Abstract
We postulated that ammonia produced byHelicobacter pylori may contribute to gastric mucosal injury. This hypothesis was evaluated inHelicobacter-positive patients with chronic renal failure in whom a high urea concentration might amplify this phenomenon. Gastric urea and ammonia were measured, and the severity of gastritis was evaluated by counting mononuclear and polymorphonuclear, cells. High gastric ammonia and low urea inHelicobacter-positive patients, and the converse inHelicobacter-negative subjects, were observed. There was a significant correlation between gastric ammonia and interstitial polymorphonuclear leukocytes infiltration (P<0.05), suggesting a causal link. Eradication ofHelicobacter pylori was associated with a decrease of ammonia and an increase of urea (P<0.01). The significant correlation between the severity of gastric inflammation and the gastric juice ammonia concentration suggests that ammonia may play a pathogenic role inHelicobacter-associated gastric injury.
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This work was supported by the Department of Health and Human Services grants AA07275, AA03508, and the Department of Veterans Affairs.
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Triebling, A.T., Korsten, M.A., Dlugosz, J.W. et al. Severity ofHelicobacter-induced gastric injury correlates with gastric juice ammonia. Digest Dis Sci 36, 1089–1096 (1991). https://doi.org/10.1007/BF01297452
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DOI: https://doi.org/10.1007/BF01297452