Published online Jul 7, 2020. doi: 10.3748/wjg.v26.i25.3673
Peer-review started: February 24, 2020
First decision: March 27, 2020
Revised: April 8, 2020
Accepted: June 4, 2020
Article in press: June 4, 2020
Published online: July 7, 2020
Processing time: 185 Days and 11.6 Hours
Type I Helicobacter pylori (H. pylori) is the major form of H. pylori infection in many areas globally. However, its infection status and role in stepwise gastric disease in this gastric cancer prevalent area have not been studied. Its impact on the commonly used gastric cancer risk markers such as gastrin-17 (G-17) and pepsinogens (PGs) is also not known.
We investigated the prevalence of type I and type II H. pylori infection in stepwise gastric diseases and the clinical implications; their impact on G-17 and PGs levels during routine clinical practice were also evaluated.
Five hundred and twenty-three hospital admitted patients were enrolled in this study. H. pylori infection was confirmed by both 13C-urea breath test and serological assay. Their serological G-17, PG I, PG II values and PG I/PG II ratio were also measured. Receiver operating characteristic curves were used to calculate the overall diagnostic performance of G-17, PG I, PG II and PG I/PG II ratio in peptic ulcers (PU), chronic atrophic gastritis (CAG) and gastric cancer (GC) patients to determine the best cutoff values, sensitivity and specificity.
The infection rate of 523 enrolled patients was 76.9%, among which type I H. pylori infection accounted for 72.4%, and type II was 27.6%. Overall, 88.4% of GC patients were H. pylori positive, 84.2% of them were type I infection, and only 11.6% of GC patients were H. pylori negative. 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 patients. PG I levels showed no difference among disease groups, and only showed a difference in stratified analysis in GC and PU patients. The diagnostic performance of G-17, PG I, PG II and PG I/PG II ratio in PU, CAG and GC patients indicated relatively low predictive value.
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 increased G-17 level, while type I H. pylori is the major strain that affects PG I, PG II levels and PG I/PG II ratio in stepwise chronic gastric diseases.
The results provide insight on H. pylori infection status in hospital admitted patients, and their impact on G-17 and PGs levels, which will be helpful to guide H. pylori eradication and explain G-17 and PGs assay results in clinical practice.