BACKGROUND
Type I
Helicobacter pylori
(
H. pylori
) infection causes severe gastric inflammation and is a predisposing factor for gastric carcinogenesis. However, its infection status in stepwise gastric disease progression in this gastric cancer prevalent area has not been evaluated; it is also not known its impact on commonly used epidemiological gastric cancer risk markers such as gastrin-17 (G-17) and pepsinogens (PGs) during clinical practice.
AIM
To explore the prevalence of type I and type II
H. pylori
infection status and their impact on G-17 and PG levels in clinical practice.
METHODS
Thirty-five hundred and seventy-two hospital admitted patients with upper gastrointestinal symptoms were examined, and 523 patients were enrolled in this study.
H. pylori
infection was confirmed by both
13
C-urea breath test and serological assay. Patients were divided into non-atrophic gastritis (NAG), non-atrophic gastritis with erosion (NAGE), chronic atrophic gastritis (CAG), peptic ulcers (PU) and gastric cancer (GC) groups. Their serological G-17, PG I and PG II values and PG I/PG II ratio were also measured.
RESULTS
A total
H. pylori
infection rate of 3572 examined patients was 75.9%, the infection rate of 523 enrolled patients was 76.9%, among which type I
H. pylori
infection accounted for 72.4% (291/402) and type II was 27.6%; 88.4% of GC patients were
H. pylori
positive, and 84.2% of them were type I infection, only 11.6% of GC patients were
H. pylori
negative. Infection rates of type I
H. pylori
in NAG, NAGE, CAG, PU and GC groups were 67.9%, 62.7%, 79.7%, 77.6% and 84.2%, respectively.
H. pylori
infection resulted in significantly higher G-17 and PG II values and decreased PG I/PG II ratio. Both types of
H. pylori
induced higher G-17 level, but type I strain infection resulted in an increased PG II level and decreased PG I/PG II ratio in NAG, NAGE and CAG groups over uninfected controls. Overall PG I levels showed no difference among all disease groups and in the presence or absence of
H. pylori;
in stratified analysis, its level was increased in GC and PU patients in
H. pylori
and type I
H. pylori-
positive groups.
CONCLUSION
Type I
H. pylori
infection is the major form of infection in this geographic region, and a very low percentage (11.6%) of GC patients are not infected by
H. pylori
. Both types of
H. pylori
induce an increase in G-17 level, while type I
H. pylori
is the ma...