Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs.
Ontology highlight
ABSTRACT:
SUBMITTER: Cullen DJ
PROVIDER: S-EPMC1891536 | biostudies-other | 1997 Oct
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Aim. Helicobacter pylori (H. pylori) infection is exceptionally rare in population from the north-eastern region of Peninsular Malaysia. This provides us an opportunity to contemplate the future without H. pylori in acute non-variceal upper gastrointestinal (GI) bleeding. Methods. All cases in the GI registry with GI bleeding between 2003 and 2006 were reviewed. Cases with confirmed non-variceal aetiology were analysed. Rockall score > 5 was considered high risk for bleeding and primary outcomes studied were in-hospital mortality, recurrent bleeding and need for surgery. Results. The incidence of non-variceal upper GI bleeding was 2.2/100,000 person-years. Peptic ulcer bleeding was the most common aetiology (1.8/100,000 person-years). In-hospital mortality (3.6%), recurrent bleeding (9.6%) and need for surgery (4.0%) were uncommon in this population with a largely low risk score (85.2% with score ?5). Elderly were at greater risk for bleeding (mean 68.5 years, P = 0.01) especially in the presence of duodenal ulcers (P = 0.04) despite gastric ulcers being more common. NSAIDs, aspirin and co-morbidities were the main risk factors. Conclusions. The absence of H. pylori infection may not reduce the risk of peptic ulcer bleeding in the presence of risk factors especially offending drugs in the elderly.
| S-EPMC3932736 | biostudies-literature
Project description:Polymorphic variability in Helicobacter pylori factors CagA and VacA contributes to bacterial virulence. The presence of one CagA EPIYA-C site is an independent risk factor for gastroduodenal ulceration (odds ratio [OR], 4.647; 95% confidence interval [CI], 2.037 to 10.602), while the presence of the vacA i1 allele is a risk factor for increased activity (OR, 5.310; 95% CI, 2.295 to 12.287) and severity of gastritis (OR, 3.862; 95% CI, 1.728 to 8.632).
| S-EPMC2884518 | biostudies-literature
Project description:IntroductionSome studies suggest that the accuracy of Helicobacter pylori diagnostic tests is decreased in peptic ulcer bleeding (PUB). We aimed to assess the accuracy of diagnostic tests for H. pylori in patients with PUB in a diagnostic test accuracy (DTA) network meta-analysis.MethodsA systematic search was carried out in seven databases until November 2019. We collected or calculated true and false positive and negative values, and constructed 2×2 diagnostic contingency tables with reference standards including histology, rapid urease test, urea breath test, serology, stool antigen test, culture, and polymerase chain reaction. We ranked the index tests by the superiority indices (SI) and calculated pooled sensitivity and specificity of each test.DiscussionOur search yielded 40 eligible studies with 27 different diagnostic strategies for H. pylori. In 32 articles, the reference standard was a combination of multiple tests. In 12 studies, the index tests were compared with a single testing method. We analyzed seven networks with the reference standards against a single or a combination of diagnostic index tests. None of the index tests had better diagnostic accuracy (SI between 9.94 and 2.17) compared with the individual index tests as all the confidence intervals included 1. Combined testing strategies had higher sensitivities (0.92-0.62) and lower specificities (0.85-0.46) while single tests proved to have higher specificities (0.83-0.77) and lower sensitivities (0.73-0.42).ConclusionUse of combined tests may have a rationale in clinical practice due to their higher sensitivities. The differences between the included DTA studies limited the comparison of the testing strategies.
| S-EPMC7747116 | biostudies-literature
Project description:Genetic factors are recognized to contribute to peptic ulcer disease (PUD) and other gastrointestinal diseases, such as gastro-oesophageal reflux disease (GORD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). Here, genome-wide association study (GWAS) analyses based on 456,327 UK Biobank (UKB) individuals identify 8 independent and significant loci for PUD at, or near, genes MUC1, MUC6, FUT2, PSCA, ABO, CDX2, GAST and CCKBR. There are previously established roles in susceptibility to Helicobacter pylori infection, response to counteract infection-related damage, gastric acid secretion or gastrointestinal motility for these genes. Only two associations have been previously reported for duodenal ulcer, here replicated trans-ancestrally. The results highlight the role of host genetic susceptibility to infection. Post-GWAS analyses for PUD, GORD, IBS and IBD add insights into relationships between these gastrointestinal diseases and their relationships with depression, a commonly comorbid disorder.
| S-EPMC7895976 | biostudies-literature
Project description:Background:Peptic ulcer disease is common with a lifetime prevalence in the general population of 5-10% and an incidence of 0.1-0.3% per year. Despite a sharp reduction in incidence and rates of hospital admission and mortality over the past 30?years, complications are still encountered in 10-20% of these patients. Peptic ulcer disease remains a significant healthcare problem, which can consume considerable financial resources. Management may involve various subspecialties including surgeons, gastroenterologists, and radiologists. Successful management of patients with complicated peptic ulcer (CPU) involves prompt recognition, resuscitation when required, appropriate antibiotic therapy, and timely surgical/radiological treatment. Methods:The present guidelines have been developed according to the GRADE methodology. To create these guidelines, a panel of experts was designed and charged by the board of the WSES to perform a systematic review of the available literature and to provide evidence-based statements with immediate practical application. All the statements were presented and discussed during the 5th WSES Congress, and for each statement, a consensus among the WSES panel of experts was reached. Conclusions:The population considered in these guidelines is adult patients with suspected complicated peptic ulcer disease. These guidelines present evidence-based international consensus statements on the management of complicated peptic ulcer from a collaboration of a panel of experts and are intended to improve the knowledge and the awareness of physicians around the world on this specific topic. We divided our work into the two main topics, bleeding and perforated peptic ulcer, and structured it into six main topics that cover the entire management process of patients with complicated peptic ulcer, from diagnosis at ED arrival to post-discharge antimicrobial therapy, to provide an up-to-date, easy-to-use tool that can help physicians and surgeons during the decision-making process.
| S-EPMC6947898 | biostudies-literature
Project description:AIM:To assess the frequency of herpes simplex virus type I in upper gastrointestinal tract ulcers and normal mucosa with the modern and better assays and also with a larger number of well characterized patients and controls and its relationship to Helicobacter pylori(H pylori). METHODS:Biopsy specimens from 90 patients (34 with gastric ulcer of the prepyloric area and 56 with duodenal ulcer) were evaluated. Biopsies from 50 patients with endoscopically healthy mucosa were considered as the control group. The method used to identify herpes simplex virus-1 (HSV-1) was polymerase chain reaction. H pylori was detected by the CLO-test and by histological method. RESULTS:Herpes simplex virus-1 was detected in 28 of 90 patients with peptic ulcer (31%) [11 of 34 patients with gastric ulcer (32.4%) and 17 of 56 with duodenal ulcer (30.4%)] exclusively close to the ulcerous lesion. All control group samples were negative for HSV-1. The likelihood of H pylori negativity among peptic ulcer patients was significantly higher in HSV-1 positive cases than in HSV-1 negative cases (P = 0.009). Gastric ulcer patients with HSV-1 positivity were strongly associated with an increased possibility of Helicobacter pylori negativity compared to duodenal ulcer patients (P = 0.010). CONCLUSION:HSV-1 is frequent in upper gastro-intestinal tract ulcers but not in normal gastric and duodenal mucosa. There is an inverse association between HSV-1 and H pylori infection.
| S-EPMC4355758 | biostudies-literature
Project description:Helicobacter pylori infection plays an important role in the pathogenesis of peptic ulcer disease (PUD). Several factors have been proposed as possible H. pylori virulence determinants; for example, bacterial adhesins and gastric inflammation factors are associated with an increased risk of PUD. However, differences in bacterial virulence factors alone cannot explain the opposite ends of the PUD disease spectrum, that is duodenal and gastric ulcers; presumably, both bacterial and host factors contribute to the differential response. Carriers of the high-producer alleles of the pro-inflammatory cytokines IL-1B, IL-6, IL-8, IL-10, and TNF-α who also carry low-producer allele of anti-inflammatory cytokines have severe gastric mucosal inflammation, whereas carriers of the alternative alleles have mild inflammation. Recent reports have suggested that the PSCA and CYP2C19 ultra-rapid metabolizer genotypes are also associated with PUD.
| S-EPMC5332543 | biostudies-literature
Project description:BackgroundNon-steroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors (PPIs) are regarded as two types of drugs that respectively increase and decrease the risk of peptic ulcer bleeding. However, their relation to occurrence, recurrence and death of bleeding in the population level is not clear.Study objectiveTo clarify recent calendar-time correlations between sales of NSAIDs and PPIs and the occurrence of peptic ulcer bleeding, re-bleeding and death.DesignEcological study.ResultsThe time trend of peptic ulcer bleeding did not correlate with PPI sales but did correlate with NSAIDs in mem (R(male)=0.6571, P(male)=0.05). Sales of PPIs (inverse) and NSAIDs correlated with re-bleeding in women (R(male)=-0.8754, P(male)=0.002 and R(female)=0.7161, P(female)=0.03, respectively), but not in men. An inverse correlation between PPI sales and 30-day death after bleeding was found (R(male)=-0.9392, P(male)=0.0002 and R(female)=-0.8561, P(female)=0.003), and NSAID sales were found to correlate with increased death after bleeding ((R(male)=0.7278, P(male)=0.03, R(female)=0.7858, P(female)=0.01).ConclusionsThe sales of NSAIDs and PPIs correlate with recurrence of peptic ulcer bleeding in women and death after peptic ulcer bleeding in both genders in the population level.
| S-EPMC3549209 | biostudies-literature
Project description:ObjectivePeptic ulcer disease is a condition in which an important role has infection with H. pylori. The most common complication of peptic ulcer is bleeding. The presence of H. pylori triggers local and systemic cytokine signaling which may affect processes such as healing, gastric or duodenal rupture, and carcinogenesis. In this study, we examined the concentrations of IL-1?, IL-6, IL-10, TNF, TGF-? and IL-17A in serum by enzyme immunoassay and their mRNA expressions in periulcer biopsies obtained from patients with bleeding peptic ulcer by means of real-time-PCR.ResultsWe have shown that pro-inflammatory IL-6 and TNF concentrations in serum were significantly higher in patients who were infected with H. pylori, while the concentrations of TGF-? and IL-17A were significantly lower compared to non-infected subjects. IL-17A expression in periulcer mucosa was significantly higher in patients who were infected with H. pylori, while the expression of other cytokines, there was no significant difference compared to non-infected controls. Considering higher serum concentrations in non-infected subjects and higher IL-17A expression in mucosal tissue of infected patients, our data support the studies that found IL-17A has protective role in eradication of H. pylori infection in infected patients.
| S-EPMC6521506 | biostudies-literature
Project description:ObjectivesThe aim of this study is to clarify the associations between IL-1B31C/T, IL-1B-511C/T, IL-8-251T/A gene polymorphisms and the risk of Helicobacter pylori (H. pylori) infection together with H. pylori-related gastric cancer (GC), peptic ulcer disease (PUD).MethodsAll eligible literature published up to July 2016 were identified by searching Pubmed, Embase, Web of Science and CNKI. Pooled odds ratio (OR) and 95% confidence interval (95% CI) were calculated using a fixed or random effects model.Results29 case-control studies were eligible, and each of them may focus on more than one gene polymorphism. Ultimately, there were 21 studies (3159 cases and 2816 controls) for IL-1B-31C/T, 16 studies (2486 cases and 1989 controls) for IL-1B-511C/T polymorphisms, 9 studies (1963 cases and 1205 controls) for IL-8-251T/A polymorphisms. Overall, an increased risk of H. pylori infection was found for IL-1B-31C/T polymorphisms in total population [OR = 1.134, 95%CI = 1.008-1.275 for recessive model; OR = 1.145, 95%CI = 1.007-1.301 for TT vs CC model]. While, for IL-1B-511C/T and IL8-251T/A polymorphisms, no evidence indicated that they were associated with the risk of H. pylori infection in all genetic models. Furthermore, we found an increased risk of H. pylori-related GC with IL-1B-511C/T polymorphisms [OR = 1.784, 95%CI = 1.289-2.469 for recessive model; OR = 1.772, 95%CI = 1.210-2.594 for TT vs CC model] and IL8-251A/T polymorphisms [OR = 1.810, 95%CI = 1.229-2.667 for recessive model; OR = 1.717, 95%CI = 1.143-2.580 for TT vs AA model], an increased risk of H. pylori-related PUD with IL8-251T/A polymorphisms [OR = 1.364, 95%CI = 1.010-1.843 for recessive model; OR = 1.427, 95%CI = 1.039-1.959 for AA vs TT model].ConclusionsIL-1B-31C/T gene polymorphisms might increase H. pylori infection risk. IL-1B-511-C/T and IL-8-251T/A gene polymorphisms might act as a risk factor to H. pylori-related diseases including GC or PUD.
| S-EPMC5409176 | biostudies-literature