| Nota di contenuto |
Intro -- Preface -- Contents -- Part I: Epidemiology -- 1: Prevalence and Transmission Routes of H. pylori -- 1.1 Introduction -- 1.2 Prevalence of H. pylori -- 1.2.1 Prevalence of H. pylori in the Adults -- 1.2.1.1 Asia Pacific Area -- 1.2.1.2 Europe -- 1.2.1.3 North America -- 1.2.1.4 Latin America -- 1.2.1.5 Africa -- 1.2.1.6 Summary -- 1.2.2 Prevalence of H. pylori in Children -- 1.2.2.1 Asia -- 1.2.2.2 Europe -- 1.2.2.3 North America -- 1.2.2.4 Latin America -- 1.2.2.5 Summary -- 1.3 Risk Factors of H. pylori Infection -- 1.4 Transmission of H. pylori -- 1.4.1 Transmission of H. pylori in the Developing Countries -- 1.4.2 Transmission of H. pylori in the Developed Countries -- 1.5 Conclusion -- References -- Part II: Pathophysiology -- 2: Gastric Colonization by H. pylori -- 2.1 Introduction -- 2.2 Gastric Environment at the Site of Infection -- 2.3 Motility -- 2.4 Adhesion -- 2.5 Acid Acclimation -- 2.6 pH Alteration and Treatment Efficacy -- 2.7 Conclusions -- References -- 3: Immunological Reactions on H. pylori Infection -- 3.1 Introduction -- 3.2 Microbiota and General Immune Mechanism in the Stomach -- 3.2.1 Microbiota in the Stomach and Their Possible Role -- 3.2.2 General Immune Mechanism of Stomach -- 3.2.2.1 IgA and IgG Response of Stomach -- 3.2.2.2 CD4+ T-Cell Responses -- 3.3 Immune Response to H. pylori -- 3.3.1 Immune Evasion -- 3.3.1.1 Inhibition of Innate Immune Recognition by H. pylori -- Evasion of Recognition by Pattern Recognition Receptors -- Inhibition of Phagocytic Killing -- Inhibition of Killing by Reactive Oxygen Species and Nitric Oxide -- 3.3.1.2 Modulation of Adaptive Immunity by H. pylori -- 3.3.1.3 Inhibition of Effective T-Cell Response -- 3.3.1.4 Evasion of Humoral Response -- 3.3.1.5 Genetic Diversity in Immune Evasion.
3.3.2 Innate Immunity Activation Due to H. pylori -- 3.3.3 Adaptive Immunity Activation Due to H. pylori -- 3.3.4 Interaction of H. pylori with Tight Junction Proteins -- 3.4 Conclusion -- References -- 4: Change of Acid Secretions, Ghrelin, and Leptin, by H. pylori -- 4.1 Introduction -- 4.2 Gastric Acid Secretion and H+, K+-ATPase with Regard to H. pylori Infection -- 4.2.1 Gastric Acid Secretion and H+, K+-ATPase -- 4.2.2 Effect of H. pylori Infection on the Gastric Acid Secretion -- 4.2.2.1 Acute Phase of H. pylori Infection Causes Hypochlorhydria -- 4.2.2.2 Effect of H. pylori Infection on H+, K+-ATPase -- 4.2.2.3 Interaction Between H. pylori Infection and Gastric Acid Secretion Determining the Pattern of Gastritis -- 4.2.2.4 Chronic Phase of H. pylori Infection and Gastric Acid Secretion -- 4.2.2.5 Gastrin and Somatostatin in Regard to H. pylori Infection -- 4.2.3 Effect of H. pylori Eradication on Gastric Acid Secretion -- 4.3 Ghrelin -- 4.3.1 Role of Ghrelin -- 4.3.2 Regulation of Ghrelin in Regard to H. pylori Infection -- 4.3.3 Effect of Eradication of H. pylori on Ghrelin -- 4.4 Leptin -- 4.4.1 Regulation and Role of Gastric Leptin -- 4.4.2 Regulation of Leptin in Regard to H. pylori Infection -- 4.5 Conclusions -- References -- 5: H. pylori Virulence Factors: Toxins (CagA, VacA, DupA, OipA, IceA) -- 5.1 Introduction -- 5.2 Cytotoxin-Associated Gene A (CagA) -- 5.2.1 cag Pathogenicity Island (cag PAI) -- 5.2.2 Diversity of the cagA Gene -- 5.2.3 The Relevance Between the EPIYA Segment and Pathogenicity of CagA -- 5.2.4 Tyrosine Phosphorylation of CagA -- 5.2.5 Phosphorylation-Independent Signaling of CagA -- 5.3 Vacuolating Cytotoxin (VacA) -- 5.3.1 VacA Structure -- 5.3.2 vacA Gene Diversity -- 5.3.3 vacA Genotype in Relation to Gastroduodenal Diseases -- 5.3.4 Biological Functions of VacA.
5.4 Outer Membrane Inflammatory Protein (OipA) -- 5.5 Induced by Contact with Epithelium (IceA) -- 5.6 Duodenal Ulcer Promoting Gene (dupA) -- 5.7 Other Virulence Factors -- 5.7.1 Shape Switch -- 5.7.2 High-Temperature Requirement A (HtrA) and Heat-Shock Proteins (Hsps) -- 5.7.3 Arginase -- 5.7.4 Catalase and Superoxidase Dismutase (SOD) -- 5.7.5 Cholesteryl α-Glucosyltransferase -- 5.8 Conclusion -- References -- 6: H. pylori Virulence Factors: Genetic Polymorphism and Disease -- 6.1 Introduction -- 6.2 Cytotoxin-Associated Gene A (cagA) -- 6.2.1 cagA Type: Western Versus East Asian -- 6.3 Vacuolating Cytotoxin (vacA) -- 6.3.1 Geographic Differences in vacA Genotypes -- 6.4 Induced by Contact with Epithelium (iceA) -- 6.5 Outer Membrane Protein -- 6.5.1 Outer Inflammation Protein (oipA) -- 6.5.2 Duodenal Ulcer Promoting Gene A (dupA) -- 6.5.3 Blood Group A Antigen-Binding Adhesion (babA) -- 6.5.4 HomA and HomB -- 6.6 Conclusion -- References -- 7: Host Factor: Genetic Polymorphism -- 7.1 Introduction -- 7.2 Interleukin-1β -- 7.3 Tumor Necrosis Factor-α -- 7.4 Interleukin-10 -- 7.5 Interleukin-8 -- 7.6 Toll-Like Receptor 4 -- 7.7 Nucleotide-Binding Oligomerization Domain-Like Receptors (NLRs) -- 7.8 Conclusions -- References -- Part III: Diagnosis -- 8: Serology -- 8.1 Introduction -- 8.2 Advantages and Disadvantages of Serological Diagnosis -- 8.3 Serological Diagnosis -- 8.3.1 Bacterial Agglutination, Complement Fixation, and Indirect Immunofluorescence Test (IIF) -- 8.3.2 EIA and ELISA -- 8.3.3 Commercial Serological ELISA Kits Depending on H. pylori Antigen -- 8.3.4 Genedia® H. pylori ELISA and Its Use on Nationwide H. pylori Epidemiological Survey in Korea -- 8.3.5 Genedia® H. pylori ELISA and Its Use on Nationwide H. pylori Epidemiological Survey in Korea -- 8.4 Conclusions -- References.
9: Histopathologic Diagnosis of H. pylori Infection and Associated Gastric Diseases -- 9.1 Introduction -- 9.2 Histological Diagnosis of H. Pylori -- 9.2.1 Hematoxylin and Eosin (H& -- E) Stain -- 9.2.2 Special Stain and Immunohistochemistry (IHC) -- 9.3 Molecular Tests -- 9.4 Pathologic Features of H. Pylori-Associated Gastritis -- 9.4.1 Acute Gastritis -- 9.4.2 Chronic Gastritis -- 9.5 Sequelae of Chronic Gastritis -- 9.5.1 Atrophic Gastritis -- 9.5.2 Intestinal Metaplasia -- 9.5.3 Mucosa-Associated Lymphoid Tissue (MALT) -- 9.5.4 Gastric Cancer -- 9.6 Pathologic Findings of Peptic Ulcer -- 9.7 Conclusion -- References -- 10: Culture -- 10.1 Introduction -- 10.2 Culture Method -- 10.2.1 Specimen Collection -- 10.2.2 Transport of Biopsy Specimens -- 10.2.3 Incubation -- 10.2.4 Identification -- 10.3 Antimicrobial Susceptibility Testing -- 10.3.1 Agar Dilution Method -- 10.3.2 Disk Diffusion Method -- 10.3.3 Broth Dilution Method -- 10.3.4 E-Test -- 10.4 Conclusions -- References -- 11: Urea Breath Test -- 11.1 Introduction -- 11.2 Principle of the Urea Breath Test -- 11.3 Urea Substrate and Measuring Equipment of the Urea Breath Test -- 11.4 Test Meal -- 11.5 Time of Breath Collection -- 11.6 Diagnostic Accuracy and Appropriate Cutoff Point of the Urea Breath Test -- 11.7 Conclusion -- References -- 12: H. pylori Stool Antigen Test -- 12.1 Introduction -- 12.2 Diagnostic Accuracy of H. Pylori Stool Antigen Test -- 12.2.1 Diagnostic Accuracy of H. Pylori Stool Antigen Test in Untreated Patients -- 12.2.2 Diagnostic Accuracy of H. Pylori Stool Antigen Test After Eradication -- 12.3 Types of H. Pylori Stool Antigen Test -- 12.3.1 H. Pylori Stool Antigen Test Based on Enzyme Immunoassay -- 12.3.2 H. Pylori Stool Antigen Test Based on Immunochromatography -- 12.3.3 Novel H. Pylori Stool Antigen Tests.
12.4 H. Pylori Stool Antigen Test in Specific Conditions -- 12.5 Conclusion -- References -- 13: Specific Conditions: Children -- 13.1 Introduction -- 13.2 Endoscopic Diagnosis of H. pylori Infection in Children -- 13.2.1 Application of Endoscopy with Biopsy in Children -- 13.2.2 Endoscopic Findings in H. pylori-Infected Children -- 13.2.3 Histopathologic Findings in H. pylori-Infected Children -- 13.3 Noninvasive Diagnosis of H. pylori Infection in Children -- 13.3.1 Urea Breath Test in Children -- 13.3.2 H. pylori Stool Antigen Test in Children -- 13.3.3 H. pylori Antibody Tests -- 13.4 Treatment of H. pylori Infection in Children -- 13.5 Conclusion -- References -- 14: Specific Conditions: Diagnosis of H. pylori Infection in Case of Upper Gastrointestinal Bleeding -- 14.1 Introduction -- 14.2 Accuracy of Diagnostic Methods for H. Pylori in Upper Gastrointestinal Bleeding -- 14.2.1 Invasive Tests -- 14.2.1.1 Rapid Urease Test (RUT) -- 14.2.1.2 Histology -- 14.2.1.3 Culture -- 14.2.1.4 Polymerase Chain Reaction (PCR) -- 14.2.2 Noninvasive Tests -- 14.2.2.1 Urea Breath Test -- 14.2.2.2 H. pylori Stool Antigen Test -- 14.2.2.3 Serology -- 14.3 Appropriate Methods for Detection of H. pylori in Upper Gastrointestinal Bleeding -- 14.4 Conclusion -- References -- 15: Diagnosis of H. pylori Infection After Gastric Surgery -- 15.1 Introduction -- 15.2 Dynamic Changes of H. pylori Status in Patients Who Underwent Gastric Cancer Surgery -- 15.2.1 Possible Mechanisms for the Dynamic Changes of H. pylori Status -- 15.2.2 Affecting Factors for H. pylori Status in Patients Who Underwent Gastric Cancer Surgery -- 15.2.2.1 Operation Methods -- 15.2.2.2 Bile Reflux -- 15.2.2.3 Postgastrectomy-Induced Hypochlorhydria -- 15.3 Diagnostic Methods -- 15.3.1 Histology -- 15.3.2 Rapid Urease Test -- 15.3.3 Serology.
15.3.4 13C-Urea Breath Test.
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Chomeurs: Anthropologie D'un Mouvement Social
