1.

Record Nr.

UNINA9910842297503321

Autore

Kim Nayoung

Titolo

Helicobacter Pylori

Pubbl/distr/stampa

Singapore : , : Springer, , 2024

©2023

ISBN

981-9700-13-2

Edizione

[2nd ed.]

Descrizione fisica

1 online resource (738 pages)

Altri autori (Persone)

Kim

Disciplina

616.33014

Lingua di pubblicazione

Inglese

Formato

Materiale a stampa

Livello bibliografico

Monografia

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&amp -- 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.