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