Gene expression of ornithine decarboxylase, cyclooxygenase-2, and gastrin in atrophic gastric mucosa infected with Helicobacter pylori before and after eradication therapy.

摘要: H. pylori (Hp) -induced atrophic gastritis is a well-known risk factor for the development of gastric cancer. Whether Hp eradication can prevent or retard progress atrophy and metaplasia has been topic numerous studies but subject remains controversial. Recently, increased expression ornithine decarboxylase (ODC), gastrin cyclooxygenase (COX)-2 shown to be in premalignant lesions mucosa play an essential role malignant transformation. The aim study assess effect therapy on analyze gene ODC, COX-2 after succesful patients with gastritis. Twenty chronic including both corpus antrum stomach were included this study. Four antral mucosal biopsy specimens obtained from four corpus. histopathologic evaluation was based Sydney classification All positive [13C] urea breath test (UBT) presence anti-Hp IgG anti-CagA-antibodies detected by ELISA. then eradicated triple consiting omeprazol (2 × 20 mg), amoxycillin 1 g) clarithromycin 500 mg) seven days vitamin C g/day three months. In samples before eradication, mRNA COX-2, assessed reverse-transcription polymerase chain reaction (RT-PCR). all secretory analysis performed measuring acid output serum levels. After successful UBT observed 95% patients. 45% infection CagA-positive strain observed. Three months significant reduction activity (neutrophilic infiltrate) severity (mononuclear score improved eradication. ODC significantly up-regulated reduced therapy. successfully increase secretion decrease We conclude that: (1) leads mucosa, may relevant prevention Hp-associated carcinogenesis. (2) ameliorates upon