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Editor,—After reading Lee and Feldman’s excellent article on the aging stomach (Gut1997;41:425–6), I have realised how many concepts we take for granted even in the absence of clear-cut scientific evidence. In their exhaustive review Lee and Feldman emphasise the paucity of human studies on the state of mucosal defence systems in the elderly. I actually had some data on file which have never been published as I felt that the results were “too obvious” to interest any medical journal. I can only blame myself for not searching Medline and not noticing earlier how little has been published on—for example, the gastric mucus-bicarbonate barrier in the elderly.
Comparative data from my laboratory on 45 patients over 65 years of age, without endoscopic gastroduodenal alterations, and 45 matched patients under 60, showed that the amount of gastric mucoproteins in fasting gastric juice was significantly reduced in the former, whereas the ratio of neutral to total mucoproteins—the so called mucoprotective index, regarded as an index of mucus quality1—was unaffected by age (Guslandi et al unpublished observations). This is in partial agreement with Lee and Feldman’s findings in the rat and apparently is the only (unpublished) experience in humans. Measurement of basal gastric bicarbonate secretion in the same patients, performed using Feldman’s method, yielded results comparable to those of Feldman and Cryer,2 namely a significant decrease in elderly patients.
Gastric mucosal blood flow is either reduced or unchanged in the elderly.3 ,4 Recent measurements of basal gastric microcirculation using laser Doppler flowmetry in 24 patients over 65 years of age showed that gastric blood flow is significantly lower than normal (Guslandi et al, unpublished observations), a finding that, although partly predictable, was previously supported only by animal studies and by a single report in humans.3
All in all, our data indicate that in the elderly, gastric mucus production, bicarbonate secretion, and gastric mucosal blood flow are indeed reduced. These observations are consistent with previous reports from Feldman’s group of a decrease in gastric prostaglandin biosynthesis in elderly subjects and accounts for the vulnerability of their gastric mucosa to damage from ingestion of non-steroidal anti-inflammatory drugs.
Editor,—We would like to thank Dr Guslandi for his interest in our paper. These unpublished observations from Dr Guslandi’s laboratory confirm and extend the findings reviewed in our article. Collectively, available data suggest that aging is associated with selective and specific changes in gastric mucosal defence mechanisms that may predispose the elderly to non-steroidal anti-inflammatory drug (NSAID) gastropathy. Future studies should be focused on the mechanisms of these age related changes in gastric mucosal function, which may help us to develop novel interventions for the treatment and prevention of NSAID induced gastrointestinal injury in susceptible elderly individuals.