Increased serum pepsinogen-I level predicts development of new duodenal erosion following eradication teraphy of H.pylori

Abstract

Aims: Eradication of Helicobacter pylori (Hp) decreases the concentrations of serum gastrin (G) and pepsinogen (PG). However, the changes in serum level of such peptides during or just after eradication therapy have not been well investigated. In this study, we evaluated the changes in serum G and PG levels at the end of eradication therapy, and then investigated the relation to the duodenal erosion following eradication. Methods: We randomly treated 318 patients (104 female and 318 men, mean age 51 years) with abdominal symptom (109 gastric ulcer (GU), 113 duodenal ulcer (DU), 32 gastro-duodenal ulcer (GDU), and 64 atrophic gastritis (AG». Before eradication, endoscopy was performed and patients with duodenal erosion were excluded. One month after eradication, endoscopy was performed to check duodenal erosion, and Hip culture, histology, and urea breath test performed to assess Hip treatment. We determined G and PG level in sera at three time points: before eradication, at the end of eradication, and one month after eradication. Results: In 272 (85.5%) cured patients, 39 (14.3%) patients had new duodenal erosions. In 46 (14.5%) patients with unsuccessful treatment, no duodenal erosion appeared. Duodenal erosion developed in 27.3%, 10.7%, 9.1%, and 0% in the patients with DU, GDU, GU, and AG. The prevalence of duodenal erosion after Hip eradication was significantly higher (p < 0.005) in DU patients than in GU, and AG patients. In cured patients, G, PG-I, II, and IIII level one month after eradication were significantly decreased compared to those measured before eradication (p < 0.005). At the end of eradication, G and PG-I level were significantly higher than before eradication (p < 0.0001). In uncured patients, no changes were seen. In the patients with new duodenal erosions, G, PG-I, II, and IIII levels were similar to non-duodenal erosion patients before eradication and one month after eradication. However, at the end of eradication, only PG-I levels were significantly higher (p < 0.0001) than in the patients with non-duodenal erosion. Conclusions: 1. Successful Hip treatment causes a temporary high G and PG-I response at the end of eradication therapy. 2. Increased PG-I might be a kind of gastric mucosal response to H.p eradication since this temporary high level of serum PG-I is strongly associated with development of new erosions in duodenum. 3. These phenomenon strongly bring about duodenal mucosal damage by excess acid secretion and PG-I following eradication therapy.