That duodenal ulcer is in some way an abnormal reaction of the duodenal mucosa to acid and pepsin is the hypothesis which underlies most current views ofthe pathophysiological basis ofduodenal ulceration and most current medical and surgical attempts at treatment. The hypothesis is accepted as a foundation for the present discussion, because the secretion of acid and pepsin by the stomach appears to be necessary for the development of duodenal ulceration, although it has not yet been proven that the exocrine secretions of the stomach are solely responsible for the pathogenesis of chronic duodenal ulcers. It is, of course, not permissible to conclude that disordered secretion of gastric juice is the cause of the ulceration from the fact that secretion of acid and pepsin is necessary for the formation of duodenal ulcer' and, in any case, abnormal secretion of acid and pepsin is not demonstrable in all patients with duodenal ulcer. The information available at present about the pathophysiology of duodenal ulceration will be analysed in terms of answers to a series of questions.

https://gut.bmj.com/content/gutjnl/15/1/59.full.pdf

The pathophysiology of duodenal ulceration.

Genetics of Hypertrophic Pyloric Stenosis

The decade since the last review of this subject in Gut has seen considerable advances in many aspects of genetics, including the influence of heredity on disease. Compared with some specialties gastroenterology has few disorders with simple Mendelian inheritance, but in most of its conditions there is some hereditary influence. Some of the best human data illustrating a quantitative type of disease liability are those on hypertrophic pyloric stenosis and Hirschsprung's disease, and the discovery of two of the genes of the genotype giving susceptibility to duodenal ulcer is still unique. There is growing realization that both heredity and environmental factors are concerned in the aetiology of most disorders.

https://gut.bmj.com/content/gutjnl/12/7/592.full.pdf

Genetics and gastroenterology.

Among 986 patients admitted to hospital in the period 1938 to 1967 for gastrointestinal haemorrhage, 882 were blood grouped. A significant excess of blood group O was found among patients with haemorrhagic gastritis and duodenal ulcer. Of 802 blood-grouped patients who left the hospital alive, 800 were retraced 2 to 31 years later. The observed deaths exceeded the expected in all groups, being most pronounced in patients previously operated on, followed by patients with gastric ulcer, duodenal ulcer, and haemorrhagic gastritis. The reason for the higher number of deaths than expected was primarily a continuing high death rate due to haemorrhage, perforation. and selective operation for ulcer. Patients with blood group O, B or AB had a higher excess death rate than patients with blood group A. The difference however was not statistically significant.

Long-term survival of patients with gastrointestinal haemorrhage with special reference to the ABO blood groups.

The aim of the present study was to determine whether blood group O and nonsecretor status are associated with gastric hyperacidity. Total output of gastric acid after maximal histamine stimulation was evaluated in 515 patients—220 males and 295 females—aged 20–50 years, with and without a familial history of duodenal ulcer. All of them were free of gastroduodenal disease. HCl output was found to be significantly higher in patients of blood group O than in those of A, B, and AB, irrespective of family history of duodenal ulcer. Furthermore HCl output was significantly higher, when blood group O was concerned, in nonsecretors than in secretors. In groups A, B, and AB there were no differences between secretors and nonsecretors. These results support the hypothesis that increased levels of acid secretion may explain partially the high incidence of duodenal ulcer among subjects possessing one or both the phenotypic traits—blood group O and nonsecretor.

Balestrieri C

Papers

Influence of blood group and secretor status on gastric acidity