OBJECTIVE: Smoking and Helicobacter pylori are both deleterious to the gastric and duodenal mucosa. Smoking also seems to modify inflammation in H. pylori infection. The aim of this study was to investigate the relationship between smoking and H. pylori in the Finnish population. MATERIAL AND METHODS: We analysed the effect of smoking on gastric inflammation, humoral response to H. pylori and peptic ulcer disease among 318 Finnish H. pylori-positive patients (age 18-75 years; 73 smokers). Gastric histology was evaluated according to the updated Sydney system. RESULTS: Smoking affected neither antral inflammation nor atrophy. In the gastric body, smokers showed milder chronic and neutrophilic inflammation and less atrophy (4% versus 17%, p=0.004). In smokers, H. pylori infiltration was denser in the atrium (mean 2.14 versus 1.87, p=0.02) but less dense in the body (mean 1.55 versus 1.84, p=0.003). Smoking thus seems to decrease inflammation in the gastric body and to delay atrophic changes in the gastric body. Subsequently, the prevalence of duodenal ulcers increased (32% versus 11%, p<0.001), but not the prevalence of gastric ulcers. Smoking also reduced serum IgG antibody titres against H. pylori (mean 8535 versus 5587, p=0.002) and their percentage decrease after successful eradication, possibly affecting serological diagnostic efficacy. Smokers were younger than non-smokers, but when age was taken into account, the differences remained the same. CONCLUSIONS: In H. pylori-positive gastritis, smoking reduced inflammation and atrophy in the gastric body as well as humoral response to H. pylori.
OBJECTIVE: Smoking and Helicobacter pylori are both deleterious to the gastric and duodenal mucosa. Smoking also seems to modify inflammation in H. pyloriinfection. The aim of this study was to investigate the relationship between smoking and H. pylori in the Finnish population. MATERIAL AND METHODS: We analysed the effect of smoking on gastric inflammation, humoral response to H. pylori and peptic ulcer disease among 318 Finnish H. pylori-positive patients (age 18-75 years; 73 smokers). Gastric histology was evaluated according to the updated Sydney system. RESULTS: Smoking affected neither antral inflammation nor atrophy. In the gastric body, smokers showed milder chronic and neutrophilic inflammation and less atrophy (4% versus 17%, p=0.004). In smokers, H. pylori infiltration was denser in the atrium (mean 2.14 versus 1.87, p=0.02) but less dense in the body (mean 1.55 versus 1.84, p=0.003). Smoking thus seems to decrease inflammation in the gastric body and to delay atrophic changes in the gastric body. Subsequently, the prevalence of duodenal ulcers increased (32% versus 11%, p<0.001), but not the prevalence of gastric ulcers. Smoking also reduced serum IgG antibody titres against H. pylori (mean 8535 versus 5587, p=0.002) and their percentage decrease after successful eradication, possibly affecting serological diagnostic efficacy. Smokers were younger than non-smokers, but when age was taken into account, the differences remained the same. CONCLUSIONS: In H. pylori-positive gastritis, smoking reduced inflammation and atrophy in the gastric body as well as humoral response to H. pylori.