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  • Title: Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans.
    Author: Konturek JW, Dembiński A, Konturek SJ, Domschke W.
    Journal: J Physiol Pharmacol; 1997 Sep; 48(3):383-91. PubMed ID: 9376621.
    Abstract:
    The gastric irritant properties of nonsteroidal anti-inflammatory drugs (NSAID) are well established but the pathogenic mechanisms by which these agents damage the mucosa or delay its repair are poorly understood. The phenomenon of gastric adaptation after repeated exposures to ASA is well documented but the involvement of Helicobacter pylori (H. pylori) in NSAID-induced gastropathy and adaptation has not been elucidated. The aim of this study was 1) to compare the gastric damage in response to repeated exposures to ASA in the same subjects before and after eradication of H. pylori and 2) to examine the morphological and functional changes of gastric mucosa during the 14 day treatment with ASA in H. pylori-infected subjects before and after eradication of this bacteria: Eight healthy volunteers (age 19-28) with H. pylori infection were given ASA 1g bd during 14 days before and after H. pylori eradication. Mucosal damage was evaluated by endoscopy before and at 3, 7 and 14 days of ASA administration using modified Lanza score. During endoscopy mucosal biopsies were obtained for determination of DNA synthesis, by measuring 3H-thymidine incorporation into DNA. Prior to each endoscopy gastric microbleeding was determined in three consecutive gastric washings. Three months after successful eradication of H. pylori confirmed by 13C-urea breath test and mucosal rapid urease test, the same subjects received again 14 day treatment with ASA and underwent the same examinations as prior to the therapy. In all subjects, ASA administration induced acute gastric damage with endoscopic Lanza score reaching maximum at 3rd day. In H. pylori-positive subjects, this damage was maintained at similar level up to day 14th, whereas in H. pylori-eradicated subjects, this damage was lessened at day 14th by about 60-75%. Gastric microbleeding also reached its maximum at 3rd day of ASA treatment being significantly higher in H. pylori-eradicated subjects than in those with H. pylori infection. This microbleeding decreased to almost normal values by the end of the study in all H. pylori-negative subjects but remained significantly elevated in H. pylori-infected subjects. DNA synthesis before and following ASA administration was significantly higher in subjects after H. pylori eradication than in those with H. pylori infection. Moreover, this DNA synthesis showed significant increase at day 7 of ASA administration only in H. pylori-eradicated subjects. We conclude that: 1) gastric adaptation to ASA is impaired in H. pylori-positive subjects but eradication of H. pylori restores this adaptation, 2) the DNA synthesis and possibly also mucosal cell turnover in response to ASA are suppressed in H. pylori infection and this can be reversed by eradication of H. pylori.
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