A study of the pathogenesis of Helicobacter pylori negative chronic duodenal ulceration.

Abstract

In the past five years 12 patients have been identified presenting with chronic duodenal ulcer (DU) disease and with no evidence of current or recent Helicobacter pylori (H pylori) infection. Four of them were taking regular non-steroidal anti inflammatory agents, one was subsequently found to have Crohn's disease of the duodenum, and one to have the Zollinger-Ellison syndrome. The remaining six patients with idiopathic DU disease were remarkable for their absence of the A1 blood antigen gene. Detailed studies of gastric function were performed in these six patients and compared with H pylon positive patients with DU and with healthy volunteers. The median integrated gastrin response in the patients with idiopathic DU (2810 (range 750-8750) ng/l min) was similar to that of the H pylori positive patients with DU (3355 (550-8725)) and higher than that of the H pylon negative healthy volunteers (560 (225-1125)). The median peak acid output in the patients with idiopathic DU (37 mmol/h, range 17-52) was similar to that of the H pylon positive patients with DU (40 (15-57)) and higher than that ofthe non-ulcer controls (22 (16-29)). The median percentage of a liquid meal retained in the stomach at 60 minutes was less in the patients with idiopathic DU (23 (15-33)) than in Hpyloni negative healthy volunteers (34 (30-53) p<0-01). The median percentage of a solid meal retained at 60 minutes was less in the patients with idiopathic DU (54 (9-83)) than in either H pylon negative healthy volunteers (87 (49-95) p<001) or H pylon positive patients with DU (79 (51-100) p<0-01). In conclusion, three abnormalities of gastric function are prevalent in patients with H pylon negative idiopathic DU disease -hypergastrinaemia, increased acid secretion, and the one feature distinguishing them from H pylon positive patients with DU -rapid gastric emptying of both liquids and solids. Each of these abnormalities will increase the exposure of the duodenal mucosa to acid and thus explain its ulceration. The absence of the blood group A1 antigen gene is consistent with a genetic basis for the disturbed gastric function linked to the ABO blood group antigen genes. (Gut 1993; 34: 762-768) More than 95% of patients with chronic duo-

Changing prevalence of upper gastrointestinal disease in 28 893 Koreans from 1995 to 2005

“…That is, the prevalence of H. pylori-negative peptic ulcers in the USA and Australia is relatively high, at 27-43%, and relatively low in Europe and Japan, at 2.7-8.0% [31][32][33][34][35][36]. This could be explained from the fact that the infection rate of H. pylori fell more rapidly in the USA and Australia.…”

Has Helicobacter pylori Eradication for Peptic Ulcer Been Overrated?

“…pylori-negative duodenal ulcer was only rare by 2.8-6.0% in developed countries in the early 1990's (Table 1) (2,3), approximately half of these were NSAID-associated ulcers. Therefore, idiopathic duodenal ulcers, which are not associated with H. pylori or NSAIDs, were extremely rare at 0.3-1.4% (2,3). Recent studies have shown a higher incidence of idiopathic duodenal ulcers in USA and Australia, while the incidence of such an ulcer is still reportedly low in other countries, including Japan (Table 2).…”

Helicobacter pylori

“…pylori, eg. in Crohn's disease, following ingestion of NSAIDs [44], and in the Zollinger-Ellison syndrome [45]. It seems logical to eradicate H .…”