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INTERACTION BETWEEN H. PYLORI AND NSAIDS: PREDICTIVE VALUE OF DENSITY OF POLYMORPHONUCLEAR LEUKOCYTES, MUCOSAL AND GASTRIC JUICE NUTRITE LEVELS
Author(s) -
Shiotani Akiko,
Yamaoka Yoshio,
ElZimaity Hala,
Saeed M. Ali,
Graham David Y.
Publication year - 2000
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2000.00a37.x
Subject(s) - medicine , gastroenterology , gastric mucosa , infiltration (hvac) , helicobacter pylori , nitrite , stomach , ecology , physics , biology , nitrate , thermodynamics
Background Although nonsteroidal anti‐inflammatory drugs (NSAIDs) use and H. pylori are the most common causes of peptic ulcers, it remains unclear whether there is an interaction between them. Aim To test whether there was a relationship between polymorphonuclear leukocyte (PMN) infiltration of the gastric mucosa and severity of NSAID‐induced gastric mucosal injury. Methods H. pylori density, mucosal interleukin‐8 (IL‐8) levels as well as gastric mucosal and juice nitrite levels were assessed in normal volunteers before and after receiving 600 mg of naproxen (twice a day for 3 days). Histology was graded using a visual analogue scale from 0 (absent/normal) to 5 (maximal intensity). IL‐8 levels were assayed by ELISA and nitrite levels by Griess reaction. Endoscopic damage was graded from none to severe (large erosions or ulcers). Results Eleven healthy volunteers with active H. pylori infection and normal appearing gastric mucosa were entered. The post‐NSAID endoscopic scores were 0 = 3, mild = 1 moderate = 4, and severe = 3. None of the pretreatment histologic or biochemical parameters (e.g., PMN density, mucosal Il‐8 or nitrite levels) predicted endoscopic outcome nor was there a significant changes from pretreatment levels. There was an inverse correlation between endoscopic score and the pH of the gastric juice post‐therapy (R‐0.669, p=0.02). Conclusions The hypothesis that the intensity of PMN infiltration in the mucosa correlated with risk of ulcer development was not confirmed. PMN infiltration is likely a surrogate for an H. pylori infection‐related increased risk of NSAID ulcers.

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