterations correlate with the changes in acid secretory capacity changes after eradication. J. Freston stated that there was probably no relationship of H. pylori to gastroesophageal reflux disease. The organism does not inhabit esophageal epithelium and, when present in Barrett's epithelium, does not appear to be associated with an inflammatory response. He suggested that H. pylori may extend in the proximal stomach with time, particularly with ppIc therapy, and may eventually interfere with LES function. There are also anecdotal reports of symptomatic remissions in patients with mild GERD after H. pylori eradication, and he speculated that this may be linked to resolution in gastrin levels following H. pylorn eradication. He did not think gastrin per se has an effect on the LES, but that the effect of gastrin on acid secretion may be relevant. Alternatively, some patients develop GERD symptoms after successful cure of the infection. Attention was drawn to the not infrequent finding of a fall in pH (from around 1.4 or 1.5 to 1.3) following H. pylori eradication. Whether this increased acidity is contributing in people who do not necessarily have frank esophagitis but have an acid sensitive esophagus requires further study. In addition, some patients do gain weight after H. pylori cure, which may also favor GERD manifestation. Finally it was noted that there are some patients with GERD in whom H. pylori eradication appears to be associated with increased acidity and a consequent increased requirement for PPIs.