PubMed · 15125688
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Kenneth E L McColl. 2004. Rebound acid hypersecretion.. https://doi.org/10.1111/j.1742-7843.2004.pto940501.x
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UNLABELLED: Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3-4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs. CONCLUSION: Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity.
Helicobacter pylori is a common gastric infection that causes serious complications in a minority of individuals. A great deal is known about the disease, but many unanswered questions remain. Among these, perhaps the most enigmatic is that we do not know how the organism is transmitted. We are uncertain why the prevalence of the disease is falling within the developed population. There is still debate as to its relationship with gastroesophageal reflux disease. It is unclear why there are differences in the international incidence of gastric cancer. Similar uncertainties relate to the reasons why the complications of H. pylori infection have changed over time. In this article, I have hypothesized that a number of these unanswered questions may be related to a putative increase in gastric acid secretion that may have taken place during the past 200 years. To date, there is little confirmatory evidence for this, and it remains a fascinating area that merits more scientific research.