Alpha(1)-antitrypsin deficiency may be a risk factor for duodenal ulcer inpatients with Helicobacter pylori infection

Background: Most individuals with Helicobacter pylori infection in Western countries have no evidence of peptic ulcer disease (PUD). We therefore asse ssed the PiZ deficiency variant of the major plasma protease inhibitor alph a(1)-antitrypsin (alpha(1)AT) as a risk factor for PUD in H. pylori-infecte d individuals. Methods: The cohort comprised 100 patients with endoscopical ly or surgically proven PUD (30 patients with duodenal ulcer (DU) and 70 pa tients with gastric ulcer (GU)) and 162 age- and sex-matched controls with PUD-negative endoscopic findings and no history of PUD. Plasma samples were screened for alpha(1)AT deficiency (PiZ) with an enzyme-linked immunosorbe nt assay (ELISA) and phenotyped by isoelectric focusing. H. pylori infectio n was evaluated with an IgG ELISA technique. Results: Among the 262 patient s 17 (6.5%) were positive for the PiZ alpha(1)AT deficiency, a frequency of the same magnitude as in the Swedish general population (4.7%). Of the PiZ carriers 76% (13 of 17)had H. pylori antibodies compared with 61% (151 of 245) of the non-PiZ carriers (NS). The prevalence of DU tended to be higher in H. pylori-positive PiZ carriers than in non-PiZ carriers (15.4%, 4 of 2 6 versus 0 of 4). Furthermore, among patients with DU a high PiZ allele fre quency (13.3%, 4 of 30) was found compared with the general population (4.7 %) (odds ratio (OR), 3.2; 95% confidence interval (CI), 1.09-8.94; P =0.02) . All. DU patients carrying the PiZ allele were positive for H. pylori. In addition, four of five PiZ carriers with H. pylori infection and PUD had DU . conclusions: The PiZ allele may be a contributing factor in the developme nt of DU in H. pylori-positive individuals.