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Abstract
Stachura J, Konturek JW. Dembinski A, Domschke W. Do infiltrating leukocytes contribute to the adaptation of human gastric mucosa to continued aspirin administration? Scand J Gastroenterol 1994:29:966-972.
Background: Aspirin (ASA)-induced gastropathy decreases with continued ASA ingestion due to the development of gastric mucosal tolerance. However, the mechanism of the gastric mucosal adaptation to repeated ASA challenge is unknown.
Methods: The aim of the present study was to determine the density of leukocytes infiltrating the gastric mucosa in healthy subjects during prolonged treatment with ASA. In eight healthy volunteers ASA treatment (2 g/day) was continued for 14 days. Endoscopy was performed before medication, on the 3rd, 7th. and 14th day of ASA treatment, and on the 16th and 18th day (2 and 4 days after medication was stopped). Gastric damage was scored (Lanza score), and gastric biopsy specimens were taken from both the oxyntic and antral mucosa.
Results: ASA administration resulted in the development of hemorrhagic erosions, which were most severe on the 3rd day of the medication; later significant reduction of severity of the damage was observed. ASA administration caused an increased mucosal infiltration of leukocytes; leukocyte margination and adherence to endothelia were commonly observed in the gastric mucosa, particularly on the 3rd day of ASA treatment but not later on. Mast cell density increased significantly on the 3rd day of ASA treatment. Density of mast cells later decreased in the antral mucosa but continued to be significantly increased in the oxyntic mucosa up to the 14th day. There was a striking correspondence between mast cell density and endoscopic score of the mucosal damage. Eosinophil density increased significantly during ASA treatment and remained high even alter medication was withdrawn.
Conclusions: 1) Initial mucosal damage by ASA is followed by gastric adaptation on continuous exposure to this agent; 2) infiltrating leukocytes appear to contribute to the development of gastric mucosal adaptation to ASA; and 3) mast cell density reflects the endoscopic score of gastric damage by ASA.
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