A total of 31 patients with FAP were assessed in this study.
The researchers determined the presence of fundic gland polyposis (FGP) and gastric adenoma (GA) by upper endoscopy with biopsies.
In addition, they assessed the degree of gastric mucosal atrophy and Helicobacter pylori status by serological and histological findings.
Furthermore, any germline mutation in the adenomatous polyposis coli (APC) gene was identified by polymerase chain reaction-based single strand conformation polymorphism and direct sequencing.
Gastric lesions were detected in 74% of the 31 patients in the study, while FGP and GA were found in 52% and 39%, respectively.
An APC gene mutation was identified in 22 of 30 patients.
|Patients infected with H. pylori:|
With FGP: 13%
It was also found that 13% of patients with FGP were infected with H. pylori, compared to 67% in those without FGP.
Patients with FGP also had a lower degree of atrophy than those without.
The research team additionally discovered that patients with GA tended to be more frequently infected with H. pylori and that they had higher degrees of atrophy than those without GA.
For further analysis, subjects were subdivided by gastric lesions (FGP alone, both FGP and GA, GA alone, and those without FGP or GA).
The GA alone group had the lowest pepsinogen I/II ratio and the highest seropositivity for H. pylori.
GA was found more frequently in patients positive for the APC mutation, whereas this trend was not observed in FGP.
To conclude, Dr S. Nakamura's team, from the Department of Medicine and Clinical Science at Kyushu University, Fukuoka, stated that, "In FAP, H. pylori-associated atrophic gastritis contributes negatively to FGP".
"It seems to contribute positively to GA, especially in patients with truncating APC gene mutation".