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Duodenal Ulcer (duodenal + ulcer)
Terms modified by Duodenal Ulcer Selected AbstractsEVALUATION OF DYSPEPTIC SYMPTOMS AND ACID SUPPRESSIVE DRUG (ASD) CONSUMPTION IN SUCCESFULLY ERADI CATED AND HEALED DUODENAL ULCER (DU) PATIENTS; RESULTS OF A ONE YEAR PROSPECTIVE STUDYJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2000Pecsi Gy To determine the upper abdominal symptoms, the use of ASD and the recurrence-rate of Helicobacter pylori in DU (Hp) patients one year after ulcer healing and successful HP eradication. Patient and methods: 37 endoscopically proven healed and successfully eradicated DU patients were successfully recruited in the study. All patients had active ulcer and showed HP positivity both by rapid urease test and histology 5 weeks before the enrollement endoscopy. The severity and character of dyspeptic symptoms and the use of ASD-s were checked by questionnaires at the start and one year after successful eradication therapy. NSAID users and reflux oesophagitis patients were excluded at inclusion. Eradication was performed by a one week LAC combination followed by 4 week ranitidine therapy. HP reinfection was controlled by C13 urea breath test at the 12 month visit. Results: 7 patients were lost for follow up by the end of the one year program. A together the data of 30 eligible patients (17 females, 13 males, mean age 49 years) were analyzed. The questionnaires represent the symptoms and ASD use of the whole year program. Only 12 out of 30 patients (40%) were permanently and completely symptoms free after the cessation of the short-term therapy. 16 patients (53.3%) had temporary and 2 patients (6.7%) had persistant symptom. About half of the patients (n=17) were taking absolutely no ASD during the follow up. The number of occasional and continuous ASD users were 7 (23.4%) and 6 (20%) respectively. HP reinfections occurred in one patient and no ulcer relaps was proven. Conclusions: 1. More than half of the patients had clinically relevant dyspeptic symptoms during the year after successful HP eradication and ulcer healing. 2. The majority of them required occasional or long term ASD therapy in this period. 3. Recurrences rate of HP was low. [source] Prevalence of Duodenal Ulcer-Promoting Gene (dupA) of Helicobacter pylori in Patients with Duodenal Ulcer in North Indian PopulationHELICOBACTER, Issue 6 2007H. S. Jayasinghe Arachchi Abstract Background: , The duodenal ulcer (DU)-promoting gene (dupA) of Helicobacter pylori has been identified as a novel virulent marker associated with an increased risk for DU. The presence or absence of dupA gene of H. pylori present in patients with DU and functional dyspepsia in North Indian population was studied by polymerase chain reaction (PCR) and hybridization analysis. Materials and Methods: , One hundred and sixty-six patients (96 DU and 70 functional dyspepsia) were included in this study. In addition, sequence diversity of dupA gene of H. pylori found in these patients was analyzed by sequencing the PCR products jhp0917 and jhp0918 on both strands with appropriate primers. Results: , PCR and hybridization analyses indicated that dupA gene was present in 37.5% (36/96) of H. pylori strains isolated from DU patients and 22.86% (16/70) of functional dyspepsia patients (p .05). Of these, 35 patients with DU (97.2%) and 14 patients with functional dyspepsia (81.25%) were infected by H. pylori positive for cagA genotype. Furthermore, the presence of dupA was significantly associated with the cagA -positive genotype (p .02). Conclusion: , Results of our study have shown that significant association of dupA gene with DU in this population. The dupA gene can be considered as a novel virulent marker for DU in this population. [source] The Interleukin-1 RN Polymorphism and Helicobacter pylori Infection in the Development of Duodenal UlcerHELICOBACTER, Issue 6 2004Ping-I Hsu ABSTRACT Background., The host genetic factors that determine the clinical outcomes for Helicobacter pylori -infected individuals remain unclear. Aims., To elucidate the relations among interleukin-1 locus polymorphisms, and H. pylori infection in the development of duodenal ulcers. Materials and methods., In a case,control study involving 168 control subjects and 147 patients with duodenal ulcer, biallelic polymorphisms of two interleukin-1 loci, IL-1B,511 and IL-1B+3954, as well as the penta-allelic variable number of tandem repeats of interleukin-1 receptor antagonist IL-1RN, were genotyped, and the H. pylori states of controls and patients were examined. Results.,Helicobacter pylori infection, male gender and the carriage of IL-1RN*2 independently increased the risk of duodenal ulcer with odds ratios of 6.4 (95% confidence interval, 3.7,11.0), 1.9 (95% confidence interval, 1.1,3.4) and 2.7 (95% confidence interval, 1.1,6.8), respectively. Statistical analysis revealed an interaction between IL-1RN*2 and H. pylori infection with the duodenal ulcer risk conferred by the H. pylori infection substantially increased (odds ratios, 22.6; 95% confidence interval, 5.9,86.5) by the carriage of IL-1RN*2. In addition, a synergistic interaction between IL-1RN*2 and blood group O existed. The combined risk of H. pylori infection, the carriage of IL-1RN*2 and blood group O for duodenal ulcer was 27.5 (95% confidence interval, 3.1,243.6). Conclusions., This work is the first to verify IL-1RN*2 as an independent factor that governs the development of duodenal ulcers. Our data indicate that H. pylori infection and IL-1RN*2 synergistically determine susceptibility to duodenal ulcer. The blood group phenotype is possibly a crucial determinant for the outcome of the impact of an interleukin-1 locus polymorphism on H. pylori -infected individuals. [source] IgG Subclass Responses in Childhood Helicobacter pylori Duodenal Ulcer: Evidence of T-Helper Cell Type 2 ResponsesHELICOBACTER, Issue 4 2004David I. Campbell ABSTRACT Background., Duodenal ulcer in adults chronically infected with Helicobacter pylori is associated with a polarized T-helper cell type 1 (Th1) mucosal immune response, with a predominantly immunoglobulin G2 (IgG2) systemic specific response. It has been suggested that children colonized by H. pylori also produce a mucosal Th1 response, but there are few studies that have measured IgG subclass responses in children with duodenal ulcer. Materials and methods., Seven children with endoscopically proven duodenal ulcer and H. pylori infection and 18 children with biopsy proven H. pylori infection but no duodenal ulcer had relative concentrations of IgG subclass responses (IgGsc) against H. pylori antigens measured by ELISA. Eighteen IgG seropositive adults acted as controls. The range of antigens recognised by IgG1 and IgG2 subclass responses were investigated by Western blots. Results., There were no differences in mean IgGsc responses between children with or without duodenal ulcer. Adults produced an IgG2 predominant response. Western blots showed no qualitative differences in antigens recognised by IgG1 or IgG2. Conclusion., Children with duodenal ulcer, in contrast to adults, produce an IgGsc response consistent with a mucosal Th2 response to H. pylori regardless of the presence of duodenal ulceration. This suggests that disease causation amongst children with H. pylori associated duodenal ulceration may not be dependant upon a mucosal Th1 biased response. [source] The risk of pancreatic cancer in patients with gastric or duodenal ulcer diseaseINTERNATIONAL JOURNAL OF CANCER, Issue 2 2007Juhua Luo Abstract Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N -nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3,38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10,40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10,110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4,3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer. © 2006 Wiley-Liss, Inc. [source] Duodenal ulcer and gastric cancer; rare association or an indication for a change of policy?INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2005Mark Wilkinson No abstract is available for this article. [source] Furazolidone-based triple ,rescue therapy' vs. quadruple ,rescue therapy' for the eradication of Helicobacter pylori resistant to metronidazole,ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2002V. Isakov Summary Background : The optimal treatment of patients with Helicobacter pylori resistant to metronidazole has not been established. Aim : To compare the efficacy of quadruple and furazolidone-based triple therapy in the eradication of H. pylori resistant to metronidazole. Methods : Duodenal ulcer patients (n = 70) in whom initial eradication therapy failed and who harboured H. pylori strains resistant to metronidazole were randomized to receive one of the following 7-day regimens: colloidal bismuth subcitrate, 240 mg, tetracycline, 750 mg, and furazolidone, 200 mg, each given twice daily (BTF), or omeprazole, 20 mg b.d., colloidal bismuth subcitrate, 240 mg b.d., tetracycline, 500 mg q.d.s., and metronidazole, 500 mg b.d. (OBTM). H.pylori status was assessed by culture, histology and rapid urease test before treatment and 4,6 weeks after therapy. Susceptibility to metronidazole was assessed by the agar dilution method. Results : H. pylori eradication rates with intention-to-treat/per protocol analyses were: BTF, 85.7%/90.9%; OBTM, 74.2%/89.6%. Duodenal ulcers were healed in nine of 10 (90%) patients in the BTF group and in all patients (12/12) (100%) in the OBTM group (P = N.S.). A significantly lower rate of adverse events was observed in the BTF group than in the OBTM group (31.4% vs. 60%, P = 0.03), but there was no difference in terms of discontinuation of treatment (2/35 vs. 6/35, P = N.S.). Conclusions : The 1-week BTF regimen was as effective as the OBTM regimen, and produced less adverse events. Thus, it may be used in patients in whom resistance of H. pylori to metronidazole is suspected. [source] Helicobacter pylori activates protein kinase C delta to control Raf in MAP kinase signalling: Role in AGS epithelial cell scattering and elongationCYTOSKELETON, Issue 10 2009Sabine Brandt Abstract Helicobacter pylori is a major etiological agent in the development of chronic gastritis, duodenal ulcer and gastric carcinoma in humans. Virulent H. pylori strains harbor a type IV secretion system (T4SS) encoded by the cag pathogenicity island. This T4SS injects the CagA protein into gastric epithelial cells leading to actin-cytoskeletal rearrangements followed by cell elongation and scattering. Here we report that PMA (4,-phorbol-12-myristate-13-acetate), a well-known cell-permeable activator of protein kinase C (PKC), induces a remarkably similar cellular phenotype as compared to infection with H. pylori. PKCs comprise a large family of serine/threonine kinases which are important for multiple physiological processes of host cells. We therefore investigated the role of individual PKC members and the signalling pathways involved in phenotypical outcome. Using isoform-specific silencing RNAs and pharmacological inhibitors we found that two isoforms, PKC-, and PKC-,, were essential for both PMA- and H. pylori -induced elongation phenotype. Furthermore, we provide evidence that PKC-, activity is profoundly stimulated during the course of infection using activation-specific antibodies against PKC phosphorylated at threonine residue 505 or serine residue 660. Infection with H. pylori wild-type and mutants showed that at least two bacterial factors activate PKC-, in a time-dependent manner, one of which is CagA. Immunofluorescence microscopy studies further demonstrated that phosphorylated PKC-, is accumulated and recruited to dynamic actin-structures at the cell membrane. Finally, we show that PKC-, specifically targets Raf kinase to stimulate the Erk1/2 kinase pathway, which is also crucial for phenotypical outcome. Thus, PKC-, is another important mediator of H. pylori -induced pathogenesis. Cell Motil. Cytoskeleton 2009. © 2009 Wiley-Liss, Inc. [source] Association of erosive esophagitis with Helicobacter pylori eradication: a role of salivary bicarbonate and glycoprotein secretionDISEASES OF THE ESOPHAGUS, Issue 4 2009D. B. Namiot SUMMARY In some populations, Helicobacter pylori eradication is associated with development of erosive esophagitis. The aim of this study was to evaluate the contribution of salivary bicarbonate and glycoprotein secretion to the pathogenesis of erosive esophagitis developing after H. pylori eradication. Gastroscopy and saliva collection were performed at recruitment and 12 months after completion of eradication therapy. Eighty-eight patients with duodenal ulcer were recruited to the study. Erosive esophagitis was found in 13 patients (grade A, 8 patients; grade B, 4 patients; grade C, 1 patient). Among the 74 subjects who completed the study, erosive esophagitis was detected in 21 patients (grade A, 15 patients; grade B, 6 patients); they all were successfully eradicated. Bicarbonate and glycoprotein secretion was not found to differ significantly between the subjects with and without erosive esophagitis both before and 1 year after H. pylori eradication. However, it was lower in H. pylori -infected (baseline) than in H. pylori -noninfected erosive esophagitis subjects (1 year after successful eradication) (bicarbonate 2.34 [1.29,3.40)]vs. 3.64 [2.70,4.58]µmol/min and glycoprotein 0.23 [0.15,0.31]vs. 0.35 [0.28,0.43] mg/min, P= 0.04 and P= 0.04, respectively). We conclude that changes in salivary bicarbonate and glycoprotein secretion related to H. pylori eradication do not promote the development of erosive esophagitis in duodenal ulcer patients. [source] Gastroesophageal reflux before and after Helicobacter pylori eradication.DISEASES OF THE ESOPHAGUS, Issue 4 2003A prospective study using ambulatory 24-h esophageal pH monitoring SUMMARY, The aim of this study was to assess prevalence of GERD before and after Helicobacter pylori (HP) eradication utilizing 24-h esophageal pH/manometry studies. Helicobacter pylori status was confirmed by the Campylobacter like organism test. Those testing positive underwent 24-h pH/manometry followed by HP eradication therapy and urea breath test. Patients were followed up at 6 months and then at 1 year when they underwent a repeat 24-h pH/manometry. Twenty patients, 10 with non-ulcer dyspepsia (NUD) and 10 with duodenal ulcer (DU) were enrolled, though only 10 patients attended for a repeat 24-h pH/manometry study. The patients were well matched, though patients with NUD had a significantly higher symptom score at entry compared with the DU group (8.5 vs 5.7, P < 0.05). The pH and esophageal manometry data were similar in the two groups. Overall nine patients (45%; DU = 5, NUD = 4) had evidence of GERD prior to HP eradication and it persisted one year after cure of the infection. The reflux disease occurred in the presence of normal LES pressure (mean 15.6 ± 3.3 mmHg). New onset GERD was uncommon after cure of HP infection, occurring in only one patient with NUD. Overall HP eradication had no impact on percentage of time pH < 4 (4.69 ± 3 vs 4.79 ± 3), episodes > 5 min (9.8 ± 16 vs 15.5 ± 25.3) and Johnson DeMeester Score (16.8 ± 7.5 vs 26.8 ± 18). In addition successful cure of HP produced no significant changes in LES pressure (17.9 ± 3.8 mmHg vs 19.3 ± 4.6 mmHg), and other esophageal manometry data. Half of HP-positive patients with NUD and DU have evidence of GERD before HP eradication. This persists after successful cure of the infection. New onset GERD occurs very uncommonly one year after HP eradication. [source] Role of Mucin Lewis Status in Resistance to Helicobacter pylori Infection in Pediatric PatientsHELICOBACTER, Issue 4 2010Sara 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] Guidelines for the Management of Helicobacter pylori Infection in Japan: 2009 Revised EditionHELICOBACTER, Issue 1 2010Masahiro Asaka Abstract Background:, Over the past few years, the profile of Helicobacter pylori infection has changed in Japan. In particular, the relationship between H. pylori and gastric cancer has been demonstrated more clearly. Accordingly, the committee of the Japanese Society for Helicobacter Research has revised the guidelines for diagnosis and treatment of H. pylori infection in Japan. Materials and Methods:, Four meetings of guidelines preparation committee were held from July 2007 to December 2008. In the new guidelines, recommendations for treatment have been classified into five grades according to the Minds Recommendation Grades, while the level of evidence has been classified into six grades. The Japanese national health insurance system was not taken into consideration when preparing these guidelines. Results:,Helicobacter pylori eradication therapy achieved a Grade A recommendation, being useful for the treatment of gastric or duodenal ulcer, for the treatment and prevention of H. pylori -associated diseases such as gastric cancer, and for inhibiting the spread of H. pylori infection. Levels of evidence were determined for each disease associated with H. pylori infection. For the diagnosis of H. pylori infection, measurement of H. pylori antigen in the feces was added to the tests not requiring biopsy. One week of proton-pump inhibitor-based triple therapy (including amoxicillin and metronidazole) was recommended as second-line therapy after failure of first-line eradication therapy. Conclusion:, The revised Japanese guidelines for H. pylori are based on scientific evidence and avoid the administrative restraints that applied to earlier versions. [source] Helicobacter pylori Stimulates a Mixed Adaptive Immune Response with a Strong T-Regulatory Component in Human Gastric MucosaHELICOBACTER, Issue 3 2007Rasmus 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] Seroprevalence of Helicobacter pylori Infection Among Schoolchildren and Teachers in TaiwanHELICOBACTER, Issue 3 2007Ding-Bang Lin Abstract Background:,Helicobacter pylori are associated with chronic antral gastritis that is related to duodenal ulcer, gastric ulcer, and probably gastric adenocarcinoma. Infection of H. pylori during childhood is considered an important risk factor for gastric carcinoma in adult life. Materials and Methods:, To examine the epidemiologic characteristics of H. pylori infection among schoolchildren in central Taiwan, a community-based survey was carried out using stratified sampling in 10 elementary schools and three junior high schools including students and theirs teachers. Serum specimens of 1950 healthy schoolchildren (aged 9,15 years old) and 253 teachers who were randomly sampled were screened for the H. pylori antibodies by enzyme-linked immunosorbent assay. Statistical analysis was performed by using the spss for Windows statistical software system. Results:, A total of 332 subjects were H. pylori antibodies positive, giving an overall prevalence of 15.1%. The age-specific seropositive rates were 11.0% in 9,12 years age group, 12.3% in 13,15 years age group, and 45.1% in the teacher group. The older the age, the higher the seroprevalence (OR = 11.53; 95% CI = 6.73,19.74; p < .001 for children vs. teachers). There was no difference in the seroprevalence of H. pylori infection by gender, ethnicity, geographical area, socioeconomic level, parental education, sibship size, family members, and source of drinking water. Conclusion:, The teachers had a much higher prevalence of H. pylori antibodies. The finding suggests that these teachers (adults) might be infected in their early childhood and implies that the poor environmental and hygienic conditions might be responsible for it. It seemed that poor water supply system, sewage disposal, and other environmental hygiene in adult might play some roles in H. pylori infection in Taiwan (before early 1980s). [source] The Interleukin-1 RN Polymorphism and Helicobacter pylori Infection in the Development of Duodenal UlcerHELICOBACTER, Issue 6 2004Ping-I Hsu ABSTRACT Background., The host genetic factors that determine the clinical outcomes for Helicobacter pylori -infected individuals remain unclear. Aims., To elucidate the relations among interleukin-1 locus polymorphisms, and H. pylori infection in the development of duodenal ulcers. Materials and methods., In a case,control study involving 168 control subjects and 147 patients with duodenal ulcer, biallelic polymorphisms of two interleukin-1 loci, IL-1B,511 and IL-1B+3954, as well as the penta-allelic variable number of tandem repeats of interleukin-1 receptor antagonist IL-1RN, were genotyped, and the H. pylori states of controls and patients were examined. Results.,Helicobacter pylori infection, male gender and the carriage of IL-1RN*2 independently increased the risk of duodenal ulcer with odds ratios of 6.4 (95% confidence interval, 3.7,11.0), 1.9 (95% confidence interval, 1.1,3.4) and 2.7 (95% confidence interval, 1.1,6.8), respectively. Statistical analysis revealed an interaction between IL-1RN*2 and H. pylori infection with the duodenal ulcer risk conferred by the H. pylori infection substantially increased (odds ratios, 22.6; 95% confidence interval, 5.9,86.5) by the carriage of IL-1RN*2. In addition, a synergistic interaction between IL-1RN*2 and blood group O existed. The combined risk of H. pylori infection, the carriage of IL-1RN*2 and blood group O for duodenal ulcer was 27.5 (95% confidence interval, 3.1,243.6). Conclusions., This work is the first to verify IL-1RN*2 as an independent factor that governs the development of duodenal ulcers. Our data indicate that H. pylori infection and IL-1RN*2 synergistically determine susceptibility to duodenal ulcer. The blood group phenotype is possibly a crucial determinant for the outcome of the impact of an interleukin-1 locus polymorphism on H. pylori -infected individuals. [source] IgG Subclass Responses in Childhood Helicobacter pylori Duodenal Ulcer: Evidence of T-Helper Cell Type 2 ResponsesHELICOBACTER, Issue 4 2004David I. Campbell ABSTRACT Background., Duodenal ulcer in adults chronically infected with Helicobacter pylori is associated with a polarized T-helper cell type 1 (Th1) mucosal immune response, with a predominantly immunoglobulin G2 (IgG2) systemic specific response. It has been suggested that children colonized by H. pylori also produce a mucosal Th1 response, but there are few studies that have measured IgG subclass responses in children with duodenal ulcer. Materials and methods., Seven children with endoscopically proven duodenal ulcer and H. pylori infection and 18 children with biopsy proven H. pylori infection but no duodenal ulcer had relative concentrations of IgG subclass responses (IgGsc) against H. pylori antigens measured by ELISA. Eighteen IgG seropositive adults acted as controls. The range of antigens recognised by IgG1 and IgG2 subclass responses were investigated by Western blots. Results., There were no differences in mean IgGsc responses between children with or without duodenal ulcer. Adults produced an IgG2 predominant response. Western blots showed no qualitative differences in antigens recognised by IgG1 or IgG2. Conclusion., Children with duodenal ulcer, in contrast to adults, produce an IgGsc response consistent with a mucosal Th2 response to H. pylori regardless of the presence of duodenal ulceration. This suggests that disease causation amongst children with H. pylori associated duodenal ulceration may not be dependant upon a mucosal Th1 biased response. [source] Effect of Helicobacter pylori Infection on Gastric Acid Secretion and Meal-Stimulated Serum Gastrin in ChildrenHELICOBACTER, Issue 2 2004Seiichi Kato ABSTRACT Background., Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal-stimulated gastrin in relation to H. pylori infection among pediatric patients. Materials and Methods., Thirty-six children aged 10,17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2,3 months after H. pylori eradication. Meal-stimulated serum gastrin response was assessed before and 12 months after eradication. Results.,H. pylori gastritis was typically antrum-predominant. Acid secretion was greater in H. pylori- positive patients with duodenal ulcer than in gastritis-only patients or controls [mean ± standard error (SE): 6.56 ± 1.4, 3.11 ± 0.4 and 2.65 ± 0.2 mEq/10 minutes, respectively; p < .001]. Stimulated acid secretion was higher in H. pylori- positive boys than girls (5.0 ± 0.8 vs. 2.51 ± 0.4 mEq/10 minutes, respectively; p < .05). Stimulated acid secretion pre- and post- H. pylori eradication was similar (5.47 ± 0.8 vs. 4.67 ± 0.9 mEq/10 minutes, respectively; p = .21). Increased basal and meal-stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p < .001 and peak from 544 to 133 pg/ml, p < .05). Conclusions.,H. pylori infection in children is associated with a marked but reversible increase in meal-stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection. [source] Recurrent Peptic Ulcers in Patients Following Successful Helicobacter pylori Eradication: A Multicenter Study of 4940 PatientsHELICOBACTER, Issue 1 2004Hiroto Miwa ABSTRACT Objective., Although curative treatment of Helicobacter pylori infection markedly reduces the relapse of peptic ulcers, the details of the ulcers that do recur is not well characterized. The aim of this study is to describe the recurrence rate and specific features of peptic ulcers after cure of H. pylori infection. Methods., This was a multicenter study involving 4940 peptic ulcer patients who were H. pylori negative after successful eradication treatment and were followed for up to 48 months. The annual incidence of ulcer relapse in H. pylori -cured patients, background of patients with relapsed ulcers, time to relapse, ulcer size, and site of relapsed ulcers were investigated. Results., Crude peptic ulcer recurrence rate was 3.02% (149/4940). The annual recurrence rates of gastric, duodenal and gastroduodenal ulcer were 2.3%, 1.6%, and 1.6%, respectively. Exclusion of patients who took NSAIDs led annual recurrence rates to 1.9%, 1.5% and 1.3%, respectively. The recurrence rate was significantly higher in gastric ulcer. Recurrence rates of patients who smoked, consumed alcohol, and used NSAIDs were significantly higher in those with gastric ulcer recurrence compared to duodenal ulcer recurrence (e.g. 125 of 149 [83.9%] relapsed ulcers recurred at the same or adjacent sites as the previous ulcers). Conclusions., Curative treatment of H. pylori infection is useful in preventing ulcer recurrence. Gastric ulcer is more likely to relapse than duodenal ulcer. Recurrent ulcer tended to recur at the site of the original ulcers. [source] Statistical Model of the Interactions Between Helicobacter pylori Infection and Gastric Cancer DevelopmentHELICOBACTER, Issue 1 2003Martin Welin ABSTRACT Background. The bacterium Helicobacter pylori is associated with a number of gastrointestinal diseases, such as gastric ulcer, duodenal ulcer and gastric cancer. Several histological changes may be observed during the course of infection; some may influence the progression towards cancer. The aim of this study was to build a statistical model to discover direct interactions between H. pylori and different precancerous changes of the gastric mucosa, and in what order and to what degree those may influence the development of the intestinal type of gastric cancer. Methods. To find direct and indirect interactions between H. pylori and different histological variables, log-linear analyses were used on a case,control study. To generate mathematically and biologically relevant statistical models, a designed algorithm and observed frequency tables were used. Results. The results show that patients with H. pylori infection need to present with proliferation and intestinal metaplasia to develop gastric cancer of the intestinal type. Proliferation and intestinal metaplasia interacted with the variables atrophy and foveolar hyperplasia. Intestinal metaplasia was the only variable with direct interaction with gastric cancer. Gender had no effect on the variables examined. Conclusion. The direct interactions observed in the final statistical model between H. pylori, changes of the mucosa and gastric cancer strengthens and supports previous theories about the progression towards gastric cancer. The results suggest that gastric cancer of the intestinal type may develop from H. pylori infection, proliferation and intestinal metaplasia, while atrophy and foveolar hyperplasia interplay with the other histological variables in the disease process. [source] Relationship Between Gastric Ulcer and Helicobacter pylori VacA Detected in Gastric Juice Using Bead-ELISA MethodHELICOBACTER, Issue 5 2002Daisuke Shirasaka Abstract Background. VacA is an important pathogenetic factor produced by Helicobacter pylori. VacA has often been detected in supernatants of liquid cultures or lysates of whole bacterial cells. However, no studies have ever tried to assay VacA produced in the human stomach. We applied a very sensitive and simple method, bead-ELISA, to detect VacA in gastric juice. Materials and Methods. Forty-eight H. pylori -positive patients (16 nonulcer dyspepsia, 16 gastric ulcer, and 16 duodenal ulcer) and four H. pylori -negative nonulcer dyspepsia patients had endoscopy performed and gastric juice were aspirated. Polystyrene beads coated with the antibody to VacA, were used in this bead-ELISA method. The nucleotide sequences of vacA in the signal and middle regions were investigated. Results. Of the 48 samples that were positive for H. pylori, 21 [43.8%] were found to be VacA positive in gastric juice. The average and maximum concentrations of detected VacA in gastric juice were 143.2 ± 216.5 and 840 pg/ml, respectively. The average density of VacA from gastric ulcer patients (227.5 ± 276.7 pg/ml) was higher than that found in nonulcer dyspepsia (51.8 ± 39.8 pg/ml) and duodenal ulcer (49.2 ± 21.5 pg/ml) patients. There was no relationship between VacA in gastric juice and vacA genotype. Conclusions. VacA in gastric juice could be directly detected by bead-ELISA. In this study, the diversity of disease outcome was associated with not the quality but the quantity of VacA. Therefore, not only the quality but also the quantity of VacA is important etiological factors in the pathogenesis of mucosal damage. [source] High Efficacy of Ranitidine Bismuth Citrate, Amoxicillin, Clarithromycin and Metronidazole Twice Daily for Only Five Days in Helicobacter pylori EradicationHELICOBACTER, Issue 2 2001Javier P. Gisbert ABSTRACT Aim. The combination of a proton pump inhibitor (PPI) or ranitidine-bismuth-citrate (Rbc) and two antibiotics for 7,10 days are, at present, the preferred treatments in Helicobacter pylori eradication. However, therapies for fewer than 7 days have been scarcely evaluated and it is unknown whether the length of treatment can be shortened, without a lost of efficacy, if three instead of two antibiotics are used. The aim of our study was to evaluate the efficacy of Rbc plus three antibiotics for only 5 days in H. pylori eradication. Methods. We prospectively studied 80 patients (34% duodenal ulcer, 66% functional dyspepsia) infected by H. pylori. At endoscopy, biopsies were obtained for histological study and rapid urease test, and a 13C-urea breath test was carried out. Urea breath test was repeated 4 weeks after completing eradication treatment with Rbc [400 mg twice a day (bid)], amoxicillin (1 g bid), clarithromycin (500 mg bid) and metronidazole (500 mg bid). All drugs were administered together after breakfast and dinner for 5 days only, and no treatment was administered thereafter. Compliance with therapy was determined from the interrogatory and the recovery of empty envelopes of medications. Results. In 79 out of the 80 patients, H. pylori eradication success or failure was assessed after therapy (one patient was lost from follow-up). All but one of these 79 patients took all the medications (one patient stopped treatment on the day 3 due to nausea/vomiting). Per protocol eradication was achieved in 72/78 (92%; 95% CI, 84,96%) and in 72/80 (90%; 81,95%) by intention-to-treat. Therapy was more effective in patients with duodenal ulcer than in those with functional dyspepsia [100% (87,100%) vs. 85% (73,92%) by intention-to-treat; p < .05]. Adverse effects were described in ten patients (12%), and included the perception of a metallic taste (eight patients), nausea/vomiting (two patients, one of them abandoned the treatment due to this), and diarrhea (two patients). Conclusion. The combination of Rbc, amoxicillin, clarithromycin and metronidazole for only 5 days represents a promising therapy for H. pylori infection, due to its high efficacy, simple posology, low cost and excellent tolerance. [source] The HOMER Study: The Effect of Increasing the Dose of Metronidazole When Given with Omeprazole and Amoxicillin to Cure Helicobacter pylori InfectionHELICOBACTER, Issue 4 2000Karna Dev Bardhan Background.Helicobacter pylori eradication with omeprazole, amoxycillin, and metronidazole is both effective and inexpensive. However, eradication rates with different dosages and dosing vary, and data on the impact of resistance are sparse. In this study, three different dosages of omeprazole, amoxycillin, and metronidazole were compared, and the influence of metronidazole resistance on eradication was assessed. Methods. Patients (n = 394) with a positive H. pylori screening test result and endoscopy-proven duodenal ulcer in the past were enrolled into a multicenter study performed in four European countries and Canada. After baseline endoscopy, patients were randomly assigned to treatment for 1 week with either omeprazole, 20 mg twice daily, plus amoxycillin, 1,000 mg twice daily, plus metronidazole, 400 mg twice daily (low M); or omeprazole, 40 mg once daily, plus amoxycillin, 500 mg three times daily, plus metronidazole, 400 mg three times daily (medium M); or omeprazole, 20 mg twice daily, plus amoxycillin, 1,000 mg twice daily, plus metronidazole, 800 mg twice daily (high M). H. pylori status at entry was assessed by a 13C urea breath test and a culture. Eradication was defined as two negative 13C-urea breath test results 4 and 8 weeks after therapy. Susceptibility testing using the agar dilution method was performed at entry and in patients with persistent infection after therapy. Results. The eradication rates, in terms of intention to treat (ITT) (population n = 379) (and 95% confidence interval [CI]) were as follows: low M 76% (68%, 84%), medium M 76% (68%, 84%), and high M 83% (75%, 89%). By per-protocol analysis (population n = 348), the corresponding eradication rates were: low M 81%, medium M 80%, and high M 85%. No H. pylori strains were found to be resistant to amoxycillin. Prestudy resistance of H. pylori strains to metronidazole was found in 72 of 348 (21%) of the cultures at entry (range, 10%,39% in the five countries). The overall eradication rate in prestudy metronidazole-susceptible strains was 232 of 266 (87%) and, for resistant strains, it was 41 of 70 (57%; p < .001). Within each group, the results were as follows (susceptible/resistant): low M, 85%/54%; medium M, 86%/50%; and high M, 90%/75%. There were no statistically significant differences among the treatment groups. 23 strains susceptible to metronidazole before treatment were recultured after therapy failed; 20 of these had now developed resistance. Conclusions.H. pylori eradication rates were similar (approximately 80%) with all three regimens. Metronidazole resistance reduced efficacy; increasing the dose of metronidazole appeared not to overcome the problem or significantly improve the outcome. Treatment failure was generally associated with either prestudy or acquired metronidazole resistance. These findings are of importance when attempting H. pylori eradication in communities with high levels of metronidazole resistance. [source] Disease-specific Helicobacter pylori Virulence Factors: The Unfulfilled PromiseHELICOBACTER, Issue S1 2000David Y. Graham A number of putative virulence factors for Helicobacter pylori have been identified including cagA, vacA and iceA. The criteria for a true virulence factor includes meeting the tests of biologically plausibility with the associations being both experimentally and epidemiologically consistent. Although disease-specific associations have been hypothesized/claimed, there are now sufficient data to conclusively state that none of these putative virulence factors have disease specificity. CagA has been claimed to be associated with increased mucosal IL-8 and inflammation, increased density of H. pylori in the antrum, duodenal ulcer (DU), gastric cancer, and protection against Barrett's cancer. Only the increase in IL-8/inflammation is direct and substantiated. Different H. pylori strains with functional cag pathogenicity islands do not vary in virulance as it has been shown that mucosal IL-8 levels are proportional to the number of cagA +H. pylori independent of the disease from which the H. pylori were obtained. It is now known that the density of either cagA + and cagA,H. pylori in the antrum of patients with H. pylori gastritis is the same. In contrast, the mean density of H. pylori in the antrum in DU is greater than in the antrum of patients with H. pylori gastritis. Of interest, the density of H. pylori is higher in the corpus of patients with H. pylori gastritis than those with DU, suggesting that acid secretion plays a critical role in these phenomena. The presence of a functional cag pathogenicity island increases inflammation and it is likely that any factor that results in an increase in inflammation also increases the risk of a symptomatic outcome. Nevertheless, the presence of a functional cag pathogenicity island has no predictive value for the presence, or the future development of a clinically significant outcome. The hypothesis that iceA has disease specificity has not been confirmed and there is currently no known biological or epidemiological evidence for a role for iceA as a virulence factor in H. pylori -related disease. The claim that vacA genotyping might prove clinically useful, e.g. to predict presentation such as duodenal ulcer, has been proven wrong. Analysis of the worldwide data show that vacA genotype s1 is actually a surrogate for the cag pathogenicity island. There is now evidence to suggest that virulence is a host-dependent factor. The pattern of gastritis has withstood the test of time for its relation to different H. pylori -related diseases (e.g. antral predominant gastritis with duodenal ulcer disease). The primary factors responsible for the different patterns of gastritis in response to an H. pylori infection are environmental (e.g. diet), with the H. pylori strain playing a lesser role. Future studies should work to eliminate potential bias before claiming disease associations. Controls must exclude regional or geographic associations related to the common strain circulation and not to the outcome. The authors must also control for both the presence of the factor and for the disease association. The study should be sufficiently large and employ different diseases and ethnic groups for the results to be robust. The findings in the initial sample (data derived hypothesis) should be tested in a new group (hypothesis testing), preferably from another area, before making claims. Finally, it is important to ask whether the results are actually a surrogate for another marker (e.g. vacA s1 for cagA) masquerading for a new finding. Only the cag pathogenicity island has passed the tests of biological plausibility (increased inflammation) and experimental and epidemiological consistency. [source] The risk of pancreatic cancer in patients with gastric or duodenal ulcer diseaseINTERNATIONAL JOURNAL OF CANCER, Issue 2 2007Juhua Luo Abstract Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N -nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3,38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10,40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10,110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4,3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer. © 2006 Wiley-Liss, Inc. [source] Different effects of polymorphisms of tumor necrosis factor-alpha and interleukin-1 beta on development of peptic ulcer and gastric cancerJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2007Mitsushige 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 trialJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006KAZUNARI 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] Determinants of basal plasma gastrin levels in the general populationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2000Hedley G Peach Abstract Background: There is considerable variation in basal plasma gastrin levels in healthy subjects. Although high plasma gastrin levels may be causally associated with duodenal ulcer and colorectal cancer, there has been little research to identify the factors that determine basal gastrin levels in the general population. Methods:Helicobacter pylori IgG antibodies and fasting basal gastrin concentrations were measured in 134 males and 137 females who had participated in a cardiovascular disease risk factor prevalence survey and for whom frozen plasma was available. Stepwise multiple linear regression analysis was used to identify the determinants of basal plasma gastrin concentration. Results: The determinants of basal plasma gastrin concentration were H. pylori infection (B = 0.12 ± 0.03; P = 0.0001), age in deciles (B = 0.02 ± 0.01; P = 0.03), hazardous drinking (B = 0.10 ± 0.05; P = 0.07) and gender (B = 0.05 ± 0.03; P = 0.06), but not education, neighborhood socioeconomic index, smoking, body mass index, vigorous exercise or medication known to affect basal plasma gastrin concentration. Ten percent (± 3) of seropositive subjects had a high basal plasma gastrin concentration > 90 pg/mL compared with only 2% (± 1) of seronegative subjects. Conclusions:Helicobacter pylori infection is one of the few modifiable determinants of basal plasma gastrin levels in the general population. [source] Rising trends of gastric cancer and peptic ulcer in the 19th centuryALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2010A. 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] Review article: Helicobacter pylori -negative duodenal ulcer diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2009J. P. GISBERT Aliment Pharmacol Ther,30, 791,815 Summary Background,Helicobacter pylori infection rates in duodenal ulcer (DU) patients may be lower than previously estimated. Aim, To review the real prevalence of H. pylori -negative DUs and its possible causes. Methods, Bibliographical searches in MEDLINE looking for the terms ,H. pylori' and ,duodenal ulcer'. Results, Mean prevalence of H. pylori infection in DU disease, calculated from studies published during the last 10 years including a total of 16 080 patients, was 81%, and this figure was lower (77%) when only the last 5 years were considered. Associations with H. pylori -negative DU were: (1) False negative results of diagnostic methods, (2) NSAID use (21% in studies with <90% infection rate), (3) Complicated DU (bleeding, obstruction, perforation), (4) Smoking, (5) Isolated H. pylori duodenal colonization, (6) Older age, (7) Gastric hypersecretion, (8) Diseases of the duodenal mucosa, (9) Helicobacter,heilmanii' infection and (10) Concomitant diseases. Conclusion, In patients with H. pylori -negative DU disease, one should carefully confirm that the assessment of H. pylori status is reliable. In truly H. pylori -negative patients, the most common single cause of DU is, by far, the use of NSAIDs. Ulcers not associated with H. pylori, NSAIDs or other obvious causes should, for the present, be viewed as ,idiopathic'. True idiopathic DU disease only exceptionally exists. [source] Review article: cellular and molecular mechanisms of NSAID-induced peptic ulcersALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2009C. MUSUMBA Summary Background, Nonsteroidal anti-inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID-induced ulcers is important to enable the development of novel and effective preventive strategies. Aims, To provide an update on recent advances in our understanding of the cellular and molecular mechanisms involved in the development of NSAID-induced ulcers. Methods, A Medline search was performed to identify relevant literature using search terms including ,nonsteroidal anti-inflammatory drugs, aspirin, gastric ulcer, duodenal ulcer, pathogenesis, pharmacogenetics'. Results, The mechanisms of NSAID-induced ulcers can be divided into topical and systemic effects and the latter may be prostaglandin-dependent (through COX inhibition) or prostaglandin-independent. Genetic factors may play an important role in determining individual predisposition. Conclusions, The pathogenesis of NSAID-induced peptic ulcers is complex and multifactorial. Recent advances in cellular and molecular biology have highlighted the importance of various prostaglandin-independent mechanisms. Pharmacogenetic studies may provide further insights into the pathogenetic mechanisms of NSAID-induced ulcers and help identify patients at increased risk. [source] | |||||||||||||||||||||||||||||||