Peptic Ulcer (peptic + ulcer)

Distribution by Scientific Domains
Distribution within Medical Sciences

Terms modified by Peptic Ulcer

  • peptic ulcer bleeding
  • peptic ulcer disease
  • peptic ulcer patient

  • Selected Abstracts


    SURGICAL INDICATIONS AND PROCEDURES FOR BLEEDING PEPTIC ULCER

    DIGESTIVE ENDOSCOPY, Issue 2010
    Nobutsugu Abe
    Recent important insights into the surgical treatment of bleeding peptic ulcer are reviewed in this article. Although the widespread use of endoscopic treatment and interventional radiology has reduced the number of surgical cases, surgery still plays a pivotal role in managing bleeding peptic ulcer. Failure to stop the bleeding by endoscopy and/or interventional radiology is the most important indication for emergency surgery. An early elective/planned surgery after the initial endoscopic control to prevent life-threatening rebleeding seems justified in patients who have risk factors for rebleeding, although its true efficacy still remains controversial. The surgical procedures in emergency situations should be limited to safe hemostasis. The addition of acid-reduction surgery may be unnecessary as a result of the increasing utilization of proton pump inhibitors. Angiographic embolization may be a less invasive alternative to surgery, and may further enhance endoscopic hemostasis. [source]


    Developments in the inhibition of gastric acid secretion

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2005
    J. Mössner
    Abstract Understanding the physiology of gastric acid secretion and the pathophysiology of acid-related diseases (e.g. gastrooesophageal reflux and peptic ulcer) has led to the development of numerous ways to decrease acid exposure. Pharmacologically one can try to neutralize secreted acid by antacids, prevent stimulation of the parietal cell, improve mucosal defences and block the functioning of the proton pump. Proton pump inhibitors (PPIs) inhibit the final step of acid secretion, and are currently the most potent acid inhibitors. Major therapeutic improvement within the PPI class appears unlikely, as agents in this class share similar chemistry, mode of action, and pharmacokinetic profiles. New approaches that block acid secretion are now being developed. Gastrin (CCK2) receptor antagonists and potassium-competitive acid blockers (P-CABs) are in clinical development. [source]


    Helicobacter pylori, T cells and cytokines: the "dangerous liaisons"

    FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2005
    Mario Milco D'Elios
    Abstract Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori -specific Th1 response, characterized by high IFN-,, TNF-,, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas,Fas ligand-mediated killing of B cells. In H. pylori -infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori -induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. [source]


    Trends in peptic ulcer pharmacotherapy

    FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2004
    Bülent Sivri
    Abstract Considering the diseases of the stomach and duodenum, peptic ulcer has been the one with a significant clinical impact. The pathophysiology of peptic ulcer has centred on an imbalance between aggressive and protective factors. The discovery of Helicobacter pylori as a cause of peptic ulcer has changed our approach greatly towards this disease. Despite the decreasing frequency of H. pylori -induced peptic ulcers, peptic ulcer remains a major clinical problem partly because nonsteroidal anti-inflammatory drug (NSAID)-related ulcers and hospital admissions for ulcer complications associated with NSAIDs have increased in frequency. The interaction between H. pylori and NSAIDs is one of the most controversial issues in peptic ulcer. In this article, current concepts of peptic ulcer etiopathogenesis and the management of peptic ulcer according to the etiology were reviewed. [source]


    Role of Mucin Lewis Status in Resistance to Helicobacter pylori Infection in Pediatric Patients

    HELICOBACTER, Issue 4 2010
    Sara Lindén
    Abstract Background:,Helicobacter pylori causes gastritis, peptic ulcer and is a risk factor for adenocarcinoma and lymphoma of the stomach. Gastric mucins, carrying highly diverse carbohydrate structures, present functional binding sites for H. pylori and may play a role in pathogenesis. However, little information is available regarding gastric mucin in children with and without stomach diseases. Materials and Methods:, Expression of mucins and glycosylation was studied by immunohistochemistry on gastric biopsies from 51 children with and without H. pylori infection and/or peptic ulcer disease. Results:, In all children, MUC5AC was present in the surface epithelium and MUC6 in the glands. No MUC6 in the surface epithelium or MUC2 was detected in any section. The Leb and Lea blood group antigens were present in the surface epithelium of 80% and 29% of children, respectively. H. pylori load was higher in Leb negative children than in Leb positive individuals (mean ± SEM 17.8 ± 3.5 vs 10.8 ± 1.5; p < 0.05), but there was no correlation between Lea or Leb status and gastritis, nodularity, and gastric or duodenal ulcer (DU). Expression of sialyl-Lex was associated with H. pylori infection, and DU. Conclusions:, Mucin expression and glycosylation is similar in children and adults. However, in contrast to adults, pediatric H. pylori infection is not accompanied by aberrant expression of MUC6 or MUC2. Furthermore, the lower H. pylori density in Leb positive children indicates that H. pylori is suppressed in the presence of gastric mucins decorated with Leb, the binding site of the H. pylori BabA adhesin. [source]


    The Effect of the cag Pathogenicity Island on Binding of Helicobacter pylori to Gastric Epithelial Cells and the Subsequent Induction of Apoptosis

    HELICOBACTER, Issue 6 2007
    Yutaka Minohara
    Abstract Background:,Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. Methods:, AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. Results:,cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. Conclusions:,cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties. [source]


    Helicobacter pylori Stimulates a Mixed Adaptive Immune Response with a Strong T-Regulatory Component in Human Gastric Mucosa

    HELICOBACTER, Issue 3 2007
    Rasmus Goll
    Abstract Background:, Host factors play an important role in the pathophysiology of Helicobacter pylori infection and development of gastritis and related disease. The established opinion is that the T-cell-mediated immune response to H. pylori infection is of Th1 type. Our earlier immune cell phenotype studies indicate a mixed Th1,Th2 profile of the effector cells. Therefore, an extensive adaptive and regulatory cytokine gene expression profile was conducted by quantitative real-time polymerase chain reaction (qPCR). Materials and Methods:, Biopsies from gastric mucosa of 91 patients diagnosed as H. pylori negative, H. pylori positive with gastritis, or H. pylori positive with peptic ulcer were obtained by endoscopy. Gene expressions of nine cytokines and CagA status were measured by qPCR. Results:, All cytokine genes showed higher expression levels in the presence of H. pylori when compared to H. pylori- negative samples (fold increase: IL8: × 11.2; IL12A: × 2.4; TNF-,: × 5.2; IFN-,: × 4.3; IL4: × 3.6; IL6: × 14.7; and IL10: × 6.7). Patients infected with CagA-positive strains had higher expression of IL1-, and IL18 compared to patients infected with CagA-negative strains (× 1.6 for IL1-, and × 2.0 for IL18). Patients with duodenal ulcer had a lower antral Th1/Th2 ratio than other H. pylori -positive patients. Conclusions:, The cytokine profile of H. pylori -infected gastric mucosa shows a mixed Th1,Th2 profile. Furthermore, a high IL10 expression may indicate that also regulatory T cells play a role in the chronic phase of H. pylori infection. [source]


    Detection of Helicobacter pylori DNA by a Simple Stool PCR Method in Adult Dyspeptic Patients

    HELICOBACTER, Issue 4 2005
    Nazime
    ABSTRACT Introduction.,Helicobacter pylori is the major agent causing peptic ulcer, gastric cancer and mucosa-associated lymphoid tissue (MALT) gastric lymphoma. A simple stool polymerase chain reaction (PCR) method was performed and compared with the gold standards for the diagnosis of H. pylori infection. Material and methods., A total of 54 adult patients (mean age, 46.41 ± 13.12 years) with dyspeptic symptoms from Gastroenterology at Dokuz Eylül University Hospital between May and November 2003 were included. Two antrum and corpus biopsies were taken from each patient. Infection by H. pylori was defined as positivity and negativity of the gold standards. DNA extraction of stool specimens was done using QIAamp DNA Stool Mini Kit (QIAGEN) and PCR conditions included amplification and reamplification steps using the H. pylori ureA gene specific primers (HPU1, HPU2) and were visualized on 1% agarose gel stained with ethidium bromide. Results., Forty-six of 54 patients (85.2%) were diagnosed positive and eight (14.8%) were negative for H. pylori infection by the gold standard methods. Thirty-two patients were positive (59.3%) and 22 of them (40.7%) were detected negative by stool PCR method. The stool PCR method and gold standard methods showed a statistical difference for the detection of H. pylori infection (p < .0001). Sensitivity, specificity, likelihood ratio, and positive and negative predictive values were 65.22%, 75%, 2.61%, 93.75%, and 27.7%, respectively. Discussion., The PCR on the stool specimens resulted as being a very specific test. We suggest that a simple stool PCR method that we developed can be used to detect H. pylori, virulence genes, and in drug resistance studies either first line diagnostic methods in the laboratory or in the clinical management of dyspeptic patients. [source]


    Usefulness of Non-invasive Tests for Diagnosing Helicobacter pylori Infection in Patients Undergoing Dialysis for Chronic Renal Failure

    HELICOBACTER, Issue 6 2004
    Thaďs López
    ABSTRACT Background.,Helicobacter pylori infection in chronic renal failure patients has been linked to peptic ulcer and gastric neoplasia after kidney transplantation. It may also contribute to the accelerated arteriosclerosis that is usual in this population. Few data are available on the usefulness of noninvasive diagnostic tests for H. pylori infection in dialyzed patients, especially regarding the new fecal antigen detection tests. The objective of this study was to determine the efficacy of a noninvasive test for H. pylori infection in patients with chronic renal failure. Methods., Eighty-six patients were included in a cross-sectional study. Urea breath test, serology and three fecal tests , FemtoLab H. pylori (Connex, Germany), Premier Platinum HpSA (Meridian, USA) and Simple H. pylori (Operon SA, Spain) were performed. Helicobacter pylori status was determined by concordance of the tests. Sensitivity, specificity and positive and negative predictive values were calculated for each test. Results., Sensitivity, specificity, positive and negative predictive values were 94%, 96%, 94% and 96% for the urea breath test; 97%, 64%, 66% and 97% for serology; 86%, 100%, 100% and 91%, for FemtoLab H. pylori; 58%, 96%, 91% and 76% for Premier Platinum HpSA and 61%, 78%, 74% and 67% for Simple H. pylori. Conclusions., The urea breath test seems to be the most reliable diagnostic method for H. pylori infection in patients with chronic renal failure. Serology has a low specificity, and the results of the fecal tests vary widely. [source]


    Pharmacoeconomics of Gastrointestinal Drug Utilisation Prior and Post Helicobacter pylori Eradication

    HELICOBACTER, Issue 1 2004
    Rogier M. Klok
    ABSTRACT Background., Eradication of Helicobacter pylori prevents recurrence of peptic ulcer. In pharmacoeconomic analyses it is often presumed that after successful eradication no more gastrointestinal drugs are used. We investigated this presumed positive monetary effect using General Practitioners prescribing data, including information in diagnosis. Methods., From the RNG-database we identified patients with a H. pylori eradication in the years 1997,2000. H. pylori eradication was defined as a prescription of two antibiotics and one gastrointestinal drug on the same day. Patients were divided into a group with diagnosed ulcers and a group without diagnosed ulcers. Gastrointestinal drug costs were calculated for 4 months prior to eradication and 9,12 months post eradication. For comparison costs in all periods were expressed per patient per period. For statistical analysis the paired t -test was used. Results., One hundred and two patients were eligible for evaluation. Of these patients 35 had a diagnosed ulcer and 67 had not. Generally the number of patients on gastrointestinal drugs decreased (61% prior vs. 33% post), however, the drug costs did not change (,33 prior vs. ,34 post). Costs for proton pump inhibitors increased post eradication (,14 prior vs. ,28 post). The ulcer and nonulcer group showed similar results. Conclusion.,Helicobacter pylori eradication is thought to be cost effective, however, we did not find a decrease in costs for all gastrointestinal drugs. There may be a great pharmacoeconomical advantage when it is possible to predict which patients are more likely to ,fail' eradication therapy. [source]


    ,Rescue' Therapy with Rifabutin after Multiple Helicobacter pylori Treatment Failures

    HELICOBACTER, Issue 2 2003
    Javier P. Gisbert
    abstract Aim. Eradication therapy with proton pump inhibitor, clarithromycin and amoxicillin is extensively used, although it fails in a considerable number of cases. A ,rescue' therapy with a quadruple combination of omeprazole, bismuth, tetracycline and metronidazole (or ranitidine bismuth citrate with these same antibiotics) has been recommended, but it still fails in approximately 20% of cases. Our aim was to evaluate the efficacy and tolerability of a rifabutin-based regimen in patients with two consecutive H. pylori eradication failures. Patients and Methods. Design: Prospective multicenter study. Patients: Consecutive patients in whom a first eradication trial with omeprazole, clarithromycin and amoxicillin and a second trial with omeprazole, bismuth, tetracycline and metronidazole (three patients) or ranitidine bismuth citrate with these same antibiotics (11 patients) had failed were included. Intervention: A third eradication regimen with rifabutin (150 mg bid), amoxicillin (1 g bid) and omeprazole (20 mg bid) was prescribed for 14 days. All drugs were administered together after breakfast and dinner. Compliance with therapy was determined from the interrogatory and the recovery of empty envelopes of medications. Outcome: H. pylori eradication was defined as a negative 13C-urea breath test 8 weeks after completing therapy. Results. Fourteen patients have been included. Mean age ± SD was 42 ± 11 years, 41% males, peptic ulcer (57%), functional dyspepsia (43%). All patients took all the medications and completed the study protocol. Per-protocol and intention-to-treat eradication was achieved in 11/14 patients (79%; 95% confidence interval = 49,95%). Adverse effects were reported in five patients (36%), and included: abdominal pain (three patients), nausea and vomiting (one patient), and oral candidiasis (one patient); no patient abandoned the treatment due to adverse effects. Conclusion. Rifabutin-based rescue therapy constitutes an encouraging strategy after multiple previous eradication failures with key antibiotics such as amoxicillin, clarithromycin, metronidazole and tetracycline. [source]


    Association of peptic ulcer with increased expression of Lewis antigens, but not vacuolating cytotoxin activity or babA2 gene status, in Helicobacter pylori strains from China

    JOURNAL OF DIGESTIVE DISEASES, Issue 1 2006
    Peng Yuan ZHENG
    OBJECTIVE: Controversies exist regarding the virulence factors, such as vacA, babA2 and Lewis blood group antigens, of Western and Asian strains of Helicobacter pylori. The aim of the present study was to determine the significance of these potential virulence factors in the Chinese population. METHODS: Seventy-two strains of H. pylori isolated from patients in Zhengzhou, China, including 43 cases of peptic ulcer (PU) and 29 cases of chronic gastritis, were determined. Vacuolating cytotoxin assay was performed by HeLa cells. The expression of Le blood group antigens (Lea, Leb, Lex and Ley) was performed by enzyme-linked immunosorbent assay (ELISA). babA2 gene was identified by polymerase chain reaction. Frequencies were compared using two-tailed Fisher's exact test. Cytotoxin activities were compared using Spearman's rank correction test. RESULTS: Vacuolating cytotoxin activity was detected in 61 of the 72 strains (84.7%), but there was no significant difference in vacuolating cytotoxin activity (83.7% vs 86.2%, P = 0.821) or titer (4.4 ± 3.8 vs 4.2 ± 4.1, P = 0.876) between the PU and gastritis strains. Significantly more PU strains expressed two or more Lewis antigens (Lex, Ley, Lea or Leb) than strains from the chronic gastritis patients (90.7% vs 65.5%, P = 0.029). Of the 43 strains from PU patients, 17 (39.5%) were positive for babA2, compared with 11 (38.5%) of the 29 strains from gastritis patients (P = 0.924). There was no significant difference in the vacuolating cytotoxin activity or titer between strains expressing two or more Lewis antigens and less than two antigens (84.5% vs 85.7%, P = 1.000; 4.4 ± 4.2 vs 4.3 ± 3.2, P = 0.965). Of the 72 H. pylori strains, 28 were babA2 positive, of which 24 were cytotoxic, compared with 37 of 44 babA2-negative strains (P = 1.000). CONCLUSION: The present study suggests that PU is associated with increased Lewis antigen expression, but not vacuolating cytotoxin production or the presence of babA2, in the H. pylori strains in the Chinese population. [source]


    GASTROENTEROLOGY: Prospective evaluation of a clinical guideline recommending early patients discharge in bleeding peptic ulcer

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2010
    María Chaparro
    Abstract Background and Aim:, To validate an early discharge policy in patients admitted with upper gastrointestinal bleeding (UGIB) due to ulcers. Methods:, Patients with gastroduodenal ulcer or erosive gastritis/duodenitis were included in a previous study aiming to develop a practice guideline for early discharge of patients with UGIB. Variables associated with unfavorable evolution were analyzed in order to identify patients with low-risk of re-bleeding. After that, a one-year prospective analysis of all UGIB episodes was carried out. Results:, A total of 341 patients were identified in the retrospective study. Variables associated with unfavorable evolution were: systolic blood pressure , 100 mmHg, heart rate , 100 bpm, and a Forrest endoscopic classification of severe. 10% of patients were immediately discharged; however, if predictive variables obtained in the multivariate analysis had been used, hospitalization could have been prevented in 34% of patients. A total of 77 patients were included in the prospective analysis. Although only 19.5% of patients were immediately discharged without complications, 29 patients (37.7%) were theoretically suitable for early discharge. Conclusions:, Patients with UGIB who have clean-based ulcers and are stable on admission can be safely discharged immediately after endoscopy. Implementation of the clinical practice guideline safely reduced hospital admission for those patients. [source]


    Overview of 50 years' progress in upper gastrointestinal diseases

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2009
    Neville D Yeomans
    Abstract There have been numerous and dramatic advances in our understanding of the mechanisms, causes and treatments of upper gastrointestinal diseases in the past 50 years. This review focuses on a few, not dealt with elsewhere in this special issue of the Journal. The early history of the recognition that nonsteroidal anti-inflammatory drugs are a major cause of peptic ulcer is described, with particular attention to the work of the pioneering Australian investigators. The story of the development of the histamine H2 -receptor antagonists and the proton pump inhibitors is also outlined. [source]


    Proteomic identification of biomarkers related to Helicobacter pylori -associated gastroduodenal disease: Challenges and opportunities

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2008
    Ming-Shiang Wu
    Abstract Helicobacter pylori colonize the stomach of over half the world's population. While 80,90% H. pylori -infected individuals have clinically asymptomatic gastritis, 10,15% develop peptic ulcer, and 1,2% gastric malignancies. These variable clinical outcomes have led to an interest in prognostic indicators. The current disease paradigm suggests that host genetics and bacterial virulence both play important roles in modulating the final outcome of H. pylori infection. Elucidation of the interaction between host and bacterium is essential to clarify pathogenesis and to develop new strategies for prevention and treatment. Proteomic technology is a powerful tool for simultaneously monitoring proteins and protein variation on a large scale in biological samples. It has provided an unprecedented opportunity to survey a cell's translational landscape comprehensively, and the results may allow in-depth analyses of host and pathogen interactions. Using this high-throughput platform and taking advantage of complete sequences for both the H. pylori and the human genome in available databases, we have identified several crucial proteins that have pathogenic and prognostic potential. Among them, antibodies to AhpC and GroEs of H. pylori could be utilized for identification of patients who are at high risk of disease complications after H. pylori infection. Evolving proteomic technologies, together with appropriate clinical phenotyping and genotype information should enhance understanding of disease pathogenesis and lead to more precise prediction of variable disease outcomes. It will also facilitate development of biomarkers for diagnosis, treatment, and prevention of H. pylori infection. [source]


    Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2007
    Sethumadhavan Santhosh
    Abstract Background:,Helicobacter pylori is the major causative factor of ulcer but the use of ibuprofen and other non-steroidal anti-inflammatory drugs have also been implicated in development of ulcer. The purpose of the present study was to determine the anti-ulcer effect of glucosamine. Methods:, The protective effect of glucosamine on ibuprofen-induced peptic ulcer in male albino rats was studied with respect to changes in the volume of gastric juice, acid output, pepsin activity, activities of membrane bound ATPases, protein content, glycoprotein components and histopathology. Results:, Oral administration of ibuprofen caused significant increase in the number of lesions in the gastric mucosa, increases in the volume of gastric juice and acidity, and decreased activity of pepsin. The levels of protein content and glycoprotein components (hexose, hexosamine and sialic acid) and ATPase activities were also observed. Oral pretreatment with glucosamine resulted in significant reduction in the number of lesions in the gastric mucosa and decreases in the volume of gastric juice and acidity. The pepsin activity was also maintained at near normalcy. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced depletion of protein and glycoprotein components and maintained the activities of membrane bound ATPases as compared to untreated ulcer induced group of rats. Conclusion:, The anti-ulcerogenic activity of glucosamine might be ascribable to its ability to neutralize the hydrochloric acid secreted into the stomach and to its capability to strengthen the mucosal barrier by increasing mucosal glycoprotein synthesis and to its free radical scavenging property. Histopathological investigations of the mucosal tissue also support the anti-ulcerogenic effect of glucosamine. [source]


    Different effects of polymorphisms of tumor necrosis factor-alpha and interleukin-1 beta on development of peptic ulcer and gastric cancer

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2007
    Mitsushige Sugimoto
    Abstract Background and Aim:, In Western countries, polymorphism of pro-inflammatory cytokine genes is associated with the development of gastric cancer and duodenal ulcer. The aim of this study was to clarify the association of polymorphisms of interleukin (IL) -1, and tumor necrosis factor (TNF) -, with susceptibility to peptic ulcer diseases and gastric cancer in Japan. Methods:, The IL-1, -511/-31 and TNF-, -308/-857/-863/-1031 genotypes were determined in Helicobacter pylori -positive patients with gastritis only (n = 164), gastric ulcers (n = 110), duodenal ulcers (n = 94), or gastric cancers (n = 105), and in H. pylori -negative controls (n = 172). Results:, Carriage of the alleles TNF-,- 857 T (odd ratio [OR], 1.826; 95% confidence interval [CI], 1.097,3.039), TNF-,- 863 A (OR, 1.788; 95% CI, 1.079,2.905) and TNF-, -1031 C (OR, 1.912; 95% CI, 1.152,3.171) was associated with increased risk for gastric ulcer development. Carriage of the alleles TNF-,- 857 T (OR, 1.686; 95% CI, 1.003,2.832), TNF-,- 863 A (OR, 1.863; 95% CI, 1.118,3.107) and TNF-, -1031 C (OR 2.074; 95% CI, 1.244,3.457) was also associated with increased risk of gastric cancer development. There was no relationship between the development of H. pylori -related diseases and polymorphisms of IL-1, -511/-31 and TNF-, -308. The simultaneous carriage of three different high-producer alleles of TNF-, -857/-863/-1031 significantly increased the risk of gastric ulcer (OR, 6.57; 95% CI, 2.34,18.40) and gastric cancer (OR, 5.20; 95% CI, 1.83,14.78). Conclusions:, Polymorphisms in TNF-, rather than IL-1, are associated with increased risk for gastric ulcers and gastric cancer in Japan. The simultaneous carriage of more than one high-producer allele of TNF-, further increased the risks for gastric ulcer and cancer. [source]


    Maintenance therapy with H2 -receptor antagonist until assessment of Helicobacter pylori eradication can reduce recurrence of peptic ulcer after successful eradication of the organism: prospective randomized controlled trial

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006
    KAZUNARI MURAKAMI
    Abstract Purpose:, This study examined the possible relationship between peptic ulcer recurrence and the presence or absence of maintenance therapy with an H2 -receptor antagonist performed until evaluation of Helicobacter pylori eradication. Methods:, The subjects were 483 patients with peptic ulcer (281 gastric ulcer and 202 duodenal ulcer) who were diagnosed as H. pylori positive. After receiving eradication therapy for H. pylori, patients were allocated at random to one of three different maintenance therapies: control group (no maintenance therapy), H2 -receptor antagonist half-dose group, and H2 -receptor antagonist full-dose group. The maintenance therapy was performed for 4 weeks until evaluation of H. pylori eradication. Results:, Among the 25 patients with a recurrent ulcer, 18 patients (72%) had a recurrence at the time of or before evaluation of H. pylori eradication. In the control group, the rate of ulcer recurrence occurring before evaluation of H. pylori eradication was 10.5% (14/133). This rate was significantly higher than those in the H2 -receptor antagonist half-dose group (2.9%, 4/136) and the full-dose group (0%, 0/135). Conclusion:, The results of this study suggest that maintenance therapy with an H2 -receptor antagonist performed after eradication therapy until evaluation of H. pylori eradication is likely to greatly reduce the ulcer recurrence rate without affecting evaluation of H. pylori eradication. [source]


    Rising trends of gastric cancer and peptic ulcer in the 19th century

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2010
    A. Sonnenberg
    Aliment Pharmacol Ther 2010; 32: 901,907 Summary Background, The risk of dying from gastric cancer appears to have increased among consecutive generations born during the 19th century. Aim, To follow the time trends of hospitalization for gastric cancer and test whether they confirm such increase. Methods, Inpatient records of the last two centuries from four hospitals in Scotland and three US hospitals were analysed. Proportional rates of hospitalization for gastric cancer, gastric ulcer and duodenal ulcer were calculated during consecutive 5-year periods. Results, The data from all seven cities revealed strikingly similar patterns. No hospital admissions for gastric cancer or peptic ulcer were recorded prior to 1800. Hospital admissions for gastric cancer increased in an exponential fashion throughout the 19th and the beginning of the 20th century. In a majority of cities, the rise in hospitalization for gastric cancer preceded a similar rise in hospitalization for gastric ulcer. Hospitalization for these two latter diagnoses clearly preceded hospitalization for duodenal ulcer by 20,40 years. Conclusions, The occurrence of gastric cancer, gastric ulcer and duodenal ulcer markedly increased during the 19th century. Improvements in hygiene may have resulted in the decline of infections by other gastrointestinal organisms that had previously kept concomitant infection by Helicobacter pylori suppressed. [source]


    Mortality from peptic ulcer bleeding: the impact of comorbidity and the use of drugs that promote bleeding

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2010
    K. Ĺhsberg
    Summary Background, Use of drugs promoting peptic ulcer bleed has increased several folds. Aim, To make a time-trend analysis of peptic ulcer bleed patients and evaluate the impact of age, gender, comorbidity and use of drugs promoting peptic ulcer bleed on outcome. Methods, Retrospective review of hospitalizations for peptic ulcer bleed at Lund University Hospital during 1984, 1994 and 2004. Univariate analyses between years and multivariable logistic regression for risk factors of fatal outcome. Results, Incidence decreased from 62.0 to 32.1 per 100 000 inhabitants between 1984 and 2004. Mortality rates were stable. Median age (70,77 years; P = 0.001), number of comorbidities (mean ± s.d.: 0.88 ± 0.96 to 1.16 ± 0.77; P = 0.021), use of aspirin (16,57%; P < 0.001) and warfarin (5,17%; P = 0.02) increased. Pharmacological and endoscopic therapy improved. Age above 65 years (OR: 1.11, 95% CI: 1.02,1.23) and number of comorbidities (OR: 6.00, 95% CI: 2.56,17.4) were independent risk factors for in-hospital mortality. Bleeding promoting drugs did not influence outcome negatively. Aspirin decreased the risk of fatal outcome (OR: 0.12, 95% CI: 0.012,0.67). Conclusions, Incidence of peptic ulcer bleed decreased despite higher prescription rates of bleeding promoting drugs. The in-hospital mortality remained unchanged. The effect of improved therapy against peptic ulcer bleed is probably outweighed by older and more comorbid patients. The decreased risk of fatal outcome in aspirin users warrants further investigations. [source]


    Uncomplicated peptic ulcer in the UK: trends from 1997 to 2005

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2009
    S. CAI
    Summary Background, Few studies have examined the incidence of uncomplicated peptic ulcer or the trends in factors affecting its incidence. Aim, To estimate the incidence rate of uncomplicated peptic ulcer in the UK from 1997 to 2005 and report temporal changes in the main known preventive and risk factors. Methods, Population-based cohort study of 1 049 689 patients enrolled in The Health Improvement Network in the UK. We estimated the incidence rate of uncomplicated peptic ulcer and evaluated temporal trends in demographic characteristics and prescription patterns for various anti-inflammatory and gastroprotective agents. Results, Overall uncomplicated peptic ulcer incidence was 0.75 cases per 1000 persons-years, declining from 1.1 to 0.52 cases per 1000 person-years between 1997 and 2005. Distributions of age, gender and alcohol habits were similar in 1997 and 2005. The proportion of documented Helicobacter pylori -negative cases increased from 5% to 12%. Monthly prevalence of subjects with prescriptions for traditional non-aspirin NSAIDs changed from 7.7% to 6.8%, Coxibs from 0% to 0.7%, and proton pump inhibitors (PPIs) from 2.4% to 7.4%. The proportion of subjects on prescription NSAIDs on PPIs increased continuously over time. Conclusion, A reduction in H. pylori -related peptic ulcers, changing patterns in NSAID use and increasing PPI use may have contributed to a decline in uncomplicated peptic ulcer incidence in the UK. [source]


    Bleeding peptic ulcer , time trends in incidence, treatment and mortality in Sweden

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009
    J. SADIC
    Summary Background, The incidence of peptic ulcer disease was expected to decrease following the introduction of acid inhibitors and Helicobacter pylori eradication. Aim, To analyse possible changes in the incidence of bleeding peptic ulcer, treatment and mortality over time. Methods, Residents of Malmö hospitalized for bleeding gastric or duodenal ulcer disease during 1987,2004 were identified in hospital databases (n = 1610). The material was divided into 6-year periods to identify changes over time. All patients who had been submitted to emergency surgery (n = 137) were reviewed. Results, The incidence rate for bleeding gastric or duodenal ulcers decreased by one half in males and by one-third in females and emergency operations decreased significantly (9.2%, 7.5% and 5.7% during the three time periods, respectively (P < 0.05). The post-operative mortality tended to decrease (9.7, 2.4 and 3.7%, respectively) and the 30-day mortality rates in the whole material were 1.2%, 3.6% and 3.4% during the different time periods. Conclusion, The incidence of bleeding gastric and duodenal ulcer disease has decreased markedly. Operative treatment has been replaced by endoscopic treatment. The bleeding ulcer-related mortality was less than 4% and has not changed over time. [source]


    Efficacy of an intravenous proton pump inhibitor after endoscopic therapy with epinephrine injection for peptic ulcer bleeding in patients with uraemia: a case-control study

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009
    G.-Y. TSENG
    Summary Background, Patients with peptic ulcer bleeding and uraemia are prone to re-bleeding. Aim, To compare the efficacy of an intravenous proton pump inhibitor in treating peptic ulcer bleeding in patients with uraemia and those without uraemia. Methods, High-risk peptic ulcer bleeding patients received endoscopic therapy with epinephrine (adrenaline) injection plus intravenous omeprazole (40 mg bolus followed by 40 mg infusion every 12 h) for 3 days. Re-bleeding, volume of blood transfusion, hospital stay, need for surgery, and mortality were analysed. Results, The uraemic group had similar 7-day re-bleeding rate (6/42, 14.29% vs. 6/46, 13.04%, P = 0.865) to that of non-uraemic patients, but more re-bleeding episodes beyond 7 days (4/42, 9.52% vs. 0/46, 0%, P = 0.032, OR [95% CI] = 1.105 [1.002,1.219]) and all-cause mortality (4/42 vs. 0/46 P = 0.032, OR [95% CI] = 1.105 [1.002,1.219]). The uraemic group also had more units of blood transfusion after endoscopic therapy (mean ± s.d. 4.33 ± 3.35 units vs. 2.15 ± 1.65 units, P < 0.001), longer hospital stay (mean ± s.d. 8.55 ± 8.12 days vs. 4.11 ± 1.60 days, P < 0.001) and complications during hospitalization (9/42 vs. 0/46, P = 0.001, OR [95% CI] = 1.273 [1.087,1.490]). Conclusion, Endoscopic therapy with epinephrine injection plus an intravenous proton pump inhibitor can offer protection against early re-bleeding in uraemic patients with peptic ulcer bleeding, but has a limited role beyond 7 days. [source]


    Time trends in peptic ulcer, erosive reflux oesophagitis, gastric and oesophageal cancers in a multiracial Asian population

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2009
    K.-L. GOH
    Summary Background, Dramatic changes in the prevalence and pattern of gastrointestinal disease has taken place in Asia in recent years. Aim, To compare the prevalence of duodenal (DU) and gastric ulcers (GU), erosive oesophagitis (EO), gastric cancer (GCA) and oesophageal cancer (OCA) and Helicobacter pylori infection over a 10-year interval of time in a multiracial South-East Asian population. Methods, Endoscopy records of first time gastroscopy in the University of Malaya Medical Centre, Kuala Lumpur, Malaysia were reviewed for 1989/1990 and 1999/2000. Results, In the period of 1989,1990, 3252 records and in 1999,2000, 4615 records were analysed. Both DU (21.1,9.5%) and GU (11.9,9.4%) had decreased significantly (P < 0.001). EO had increased significantly from 2.0% to 8.4% (P < 0.001). Both GCA and OCA had declined in the 10-year interval. Helicobacter pylori prevalence had decreased from 51.7% to 30.3% (P < 0.001). The decrease in DU and GU was seen in all racial groups. The increase in EO was most marked in Indians and the decrease in GCA in Chinese. The proportion of H. pylori- associated DU and GU had also decreased with time. Conclusions, Peptic ulcers and H. pylori infection had declined over a 10-year period of time and showed an opposing time trend with EO, which had increased dramatically. Both GCA and OCA had declined in prevalence. [source]


    Recurrence of peptic ulcer in uraemic and non-uraemic patients after Helicobacter pylori eradication: a 2-year study

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2007
    G.-Y. TSENG
    Summary Background The role of Helicobacter pylori in the pathogenesis of peptic ulcer disease in patients with uraemia remains unclear. Aim To evaluate the long-term effect of H. pylori eradication in these patients. Methods Uraemic and non-uraemic patients with peptic ulcer were enrolled in this study. Patients having history of non-steroidal anti-inflammatory drugs use or cardiovascular disease that need aspirin use were excluded. After confirmation of H. pylori infection, they received a triple therapy and were followed up for 2 years. Results Between September 1999 and December 2005, 34 patients (41%) of the end-stage renal disease [H. pylori (+) group] and 67 (84%) of the non-uraemic patients with peptic ulcer disease (PU group) received anti- H. pylori therapy. After triple therapy, 32 (94%) from the end-stage renal disease group and 64 (96%) from the peptic ulcer group obtained successful eradication. During the 2-year follow-up, three patients in the end-stage renal disease group were excluded because of the presence of cardiovascular disease and aspirin use in two cases and died of heart failure in one case; two patients in peptic ulcer group refused follow-up. Finally, 29 uraemic and 62 non-uraemic patients had achieved the follow-up. Recurrence of peptic ulcer was more in the end-stage renal disease group than in the peptic ulcer group with intention-to-treat analysis (eight of 32, 25% vs. two of 64, 3%, P = 0.001, OR: 10.0, 95% CI: 1.979,50.540) or per-protocol analysis (eight of 29, 28% vs. two of 62, 3%, P < 0.001, OR: 11.4, 95% CI: 2.245,58.168). Conclusions Peptic ulcer recurrence after H. pylori eradication is higher in end-stage renal disease patients with peptic ulcer than in peptic ulcer patients without renal disease. Factors aside from H. pylori play an important role in peptic ulcer recurrence in end-stage renal disease patients. [source]


    Helicobacter pylori in patients can be killed by visible light

    LASERS IN SURGERY AND MEDICINE, Issue 4 2005
    Robert A. Ganz MD
    Abstract Background Helicobacter pylori colonizes the mucus layer of the human stomach and may cause peptic ulcer and adenocarcinoma. Novel antimicrobial approaches are sought due to the occurrence of antibiotic resistance and consequent treatment failure. We report here that H. pylori is susceptible to inactivation by blue light. Study Design/Materials and Methods A controlled, prospective, blinded, trial of endoscopically delivered blue light to eradicate H. pylori in regions of the gastric antrum, in 10 patients between the ages of 21 and 80 who tested positive for H. pylori. Light (405 nm) (40 J/cm2) was delivered to a 1-cm diameter spot in the gastric antrum via optical fiber passed through the endoscope and weighed biopsies were taken from treated and control spots and colonies quantitatively cultured. Results Blue light killed 5 logs of bacteria in vitro. The mean reduction in H. pylori colonies per gram tissue between treated and control spots was 91% (7.4±4.8×106 vs. 8.1±1.9×107, two-tailed P<0.0001). Some patients had reductions approaching 99%. No differences were observed on histological examination of light-treated and control gastric tissue. Conclusion Blue light phototherapy may represent a novel approach to eradication of H. pylori, particularly, in patients who have failed standard antibiotic treatment. © 2005 Wiley-Liss, Inc. [source]


    Review article: from 1906 to 2006 , a century of major evolution of understanding of gastro-oesophageal reflux disease

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2006
    J. DENT
    Summary Background Our understanding of gastro-oesophageal reflux disease has undergone significant changes over the last century. Aim To trace the rise in understanding of gastro-oesophageal reflux disease and highlight remaining areas of uncertainty. Methods Literature review. Results In 1906, Tileston published his observations on ,peptic ulcer of the oesophagus'. Winkelstein, in 1934, first correlated symptoms of heartburn with acid regurgitation and reflux oesophagitis. In 1946, Allison described hiatus hernia as a causal factor in the development of gastro-oesophageal reflux disease. In 1958, Bernstein and Baker showed a direct relationship between oesophageal acidification and heartburn in patients with gastro-oesophageal reflux disease, irrespective of endoscopic findings, leading to the recognition of non-erosive gastro-oesophageal reflux disease. In the 1980s, continuous recordings of the lower oesophageal sphincter showed that episodes of reflux were related to transient relaxations of lower oesophageal sphincter tone. There is now increasing recognition that gastro-oesophageal reflux disease arises from the interaction of several anatomical and physiological factors. A turning point in the medical treatment of gastro-oesophageal reflux disease came with the introduction of the first proton pump inhibitor, omeprazole, in 1989. Conclusions Future efforts need to identify the multifactorial interactions of gastro-oesophageal junction anatomy and physiology in patients with gastro-oesophageal reflux disease. Increased understanding of the disease will guide development of new therapies. [source]


    Systematic review and meta-analysis: enhanced efficacy of proton-pump inhibitor therapy for peptic ulcer bleeding in Asia , a post hoc analysis from the Cochrane Collaboration

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2005
    G. I. Leontiadis
    Summary Background :,Proton-pump inhibitors reduce re-bleeding rates after ulcer bleeding. However, there is significant heterogeneity among different randomized-controlled trials. Aim :,To see whether proton-pump inhibitors for ulcer bleeding produced different clinical outcomes in different geographical locations. Methods :,This was a post hoc analysis of our Cochrane Collaboration systematic review and meta-analysis of proton-pump inhibitor therapy for ulcer bleeding. Sixteen randomized-controlled trials conducted in Europe and North America were pooled and re-analysed separately from seven conducted in Asia. We calculated pooled rates for 30-day all-cause mortality, re-bleeding and surgical intervention and derived odds ratios and numbers needed to treat with 95% confidence intervals. Results :,There was no significant heterogeneity for any outcome. Reduced all-cause mortality was seen in the Asian randomized-controlled trials (odds ratios = 0.35; 95% confidence interval: 0.16,0.74; number needed to treat = 33), but not in the others (odds ratios =,1.36; 95% confidence interval: 0.94,1.96; number needed to treat , incalculable). There were significant reductions in re-bleeding and surgery in both sets of randomized-controlled trials, but the effects were quantitatively greater in Asia. Conclusions :,Proton-pump inhibitor therapy for ulcer bleeding has been more efficacious in Asia than elsewhere. This may be because of an enhanced pharmacodynamic effect of proton-pump inhibitors in Asian patients. [source]


    Systematic review and meta-analysis: is 1-week proton pump inhibitor-based triple therapy sufficient to heal peptic ulcer?

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2005
    J. P. Gisbert
    Summary Aims :,To systematically review the efficacy on ulcer healing of 1-week combination of a proton pump inhibitor plus two antibiotics and to perform a meta-analysis of randomized clinical trials to evaluate whether 7 days of proton pump inhibitor-based triple therapy is sufficient to heal peptic ulcer. Methods :,Studies where 1-week proton pump inhibitor-based triple therapy was administered to heal peptic ulcer were included. Randomized clinical trials comparing the efficacy on ulcer healing of 7-day proton pump inhibitor-based triple therapy versus this same regimen but prolonging the proton pump inhibitor for several more weeks were included in the meta-analysis. Electronic and manual bibliographical searches were conducted. Meta-analysis was performed combining the odds ratios of the individual studies. Results :,Twenty-four studies (2342 patients) assessed ulcer healing with 1-week proton pump inhibitor-based triple therapy. Mean healing rate was 86%, and 95% in Helicobacter pylori -eradicated patients. Six studies (862 patients), were included in the meta-analysis. Mean ulcer healing rate with a 7-day treatment was 91% versus 92% when proton pump inhibitor was prolonged for 2,4 more weeks (odds ratio = 1.11; 95% confidence interval = 0.71,1.74). Conclusion :,In patients with peptic ulcer and H. pylori infection, prolonging therapy with proton pump inhibitor after a triple therapy for 7 days with a proton pump inhibitor and two antibiotics is not necessary to induce ulcer healing. [source]


    Clinical trends in ulcer diagnosis in a population with high prevalence of Helicobacter pylori infection

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2005
    M. A. Pérez-Aisa
    Summary Background :,It is unknown whether the incidence of peptic ulcer changes in areas with a high prevalence of Helicobacter pylori infection. Aim :,To determine trends in peptic ulcer complications in a community with a high prevalence of H. pylori infection. Methods :,New endoscopic diagnoses of peptic ulcers and their complications from 1985 to 2000 were obtained. H. pylori infection in the adult population, the number of prescriptions for anti-secretory drugs and non-steroidal anti-inflammatory drugs were also evaluated. Results :,Although the global prevalence of H. pylori infection remains high in this population (>60%), a 41.4 to 25.4% decrease in the incidence of peptic ulcers and ulcer complications was observed. This was associated with a decrease in the prevalence of H. pylori infection in people under 65 years of age, a 3.5-fold increase in the number of prescriptions of proton-pump inhibitors and an increase in the number of prescriptions of non-steroidal anti-inflammatory drugs, especially coxibs. Conclusions :,In an area with a high prevalence of H. pylori infection, the incidence of peptic ulcer and associated complications is declining rapidly. This was associated with a reduction of the prevalence of H. pylori infection in the young and a widespread use of proton-pump inhibitors. The increase in the use of non-steroidal anti-inflammatory drugs, especially coxibs, has not changed the tendency. [source]