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  • Title: Role of Helicobacter pylori infection and duodenogastric reflux in the pathogenesis of alkaline reflux gastritis after gastric operations.
    Author: Robles-Campos R, Lujan-Mompean JA, Parrilla-Paricio P, Bermejo-Lopez J, Liron-Ruiz R, Torralba-Martinez JA, Morales-Cuenca G, Molina-Martinzez JA.
    Journal: Surg Gynecol Obstet; 1993 Jun; 176(6):594-8. PubMed ID: 8322136.
    Abstract:
    In patients undergoing gastric operations, we studied the relationship between data suggesting alkaline reflux gastritis (symptoms, endoscopic alterations and histologic lesions) and two factors that produce chronic gastritis (helicobacter pylori and duodenogastric reflux). Of 225 patients who underwent operations for gastroduodenal gastric ulcer at our General Surgery Unit between 1980 and 1982, 63 agreed to undergo endoscopy and biopsies. Of these 63 patients, 38 agreed to a test to quantify duodenogastric reflux (24 hour gastric pH monitoring associated with the determination of bile acids in gastric juice). According to the clinical questionnaire, patients were classified as symptomatic and asymptomatic. Endoscopy was considered either normal with mucosal lesions or mucosal lesions plus bile. In the histologic study, we considered normal mucosa, superficial chronic gastritis and atrophic chronic gastritis. Furthermore, the presence of atrophy, metaplasia, foveolar hyperplasia and helicobacter pylori was studied. Symptoms, endoscopic alterations and histologic lesions were not significantly related to helicobacter pylori, but were significantly related to the quantity of duodenogastric reflux. The symptomatic patients presented with a greater quantity of reflux than the asymptomatic patients (p < 0.05). The patients with mucosal lesions plus bile who had endoscopy showed a greater quantity of reflux than those with normal endoscopy (p < 0.001) and those with mucosal lesions without bile (p < 0.02 for pH values and p < 0.001 for bile acids). The patients with atrophic chronic gastritis presented with a greater quantity of reflux than those with normal mucosa and superficial chronic gastritis (p < 0.05, respectively), and the patients with atrophy and metaplasia and foveolar hyperplasia had more reflux than those without (p < 0.001, respectively). The patients who were helicobacter positive and negative presented with similar quantities of reflux.
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