Prospective multi-center trial for the efficacy of ecabet sodium on the relief of dyspepsia in korean patients with chronic gastritis

一项前瞻性多中心试验,旨在评估依卡贝钠对韩国慢性胃炎患者消化不良症状的缓解效果

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Abstract

Anti-peptic and anti-inflammatory actions of ecabet sodium might be beneficial in either improving gastritis or relieving dyspeptic symptoms. This study was designed to evaluate the clinical efficacy of ecabet sodium on dyspeptic symptoms and to elucidate the molecular mechanism attributable to symptom relief in patients with chronic gastritis. Two hundred and sixty eight chronic gastritis patients with persistent dyspepsia received ecabet sodium 1 g b.i.d. for 2 weeks, after which dyspeptic symptoms were reassessed with a questionnaires as before. The changes of interleukin-8 (IL-8), inducible nitric oxide synthase (iNOS), prostaglandin E(2) (PGE(2)), and vascular endothelial growth factor (VEGF) levels in gastric juices were measured by ELISA. The changes of nitrotyrosine in gastric mucosa were measured by immunohistochemical staining. The most common dyspeptic symptom in Korean patients with chronic gastritis was epigastric soreness (76.8%), which was improved significantly after ecabet sodium treatment (81.7%, p<0.001). Ecabet sodium was more effective in patients with epigastric pain than vague abdominal discomfort (p = 0.02), especially in patients with old age. Complete relief of discomfort was more highly achieved in patients with positive Helicobacter pylori than without (p = 0.01). In spite of clear tendency that the decreased levels of IL-8, iNOS, and PGE(2) and increased levels of VEGF were measured in gastric juices after ecabet sodium treatment, no statistical significance was noted, which might be due to high inter-individual variations. The nitrotyrosine expressions were significantly decreased after ecabet sodium treatment than before (p<0.01). In conclusion, ecabet sodium treatment was very useful for the relief of dyspeptic symptoms in chronic gastritis, to which both attenuated inflammatory and enhanced regenerative mechanisms were contributive.

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