# Elevated fasting glucose levels associated with H. pylori acute gastritis: an observational study

## TL;DR

This study found that people infected with H. pylori had higher fasting glucose levels, suggesting a link between the infection and prediabetes.

## Contribution

The study identifies a novel association between H. pylori-induced acute gastritis and elevated fasting glucose levels.

## Key findings

- H. pylori infection was associated with higher fasting glucose levels (OR = 3.3).
- High HbA1c levels were significantly linked to H. pylori infection (OR = 4.1).
- Acute gastritis caused by H. pylori was specifically associated with elevated fasting glucose (OR = 8.3).

## Abstract

Helicobacter pylori (H. pylori) is one of the world’s most prevalent infections, being responsible for 90% of gastric MALT lymphomas along with multiple other extra-gastric manifestations. Its role in insulin resistance and glycemic metabolism has been debated in the last few years. The study included a retrospective analysis of 131 patients with dyspeptic symptoms who underwent gastroscopy with biopsies in two hospitals in Northwestern Romania. Our study analyzed the overall prevalence of H. pylori infection, its association with high glycemic values and glycosylated hemoglobin values, as well as histopathology results and their association with modified glycemic values. Fasting glucose levels were higher in patients with H. pylori than in patients without H. pylori (OR = 3.3; 95% CI, 1.6–6.8; P = 0.001). High HbA1c levels were associated with H. pylori infection (OR = 4.1; 95% CI, 1.9–8.7; P < 0.001). Histologically confirmed acute gastritis due to H. pylori was associated with high fasting glucose levels (OR = 8.3; 95% CI, 1–68; P = 0.028), and more specifically with antral acute gastritis (OR = 16.4; 95% CI, 1–290; P = 0.007), while no association between confirmed chronic gastritis and high fasting glucose values was found. Within the limitations of this study, our results support the findings that H. pylori infection represents a risk factor for prediabetes, highlighting the need for special attention to be given to those vulnerable patients. To fully understand the involved mechanisms and the potential therapeutic strategies and management implications, further investigations are required.