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  • 1
    Keywords: Helicobacter pylori. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (209 pages)
    Edition: 1st ed.
    ISBN: 9780323395663
    Series Statement: The Clinics: Internal Medicine Series ; v.Volume 44-3
    DDC: 616.33014
    Language: English
    Note: Front Cover -- Managementof Helicobacterpylori-Related Diseases -- Copyright -- Contributors -- CONSULTING EDITOR -- EDITORS -- AUTHORS -- Contents -- Foreword: Helicobacter pylori -- Preface: Helicobacter pylori: New Thoughts and Practices -- Diagnosis of Helicobacter pylori Infection in the Proton Pump Inhibitor Era -- Practical Aspects in Choosing a Helicobacter pylori Therapy -- How to Effectively Use Bismuth Quadruple Therapy: The Good, the Bad, and the Ugly -- Is There a Role for Probiotics in Helicobacter pylori Therapy? -- Molecular Approaches to Identify Helicobacter pylori Antimicrobial Resistance -- When Is Endoscopic Follow-up Appropriate After Helicobacter pylori Eradication Therapy? -- Gastric Cancer Risk in Patients with Helicobacter pylori Infection and Following Its Eradication -- Molecular Pathogenesis of Helicobacter pylori-Related Gastric Cancer -- Helicobacter pylori Eradication to Eliminate Gastric Cancer: The Japanese Strategy -- Treatment Strategy for Gastric Mucosa-Associated Lymphoid Tissue Lymphoma -- Rationale for a Helicobacter pylori Test and Treatment Strategy in Gastroesophageal Reflux Disease -- Screening to Identify and Eradicate Helicobacter pylori Infection in Teenagers in Japan -- Current Status and Prospects for a Helicobacter pylori Vaccine -- GASTROENTEROLOGY CLINICS OF NORTH AMERICA -- FORTHCOMING ISSUES -- December 2015 -- March 2016 -- June 2016 -- RECENT ISSUES -- June 2015 -- March 2015 -- December 2014 -- Helicobacter pylori -- Helicobacter pylori: New Thoughts and Practices -- Diagnosis of Helicobacter pylori Infection in the Proton Pump Inhibitor Era -- Key points -- INTRODUCTION -- INVASIVE TESTS -- Histology -- Culture -- Rapid urease test -- Molecular tests -- Noninvasive Tests -- Urea breath test -- Stool antigen tests -- SEROLOGY. , SUMMARY: DIAGNOSIS OF HELICOBACTER PYLORI INFECTION IN THE PROTON PUMP INHIBITORS ERA -- ACKNOWLEDGMENTS -- REFERENCES -- Practical Aspects in Choosing a Helicobacter pylori Therapy -- Key points -- INTRODUCTION -- Why Is Helicobacter pylori Difficult to Treat? -- CHOICE OF THERAPY -- FIRST-LINE REGIMENS -- Nonbismuth Quadruple Therapies -- Sequential therapy -- Concomitant therapy -- Hybrid (sequential-concomitant) therapy -- Bismuth Quadruple Therapy -- RESCUE THERAPY -- Fluoroquinolone-Containing Therapy -- Bismuth Quadruple Therapy, Including Furazolidone-Containing Regimens -- Rifabutin-Containing Therapy -- PROBIOTICS -- SUMMARY -- REFERENCES -- How to Effectively Use Bismuth Quadruple Therapy -- Key points -- BACKGROUND -- BISMUTH IN THE ERA OF NEW CONCEPTS REGARDING PATHOGENESIS AND TREATMENT OF PEPTIC ULCER -- BISMUTH QUADRUPLE THERAPY FOR H PYLORI ERADICATION -- THE EFFECT OF METRONIDAZOLE RESISTANCE AS EXAMINED BY META-ANALYSIS -- CALCULATION OF THE EFFECTIVENESS OF BISMUTH QUADRUPLE THERAPY -- ADHERENCE (COMPLIANCE) WITH BISMUTH QUADRUPLE THERAPY -- Adherence to the Protocol -- HOW TO MAKE BISMUTH QUADRUPLE THERAPY MORE ACCEPTABLE -- DOXYCYCLINE -- EXAMINATION OF OUTCOME IN REGIONS WHERE BISMUTH QUADRUPLE THERAPY FREQUENTLY FAILS (EG, TURKEY AND IRAN) -- BISMUTH, TETRACYCLINE, AMOXICILLIN, PROTON PUMP INHIBITORS QUADRUPLE THERAPY -- BISMUTH SEQUENTIAL THERAPIES -- INFORMATION NEEDED TO OBTAIN GENERALIZABLE RESULTS -- ISSUES RIPE FOR SYSTEMATIC STUDY -- Relation of Drug Administration and Meals -- Reduction of Side Effects with Bismuth Quadruple Therapy -- PROTON PUMP INHIBITORS DOSAGE -- EFFICIENT STUDY DESIGN -- RECOMMENDATIONS -- REFERENCES -- Is There a Role for Probiotics in Helicobacter pylori Therapy? -- Key points -- WHAT PROBIOTICS ARE -- PROBIOTICS -- Use of Probiotics Clinically. , PROBIOTICS AS ADJUVANT THERAPY FOR HELICOBACTER PYLORI ERADICATION -- PROBIOTICS AS CURE FOR HELICOBACTER PYLORI INFECTION -- SUMMARY -- REFERENCES -- Molecular Approaches to Identify Helicobacter pylori Antimicrobial Resistance -- Key points -- MOLECULAR DETERMINATION OF HELICOBACTER PYLORI RESISTANCE TO MACROLIDES -- Mechanisms -- Methods -- Real-time polymerase chain reaction for detection of Helicobacter pylori resistance to macrolides -- Principle -- Advantages of this procedure -- Variants of the method -- The TaqMan format -- Advantages and limitations -- The scorpion format -- Multiplex polymerase chain reaction followed by strip hybridization -- Advantages and limits -- Dual priming oligonucleotide-polymerase chain reaction -- Other polymerase chain reaction-based assays -- Nested polymerase chain reaction followed by sequencing or standard polymerase chain reaction followed by sequencing or res ... -- Allele-specific primer polymerase chain reaction -- Primer mismatch polymerase chain reaction -- Invader assay for single nucleotide polymorphism genotyping -- Non-polymerase chain reaction-based assays -- Fluorescence in situ hybridization -- Advantages -- Peptide nucleic acid-fluorescence in situ hybridization -- Other methods -- Correlation with Clinical Outcome -- MOLECULAR DETERMINATION OF HELICOBACTER PYLORI RESISTANCE TO FLUOROQUINOLONES -- Mechanisms -- Methods -- Real-time polymerase chain reaction -- Multiplex polymerase chain reaction followed by strip hybridization -- Other polymerase chain reaction-based assays -- Sequencing of the gyrA quinolone resistance-determining region -- Allele-specific polymerase chain reaction -- Correlation with Clinical Outcome -- MOLECULAR DETERMINATION OF HELICOBACTER PYLORI RESISTANCE TO TETRACYCLINE -- Mechanisms -- Methods -- Real-time polymerase chain reaction. , Standard polymerase chain reaction followed by sequencing or polymerase chain reaction-restriction length polymorphism -- MOLECULAR DETERMINATION OF HELICOBACTER PYLORI RESISTANCE TO OTHER ANTIBIOTICS -- Rifampins -- Amoxicillin -- 5-Nitroimidazoles -- REFERENCES -- When Is Endoscopic Follow-up Appropriate After Helicobacter pylori Eradication Therapy? -- Key points -- INTRODUCTION -- HELICOBACTER PYLORI ERADICATION -- UNINVESTIGATED AND NONULCER DYSPEPSIA -- PEPTIC ULCER -- PREMALIGNANT GASTRIC LESIONS AND EARLY GASTRIC CANCER -- HEREDITARY RISK FOR GASTRIC CANCER -- MUCOSA-ASSOCIATED LYMPHOID TISSUE LYMPHOMA -- SUMMARY -- REFERENCES -- Gastric Cancer Risk in Patients with Helicobacter pylori Infection and Following Its Eradication -- Key points -- INTRODUCTION -- HELICOBACTER PYLORI INFECTION IS THE MOST IMPORTANT DETERMINANT OF GASTRIC CANCER RISK -- GASTRIC CANCER RISK: EPIDEMIOLOGIC TRENDS -- GASTRIC CANCER RISK: THE ASSESSMENT -- Demographics -- Noninvasive Methods -- Invasive Methods -- Endoscopy and biopsy protocols -- Histology -- GASTRIC CANCER RISK IN ERADICATED PATIENTS -- Helicobacter pylori Eradication as a Primary Prevention of Gastric Cancer -- How to Assess/Quantify Cancer Risk After Helicobacter pylori Eradication -- SUMMARY -- REFERENCES -- Molecular Pathogenesis of Helicobacter pylori-Related Gastric Cancer -- Key points -- INTRODUCTION -- CLASSIFICATIONS AND CHARACTERIZATIONS OF GASTRIC CANCER -- HELICOBACTER PYLORI VIRULENCE FACTORS ON GASTRIC EPITHELIUM DURING GASTRIC CARCINOGENESIS -- Roles of CagA in Gastric Carcinogenesis -- Roles of Vacuolating Cytotoxin A in Gastric Carcinogenesis -- Role of Peptidoglycan in Gastric Carcinogenesis -- HELICOBACTER PYLORI-INDUCED INFLAMMATORY RESPONSES DURING GASTRIC CARCINOGENESIS -- GENETIC AND EPIGENETIC ALTERATIONS DURING GASTRIC CARCINOGENESIS. , Mechanisms of Induction of Genetic Alterations -- Deamination -- Oxidative stress -- Chromosomal instability -- Mechanisms of Induction of Epigenetic Alterations -- Mechanisms of Induction of microRNA Alterations -- SUMMARY -- REFERENCES -- Helicobacter pylori Eradication to Eliminate Gastric Cancer -- Key points -- INTRODUCTION -- PREVIOUS PREVENTIVE MEASURES FOR GASTRIC CANCER IN JAPAN -- CURRENT STATUS AND CHARACTERISTICS OF SCREENING FOR GASTRIC CANCER IN JAPAN -- THE EFFECT OF HELICOBACTER PYLORI ERADICATION FOR GASTRIC CANCER PREVENTION -- HEALTH INSURANCE COVERAGE FOR HELICOBACTER PYLORI ERADICATION THERAPY IN JAPAN -- STRATEGY FOR THE ELIMINATION OF GASTRIC CANCER IN JAPAN -- REFERENCES -- Treatment Strategy for Gastric Mucosa-Associated Lymphoid Tissue Lymphoma -- Key points -- INTRODUCTION -- PATHOGENESIS -- Helicobacter pylori -- Genetic Aberrations -- DIAGNOSIS -- Histopathology -- Endoscopic Findings -- Clinical Staging -- TREATMENTS -- Helicobacter pylori Eradication -- Strategies for Patients not Responding to Helicobacter pylori Eradication -- SUMMARY/DISCUSSION -- REFERENCES -- Rationale for a Helicobacter pylori Test and Treatment Strategy in Gastroesophageal Reflux Disease -- Key points -- INTRODUCTION -- THE EFFECT OF PROTON PUMP INHIBITOR TREATMENT ON CHRONIC HELICOBACTER PYLORI-RELATED GASTRITIS -- THE EFFECT OF HELICOBACTER PYLORI ERADICATION ON CHRONIC GASTRITIS AND ATROPHY RELATED TO HELICOBACTER PYLORI INFECTION -- GASTRITIS AND ADENOCARCINOMA IN MONGOLIAN GERBILS -- A CONTROLLED TRIAL OF PROTON PUMP INHIBITOR THERAPY IN INFECTED SUBJECTS WITH GASTROESOPHAGEAL REFLUX DISEASE -- THE CASE AGAINST HELICOBACTER PYLORI ERADICATION THERAPY IN GASTROESOPHAGEAL REFLUX DISEASE -- COST-EFFECTIVENESS ANALYSIS -- SUMMARY -- REFERENCES -- Screening to Identify and Eradicate Helicobacter pylori Infection in Teenagers in Japan. , Key points.
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  • 2
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The objective of this research was to evaluate the outcomes and costs of alternative approaches to managing patients previously treated for peptic ulcer disease and Helicobacter pylori infection.〈section xml:id="abs1-3"〉〈title type="main"〉Materials and Methods.A decision-analytic model was used to compare (1a) urease breath testing (UBT) for assessment of H. pylori status versus (1b) observation without further testing or treatment, among patients who were symptom-free following initial antimicrobial and antisecretory therapy for endoscopically demonstrated ulcer and H. pylori infection; and (2a) UBT versus (2b) repeat endoscopy with H. pylori testing, and versus (2c) repeat antimicrobial and antisecretory therapy without further testing, among patients who remained symptomatic following initial therapy.〈section xml:id="abs1-4"〉〈title type="main"〉Results.Among patients who were symptom free after initial therapy, 6.1% receiving UBT had symptomatic ulcer at one year, compared to 18.2% of those simply observed. The expected first-year cost per symptom-free patient following initial therapy was $591 for UBT compared to $480 for observation. Among patients with persistent symptoms after initial therapy, 21% receiving repeat therapy had symptomatic ulcer at one year, compared to 23.8% receiving repeat endoscopy, and 23.3% receiving UBT. Corresponding medical costs per patient were, respectively, $766, $1787 and $1122.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions.The optimal approach to managing patients following initial treatment for ulcer and H. pylori infection depends on symptom status following initial therapy. For symptomatic patients, the preferred approach is to prescribe a repeat course of antimicrobial and antisecretory therapy. For patients without symptoms following initial therapy, UBT is the preferred approach because it is associated with a threefold lower risk of symptomatic ulcer at one year, although it costs an additional $110 per patient, compared with observation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Childhood is known to be a major risk period for acquiring Helicobacter pylori infection. Studies of the epidemiology of H. pylori infection depend on the validity of the diagnostic tools used to detect the infection in the pediatric setting. This study aims to conduct a combination of diagnostic tests on the same children, evaluate the sensitivity and the specificity of IgG antibody testing compared with the 13C-urea breath test, and examine the variability in the prevalence of H. pylori infection in asymptomatic children based on the use of different diagnostic tests.Methods. 13C-urea breath test (13C-UBT), whole blood FlexSure (systemic antibodies), and OraSure (salivary antibodies) tests were conducted on 287 asymptomatic children (151 boys, 136 girls; ages 2–18 years). The three tests were conducted on each child during the same day. The prevalence was calculated using each test independently.Results. H. pylori infection was detected in 32%, 22%, or 18% of the studied children, based on UBT, OraSure, or FlexSure, respectively. A total of 103 children tested positive for any one test (92 on UBT, 8 on FlexSure, 3 on OraSure), giving a prevalence of 35% based on the “parallel” method. Only 39 children tested positive in all three tests, giving a prevalence of 14% based on the “serial” method. Using the UBT as the gold standard, the sensitivity of FlexSure and OraSure were 48% and 65%, respectively, and the specificity of both tests was greater than 95%. When we applied the parallel method, the sensitivity and specificity of the combined antibody tests (FlexSure+OraSure) compared to the UBT were 71% and 95%, respectively.Conclusions. Among asymptomatic children, there is a wide variation in the prevalence of H. pylori infection based on the diagnostic test used. The study shows that antibody assays are less suitable than the UBT. However, under certain conditions, the IgG assays (combined systemic, salivary, or both) are less expensive alternative tools to the UBT for epidemiological studies in children.
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  • 4
    Electronic Resource
    Electronic Resource
    Cambridge, MA, USA : Blackwell Science, Inc.
    Helicobacter 2 (1997), S. 0 
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and Methods.Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. Sucrose permeability was assessed both before and approximately 4 weeks after anti–H. pylori therapy.〈section xml:id="abs1-3"〉〈title type="main"〉Results.Seventeen asymptomatic H. pylori–infected volunteers participated; 8 were cured. Sucrose permeability was in the range commonly found in normal controls both before and after anti–H. pylori therapy (mean excretion, 76.3 mg; range, 13–171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 ± 18 mg to 51.7 ± 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 ± 4 vs 71.4 ± 13 for those with scores ≥ 5 compared to scores ≤ 4;p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 ± 13 mg–99.7 ± 19 mg pretreatment vs posttreatment, respectively;p = .031).〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion. H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Boston, MA, USA : Blackwell Science Inc
    Helicobacter 4 (1999), S. 0 
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. The β-lactam group of antibiotics kills bacteria by inhibiting the terminal stages of peptidoglycan metabolism. We have recently identified amoxicillin-resistant Helicobacter pylori, none of which expressed β-lactamase. Penicillin-binding proteins (PBPs) represent a group of target enzymes for the β-lactam antibiotic family, and alterations in PBPs have been described in other penicillin-resistant bacteria. The amoxicillin-resistant phenotype characteristically was lost after freezing but could be restored by consecutive transfers into gradient plates.Materials and Methods. To determine whether amoxicillin resistance in H. pylori was related to alterations in any of the H. pylori PBPs, five H. pylori strains resistant to amoxicillin and three amoxicillin-sensitive strains were tested. PBPs were extracted from bacteria grown to logarithmic phase, labeled in vivo with 3H-benzylpenicillin, and analyzed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) and fluorography. Four main PBPs were separated from all amoxicillin-sensitive H. pylori strains.Results. Only three of the four main PBPs were found in the amoxicillin-resistant H. pylori strains. The differentially detectable PBP (PBP D) had an apparent molecular weight of 30 to 32 kD.Conclusion. These results suggest that PBP D might play a role in the amoxicillin-resistant phenotype of H. pylori strains lacking β-lactamase activity.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 6 (2001), S. 0 
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 5 (2000), S. 0 
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A number of putative virulence factors for Helicobacter pylori have been identified including cagA, vacA and iceA. The criteria for a true virulence factor includes meeting the tests of biologically plausibility with the associations being both experimentally and epidemiologically consistent. Although disease-specific associations have been hypothesized/claimed, there are now sufficient data to conclusively state that none of these putative virulence factors have disease specificity. CagA has been claimed to be associated with increased mucosal IL-8 and inflammation, increased density of H. pylori in the antrum, duodenal ulcer (DU), gastric cancer, and protection against Barrett’s cancer. Only the increase in IL-8/inflammation is direct and substantiated. Different H. pylori strains with functional cag pathogenicity islands do not vary in virulance as it has been shown that mucosal IL-8 levels are proportional to the number of cagA +H. pylori independent of the disease from which the H. pylori were obtained. It is now known that the density of either cagA + and cagA–H. pylori in the antrum of patients with H. pylori gastritis is the same. In contrast, the mean density of H. pylori in the antrum in DU is greater than in the antrum of patients with H. pylori gastritis. Of interest, the density of H. pylori is higher in the corpus of patients with H. pylori gastritis than those with DU, suggesting that acid secretion plays a critical role in these phenomena. The presence of a functional cag pathogenicity island increases inflammation and it is likely that any factor that results in an increase in inflammation also increases the risk of a symptomatic outcome. Nevertheless, the presence of a functional cag pathogenicity island has no predictive value for the presence, or the future development of a clinically significant outcome. The hypothesis that iceA has disease specificity has not been confirmed and there is currently no known biological or epidemiological evidence for a role for iceA as a virulence factor in H. pylori-related disease. The claim that vacA genotyping might prove clinically useful, e.g. to predict presentation such as duodenal ulcer, has been proven wrong. Analysis of the worldwide data show that vacA genotype s1 is actually a surrogate for the cag pathogenicity island. There is now evidence to suggest that virulence is a host-dependent factor. The pattern of gastritis has withstood the test of time for its relation to different H. pylori-related diseases (e.g. antral predominant gastritis with duodenal ulcer disease). The primary factors responsible for the different patterns of gastritis in response to an H. pylori infection are environmental (e.g. diet), with the H. pylori strain playing a lesser role. Future studies should work to eliminate potential bias before claiming disease associations. Controls must exclude regional or geographic associations related to the common strain circulation and not to the outcome. The authors must also control for both the presence of the factor and for the disease association. The study should be sufficiently large and employ different diseases and ethnic groups for the results to be robust. The findings in the initial sample (data derived hypothesis) should be tested in a new group (hypothesis testing), preferably from another area, before making claims. Finally, it is important to ask whether the results are actually a surrogate for another marker (e.g. vacA s1 for cagA) masquerading for a new finding. Only the cag pathogenicity island has passed the tests of biological plausibility (increased inflammation) and experimental and epidemiological consistency.
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  • 8
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Although combinations of antibiotics and antisecretory drugs are useful for treatment of Helicobacter pylori infection, treatment failure is common. The aim of this study was to evaluate the relation between pretreatment antibiotic resistance and outcome by using six different treatment regimens for H. pylori infection.Patients and Methods. Three hundred sixty-nine consecutive H. pylori–infected patients with dyspeptic symptoms were enrolled in three consecutive randomized, controlled, single-center clinical trials: trial A, 128 patients; trial B, 125 patients; trial C, 116 patients. Treatments consisted of (A) a 15-day course of dual therapy (omeprazole, 20 mg bid, and amoxicillin, 1 gm bid, or clarithromycin, 500 mg tid) (OA vs OC); (B) a 7-day triple therapy of omeprazole, 20 mg bid, plus metronidazole, 500 mg bid, and amoxicillin, 1,000 mg bid, or clarithromycin, 500 mg tid (OMA vs OMC); or (C) omeprazole, 20 mg bid, plus metronidazole, 500 mg bid, plus tetracycline, 500 mg qid, or doxycycline, 100 mg tid (OMT vs OMD). Diagnostic endoscopy was made in all patients before and 5 to 6 weeks after therapy. Six biopsies were taken from each patient for histology, rapid urease test, and H. pylori culture; antibiotic susceptibility testing was performed using the E-test method.Results. Overall cure rates were poor for both dual therapies OA and OC (38% and 37%, respectively) and for triple therapies OMA, OMC, and OMD (57%, 55%, and 58%, respectively). The OMT combination was successful in 91% (95% confidence interval [CI], 80.4%–97%). Metronidazole resistance was present in 29.7% (95% CI, 24%–35%), amoxicillin resistance was present in 26% (95% CI, 21%–32%), clarithromycin resistance was present in 23.1% (95% CI, 18%–29%), tetracycline resistance was present in 14% (95% CI, 10%–20%), and doxycycline resistance was present in 33.3% (95% CI, 21%–47%). Antibiotic resistance markedly reduced the cure rates and accounted for most of the poor results with the triple therapies: 89% versus 23%; 77% versus 26%; 100% versus 60%; and 67% versus 23% for OMC, OMA, OMT, and OMD, respectively. OMT appeared to be the best because of the high success rate with metronidazole-resistant H. pylori (71%) and in low-level tetracycline resistance.Conclusions. Pretreatment antibiotic-resistant H. pylori can, in part, explain the low cure rate of the infection and the variability in outcome in reported trials.
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 5 (2000), S. 0 
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has been suggested that H. pylori infection is associated with abnormalities in total leukocyte count as well as the number of basophils and lymphocytes. In addition, CagA seropositivity has been associated with an increase in serum transaminase (SGOT) values. The aim of this study was to confirm the findings of previous subgroup analyses in patients before and after treatment for H. pylori infection and to ascertain whether the abnormalities reversed following successful treatment.〈section xml:id="abs1-2"〉〈title type="main"〉Methods.Blood counts and serum transaminase levels were obtained prior to and following treatment of H. pylori infection of H. pylori-infected duodenal ulcer patients. CagA status was assessed by Western blot of the H. pylori isolates obtained from the patients.〈section xml:id="abs1-3"〉〈title type="main"〉Results.Ninety-four ulcer patients were studied, including 77 with CagA-positive H. pylori isolates (82%) and 17 with CagA-negative H. pylori isolates. All study parameters remained within normal limits both before and after therapy. There were no significant changes in any study parameter in those who failed therapy. Successful therapy resulted in a significant fall in total white cell count (7413 ± 520 cmm to 6738 ± 410 cmm, for pretreatment vs. cured, respectively, p = 0.04) and was almost entirely accounted for by a reduction in the number of circulating polymorphonuclear leukocytes (4595 ± 370 cmm to 3855 ± 270 cmm for pretreatment vs. cured, respectively, p = 0.015). The pretreatment SGOT and basophil count were significantly higher in those with CagA-positive H. pylori (SGOT = 23 ± 1 vs. 18.5 ± 1 U). Successful or failed therapy with follow-up for 3 months post therapy did not result in a significant change of SGOT levels.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.We confirmed an increase in total leukocyte count and number of polymorphonuclear leukocytes in those with H. pylori infection. We also confirmed higher SGOT levels with CagA-positive H. pylori infection, but the failure to resolve within 3 months of cure of the infection makes it unlikely to be a direct result of the H. pylori infection.
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