Relation of Serum Gastrin and Pepsinogen Levels to Serologic Recognition of CagA and VacA in Helicobacter pylori Infection

Kim, Kyung Chul; Park, Hyo Jin; Lee, Hong Woo; Jung, Jun Keun; Chung, Jun Pyo; Lee, Kwan Sik; Chon, Chae Yoon; Lee, Sang In; Park, In Suh

Abstract

BACKGROUND/AIMS: Helicobacter pylori(H. pylori) infection is associated with increases in serum gastrin and pepsinogen(PG) in patients with gastritis and peptic ulcer disease. H. pylori strains show phenotypic heterogeneity in their ability to express CagA(cytotoxin-associated protein) and VacA(vacuolating cytotoxin), which are tbought to be virulence factors. The aim of the study was to investigate whether the biochemical(serum gastrin and PG) changes in H. pylori infection are related to the bacterial expression of CagA and VacA.
METHODS
The subjects were 80 patients who had underwent diagnostic esophagogastroduodenoscopy; 49 with functional dyspepsia(FD), 10 with gastric ulcer(GU), 10 with duodenal ulcer(DU) and 11 with gastric cancer(GC). H. pylori infection was assessed by rapid urease(CLO) test and histology. Bacterial expression of CagA and VacA was determined indirectly by assaying serum IgG antibodies to these proteins by Western blotting using a Helico Blot 2.0 kit. Basal serum levels of gastrin, PG I and PG II were determined by radioimmunoassay.
RESULTS
The serologic positive rate for CagA in H. pylori-positive patients with FD, GU, DU and GC, was 80%, 88%, 100% and 88% respectively. For VacA, positive rate was 41%, 38%, 88%, and 63%, respectively(FD vs DU, p<0.05). Serum level of gastrin and PG were increased in patients with H. pylori-positive FD, GU, DU, and GC compared with patients with H. pylori-negative FD. In the patients with H. pylori-positive FD(n=34), the changes of serum levels of gastrin and PG were more prominent in serologic type I(CagA+/VacA+) infection than either type II(CagA-/VacA-) or type III(CagA+/VacA-) infection, especially the increase in PG I level being significant, Serologic recognition of VacA was associated with increased levels of serum PG I and PG II, whereas serologic recognition of CagA had no significant relation to the changes in serum level of either gastrin or PG.
CONCLUSIONS
Biocbemical changes in patients with H. pylori infection, especially the increase in serum PG I level, were prominent in serologic type I(CagA+/VacA+) infection. Serologic recognition of VacA, which was more prevalent among DU patients than among FD patients, was associated with increases in serum level of PG I and PG II. Serologic recognition of VacA, as well as the increased level of serum PG, may serve as useful serum markers to predict the clinical status of H. pylori infection.