IL-1beta and IL-8 levels in the antrum were greater in DU than in gastritis; in the corpus the cytokine level/H pylori differed irrespective of similar H pylori densities.
In summary, the present meta-analysis suggests that IL-8 gene -251 T/A polymorphism is associated with increased PUD risk among Asians, and especially for the subgroups of H. pylori+, DUD and GUD.
A total of 153 H. pylori isolates from patients with chronic gastritis (n = 74) or gastro-duodenal ulcers (n = 79) was examined for vacA genotypes and cagA status by polymerase chain reaction (PCR) and dot blot, and for their ability to induce IL-8 secretion by HEp-2 cells.
The IL-8 heterozygote mutant variant was detected with a significantly higher frequency among the DU patients and those with gastritis than among the H. pylori-positive controls.
The IL-8 heterozygote mutant variant was detected with a significantly higher frequency among the DU patients and those with gastritis than among the H. pylori-positive controls.
The clinical outcome of duodenal ulcer treated with proton pump inhibitor (PPI)-based, anti-Helicobacter pylori (H.p.) regimens varies according to cytochrome P450 2C19 (CYP2C19) genotype.
The cagA gene was significantly associated with the presence of DU (p = .004) and GC (p = .003), and the cagE gene, too, was significantly associated with the presence of DU (p = .002) and GC (p = .000).
This study was undertaken to determine whether infection with Helicobacter pylori strains that contain the cagE gene was associated with duodenal ulceration in children.
The aims of the present study were to clarify the association between the cagE gene and clinical outcome and to analyze the relationship between the cagE gene and two other virulence factors--cagA and vacA--in two areas in Japan (Fukui and Okinawa) where the prevalence of duodenal ulcer and gastric cancer risk are quite different.
But a 670 bp DNA fragment (GU198) that was a bit homologous to the 3'-end of the gene of thymidylate kinase was positive in 7 GU strains (7/8), 3 GU-DU strains (3/4) and 3 DU strains (3/12).
The epidermal growth factor (EGF) has been shown to promote the proliferation of various types of cells, to maintain the physiological function of the mucosa of the digestive tract, and to promote the healing of the gastric and duodenal ulcers.
Thus, our research during the last three decades focused on the molecular mechanisms of duodenal ulcer in rodent models of chemically induced duodenal ulceration, and here we review our three recent findings: Endothelins (ET-1), the immediate early gene egr-1 and imbalance of angiogenic/antiangiogenic molecules.
The proportion of cases requiring EI and clinical factors (age, gender, antiplatelet/anticoagulant therapy, history of gastro-duodenal ulcer (GDU), systolic blood pressure, heart rate, hemoglobin, mean corpuscular volume, blood urea nitrogen-creatinine ratio (BUN/Cr ratio), prothrombin time-international normalized ratio, and Glasgow-Blatchford Score (GBS) were analyzed using logistic regression models.
This study aimed to investigate the intestinal microbiota in duodenal ulcer (DU) patients, effects of proton pump inhibitors,clarithromycin and amoxicillin, PCA) for Helicobacter pylori (H. pylori) and Bacillus subtilis and Enterococcus faecium (BSEF) on intestinal microbiota.
Upon depletion of FUCA2 by RNA interference and detection of translocated CagA (a virulence factor of H. pylori) in host cells, FUCA2 was found to be essential for H. pylori adhesion, in particular to the gastric cancer- and duodenal ulcer-specific strains.
On the other hand, infection with H. pylori and male gender were significantly associated with the development of duodenal ulcer, whereas Nrf2 promoter polymorphisms were not.
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.
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.
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).
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.
A 53-year old female patient with duodenal ulcer and Helicobacter pylori infection was treated three times with a proton pump inhibitor-based triple therapy, such as lansoprazole-clarithromycin-amoxicillin (INN, amoxicilline) and lansoprazole-minocycline-cefaclor.