Effect of gastric acid on Helicobacter pylori ecology
The discovery of Helicobacter pylori has altered for ever our perceptions of gastro-duodenal disease, and has dramatically influenced patient management. However, we have much to learn. We still cannot explain the rather politically incorrect observation of nearly 40 years ago which was referring to differences in distribution of peptic ulcers between the rich and the poor. While all would now accept H. pylori as a cause of peptic ulcer, most gastric ulcers (GU), many gastric cancers (GC) and all mucosa-associated lymphoid tissue (MALT) lymphomas, we cannot explain what is illustrated in Figure 1, i.e., that there are different patterns of H. pylori-associated disease and these patterns vary in different populations. Indeed, some of the pathways of disease appear to be mutually exclusive. In the developed world the pattern tends towards duodenal ulcer (DU), while in the developing world gastric cancer may be more likely to develop. In this latter group, gastric ulcers will outnumber duodenal ulcers, as is implied in the opening quote. This chapter attempts to address this issue by suggesting that a major difference in these populations is variation in local acid output.
KeywordsDuodenal Ulcer Gastric Ulcer Pylorus Infection Parietal Cell Transitional Zone
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