THE RELATIONSHIPS BETWEEN CHRONIC GASTRITIS AND GASTRIC-ACID SECRETION

Citation
P. Sipponen et al., THE RELATIONSHIPS BETWEEN CHRONIC GASTRITIS AND GASTRIC-ACID SECRETION, Alimentary pharmacology & therapeutics, 10, 1996, pp. 103-118
Citations number
150
Categorie Soggetti
Pharmacology & Pharmacy","Gastroenterology & Hepatology
ISSN journal
02692813
Volume
10
Year of publication
1996
Supplement
1
Pages
103 - 118
Database
ISI
SICI code
0269-2813(1996)10:<103:TRBCGA>2.0.ZU;2-6
Abstract
Helicobacter pylori is the main cause of chronic gastritis in humans, Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspec tive. Atrophic gastritis is a quite common late consequence of H. pylo ri gastritis and will develop on a multifactorial basis, but not in al l infected persons, The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum a nd corpus are affected to dissimilar extent and degree. The distal par t of the stomach is the site where the atrophic sequelae (atrophic gas tritis and intestinal metaplasia) of H. pylori infection occur most of ten. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis, Along with the worsening of atrophic gastritis, i nflammation and density of colonization of the mucosa by H. pylori ten d to decrease in grade. In general, the degree of gastric mucosal infl ammation, acute and chronic, is positively related to the degree of co lonization of the mucosa by H. pylori. Acid secretion and local acidit y are factors which modulate the ecology and density of colonization o f H. pylori in the stomach, and may thus also modulate the evolution o f chronic gastritis into topographically dissimilar subtypes. Acid sec retion varies among individuals, this variation being perhaps caused b y hereditary differences in parietal cell mass, or by differences in t he sensitivity of parietal cells to hormonal or neural stimuli, It is hypothesized that in genuine hypersecretors, H. pylori colonization an d subsequent gastritis with atrophic and metaplastic sequelae may be l imited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then lead s to further impairment of acid output. In these cases, H. pylori infe ction and gastritis may, finally, heal in the antrum, resulting in hyp ochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.