Endoscopic characteristics and Helicobacter pylori infection in NSAID-associated gastric ulcer.

BACKGROUND AND AIM: Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are deeply involved in the etiology of gastric ulcers. The aim of our study was to clarify the endoscopic characteristics and H. pylori infection status of NSAID-associated gastric ulcers. METHODS: The study group comprised 50 patients (23 men, 27 women; mean age 66.5 years) with NSAID-associated gastric ulcers and 100 sex- and age-matched patients with gastric ulcer associated with other factors (control group). Ulcer morphology, size and number of lesions, onset site and incidence of hemorrhagic ulcers were investigated endoscopically in both groups. H. pylori infection was diagnosed by serology, histology and (13)C-urea breath test. RESULTS: Multiple lesions (68% vs 20%, P<0.001), occurrence in the antrum (56% vs 6%, P<0.001), and hemorrhagic ulcer (34% vs 4%, P<0.001) were significantly more prevalent in patients with NSAID-associated gastric ulcers than in patients with non-NSAID-associated gastric ulcer. The H. pylori infection rate was significantly lower in NSAID-associated gastric ulcer patients than in non-NSAID-associated gastric ulcer patients (48% vs 96%, P<0.001). In the NSAID-associated gastric ulcer group, the prevalence of H. pylori infection was significantly lower in patients with ulcers in the antrum than in those with ulcers in the angulus or corpus (25% vs 77.3%, P<0.001). CONCLUSIONS: In contrast to non-NSAID-associated gastric ulcers, NSAID-associated gastric ulcers frequently occur in the antrum with bleeding. The rate of H. pylori infection in NSAID-associated gastric ulcers is significantly lower than that in non-NSAID-associated gastric ulcers.

Cigarette smoking promotes atrophic gastritis in Helicobacter pylori-positive subjects.

Aging and smoking are known to promote atrophic gastritis (AG) and intestinal metaplasia (IM). This study investigated the relationship between Helicobacter pylori (Hp) infection, aging, smoking, and AG/IM. Ninety-six Hp-negative and 231 Hp-positive subjects were divided according to age; (< or = 39 years, 40-59 years, and > or = 60 years) and smoking history (never smoked, or currently smoking). Histologic grading was performed according to the updated Sydney system. Fasting pH, total bile acid (TBA) concentration, and ammonia (NH3) concentration in gastric juice were measured. Comparisons were made based on Hp status, age, and smoking. Independent relative risks for severe AG and IM were calculated. Grades of atrophy and IM were significantly higher in Hp-positive subjects, and these increased with age. Within Hp-positive subjects, grades of atrophy and IM were higher in smokers and in the middle and upper age groups. Within Hp-positive subjects, gastric pH and TBA were similarly higher in smokers and older subjects. An increased risk of severe AG/IM was statistically associated with smoking (OR 9.31, 3.85-22.50/OR 4.91, 1.90-12.68) and high TBA concentrations (OR 2.92, 1.19-7.17/OR 3.28, 1.25-8.62). Both Hp infection and aging are closely related to the development of AG and IM. Cigarette use and high TBA concentrations may play a role in the progression of AG and IM in Hp-positive subjects.