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Gastric Ulcer (gastric + ulcer)
Selected AbstractsRelationship 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] 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] 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] CLINICAL INVESTIGATION OF UPPER GASTROINTESTINAL HEMORRHAGE AFTER PERCUTANEOUS ENDOSCOPIC GASTROSTOMYDIGESTIVE ENDOSCOPY, Issue 3 2010Shinji Nishiwaki Background:, Upper gastrointestinal (GI) hemorrhage after percutaneous endoscopic gastrostomy (PEG) is sometimes reported as one of the serious complications. Our purpose was to clarify the cause of upper GI hemorrhage after PEG. Patients and Methods:, We retrospectively investigated the causes of upper GI hemorrhage among a total of 416 patients out of 426 consecutive patients who underwent PEG in our institution, excluding 10 patients who showed upper GI tumors on PEG placement. Results:, Among 17 patients who developed upper GI hemorrhage after PEG, three and four patients showed PEG tube placement and replacement-related hemorrhage, respectively; these lesions were vascular or mucosal tears around the gastrostomy site. Ten patients experienced 12 episodes of upper GI hemorrhage during PEG tube feeding. The lesions showing bleeding were caused by reflux esophagitis (five patients), gastric ulcer (two patients), gastric erosion due to mucosal inclusion in the side hole of the internal bolster (two patients), and duodenal diverticular hemorrhage (one patient). Anticoagulants were administered in six patients, including four patients with replacement-related hemorrhage and one patient each with reflux esophagitis and gastric ulcer. Conclusions:, Reflux esophagitis was the most frequent reason for upper GI hemorrhage after PEG. The interruption of anticoagulants should be considered for the prevention of hemorrhage on the placement as well as replacement of a gastrostomy tube. [source] Gastric bleeding due to Dieulafoy's ulcer successfully treated with an esophageal variceal ligation (EVL) kitDIGESTIVE ENDOSCOPY, Issue 3 2001Yoshihide Chino Dieulafoy's ulcer is a cause of life-threatening upper gastrointestinal hemorrhage. With advanced endoscopic procedures, Dieulafoy's ulcer is easily diagnosed and treated. However, a few patients still need surgery to stop bleeding or they will die of shock. Further improved procedures are therefore required to treat bleeding in Dieulafoy's ulcer. A 77-year-old man was admitted to our hospital with hematemesis and general malaise. He had moderate anemia and azotemia but no past history of gastric ulcer. He was diagnosed with Dieulafoy's ulcer endoscopically. Dieulafoy's ulcer was ligated with an endoscopic variceal ligation kit without surgery. Although an ulcer was found at the ligation point after 1 week, the ulcer changed to the scar on administration of Histamine H2 receptor blockers. The patient has suffered no recurrent ulcer and no bleeding for 24 months. Endoscopic variceal ligation may be an alternative new method for hemostasis of Dieulafoy's ulcer. [source] Helicobacter pylori infection in patients with haemophilia in Poland: prevalence and risk of upper gastrointestinal bleedingHAEMOPHILIA, Issue 4 2005A. B. Szczepanik Summary., Infection with Helicobacter pylori is the main aetiological factor for erosive gastritis and duodenal or gastric peptic ulcers often complicated with life-threatening bleeding in patients with coagulation disorders. The aim of this prospective study was to evaluate the prevalence of Helicobacter pylori infection in haemophilia patients, and to assess the risk of gastrointestinal bleeding associated with this infection. From 2000 to 2002, 146 patients with haemophilia (129, haemophilia A; 13, haemophilia B), mean age, 39.9 years (±7.3), were investigated for H. pylori infection using IgG and IgA latex serological test. The control group included 100 men with no coagulation disorders, mean age, 40.9 years (±9.2). For 72 (49.3%) patients with haemophilia and 39 controls (39.0%) serological tests were positive indicating the presence of H. pylori infection (P =0.1112). A history of gastrointestinal bleeding was reported in 46 patients (31.5%) with haemophilia and in two control group patients (2.0%) (P < 0.0001). Gastrointestinal bleeding was significantly more frequent in patients with haemophilia infected with H. pylori (33/46; 71.7%) than in patients with no H. pylori infection (13/46; 28.3%; P = 0.0002). In conclusion, the prevalence of H. pylori infection in haemophilic patients in Poland is comparable with that in patients with no coagulation disorders. Helicobacter pylori infection is a risk factor for duodenal and gastric ulcer bleeding in haemophilia patients. In view of the high frequency of upper gastrointestinal bleeding associated with H. pylori infection, we believe that screening and eradication therapy are appropriate in haemophilia patients. [source] Helicobacter pylori Eradication Therapy May Facilitate Gastric Ulcer Healing After Endoscopic Mucosal Resection: A Prospective Randomized StudyHELICOBACTER, Issue 6 2008Jae Hee Cheon Abstract Background and Aim:, It remains unclear whether Helicobacter pylori eradication therapy affects the healing rate of iatrogenic ulcers following endoscopic mucosal resection (EMR) for gastric tumors. The aim of our study was to prospectively evaluate the effect of H. pylori eradication therapy on gastric ulcer healing after EMR. Methods:, After EMR, patients were randomly assigned to either the H. pylori eradication group (Hp group) (lansoprazole 30 mg, amoxicillin 1000 mg, and clarithromycin 500 mg, twice a day for 7 days) or the noneradication group (proton pump inhibitor, PPI group) (lansoprazole 30 mg, twice a day for 7 days). Four weeks after EMR, the ulcer stages and size were compared between the two groups. Moreover, ulcer-related symptoms, bleeding rates, adverse effects, and drug compliance were compared. Results:, A total of 64 patients were enrolled. Of these, 17 patients were excluded from the study. The two groups were comparable in terms of baseline clinicopathologic characteristics. Four weeks after EMR, the two groups did not differ with respect to ulcer stage (p = .475) or ulcer-related symptoms (p = .399). However, the ulcer reduction ratio was significantly higher in the Hp group (0.028 ± 0.024 vs. 0.065 ± 0.055, p < .05). No differences were observed between the two groups with regard to drug compliance, adverse drug event rates, or bleeding rates. Conclusions:, Our results suggest that H. pylori eradication therapy might improve the ulcer healing rate after EMR. [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] 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] Immune Response to a 26-kDa Protein, Alkyl Hydroperoxide Reductase, in Helicobacter pylori-Infected Mongolian Gerbil ModelHELICOBACTER, Issue 4 2001Jing Yan ABSTRACT Background. The host immune response is thought to play an important role in the outcome of Helico-bacter pylori infection. The successful development of the H. pylori -infected Mongolian gerbil model that mimics human disease has enabled study of the antibody response against H. pylori antigens. Materials and Methods. Serum samples from ulcer and carcinogenesis models of H. pylori -infected gerbils were used to screen for H. pylori antigens that cause a humoral immune response in the infected hosts. H. pylori alkyl hydroperoxide reductase (AhpC) is one such antigen on which we report here. The tsaA gene encoding AhpC was amplified by PCR from H. pylori ATCC 43504 strain, cloned into pMALTM -c2 expression vector and expressed in Escherichia coli. Maltose-binding protein fusion protein (MBP-AhpC) was purified by a MBP affinity column. Using purified recombinant AhpC protein as an antigen, the antibody response and changes of antibody levels against AhpC in the gerbil models were studied by Western blotting and ELISA. Results. Antibody against AhpC was negative in the early stages of infection, and became positive in the gerbils with the emergence of gastric diseases such as chronic active gastritis, gastric ulcer and gastric cancer. The antibody levels (ELISA) increased gradually over time and were higher in gerbils with gastric ulcer than that in gerbils without ulcers. Conclusions. Use of the gerbil model that mimics human H. pylori infection is likely to provide insights into the role of H. pylori -specific antigens possibly related to the subsequent development of gastric diseases. [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] Combined histology and molecular biology for diagnosis of early stage gastric MALT lymphomaJOURNAL OF DIGESTIVE DISEASES, Issue 1 2006Zhi Hui YI OBJECTIVE: To establish a sequential diagnostic procedure of gastric mucosa-associated lymphoid tissue (MALT) lymphoma and provide evidence for selected optimal cases to be treated in the early stage. METHODS: Thirty-one cases of gastric lymphoid hyperplasia (GLH) were selected and multiple investigations including histology, protein level, DNA and chromosome levels, combined with clinical follow-up were performed. Histological grade was according to Isaacson's criteria of GLH; CD20, UCHL-1 (CD45RO), anti-kappa (,), anti-lambda (,) and Ki-67 were used for immunohistochemical staining; semi-nested polymerase chain reaction (PCR) was used to detect IgH gene rearrangement and reverse-transcription PCR (RT-PCR) was used to detect API2-MALT1 fusion of the chromosome translocation t(11;18)(q21;q21). Twenty-nine cases underwent eradication therapy for Helicobacter pylori. Changes in histological grade, endoscopic appearance, expression of Ki-67 and IgH gene rearrangement were compared after eradication treatment. RESULTS: Of the 31 cases of GLH with predominant chronic gastritis and gastric ulcer most were histological grade 2 and 3. Only one case had , light chain restriction and 10 cases had monoclonal IgH gene rearrangement. Expression of Ki-67 and monoclonal IgH gene rearrangement were significantly increased with increased lymphoid hyperplasia (P < 0.05). Two cases had API2-MALT1 fusion. Helicobacter pylori was eradicated in 25 cases and another course of treatment had to be given in 4 cases. All cases were followed up for 1.5,37 months. Of the 27 successful eradication cases, 18 showed complete regression both histologically and endoscopically, 4 had partial regression and 7 were unchanged. CONCLUSIONS: A sequential diagnostic procedure based on histology, expression of Ki-67 combined with clonality of IgH rearrangement and API2-MALT1 fusion helps to diagnosis of early stage gastric MALT lymphoma and choose the best treatment strategy. [source] Are repeat upper gastrointestinal endoscopy and colonoscopy necessary within six months of capsule endoscopy in patients with obscure gastrointestinal bleeding?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2008David Gilbert Abstract Background and Aim:, Medicare reimbursement for capsule endoscopy for the investigation of obscure gastrointestinal bleeding in Australia requires endoscopy and colonoscopy to have been performed within 6 months. This study aims to determine the diagnostic yield of repeating these procedures when they had been non-diagnostic more than 6 months earlier. Methods:, Of 198 consecutive patients who were referred for the investigation of obscure gastrointestinal bleeding, 50 underwent repeat endoscopy and colonoscopy solely to enable reimbursement (35 females and 15 males; mean age 59.4 [range: 21,82] years). The average duration of obscure bleeding was 50.16 (range: 9,214) months. The mean number of prior endoscopies was 3 (median: 2) and 2.8 colonoscopies (median: 2). The most recent endoscopy had been performed 18.9 (median: 14; range: 7,56) months, and for colonoscopy, 19.1 (median 14; range 8-51) months earlier. Results:, A probable cause of bleeding was found at endoscopy in two patients: gastric antral vascular ectasia (1) and benign gastric ulcer (1). Colonoscopy did not reveal a source of bleeding in any patient. Capsule endoscopy was performed in 47 patients. Twenty four (51%) had a probable bleeding source identified, and another five (11%) a possible source. These included angioectasia (17 patients), mass lesion (2), non-steroidal anti-inflammatory drug enteropathy (2), Cameron's erosions (2), and Crohn's disease (1). Four patients undergoing repeat capsule endoscopy had a probable bleeding source detected. Conclusion:, The yield of repeat endoscopy and colonoscopy immediately prior to capsule endoscopy is low when these procedures have previously been non-diagnostic. Such an approach is also not cost-effective. [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] Influence of gender difference and gastritis on gastric ulcer formation in ratsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2001Edgar SL Liu Abstract Background: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. Methods: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E2 (PGE2) level were also determined. Results: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE2 level was higher in female rats with acute gastritis. Both mucus and PGE2 were increased during ulcer healing in both genders. Conclusions: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE2 not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach. [source] HISTOPATHOLOGICAL PATTERN OF GASTRIC BIOPSIES OF HELICOBACTER PYLORI POSITIVE PATIENTS IN SARDJITO GENERAL HOSPITAL, YOGYAKARTA, INDONESIAJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2000Siti Nurdjanah Objective: To determine the gastric histopathological types distribution of H. pylori positive patients who were detected histopathologically. Material& Methods: Study design was prospective study. Consecutive patients who were suffering chronic dyspepsia underwent endoscopy examination between August 1998 and December 1999. The biopsy specimens were taken from gastric antrum and corpus and sent to the pathologist for histopathology type and H. pylori examinations. H. pylori were also confirmed with CLO and IgG-Helicobacter pylori tests. Results: There were 92 patients (48 male (M) and 44 Female (F) who underwent gastric biopsies endoscopically between August 1998 and December 1999. Fifty-six (60.87%) patients were chronic superficial gastritis, 11(11.96%) chronic antropic gastritis, 18 (19.56%) chronic gastritis 2 (2.17%) chronic gastritis with metaplasia, 3 (3.27%) gastric ulcer, and 2 (2.17%) gastric signet-ring cell carcinoma. Twenty one (22.8%) patients with H. pylori positive by histopathology examination with CLO and IgG-H.pylori tests. Those were 5 (8.90%) patients with chronic superficial gastritis, 7(63.63%) chronic atrophic gastritis, 3(100%) gastric ulcer, 2 (100%) chronic gastritis with metaplasia, 3(16.67%) chronic gastritis, 1(50%) signet-ring cell carcinoma. The age range of the H. pylori positive patients were between 16 and 76 years old. Conclusion: Twenty one (22.8%) H. pylori positive patients out of 92 endoscopied patients and the high percentage tendency of H. pylori positively in chronic atrophic gastritis, gastric ulcer, and chronic gastritis with metaplasia, although most of the patients had chronic superficial gastritis. Further study is needed with larger with larger sample to get the clearer picture of H. pylori distribution based on gastric histopathological types. [source] The role of erythropoietin in the protection of gastric mucosa from indometacin-induced gastric injury and its relationship with oxidant and antioxidant parameters in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2010Fatih Albayrak Abstract Objectives Erythropoietin has anti-oxidative and anti-inflammatory activity. We wanted to evaluate its activity in preventing damage to the gastric mucosa. Methods We examined the protective effect of erythropoietin on indometacin-induced gastric mucosa damage in the rat stomach and compared its potency with that of famotidine. We also measured effects on oxidant and antioxidant parameters in the rat stomach. Key findings Famotidine and erythropoietin 2500 and 5000 IU/kg reduced the ulcer area by 98%, 31% and 58%, respectively, compared with the indometacin group. Superoxide dismutase activity and glutathione level were decreased and myeloperoxidase activity increased in the indometacin group compared with healthy rats. Famotidine and erythropoietin at all doses increased superoxide dismutase and glutathione levels significantly compared with the indometacin group. Myeloperoxidase activity was decreased by erythropoietin and famotidine. Conclusions These results support the view that erythropoietin counteracts the effects of indometacin in inducing gastric ulcer and could be used as a an antiulcer compound. Its antiulcer effect is less potent than that of famotidine. The antiulcerogenic effects of erythropoietin may be related to its intrinsic ability to sustain the activities of free-radical scavenging enzymes and the bioavailability of glutathione. [source] Effect of methanolic extract of Terminalia arjuna against Helicobacter pylori 26695 lipopolysaccharide-induced gastric ulcer in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2008Rethinam Sundaresan Devi Helicobacter pylori lipopolysaccharide (HP-LPS) is a potent virulence factor in the causation of gastric ulcer and gastritis. H. pylori -induced gastric pathology is prevalent throughout the world. Herbal medicines are attracting attention because of their traditional values, popularity and belief, as well as for their advantages such as less toxicity, affordability and medicinal value. The present study aimed to evaluate the anti-ulcer effect of a methanolic extract of Terminalia arjuna (TA) against HP-LPS-induced gastric damage in rats. Ulcers were induced with HP-LPS (50 ,g per animal) administered orally daily for 3 days. The efficacy of TA on gastric secretory parameters such as volume of gastric juice, pH, free and total acidity, pepsin concentration, and the cytoprotective parameters such as protein-bound carbohydrate complexes in gastric juice and gastric mucosa was assessed. The protective effect of TA was also confirmed by histopathological examination of gastric mucosa. HP-LPS-induced alterations in gastric secretory parameters were altered favourably in rats treated with TA, suggesting that TA has an anti-secretory role. Furthermore, HP-LPS-induced impairments in gastric defence factors were also prevented by treatment with TA. These results suggest that the severe cellular damage and pathological changes caused by HP-LPS are mitigated by TA; these effects are comparable with those of sucralfate. The anti-ulcer effect of TA may reflect its ability to combat factors that damage the gastric mucosa, and to protect the mucosal defensive factors. [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] Clinical trial: irsogladine maleate, a mucosal protective drug, accelerates gastric ulcer healing after treatment for eradication of Helicobacter pylori infection , the results of a multicentre, double-blind, randomized clinical trial (IMPACT study)ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010H. HIRAISHI Aliment Pharmacol Ther,31, 824,833 Summary Background,Helicobacter pylori eradication therapy alone is not sufficient to heal all gastric ulcers. Aim, To verify the efficacy of treatment with irsogladine maleate between the termination and assessment of treatment for eradicating H. pylori in a double-blind study. Methods Three hundred and twenty-two patients with a single H. pylori -positive gastric ulcer were given eradication treatment, then assigned randomly to a treatment group [given 4 mg/day irsogladine maleate (n = 150)] or a control group [given a placebo (n = 161)]. The gastric ulcer healing rates were compared after 7 weeks of treatment. Results, The healing rate was significantly higher in the irsogladine maleate group (83.0%) than in the placebo group (72.2%; ,2 test, P = 0.0276). In the subgroup analysis of cases of eradication failure, the gastric ulcer healing rate was significantly higher in the irsogladine maleate group (57.9%) than in the placebo group (26.1%; ,2 test, P = 0.0366). Conclusions, Irsogladine maleate was effective for treating gastric ulcer after H. pylori eradication. The high healing rates observed in patients with or without successful eradication demonstrate the usefulness of irsogladine maleate treatment regardless of the outcome of eradication. [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] Incidence of bleeding lesions within reach of conventional upper and lower endoscopes in patients undergoing double-balloon enteroscopy for obscure gastrointestinal bleedingALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2009L. C. FRY Summary Background, Double-balloon enteroscopy (DBE) is a useful method for evaluation of obscure gastrointestinal bleeding (OGIB). Aim To determine the incidence of lesions within reach of conventional upper and lower endoscopes as the cause of OGIB in patients referred for DBE. Methods All patients undergoing DBE for OGIB during a 3.5-year period at a university hospital were studied. OGIB was defined according to American Gastroenterological Association (AGA) guidelines. Results One hundred and forty-three DBEs were performed in 107 patients for obscure overt (n = 85) and obscure occult (n = 22) GIB. Lesions outside the SB as possible sources of GIB were found in 51 patients (47.6%) and a definite source of bleeding outside the small bowel (SB) was detected in 26 patients (24.3%). Lesions considered to explain a definite source of GIB were: gastric ulcer (n = 3), duodenal ulcer (n = 3), Cameron's lesions (n = 2), gastric antral vascular ectasias (n = 4), radiation proctitis (n = 1), radiation ileitis (n = 2), duodenal angiodysplasias (n = 1), haemorrhoids with stigmata of recent bleed (n = 1), colon angiodysplasias (n = 3), colon diverticulosis (n = 3), colonic Crohn's disease (n = 1), anastomotic ulcers (n = 1). Conclusions The frequency of non-SB lesions definitely explaining the source of GIB in patients referred for DBE was 24.3%. Therefore, repeat esophago-gastroduodenoscopy (EGD) and ileocolonoscopy should be taken into consideration before DBE. [source] Clinical features of gastric cancer discovered after successful eradication of Helicobacter pylori: results from a 9-year prospective follow-up study in JapanALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2005T. Kamada Summary Background :,Eradication of Helicobacter pylori is expected to prevent the development of gastric cancer. However, gastric cancer is sometimes discovered after successful eradication of H. pylori. Aim :,To conduct a prospective study to determine the clinical features of patients who underwent successful eradication and were later diagnosed with gastric cancer. Methods :,A total of 1787 patients (1299 males and 488 females; mean age, 58.2 years; range: 15,84) who underwent successful eradication therapy between April 1994 and March 2001 were our study subjects. Results :,Gastric cancer occurred at a rate of 1.1% (20 of 1787) during the follow-up period. Gastric cancer comprises six of 105 (5.7%) with early gastric cancer after endoscopic resection, 12 of 575 (2.1%) with gastric ulcer and two of 453 (0.4%) with atrophic gastritis. Gastric cancer did not develop in any patient with duodenal ulcer. All patients with gastric cancer had baseline severe atrophic gastritis in the corpus. Conclusion :,Careful endoscopic examination is necessary even after successful eradication of H. pylori in patients with early gastric cancer or gastric ulcer with severe mucosal atrophy in the corpus. [source] Treatment with a proton pump inhibitor promotes corpus gastritis in patients with Helicobacter pylori -infected antrum-predominant gastritisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2002M. Suzuki Background: Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis. Aim: To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction. Methods: Forty-six H. pylori -infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme-linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks. Results: In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase > corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase > antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus. Conclusions: Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density. [source] Evaluation of the cost-effectiveness of Helicobacter pylori eradication triple therapy vs. conventional therapy for ulcers in JapanALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2001S. Ikeda Background: Helicobacter pylori eradication triple therapy with a combination of lansoprazole, amoxicillin and clarithromycin was approved in Japan in September 2000. Aim: To compare the cost-effectiveness of this eradication therapy with conventional histamine-2 receptor antagonist therapy in Japan. Methods: We established two Markov models for gastric and duodenal ulcers. The model design was based on the Japanese H. pylori eradication guideline and a specialist's opinions, and the model inputs were obtained from a literature review. The models predict the direct medical costs, number of disease-free days and cost per disease-free day for 5 years. Results: In the gastric ulcer model, the expected total costs of eradication and conventional therapies per patient were ¥169 719 and ¥390 921, respectively; the expected numbers of disease-free days were 1454 days and 1313 days, respectively. In the duodenal ulcer model, the expected total costs were ¥134 786 and ¥324 689, respectively; the expected numbers of disease-free days were 1503 days and 1387 days, respectively. The sensitivity analyses showed that the results of the base case analysis were robust. Conclusions: This eradication therapy is less costly and more effective than conventional therapy for the treatment of gastric and duodenal ulcers in a Japanese medical setting. [source] Duodenogastric reflux following cholecystectomy in the dog: role of antroduodenal motor functionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2001K. Nogi Background : Duodenogastric reflux has been implicated in the pathogenesis of gastric ulcer and gastritis. Duodenogastric reflux after cholecystectomy is also a possible cause of post-cholecystectomy syndrome. Aim : To investigate the role of antroduodenal motor function in increased duodenogastric reflux following cholecystectomy and the effect of trimebutine maleate (trimebutine) on the duodenogastric reflux in conscious dogs. Methods : Antropyloric and duodenal motility and bile acids content in the gastric juice were measured for 3 h during the inter-digestive state in dogs with or without cholecystectomy. Results : Bile acids content in the gastric juice of cholecystectomized dogs was significantly higher than that of non-cholecystectomized dogs. The frequency of pyloric relaxation during phase II of the migrating motor complex was significantly increased following cholecystectomy. Intravenous infusion of trimebutine inhibited both the increased duodenogastric reflux and the frequency of pyloric relaxation in the cholecystectomized dog. Conclusion : Duodenogastric reflux and frequency of pyloric relaxations were increased in cholecystectomized dogs and trimebutine suppressed both of them. These findings suggest that the increased frequency of pyloric relaxation contributes to the duodenogastric reflux following cholecystectomy. [source] Gastric epithelial cell proliferation and apoptosis in Helicobacter pylori-infected miceALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000T. Yamaguchi Summary Background: Helicobacter pylori causes gastritis and is strongly associated with gastroduodenal ulcer and gastric cancer. The bacterium is associated with an increased rate of epithelial proliferation, which can be reversed by eradication of the organism. The mechanism of this response is not known, but this epithelial proliferation is one of the risk factors for developing gastric carcinoma. Recently, apoptosis also was found to be increased in the gastric mucosa of persons carrying H. pylori. Methods: cagA -positive H. pylori isolated from a human gastric ulcer was inoculated into BALB/C mice. At 4, 6, 12, 18 and 24 weeks, mice were injected with bromodeoxyuridine 5 mg/kg and killed 1 h later. Proliferation was analysed by histochemical staining for BrdU; apoptosis was examined by the TUNEL assay. Results: The number of BrdU-labelled cells in the antrum was significantly increased by H. pylori infection beginning 12 weeks after infection. The number of apoptotic cells in this tissue was increased significantly by 6 weeks after inoculation. Conclusion: The proliferation observed in H. pylori infection may be a response to increased apoptosis. [source] | ||||||||||||||||||||||||||||