Objective: Histopathological and clinical data strongly suggest that Helicobacter pylori is the cause of chronic gastritis and peptic ulceration. However, little has been written about the potential causal relation of H. pylori infection to hyperplastic and adenomatous gastric polyps. We therefore carried out a prospective study to determine the effect of eradicating H. pylori infection on the course of hyperplastic and adenomatous gastric polyps.
Methods: From November 1996 to December 1997, 6700 patients who had undergone upper gastrointestinal endoscopy at the two centres in Zagreb, Croatia, were candidates for participation in the study. Hyperplastic and adenomatous polyps were diagnosed on a basis of at least three histological samples taken from the polyp. In seven patients endoscopy had to be repeated because forceps biopsy sampling either provided inadequate tissue for correct histological diagnosis, or accurate characterization of gastric polyp histology was not possible. Upon completion of all endoscopic examinations before and after treatment, biopsy samples were taken from the antrum (two) and the body of the stomach (two) so that gastritis could be graded and classified, and the presence of H. pylori sought by histology. Two other samples were taken from the antrum for a rapid urease test. Follow-up examinations were performed by using endoscopy. Control endoscopy was performed at least 4 weeks after the treatment of H. pylori infection had been completed, and then every 3-4 months. The follow-up ranged from 4 to 17 months, with a median of 14 months. The treatment of H. pylori infection consisted of a 1-week course of either omeprazole (20 mg twice daily) or pantoprazole 40 mg twice daily), and a 1-week course of amoxicillin 2g twice daily) and metronidazole (400 mg three times daily), and clarithromycin (500 mg twice daily). Eradication of H. pylori infection was assessed by repeated histology and rapid urease test.
Results: Twenty-one patients (nine women, 12 men; median age 52 years) with histologically proven hyperplastic gastric polyps, and seven patients (two women, five men; median age, 67 years) with adenomatous gastric polyps were included in the study. Among 21 patients with hyperplastic gastric polyps, 16 patients (76%) were positive for H. pylori infection. Only two patients (29%) with adenomatous gastric polyps were positive for the infection. Complete eradication of H. pylori was initially achieved in all patients positive for H. pylori. Total regression of the gastric polyps was observed only among the patients with hyperplastic gastric polyps in whom H. pylori had been eradicated. Complete regression of the hyperplastic gastric polyps was observed in seven of the 16 evaluable patients (44%; 95% CI, 19-68%) after H. pylori eradication. The endoscopic snare polypectomy was carried out in nine patients with hyperplastic polyps and two patients with adenomatous gastric polyps in whom regression of the polyps was not observed after H. pylori eradication, as well as in five patients with hyperplastic and four with adenomatous gastric polyps who were negative for H. pylori. Exploratory laparotomy and gastrotomy with polyps excision were carried out in one patient with multiple adenomatous gastric polyps. In only one patient who was not positive for H. pylori recurrence of hyperplastic gastric polyp was recorded during follow-up, and no re-infection with H. pylori has been detected.
Conclusions: Our results suggest that the development of hyperplastic gastric polyps may be directly related to chronic active gastritis and concomitant H. pylori infection. Cure of H. pylori infection associated with hyperplastic gastric polyps resulted in complete polyp regression in more than 40% of patients. Therefore, for patients with hyperplastic gastric polyps and concurrent H. pylori infection an antibiotic treatment designed to eradicate H. pylori appears to be recommended before further therapeutic options are consi