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Eradication Therapy (eradication + therapy)
Kinds of Eradication Therapy Selected AbstractsImpact of Helicobacter pylori Eradication Therapy on Histologic Change in the Distal EsophagusHELICOBACTER, Issue 4 2006Masanori Toyoda Abstract Background:, Although cases of reflux esophagitis (RE) developing after treatment to eradicate Helicobacter pylori have been discussed in some detail, no reports are available concerning the histologic examination of RE both before and after eradication therapy. Materials and methods:, Sixty-one patients and 111 specimens were investigated using endoscopic and histologic techniques. The histologic findings including basal zone height, papillar height, Ki-67 labeling index, and COX-2 expression before and after treatment for H. pylori infection were compared with those in normal controls and patients with endoscopic RE. Results:, Twelve months after eradication therapy, the incidence of newly developed endoscopic RE was 20% (5/25). Basal zone height and papillar height had increased at 1 month, but had returned to pretreatment levels after 12 months of eradication therapy. The Ki-67 labeling index was significantly increased 1 and 12 months after eradication therapy compared to values before treatment. COX-2 expression gradually increased after the treatment. The phenomena linked to esophagitis appeared after eradication therapy. However, the severity and extent of these signs were not so high after the treatment of H. pylori than those in patients with overt reflux esophagitis. Focusing on the patients with hiatal hernia, papillar height and Ki-67 labeling index increased significantly after eradication therapy, values being almost the same as those in the patients with endoscopic RE. Conclusions:, Hiatal hernia plays an important role in the possible occurrence of hidden RE after treatment for a H. pylori infection. [source] ,Rescue' Therapy with Rifabutin after Multiple Helicobacter pylori Treatment FailuresHELICOBACTER, Issue 2 2003Javier P. Gisbert abstract Aim. Eradication therapy with proton pump inhibitor, clarithromycin and amoxicillin is extensively used, although it fails in a considerable number of cases. A ,rescue' therapy with a quadruple combination of omeprazole, bismuth, tetracycline and metronidazole (or ranitidine bismuth citrate with these same antibiotics) has been recommended, but it still fails in approximately 20% of cases. Our aim was to evaluate the efficacy and tolerability of a rifabutin-based regimen in patients with two consecutive H. pylori eradication failures. Patients and Methods. Design: Prospective multicenter study. Patients: Consecutive patients in whom a first eradication trial with omeprazole, clarithromycin and amoxicillin and a second trial with omeprazole, bismuth, tetracycline and metronidazole (three patients) or ranitidine bismuth citrate with these same antibiotics (11 patients) had failed were included. Intervention: A third eradication regimen with rifabutin (150 mg bid), amoxicillin (1 g bid) and omeprazole (20 mg bid) was prescribed for 14 days. All drugs were administered together after breakfast and dinner. Compliance with therapy was determined from the interrogatory and the recovery of empty envelopes of medications. Outcome: H. pylori eradication was defined as a negative 13C-urea breath test 8 weeks after completing therapy. Results. Fourteen patients have been included. Mean age ± SD was 42 ± 11 years, 41% males, peptic ulcer (57%), functional dyspepsia (43%). All patients took all the medications and completed the study protocol. Per-protocol and intention-to-treat eradication was achieved in 11/14 patients (79%; 95% confidence interval = 49,95%). Adverse effects were reported in five patients (36%), and included: abdominal pain (three patients), nausea and vomiting (one patient), and oral candidiasis (one patient); no patient abandoned the treatment due to adverse effects. Conclusion. Rifabutin-based rescue therapy constitutes an encouraging strategy after multiple previous eradication failures with key antibiotics such as amoxicillin, clarithromycin, metronidazole and tetracycline. [source] Long-term treatment of localized gastric marginal zone B-cell mucosa associated lymphoid tissue lymphoma including incidence of metachronous gastric cancerJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2010Shouko Ono Abstract Background and Aim:, According to a few recent reports on the long-term clinical outcome of gastric marginal zone B-cell mucosa associated lymphoid tissue lymphoma (MALT lymphoma); localized gastric MALT lymphoma generally has a favorable prognosis. However, the risk of metachronous gastric cancer has not been evaluated. In this study, we analyzed long-term outcomes of localized gastric MALT lymphoma including the incidence of metachronous gastric cancer. Methods:, Between April 1996 and May 2008, 60 patients (31 men and 29 women; mean age 58.1 years) with localized gastric MALT lymphoma (stage I and II1 according to Lugano classification) were analyzed retrospectively. Results:, Forty-eight patients (82.6%) achieved complete remission by eradication therapy. Radiation therapy was conducted on eight patients as second-line treatment, and all of them achieved remission. The median follow-up period was 76 months (range, 12,157 months). One patient had local relapse after remission for 5 years and three patients developed early gastric cancer without recurrence of lymphoma (5%). All of the three gastric cancers appeared in the same areas where MALT lymphoma had been eradicated. Conclusion:, Eradication therapy and radiation therapy for localized gastric MALT lymphoma have a favorable long-term outcome, though regular follow-up endoscopy should be performed for detecting metachronous early gastric cancer. [source] The long-term efficacy of Helicobacter pylori eradication therapy in patients with idiopathic thrombocytopenic purpuraJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2007Masaaki Satake Abstract Background and Aim:, A beneficial effect of Helicobacter pylori (H. pylori) eradication in patients with H. pylori -positive idiopathic thrombocytopenic purpura (ITP) has been reported by several investigators; however, it was not clear whether the recovered platelet count after H. pylori eradication was maintained for a long period. Method:, Thirty-eight ITP patients who were examined for H. pylori infection were assessed. H. pylori -positive patients received a standard antibiotic therapy for H. pylori eradication. We investigated the long-term effect of H. pylori eradication on platelet recovery in patients with H. pylori -positive ITP. Results:, Of the 38 ITP patients, 26 (68.4%) were positive for H. pylori. The response rate of platelet recovery was 56.5% (13/23 patients). Twelve patients showed complete response (CR) and one showed partial response (PR). The mean platelet counts 6 months after eradication significantly increased from 31 × 109/L to 129 × 109/L in 23 H. pylori -eradicated patients (P < 0.001). The median platelet counts of responders 1, 2, 3, and 4 years after eradication were 168 × 109/L (n = 10), 193 × 109/L (n = 9), 168 × 109/L (n = 7), and 243 × 109/L (n = 4) after a mean follow-up of 25.8 months. Conclusion:, Eradication therapy for H. pylori -positive patients with ITP was effective and a favorable effect was maintained for long periods. [source] Clinical trial: the combination of rifaximin with partially hydrolysed guar gum is more effective than rifaximin alone in eradicating small intestinal bacterial overgrowthALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010M. Furnari Aliment Pharmacol Ther 2010; 32: 1000,1006 Summary Background, Abnormal intestinal clearance is involved in the pathogenesis of small intestinal bacterial overgrowth (SIBO). It is known that partially hydrolysed guar gum affects intestinal motility. Eradication therapy of SIBO is based on antibiotic treatment: no data are available on the role of fibre supplementation in eradicating SIBO. Aim, To assess whether the combination of partially hydrolysed guar gum and rifaximin is more effective than rifaximin alone in the treatment of SIBO. Methods, A 50 g-glucose breath test was given to 500 consecutive patients. Patients with a positive glucose breath test and predisposing conditions to SIBO entered into the study, and were randomized to receive rifaximin 1200 mg/day or rifaximin 1200 mg/day plus partially hydrolysed guar gum 5 g/day for 10 days. Patients completed a symptom questionnaire and glucose breath test both in basal condition and 1 month after withdrawal of therapy. Results, Seventy-seven patients had SIBO. Eradication rate of SIBO was 62.1% in the rifaximin group (both on per-protocol and intention-to-treat analyses), and 87.1% (per-protocol, P = 0.017) and 85.0% (intention-to-treat, P = 0.036) in the rifaximin-plus-partially hydrolysed guar gum group. Clinical improvement was observed in 86.9% and 91.1% of eradicated cases in rifaximin and rifaximin-plus-partially hydrolysed guar gum groups respectively (P = 0.677). Conclusion, The combination of rifaximin with partially hydrolysed guar gum seems to be more useful in eradicating SIBO compared with rifaximin alone. [source] Effect of triple therapy on eradication of canine gastric helicobacters and gastric diseaseJOURNAL OF SMALL ANIMAL PRACTICE, Issue 1 2000I. Happonen Nine helicobacter-positive pet dogs with upper gastrointestinal signs were studied to evaluate the effect of a triple therapy, normally applied to humans for the eradication of gastric helicobacters, on clinical signs and gastric histology, as well as the recurrence of helicobacters after eradication in an extended follow-up in four dogs. Endoscopy was performed at entry to the study and repeated after eradication therapies and additional treatments. If the triple therapy (amoxycillin, metronidazole and bismuth subcitrate) failed, tetracycline and omeprazole were prescribed. Additional therapies were instituted if clinical signs persisted after eradication therapies. Helicobacter status was verified from gastric biopsy specimens by the urease test and histological examination, and in a few dogs also by brush cytology. Triple therapy eradicated gastric helicobacters in 7/9 dogs; gastric helicobacters were also eradicated in one dog treated with tetracycline and omeprazole. Eradication of helicobacters resulted in significant improvement, but not total resolution, of clinical signs. Subsequent additional therapies resulted in further alleviation of clinical signs. Neither triple therapy nor additional therapies had a significant effect on gastric histological changes. Gastric helicobacters recurred in 4/4 dogs within three years of the eradication treatment. Because canine gastric helicobacters alone were not definitively shown to induce clinical signs, routine eradication therapy seems not to be warranted at present. [source] Comparison of efficacies of dual therapy and triple therapy using rabeprazole in second-line eradication of Helicobacter pylori in JapanALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2006T. KAWAI Summary Background The only authorized second-line Helicobacter pylori regimen in Japan is proton pump inhibitor + amoxycillin + clarithromycin. However, it has been reported that this second-line regimen is not effective. In this study, we evaluated the efficacy of dual and triple eradication therapies using rabeprazole as second-line H. pylori eradication regimens. Aim To evaluate the efficacy of dual and triple eradication therapies using rabeprazole as second-line H. pylori eradication therapy. Methods Sixty-two H. pylori -positive patients with first-line eradication failure were randomly assigned to two groups. The RAM group was administered rabeprazole 20 mg + amoxycillin 1500 mg + metronidazole 500 mg daily for 1 week. The RA group was administered rabeprazole 40 mg + amoxycillin 2000 mg daily for 2 weeks. Eradication of H. pylori infection was determined by 13C-urea breath testing at 8 weeks after completion of treatment. Prior to treatment, amoxycillin, clarithromycin and metronidazole susceptibility, and CYP2C19 phenotype status were determined. Results Eradication rates for the RAM and RA groups were 97% and 74%, respectively. Eradication rates were not influenced by CYP2C19 phenotype in either group. Eradication rates for clarithromycin-resistant patients were 100% in the RAM group and 77% in the RA group. Conclusions One week with RAM therapy and 2 weeks with RA therapy were effective as second-line eradication therapy for H. pylori infection; moreover, RAM was more effective than RA therapy. [source] Effectiveness of Helicobacter pylori eradication treatments in a primary care setting in ItalyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2002P. Della Monica To evaluate the choice and relative effectiveness of Helicobacter pylori eradication regimens in a primary care setting. Patients and methods: Patients referred to our department, who had been treated for H. pylori infection during the preceding 6 months, were enrolled between September 1998 and July 1999. H. pylori status was assessed by urea breath test. Information on the drugs administered, compliance and side-effects was recorded. Results: The mean eradication rate was 72% in patients receiving their first course of treatment (1863 cases; 45% male; mean age, 53 ± 14 years); a double therapy regimen was prescribed to 14% of patients, triple therapy to 85% and quadruple therapy to 1%. Maastricht Consensus proton pump inhibitor-based regimens were prescribed in 80% of cases, with a mean eradication rate of 73%. No statistically significant correlation was found between eradication failure and sex, age, endoscopic findings or administered treatment. Conclusions: In Italy, in a primary care setting, first-line H. pylori eradication therapies reflect international guidelines. The efficacy of such regimens is lower than that reported by controlled trials. These results are relevant when making pharmacoeconomic evaluations of H. pylori management. [source] Current concepts in the management of Helicobacter pylori infection,The Maastricht 2-2000 Consensus ReportALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2002P. Malfertheiner Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21,22 September 2000. A ,test and treat' approach is recommended in adult patients under the age of 45 years (the age cut-off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro-oesophageal reflux disease symptoms, non-steroidal anti-inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test. As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low-grade gastric mucosa-associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first-degree relatives of gastric cancer patients and according to patients' wishes after full consultation. It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long-term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro-oesophageal reflux disease in most cases, and does not exacerbate existing gastro-oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non-steroidal anti-inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non-steroidal anti-inflammatory drugs. Treatment should be thought of as a package which considers first- and second-line eradication therapies together. First-line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second-line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second-line therapy should be with proton pump inhibitor-based triple therapy. If second-line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case-by-case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradica- tion should always be confirmed by urea breath test or an endoscopy-based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available. [source] ORIGINAL ARTICLE: In vitro and in vivo effects of the Mongolian drug Amu-ru 7 on Helicobacter pylori growth and viabilityMICROBIOLOGY AND IMMUNOLOGY, Issue 9 2010Cui Lan Bai ABSTRACT Amu-ru 7, a Mongolian folk medicine, is used to treat digestive diseases such as gastritis and gastric and duodenal ulcers. We examined the effect of Amu-ru 7 on the growth and viability of Helicobacter pylori in vivo and in vitro. By the agar dilution method, the MIC of Amu-ru 7 for H. pylori strains was shown to be 100,200 ,g/mL with a MIC90 of 200 ,g/mL. Two hundred micrograms per milliliter of Amu-ru 7 exhibited potent bactericidal activity against H. pylori in the stationary phase of growth 6 hr after treatment. Amu-ru 7 inhibited the growth of both AMPC-resistant and CAM-resistant strains, and also had a combined effect with AMPC on AMPC-resistant strain 403. The Amu-ru 7 inhibited biofilm formation by H. pylori and induced morphological changes, such as bleb-like formation and shortening of the cell. Although colonization of the stomach of the Mongolian gerbil by H. pylori was not cured by treatment with Amu-ru 7, both the mean number of H. pylori colonized and the colonization rate were decreased in Amu-ru 7 treated gerbils. These results suggest the effectiveness Amu-ru 7 as an adjunct therapy for eradication therapies consisting of a PPI combined with antibiotics. [source] RECENT PROGRESS IN ENDOSCOPY-BASED DIAGNOSIS OF HELICOBACTER PYLORI INFECTIONDIGESTIVE ENDOSCOPY, Issue 1 2001Tadashi Sato Numerous invasive and non-invasive tests are available in the detection of Helicobacter pylori. Endoscopy-based tests that include rapid urease test, histological examination and culture are important generally in the assessment of H. pylori status before eradication therapy. Recently, several new endoscopy-based diagnostic methods have been developed aiming at rapid and accurate detection of the organisms. It would be possible to diagnose H. pylori infection in treated patients by using these new highly sensitive tests. Although the diagnosis of H. pylori infection itself is possible by using non-invasive diagnostic tests, endoscopy-based tests provide not only the diagnosis of the organisms, but also the exclusive information such as treatment indications and the susceptibility for the antimicrobial drugs. Recently, new triple therapy including clarithromycin has been widely performed in Japan. Along with an increase in the prevalence of the antibiotic-resistant strains, culture may become a more important diagnostic method in the future. The inappropriate application of the tests may increase the potential risk of the misdiagnosis and the treatment failures. The diagnostic method should be selected by taking into account the circumstances in which a diagnosis is to be performed. [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] Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in JapanEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2005T. Inaba Abstract Background, The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients. Materials and methods, Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 × 109 L,1 were defined as idiopathic thrombocytopenic purpura responders. Results,Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 × 109 L,1 in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori -negative patients experienced the same improvement (P = 0·015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0·015). Conclusions,Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity. [source] Laboratory identification of factor VIII inhibitors in the real world: the experience from AustralasiaHAEMOPHILIA, Issue 4 2010E. J. FAVALORO Summary., The laboratory has a key role in the initial detection of factor inhibitors and an ongoing role in the measurement of inhibitor titres during the course of inhibitor eradication therapy. The most commonly seen factor inhibitors are those directed against factor VIII (FVIII), usually detected either using the original or Nijmegen-modified Bethesda assay. In view of previously demonstrated high variability in laboratory results for inhibitor assays, we have more extensively examined laboratory performance in the identification of FVIII inhibitors. Over the past 3 years, we conducted two questionnaire-based surveys and two wet-challenge surveys utilizing eight samples comprising no FVIII inhibitor (n = 1), or low-titre (n = 2), medium-titre (n = 3) or high-titre (n = 2) FVIII inhibitor. Four samples were tested by 42 laboratories in 2007, and four by 52 laboratories in 2009. High inter-laboratory variation was evident, with CVs around 50% not uncommon, and some 10% of all laboratories (or around 15% of laboratories using Bethesda method) failed to detect low-level inhibitors of around 1 BU mL,1. Laboratories using the Nijmegen method appeared to perform better than those using a standard Bethesda assay, with lower evident assay variation and no false negatives. There was a wide variety of laboratory practice, with no two laboratories using exactly the same process for testing and interpretation of factor inhibitor findings. In conclusion, our study indicates that there is still much need for standardization and improvement in factor inhibitor detection, and we hope that our findings provide a basis for future improvements in this area. [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] 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] Annual Change of Primary Resistance to Clarithromycin among Helicobacter pylori Isolates from 1996 through 2008 in JapanHELICOBACTER, Issue 5 2009Noriyuki Horiki Abstract Background:, Recent studies have shown that the combination of proton pump inhibitor, amoxicillin and clarithromycin is one of the best choices for Helicobacter pylori eradication therapy. However, increasing number of cases of H. pylori infection showing resistance to clarithromycin therapy has been reported and this is currently the main cause of eradication failure. We investigated the annual changes of the antimicrobial susceptibility to clarithromycin, amoxicillin and minocycline during a period of 12 years in Japan. Methods:, This study comprised 3521 patients (mean age (SD), 55.4 (13.7) years-old, 2467 males and 1054 females) positive for H. pylori as assessed by microaerobic bacterial culture from 1996 through 2008. All patients were previously untreated for H. pylori and were enrolled in the study to assess primary resistance to the three antibiotics. Results:, The overall primary resistance to clarithromycin, amoxicillin and minocycline were 16.4%, (577/3521), 0.03% (1/3521) and 0.06% (2/3521), respectively. From1996 through 2004, the resistance rate to clarithromycin increased gradually to approximately 30% and then it remained without marked fluctuation since 2004. Analysis by gender showed a significant increase (p < .0001) in resistance rate to clarithromycin among females (217/1057, 20.6%) compared to males (360/2467, 14.6%). Analysis by age, disclosed significantly (p < .0001) higher resistance rate to clarithromycin in patients of more than 65-years-old compared to the younger population. Conclusions:, The resistance rate of H. pylori infection to clarithromycin in Japan has increased gradually to approximately 30% from 1996 through 2004, and remained unchanged since 2004. Elderly and females were at high risk of having resistance to clarithromycin. Our results suggested that the level of clarithromycin resistance in Japan has now risen to the point where it should no longer be used as empiric therapy. [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] Rabeprazole- versus Esomeprazole-Based Eradication Regimens for H. pylori InfectionHELICOBACTER, Issue 6 2007I-Chen Wu Abstract Background: Different kinds of proton pump inhibitor-based triple therapies could result in different Helicobacter pylori eradication rates. Aim: The aims of this study were to compare the efficacy and safety of rabeprazole- and esomeprazole-based triple therapy in primary treatment of H. pylori infection in Taiwan. Patients and Methods: From June 2005 to March 2007, 420 H. pylori -infected patients were randomly assigned to receive a 7-day eradication therapy with either esomeprazole 40 mg daily (EAC group, n = 209) or rabeprazole 20 mg b.i.d. (RAC group, n = 211) in combination with amoxicillin 1 g b.i.d. and clarithromycin 500 mg b.i.d.. Follow-up endoscopy with biopsy was done 12,16 weeks after completion of eradication therapy. Those who refused endoscopic exams underwent 13C-urea breath test to assess the treatment response. Results: Intention-to-treat analysis revealed that the eradication rate was 89.4% in the EAC group and 90.5% in RAC groups (p -value = .72). All of the subjects returned for assessment of compliance (100% in EAC group vs. 99.5% in RAC group, p -value = .32) and adverse events (3.83% in EAC group vs. 6.16% in RAC group, p -value = .27). Sixty (28.7%) and 37 (17.6%) patients in EAC and RAC group, respectively, refused endoscopy and underwent a 13C-urea breath test to determine the treatment effect. Conclusion: In conclusion, rabeprazole- and esomeprazole-based primary therapies for H. pylori infection are comparable in efficacy and safety. [source] Double-Dose, New-Generation Proton Pump Inhibitors Do Not Improve Helicobacter pylori Eradication RateHELICOBACTER, Issue 6 2007Hyo Sun Choi Abstract Background: Up to present, omeprazole plus two antibiotics are used for Helicobacter pylori eradication therapy . Few studies have compared double-dose new-generation, proton pump inhibitors (PPI) with omeprazole. Therefore, we conducted a randomized, prospective study to evaluate differences in H. pylori eradication rates by PPI type. Material and Methods: Between January 2006 and December 2006, 576 consecutive patients with proven H. pylori infection were enrolled prospectively. Four different PPIs [omeprazole 20 mg b.i.d. (old generation), or pantoprazole 40 mg b.i.d., rabeprazole 20 mg b.i.d., or esomeprazole 40 mg b.i.d. (new generation)] were added to clarithromycin (500 mg b.i.d.) and amoxicillin (1 g b.i.d.) for 1 week. Results: By intention-to-treat analysis, no difference was found between the eradication rates of these four PPIs: 64.9% (omeprazole, n = 148), 69.3% (pantoprazole, n = 140), 69.3% (rabeprazole, n = 140), and 72.9% (esomoprazole, n = 148). When eradication rates were analyzed according to whether patients had an ulcer or not on a per-protocol basis, no difference was found between the eradication rates of the four PPIs. However, side-effects were more common in the esomeprazole-based triple therapy group than in the other groups (p < .05). Conclusions: No convincing evidence was obtained that double-dose new-generation PPIs have better H. pylori eradication rates and tolerability than omeprazole. [source] Eradication of Helicobacter pylori Does Not Reduce the Incidence of Gastroduodenal Ulcers in Patients on Long-term NSAID Treatment: Double-Blind, Randomized, Placebo-Controlled TrialHELICOBACTER, Issue 5 2007Helena T.J.I. De Leest Abstract Background:,,Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are the major causes of gastroduodenal ulcers. Studies on the benefit of eradication of H. pylori in NSAID users yielded conflicting results. Objective:, To investigate whether H. pylori eradication in patients on long-term NSAIDs reduces the incidence of gastroduodenal ulcers. Methods:, Patients on long-term NSAID treatment and who are H. pylori positive on serologic testing, were randomly assigned to either H. pylori eradication (omeprazole, amoxicillin, and clarithromycin) or placebo. Primary endpoint was the presence of endoscopic gastric or duodenal ulcers 3 months after randomization. Results:, One hundred sixty-five (48%) of a total of 347 patients were on gastroprotective medication. At endoscopy, gastroduodenal ulcers were diagnosed in 6 (4%) and 8 (5%) patients in the eradication and placebo group, respectively (p = .65). During follow-up of 12 months, no symptomatic ulcers or ulcer complications developed. No significant differences were found in the development of gastroduodenal erosions, dyspepsia, or in quality of life. Conclusion:,H. pylori eradication therapy in patients on long-term NSAID treatment had no beneficial effect on the occurrence of ulcers, erosions, or dyspepsia. Ulcer rates in both study arms are remarkably low, in both patients with and without gastroprotective therapy. [source] Impact of Helicobacter pylori Eradication Therapy on Histologic Change in the Distal EsophagusHELICOBACTER, Issue 4 2006Masanori Toyoda Abstract Background:, Although cases of reflux esophagitis (RE) developing after treatment to eradicate Helicobacter pylori have been discussed in some detail, no reports are available concerning the histologic examination of RE both before and after eradication therapy. Materials and methods:, Sixty-one patients and 111 specimens were investigated using endoscopic and histologic techniques. The histologic findings including basal zone height, papillar height, Ki-67 labeling index, and COX-2 expression before and after treatment for H. pylori infection were compared with those in normal controls and patients with endoscopic RE. Results:, Twelve months after eradication therapy, the incidence of newly developed endoscopic RE was 20% (5/25). Basal zone height and papillar height had increased at 1 month, but had returned to pretreatment levels after 12 months of eradication therapy. The Ki-67 labeling index was significantly increased 1 and 12 months after eradication therapy compared to values before treatment. COX-2 expression gradually increased after the treatment. The phenomena linked to esophagitis appeared after eradication therapy. However, the severity and extent of these signs were not so high after the treatment of H. pylori than those in patients with overt reflux esophagitis. Focusing on the patients with hiatal hernia, papillar height and Ki-67 labeling index increased significantly after eradication therapy, values being almost the same as those in the patients with endoscopic RE. Conclusions:, Hiatal hernia plays an important role in the possible occurrence of hidden RE after treatment for a H. pylori infection. [source] Gastric Acidity in Patients with Follicular Gastritis is Significantly Reduced, but Can be Normalized After Eradication for Helicobacter pyloriHELICOBACTER, Issue 3 2005Tomohiko Shimatani ABSTRACT Background., Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear. Materials and methods., We assessed gastric acidity in 15 patients with follicular gastritis, aged 20,37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori -positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori -negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori. Results., During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p < .0001), and in antrum-predominant gastritis (p < .001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p < .001), in antrum-predominant gastritis (p < .001), and in pangastritis (p < .05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p < .0001) and in antrum-predominant gastritis (p < .001), whereas serum gastrin was significantly higher than that in normals (p < .0001), in antrum-predominant gastritis (p < .01) and in pangastritis (p < .05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals. Conclusions., In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori -infection,induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis. [source] Amoxicillin Resistance in Helicobacter pylori: Studies from Tokyo, Japan from 1985 to 2003HELICOBACTER, Issue 1 2005Kazuhiro Watanabe ABSTRACT Background., Previous reports revealed no resistant strains of amoxicillin (AMPC), which is usually used in eradication therapy for H. pylori infection. However, the frequency and evolution of natural AMPC-resistant strains in the Japanese population remains unknown. Aim., To assess the prevalence of H. pylori resistance against AMPC in the Tokyo area, a collection of 648 H. pylori strains isolated from patients with GI diseases from 1985 to 2003 was tested for their sensitivity to AMPC. Methods., The susceptibility of the strains was assessed by determination of the minimal inhibitory concentration (MIC) using the E -test and/or the Dry-plate method. The susceptibility breakpoints of AMPC for H. pylori were: sensitive (AMPC-S); MIC < 0.04 µg/ml, intermittent resistance (AMPC-I); 0.04,1, resistant (AMPC-R); > 1. Results., No AMPC-R strains were detected in the strains isolated between 1985 and 1996, while the rate of resistance was determined to be 1.1%, 2.1%, 5.4%, 5.6%, 0%, 8.8%, and 1.5% every year, respectively, from 1997 to 2003. The percentage of AMPC-I strains increased from 2000 to 2003. The total eradication rate of H. pylori in the patients who received triple therapy containing AMPC was 81.4% (214/263). Classified as above, the rates of AMPC-S, AMPC-I, and AMPC-R were 84.6%, 77.8%, 25%, respectively. Conclusion.,H. pylori resistance to AMPC is still rare in Japan, although the percentage of AMPC-I strains has increased over the last 4 years. The frequency of isolation of strains showing true resistance to AMPC may increase in the future, along with an increase in the frequency of isolation of AMPC-I strains. [source] Serum Antibodies to Helicobacter pylori and its Heat-Shock Protein 60 Correlate with the Response of Gastric Mucosa-Associated Lymphoid Tissue Lymphoma to Eradication of H. pyloriHELICOBACTER, Issue 3 2004Ryuta Takenaka ABSTRACT Background and aims., Eradication of Helicobacter pylori leads to regression of mucosa-associated lymphoid tissue (MALT) lymphomas. In this study, we measured serum antibodies to H. pylori and H. pylori- recombinant heat-shock protein 60 (rHSP60) in patients with gastric MALT lymphoma to determine whether humoral immune responses to the bacterial antigens correlate with the efficacy of eradication therapy. Methods., Serum samples were obtained from 33 patients with H. pylori -positive gastric MALT lymphoma before undergoing therapy to eradicate the bacteria. Anti- H. pylori antibodies were measured in a commercial assay and in immunoassays to lysates and rHSP60 which were prepared from ATCC 43504 strain. Results.,Helicobacter pylori were eradicated in all 33 patients, and the lymphoma completely regressed histologically in 26 patients (79%). Pre-treatment titers of serum antibody to H. pylori and to rHSP60 in the patients whose tumor regressed were significantly higher than titers in patients whose tumors did not regress (p = .0011 and .035, respectively). By logistic regression analysis, age (odds ratio = 0.88, 95% confidence interval = 0.80,0.99), endoscopic appearance (0.053, 0.004,0.65), titers of anti- H. pylori antibodies (67.6, 2.5,1800), and titers of anti-rHSP60 antibody (6.4, 1.2,36) were identified as significantly associated factors with the outcome of MALT lymphoma. Conclusions., Measurement of serum antibodies to H. pylori and HSP60 might be useful for predicting the response of gastric MALT lymphoma to eradication of H. pylori. [source] Pharmacoeconomics of Gastrointestinal Drug Utilisation Prior and Post Helicobacter pylori EradicationHELICOBACTER, Issue 1 2004Rogier M. Klok ABSTRACT Background., Eradication of Helicobacter pylori prevents recurrence of peptic ulcer. In pharmacoeconomic analyses it is often presumed that after successful eradication no more gastrointestinal drugs are used. We investigated this presumed positive monetary effect using General Practitioners prescribing data, including information in diagnosis. Methods., From the RNG-database we identified patients with a H. pylori eradication in the years 1997,2000. H. pylori eradication was defined as a prescription of two antibiotics and one gastrointestinal drug on the same day. Patients were divided into a group with diagnosed ulcers and a group without diagnosed ulcers. Gastrointestinal drug costs were calculated for 4 months prior to eradication and 9,12 months post eradication. For comparison costs in all periods were expressed per patient per period. For statistical analysis the paired t -test was used. Results., One hundred and two patients were eligible for evaluation. Of these patients 35 had a diagnosed ulcer and 67 had not. Generally the number of patients on gastrointestinal drugs decreased (61% prior vs. 33% post), however, the drug costs did not change (,33 prior vs. ,34 post). Costs for proton pump inhibitors increased post eradication (,14 prior vs. ,28 post). The ulcer and nonulcer group showed similar results. Conclusion.,Helicobacter pylori eradication is thought to be cost effective, however, we did not find a decrease in costs for all gastrointestinal drugs. There may be a great pharmacoeconomical advantage when it is possible to predict which patients are more likely to ,fail' eradication therapy. [source] Impact of Helicobacter pylori on the Development of Vitamin B12 Deficiency in the Absence of Gastric AtrophyHELICOBACTER, Issue 6 2002Ender Serin Abstract Background. Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Materials and Methods. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori -infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. Results. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p < .01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p < .001). Conclusion. The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with nonulcer dyspepsia and minimal or no gastric atrophy. [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] Effect of Helicobacter pylori infection on cyclooxygenase-2 expression in gastric antral mucosaJOURNAL OF DIGESTIVE DISEASES, Issue 2 2002Hong LU OBJECTIVE: Helicobacter pylori infection is a major etiological cause of chronic gastritis. Inducible cyclooxygenase (COX-2) is an important regulator of mucosal inflammation. Recent studies indicate that expression of COX-2 may contribute to gastrointestinal carcinogenesis. The aim of this study was to investigate the effects of H. pylori infection and eradication therapy on COX-2 expression in gastric antral mucosa. METHODS: Antral biopsies were taken from 46 H. pylori- infected patients, who also had chronic gastritis, both before and after anti- H. pylori treatment. The COX-2 protein was stained by using immunohistochemical methods and COX-2 expression was quantified as the percentage of epithelial cells expressing COX-2. Gastritis and H. pylori infection status were graded according to the Sydney system. RESULTS: Cyclooxygenase-2 expression was detected in the cytoplasm of gastric antral epithelial cells both before and after the eradication of H. pylori. Cyclooxygenase-2 expression in mucosa with H. pylori infection was compared with the corresponding mucosa after successful H. pylori eradication (20.1 ± 13.1%vs 13.8 ± 5.9%; P < 0.05). At the same time, COX-2 expression in H. pylori -infected mucosa was compared with the normal controls (18.0 ± 14.1%vs 12.3 ± 4.6%, P < 0.05). Expression of COX-2 was correlated with the degree of chronic inflammation (r= 0.78, P < 0.05). CONCLUSIONS: Our results showed that H. pylori infection leads to gastric mucosal overexpression of COX-2 protein, suggesting that the enzyme is involved in H. pylori -related gastric pathology in humans. [source] |