intragastric acidity in patients with gastritis and duodenal ulcer

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. Hpylon was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower inHpylon negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p<0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmolll, 19 (7.1-33.1) mmolll, 44 (25-1-63.1) mmol/l, and 36 (31.6-39.8) mmoVIl respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During ali predefined time periods, intragastric acidity was significantly higher in patients withHpylon positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between theH pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylon infection have normal gastric acidity. (Gut 1992; 33: 1024-1028) Department of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, D-3000 Hannover, 61 Germany S Wagner M Varrentrapp M Gebel Department of Medicine, Rheinisch-Westfalische Technische Hochschule Aachen, D-5100 Aachen, Germany U Gladziwa The First Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima 734, Japan K Haruma Correspondence to: Dr Siegfried Wagner, Dept of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, Konstanty Gutschowstr 8, D-3000 Hannover 61, Federal Republic of Germany. Accepted for publication 19 November 1991 A causative role is now generally accepted for Helicobacter pylon in type B gastritis, and evidence is accumulating that H pylori infection plays a major contributory part in peptic ulcer disease. 2 It has been shown that eradication ofH pylori is associated with a significant reduction in the duodenal ulcer relapse rate.3'5 Since, on average, duodenal ulcer patients secrete more acid than control subjects, Levi et al have suggested that H pyloni causes duodenal ulcer disease by stimulating antral mucosal gastrin release which increases gastric acid secretion.6 While inappropriate hypergastrinaemia has been shown in subjects infected with H pylori, the effect of H pylori infection on gastric acidity remains controversial.7'Acute infections may lead to a transient hypochlorhydria. 15-1X By contrast, in chronic infections large variations in gastric acidity have been reported, including hypochlorhydria, hyperchlorhydria, and normal acid secretion.`-4 1' There is, however, a paucity of data relating gastric acidity to the presence of chronic H pylori infection. Because of this we have studied the effect of gastric H pylori infection on the circadian pattern of gastric acidity in patients with gastritis and active duodenal ulcer disease.