Abstract

Background:Non-steroidal anti-inflammatory drugs (NSAIDs) are implicated in several diseases showing altered tissue and leukocyte eicosanoid patterns, such as nasal polyposis and asthma. NSAIDs are also associated with gastrointestinal lesions, but it is unknown whether there is an altered eicosanoid pattern.Material/Methods: The ex vivo modulated syntheses of prostaglandin E[sub]2[/sub] (PGE[sub]2[/sub]) and peptido-leukotrienes (pLT) by leukocytes from 41 patients with gastroduodenal ulcer were compared with those of 61 healthy controls. Samples were incubated with diluent, arachidonic acid, or acetylsalicylic acid. The individual syntheses of PGE[sub]2[/sub] and pLT were quantified using competitive enzyme-immuno-assays followed by calculation of individual eicosanoid patterns.Results: Controls synthesized ~4.9-fold whereas patients only ~2.9-fold more PGE2 than pLT due to higher basal synthesis of pLT (67 and 125 pg/ml, respectively). The baseline PGE[sub]2[/sub]/pLT ratio was slightly higher in patients (6.1) than in controls (5.7). The arachidonic acid-induced PGE[sub]2[/sub]/pLT ratio in patients (14.2) was significantly higher than in controls (3.3). The acetylsalicylic acid-induced PGE[sub]2[/sub]/pLT ratio in patients (3.5) was significantly lower than in controls (8.3) due to diminished PGE[sub]2[/sub] and elevated pLT. Integrated individual PGE[sub]2[/sub] and pLT values revealed a highly significantly altered eicosanoid pattern score in ~95% patients and ~12% controls.Conclusions: There is strong evidence of an altered eicosanoid pattern generated by leukocytes of gastroduodenal ulcer patients, which became obvious upon in vitro modulation by arachidonic or acetylsalicylic acid. The phenomenon of an abnormal eicosanoid pattern in gastroduodenal ulcer is yet not fully understood, but may have implications in pathophysiology and diagnostics.

Keywords: Eicosanoids - metabolism, Health, Leukocytes - metabolism, Peptic Ulcer - metabolism, Eicosanoids - metabolism, Health, Leukocytes - metabolism, Peptic Ulcer - metabolism