Genetic markers and duodenal ulcer

Serum pepsinogen, α₁-antitrypsin (α₁-AT) and blood groups were studied as genetic marken in 32 patients with endoscopically proven duodenal ulcer and 44 control subjects with no family history of ulcer disease. Serum pepsinogen was determined by the modified method of Edward et al⁷, α₁-AT by single radial unmunodiffusion⁸ (RID) and phenotyping was carried out by isoelcctric focusing (IEF)⁹. Duodenal ulcer patients with hyper-pepsinogenemia (28%) and low serum α₁-AT (35%) had a dominant blood group O, lower mean age, an early onset of disease, a higher frequency of gastrointestinal (GI) bleeding and ulcer perforation. These parameters were found considerably different in patients with normal serum pepsinogen and α₁-AT. Phenotype analysis of α₁-AT revealed that four duodenal ulcer patients had partial deficiency of the protease inhibitor and none of the normal exhibited the deficiency pattern. The etiology of the disease appears to be genetic anomaly in 28% of patients while the rest (72%) had ulcers as a result of neuroendocrinological or environmental factors.