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Alpha1-antitrypsin deficiency may be a risk factor for duodenal ulcer in patients with Helicobacter pylori infection
A N Elzouki1, E Tóth, C H Florén
1Dept. of Medicine, Malmö University Hospital, Sweden.
Insights
Alpha-1 antitrypsin (AAT) PiZ deficiency may increase duodenal ulcer risk in individuals with H. pylori infection. This genetic factor, combined with H. pylori, appears to contribute to duodenal ulcer development.
Area of Science:
- Gastroenterology
- Genetics
- Infectious Disease
Background:
- Most individuals with Helicobacter pylori infection do not develop peptic ulcer disease (PUD).
- The role of alpha1-antitrypsin (alpha1AT) PiZ deficiency variant in PUD development among H. pylori-infected individuals is unclear.
Purpose of the Study:
- To investigate alpha1-antitrypsin (alpha1AT) PiZ deficiency as a potential risk factor for peptic ulcer disease (PUD) in H. pylori-infected individuals.
Main Methods:
- A cohort study involving 100 PUD patients (30 duodenal ulcer [DU], 70 gastric ulcer [GU]) and 162 controls.
- Plasma alpha1AT PiZ deficiency was assessed using ELISA and isoelectric focusing.
- H. pylori infection was determined via IgG ELISA.
Main Results:
- The PiZ allele frequency in the study cohort was similar to the general population.
- H. pylori positivity was higher in PiZ carriers (76%) than non-carriers (61%).
- A significantly higher PiZ allele frequency was observed in duodenal ulcer patients (13.3%) compared to the general population (4.7%) (OR, 3.2; P = 0.02).
- All H. pylori-positive DU patients carrying the PiZ allele developed DU.
Conclusions:
- The alpha1-antitrypsin (alpha1AT) PiZ allele may be a contributing factor in the development of duodenal ulcers in H. pylori-positive individuals.
Background:
Most individuals with Helicobacter pylori infection in Western countries have no evidence of peptic ulcer disease (PUD). We therefore assessed the PiZ deficiency variant of the major plasma protease inhibitor alpha1-antitrypsin (alpha1AT) as a risk factor for PUD in H. pylori-infected individuals.
Methods:
The cohort comprised 100 patients with endoscopically or surgically proven PUD (30 patients with duodenal ulcer (DU) and 70 patients 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 alpha1AT deficiency (PiZ) with an enzyme-linked immunosorbent assay (ELISA) and phenotyped by isoelectric focusing. H. pylori infection was evaluated with an IgG ELISA technique.
Results:
Among the 262 patients 17 (6.5%) were positive for the PiZ alpha1AT 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 26 versus 0 of 4). Furthermore, among patients with DU a high PiZ allele frequency (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 development of DU in H. pylori-positive individuals.
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