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Duodenal Ulcer Patients (duodenal + ulcer_patient)
Selected AbstractsDifferent Helicobacter pylori Strains Colonize the Antral and Duodenal Mucosa of Duodenal Ulcer PatientsHELICOBACTER, Issue 2 2000Ann-Catrin E. Thoreson Background. We have investigated the possibility that the same patients may be colonized by Helicobacter pylori strains of different genotypes or phenotypes in the antrum as compared to in the duodenum. The strains were typed for DNA fingerprints, different lipopolysaccharides (LPS), and Lewis antigen expression on the O,side chains of LPS. Materials and Methods. Polymerase chain reaction (PCR) amplifications using primer sequences (i.e., the Enterobacterial Repetitive Intergenic Consensus [ERIC]) and randomly amplified polymorphic DNA (RAPD) elements were performed to asses chromosomal DNA diversity between H. pylori strains. The expression of different LPS types and Lewis antigens in the various H. pylori isolates were determined by whole bacterial enzyme-linked immunosorbent assays using monoclonal antibodies. Results. Duodenal ulcer patients had different H. pylori genotypes in the duodenum as compared to in the antrum as shown by ERIC-PCR (44%) and by RAPD-PCR (75%). Different DNA patterns were found among the strains that were isolated from various regions of the duodenum in 4 of 16 patients (25%) as shown by ERIC-PCR and in 8 of 16 patients (50%) as shown by RAPD-PCR. Sixty-three percent of the duodenal ulcer patients had H. pylori strains with a different Lewis antigen phenotype in the duodenum as compared to in the antrum, and 3 of 16 patients (19%) had strains with different Lewis antigens expressed by strains from different duodenal biopsies from the same patient. Conclusion. The results suggest that a mixed population of different H. pylori strains with marked variation, both genotypically and phenotypically, colonize the same patient. [source] New once-daily, highly effective rescue triple therapy after multiple Helicobacter pylori treatment failures: a pilot studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2005L. G. V. Coelho Summary Background:,Helicobacter pylori treatment failure is a growing problem in daily practice. Aim:, To determine the efficacy of the combination of rabeprazole, levofloxacin and furazolidone as a rescue therapy. Methods:, Duodenal ulcer patients previously submitted, without success, to at least two H. pylori treatment regimens were included. Gastroscopy (urease test, histological examination and culture) and 13C-urea breath test were performed. All patients received a combination of rabeprazole 20 mg, levofloxacin 500 mg and furazolidone 200 mg (two tablets) administered in a single dose in the morning for 10 days. Clinical examination and a new 13C-urea breath test were performed 90 days after therapy. Results:, Twelve patients (eight females and four males), mean age 43 (30,58) years were included. Two patients failed to complete the treatment because of nausea and vomiting. Ten patients completed the study and took all the medications as advised. Culture was obtained in six patients: 100 and 83% of the samples were sensitive to furazolidone and levofloxacin, respectively. Per-protocol and intention-to-treat eradication rates were 100 and 83% (P = 0.019). Conclusions:, the combination of rabeprazole, levofloxacin and furazolidone in a single daily dose for 10 days constitutes a highly-effective and low-cost alternative as a third-line therapy in patients infected with H. pylori. [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] 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] Different Helicobacter pylori Strains Colonize the Antral and Duodenal Mucosa of Duodenal Ulcer PatientsHELICOBACTER, Issue 2 2000Ann-Catrin E. Thoreson Background. We have investigated the possibility that the same patients may be colonized by Helicobacter pylori strains of different genotypes or phenotypes in the antrum as compared to in the duodenum. The strains were typed for DNA fingerprints, different lipopolysaccharides (LPS), and Lewis antigen expression on the O,side chains of LPS. Materials and Methods. Polymerase chain reaction (PCR) amplifications using primer sequences (i.e., the Enterobacterial Repetitive Intergenic Consensus [ERIC]) and randomly amplified polymorphic DNA (RAPD) elements were performed to asses chromosomal DNA diversity between H. pylori strains. The expression of different LPS types and Lewis antigens in the various H. pylori isolates were determined by whole bacterial enzyme-linked immunosorbent assays using monoclonal antibodies. Results. Duodenal ulcer patients had different H. pylori genotypes in the duodenum as compared to in the antrum as shown by ERIC-PCR (44%) and by RAPD-PCR (75%). Different DNA patterns were found among the strains that were isolated from various regions of the duodenum in 4 of 16 patients (25%) as shown by ERIC-PCR and in 8 of 16 patients (50%) as shown by RAPD-PCR. Sixty-three percent of the duodenal ulcer patients had H. pylori strains with a different Lewis antigen phenotype in the duodenum as compared to in the antrum, and 3 of 16 patients (19%) had strains with different Lewis antigens expressed by strains from different duodenal biopsies from the same patient. Conclusion. The results suggest that a mixed population of different H. pylori strains with marked variation, both genotypically and phenotypically, colonize the same patient. [source] Erythrocyte Lewis (A+B,) host phenotype is a factor with familial clustering for increased risk of Helicobacter pylori -related non-cardiac gastric cancerJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006MING-JEN SHEU Abstract Background:, The purpose of the present study was to test whether host erythrocyte Lewis phenotypes correlated with the risk of gastric cancers. Because of the association of gastric cancer with familial clustering, cancer relatives were investigated as to whether they had unique distribution of Lewis phenotypes. Methods:, The study prospectively enrolled 74 Helicobacter pylori -positive gastric cancer patients and 100 H. pylori -positive duodenal ulcer patients to serve as non-cancer controls after panendoscopy. In addition, 433 family members from the 74 index cancer and 100 non-cancer control patients were enrolled. All enrolled cases were checked for their H. pylori status and erythrocyte Lewis phenotypes, defined as Lea,b,, Lea,b+, Lea+b,, and Lea+b+ subtypes by the anti-Lea and anti-Leb monoclonal antibodies. Results:, These H. pylori -infected patients with gastric cancer had a higher rate of Lea+b, phenotype and a lower rate of Lea,b+ phenotype than the non-cancer duodenal ulcer controls (20.3% vs 9%; 51.4% vs 72%, P < 0.05). Among these H. pylori -infected patients, the risk of the patients with Lea+b, phenotype having gastric cancer was 3.15-fold higher as compared with those with the Lea,b+ phenotype (P = 0.02, 95% confidence interval: 1.26,7.87). The offspring and cousins of the cancer patients had a higher rate of Lea+b, phenotype as compared to either that of the spouses of cancer index patients or to that of the family members of the non-cancer control (P < 0.05). Conclusion:, Lea+b, phenotype of the H. pylori -infected host could be a risk factor (with familial clustering) for gastric carcinogenesis. [source] Anti- Helicobacter pylori therapy in India: Differences in eradication efficiency associated with particular alleles of vacuolating cytotoxin (vacA) geneJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2003SUJIT CHAUDHURI Abstract Background and Aims:, The efficiency of Helicobacter pylori eradication varies geographically, as do many parameters that might affect therapeutic efficiency, including bacterial genotype. The aim of the present study was to determine the efficiency of H. pylori eradication using a 10-day proton pump inhibitor-based triple-therapy regimen (omeprazole, clarithromycin and amoxycillin) in an eastern Indian patient population, and to find out the relationship, if any, of the success or failure of the therapy to known features of bacterial genotype. Methods,Helicobacter pylori infections were analyzed in 66 duodenal ulcer patients by upper gastrointestinal endoscopy, rapid urease tests, histology and culture. The cytotoxin-associated gene (cagA) and vacuolating cytotoxin (vacA) gene status of cultured strains were studied by polymerase chain reaction. Treatment was given for 10 days and endoscopy was repeated at 4 and 12 weeks post therapy to monitor ulcer healing and H. pylori eradication. Results:, Ulcer healing was observed in 60 patients (96.77%). Helicobacter pylori was eradicated in 41 (62.12% intention to treat, 66.13% per protocol) of the 66 duodenal ulcer patients, but not in the other 25. The bacteria from 47 patients were genotyped. The only significant disease-associated difference in patterns observed was that the vacA m1 allele was represented more disproportionately among patients with eradication failures (68%) than in those with successful eradication (39%) (P < 0.05) No significant association of vacAs1 (signal sequence allele) or cag pathogenicity island status with persistence was detected. Conclusions:, This study highlights the public health need for cheaper, more cost-effective anti- H. pylori therapies for developing countries, and suggests that subtle features of bacterial genotype can influence therapeutic efficiency. The possibility that particular vacA mid region alleles affect persistence, perhaps through toxin action on particular gastric cell types, merits further study. [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] Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infectionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2001G. Capurso Background: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer. Aim: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer. Patients and methods: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger,Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger,Ellison Syndrome patients were H. pylori -positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes. Results: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger,Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2,21). In the follow-up period, three out of 83 (3.3%) non-Zollinger,Ellison Syndrome patients had a H. pylori -negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2). Conclusions: In H. pylori -positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal. [source] Triple therapy with clarithromycin, omeprazole, and amoxicillin for eradication of Helicobacter pylori in duodenal ulcer patients in Asia and AfricaALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2000B. C. Y. Wong Background: Studies assessing the efficacy of triple therapy containing clarithromycin and amoxicillin for the eradication of Helicobacter pylori infection and healing of duodenal ulcers in Asian and African countries are limited. Aim: To determine the efficacy and safety of 1-week triple therapy with omeprazole, amoxicillin and clarithromycin for eradicating H. pylori infection in patients with active duodenal ulcer living in Asian and African regions. Methods: This was an open-label, multicentre study in 11 centres in Asia and Africa. Patients with endoscopy-proven duodenal ulcer and who were H. pylori -positive were treated with clarithromycin 500 mg, omeprazole 20 mg, and amoxicillin 1000 mg, all given twice daily for 7 days. Upper endoscopy was repeated at week 6 to check for ulcer healing and H. pylori status. Results: A total of 117 patients were recruited. H. pylori eradication rates were 85% by per protocol analysis and 80% by intention-to-treat analysis. Ulcer healing was found in 94% of subjects (per protocol analysis). Clinical success, measured by change of pre-treatment ulcer symptoms, was strongly supported by complete resolution or improvement in 100% of the evaluable patients (per protocol analysis). Since treatment-related adverse events, when present, were largely mild or moderate, the triple therapy regimen was considered safe. Conclusion: Seven-day triple therapy with omeprazole, amoxicillin, and clarithromycin was efficacious for treating Asian and African patients with duodenal ulcer disease associated with H. pylori infection, and the treatment regimen was well-tolerated. [source] | ||||||||||