Relationship of postprandial serum gastrin response to sex, body weight, blood group status, familial dyspepsia, duration, and age of onset of ulcer symptoms in duodenal ulcer.
Pentagastrin-stimulated maximal acid output and postprandial integrated gastrin response (sigma gastrin) were measured in 170 consecutive patients with duodenal ulcers.
To assess the influence of ethnic origin on the incidence of HLA antigens in duodenal ulcer, we typed 160 white Australian patients (including 22 born in Greece or Italy) and 320 blood donor controls for the HLA-A and -B loci.
These findings suggest that gastrin hypersensitivity is a distinct physiological abnormality in duodenal ulcer, the increased gastrin sensitivity in some patients with normal MAO has a genetic basis but the lateness in onset of their disease also suggests an environmental origin, and the increased gastrin sensitivity in some patients with abnormally large MAO is related to environmental factors encountered early in life.
This study does not support an association between hereditary alpha 1-AT deficiency and duodenal ulcer disease, and makes therefore a possible role of such a deficiency in the etiology of peptic ulcer disease highly unlikely.
An alpha-1-antitrypsin study was carried out on 184 patients with endoscopically proven duodenal ulcer, 66 first degree relatives of the patients and in 150 healthy controls, to establish the role of genetic factors in the etiology of duodenal ulcer.
Basal acid output and maximal acid output were significantly higher in our duodenal ulcer patients than in controls without ulcer (both, p < 0.01), and patients with duodenal ulcer showed significantly higher serum levels of PG I and gastrin than the controls (both, p < 0.001).
To further investigate the possible role of acetaldehyde in the pathogenesis of alcoholic liver disease, we determined the ADH and ALDH genotype frequencies in patients with alcohol-related cirrhosis (n = 27), viral hepatitis-related cirrhosis (n = 29) and gastric and duodenal ulcer without relevance to alcohol (n = 30).
These results suggest that there is genetic heterogeneity in combined gastric and duodenal ulcers depending upon the location of gastric ulcer, and that combined gastric body and duodenal ulcers are associated with the small fragment allele of the PGC RFLP in the same way as solitary gastric body ulcers.
In this study, the cagA gene was detected in H. pylori isolates from 26 (81.3%) of 32 patients with duodenal ulcers (DU), 17 (68.0%) of 25 patients with gastric ulcers, and 23 (59.0%) of 39 patients with nonulcer dyspepsia (NUD).
In contrast, the allele frequency of DQA1*0301 was significantly lower in H. pylori-negative controls (0.214) than in H. pylori-positive duodenal ulcer patients (0.418).
Genomic DNA was amplified by PCR, using synthetic oligonucleotide primers to the cagA gene to determine the prevalence of the cagA gene in 60 H. pylori isolates obtained from well-documented duodenal ulcer or asymptomatic gastritis patients (30 each).
In the IgG-positive, IgA-low group, the rate of peptic ulcers (especially duodenal ulcers) in endoscopic findings was higher (P < 0.05); the score of activity and the density of H. pylori were higher (P < 0.001 and P < 0.05, respectively); the score of metaplasia was lower (P < 0.05); and the level of interleukin-1 beta was lower (P < 0.05) than in the IgG-positive, IgA-high group.
In order to study the association between gastrin and H. pylori infection the density of antral G cells was evaluated by transcriptional expression of gastrin mRNA using a sensitive cold probe labelled with digoxigenin. the study group included 22 patients with symptomatic H. pylori positive gastritis and/or duodenal ulcer, 12 of whom were re-evaluated after eradication of H. pylori and 6 controls.
The CagA protein of Helicobacter pylori is an immunogenic antigen of variable size and unknown function that has been associated with increased virulence as well as two mutually exclusive diseases, duodenal ulcer and gastric carcinoma.
The cagA gene was detected in 100% of 16 Helicobacter pylori isolates from patients with gastric carcinoma versus 78% of 18 isolates from patients with duodenal ulcers (P = 0.344) and only 64% of 22 isolates from patients with gastritis only (P = 0.005) in Brazil.
The genotype TNF1/TNF1 of the polymorphism TNF-308 is a risk factor for duodenal ulcer in H. pylori+ females; p = 0.01; relative risk (RR) = 10.7; corrected p-value (Pc) = 0.05.