Helicobacter pylori

✍ Scribed by Nayoung Kim (editor)

• Publisher: Springer
• Year: 2024
• Tongue: English
• Leaves: 738
• Edition: 2
• Category: Library

✦ Table of Contents

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
15.3.4.1 Efficacy of 13C-Urea Breath Test in the Remnant Stomach After Partial Gastrectomy
15.3.4.2 Clinical Factors that Caused False Positive 13C-UBT Results After H. pylori Eradication in the Remnant Stomach
15.4 Conclusion
References
Part IV: Symptom
16: Symptoms of Acute and Chronic H. pylori Infection
16.1 Introduction
16.2 The Induction Mechanisms of Symptoms After H. pylori Infection
16.3 Brain-Gut Axis, a Possible Mechanism of Symptoms of H. pylori Infection
16.4 Symptoms and Endoscopic and Histological Findings of Acute H. pylori Infection
16.5 Symptoms of Chronic H. pylori Infection
16.5.1 Brain-Gut Axis Relationship with Chronic H. pylori Infection
16.5.2 Extragastric Diseases of Chronic H. pylori Infection
16.6 Conclusions
References
Part V: Disease
17: Synopsis of H. pylori-Associated Diseases
17.1 Introduction
17.2 H. pylori-Associated Gastric Diseases
17.2.1 Acute and Chronic Gastritis
17.2.1.1 Acute Gastritis
17.2.1.2 Chronic Gastritis
17.2.2 Nonulcer Dyspepsia
17.2.3 Gastric or Duodenal Ulcers
17.2.4 Gastric MALT Lymphoma
17.2.5 Gastric Cancer
17.3 Gastroesophageal Reflux Disease, Barrett’s Esophagus, and Esophageal Adenocarcinorma
17.4 Extraintestinal Manifestations of H. pylori Infection
17.5 Conclusions
References
18: Atrophic Gastritis and Intestinal Metaplasia
18.1 Introduction
18.2 Atrophic Gastritis and Intestinal Metaplasia as Precursor Lesions of Gastric Cancer
18.3 Prevalence of Atrophic Gastritis and Intestinal Metaplasia
18.4 Risk Factors of Atrophic Gastritis and Intestinal Metaplasia
18.5 Classification of Atrophic Gastritis and Intestinal Metaplasia
18.6 Diagnosis of Atrophic Gastritis and Intestinal Metaplasia
18.6.1 Endoscopic Diagnosis
18.6.2 Histological Diagnosis
18.6.3 Diagnosis by Serum Pepsinogen I/II Ratio
18.7 Management for Atrophic Gastritis and Intestinal Metaplasia
18.8 Conclusions
References
19: Functional Dyspepsia
19.1 Introduction
19.2 Definition of Functional Dyspepsia
19.3 Pathophysiology of Functional Dyspepsia
19.4 Diagnostic Approach to Functional Dyspepsia
19.5 Treatment of Functional Dyspepsia
19.6 Conclusions
References
20: Peptic Ulcer
20.1 Introduction
20.2 Epidemiology
20.3 Causative Factors
20.3.1 H. pylori Infection
20.3.2 NSAIDs
20.3.3 Non-H. pylori, Non-NSAID Ulcer
20.4 Clinical Features
20.5 Diagnosis
20.6 Treatment
20.7 Complications
20.7.1 Gastroduodenal Hemorrhage
20.7.2 Intestinal Perforation
20.7.3 Gastric Outlet Obstruction
20.7.4 Penetration and Fistula
20.7.5 Prevention of Peptic Ulcer
20.8 Conclusions
References
21: Gastric Extranodal Marginal Zone B-Cell Lymphoma of MALT
21.1 Introduction
21.2 Pathogenesis of Gastric MALT Lymphoma
21.2.1 H. pylori
21.2.2 Genetic Variation
21.3 Clinical Feature and Diagnosis
21.3.1 Clinical Characteristics and Endoscopic Features
21.3.2 Diagnosis and Pathology
21.3.3 Staging
21.4 Therapeutic Options
21.4.1 Anti-H. pylori Therapy
21.4.1.1 Indication and the Effect
21.4.1.2 The Predictive Factors for Regression After Anti-H. pylori Therapy
21.4.1.3 Assessment of the Response to Treatment
21.4.1.4 Long-Term Outcome after Successful Eradication
21.4.1.5 Histological Residual Disease
21.4.2 Nonresponder to Anti-H. pylori Therapy
21.4.2.1 Radiotherapy
21.4.2.2 Chemotherapy
21.4.3 H. pylori-Negative Gastric MALT Lymphoma
21.5 Surveillance After Remission
21.6 Recurrent Disease
21.7 Conclusions
References
22: Gastric Cancer: Synopsis and Epidemiology of Gastric Cancer
22.1 Introduction
22.2 Incidence and Mortality
22.2.1 Incidence
22.2.2 Mortality
22.2.3 Incidence and Mortality in Lynch Syndrome Carriers
22.3 Risk Factors
22.3.1 Helicobacter pylori
22.3.2 Other Risk Factors
22.4 Future Trends
22.5 Conclusions
References
23: Gastric Cancer: Genetic Alternations Induced by H. pylori Infection: The Role of Activation-Induced Cytidine Deaminase
23.1 Introduction
23.2 Genetic Alternations in Gastric Carcinogenesis
23.3 Chronic Inflammation and Genetic Alternations
23.3.1 Free Radicals
23.3.2 Activation-Induced Cytidine Deaminase
23.4 Genetic Alternations in H. pylori-Associated Gastric Carcinogenesis
23.5 Conclusions
References
24: Gastric Cancer: Epigenetic Mechanisms: Aberrant DNA Methylation and Dysregulation of MicroRNA
24.1 Introduction
24.2 H. pylori-Induced Gastric Carcinogenesis and Aberrant DNA Methylation
24.2.1 Underlying Mechanisms of Induction of Aberrant DNA Methylation by H. pylori Infection
24.2.2 Reversibility of Aberrant DNA Methylation Following H. pylori Eradication
24.2.3 Epigenetic Fingerprint of H. pylori Infection and Epigenetic Field for Cancerization
24.3 H. pylori-Induced Gastric Carcinogenesis and miRNA
24.3.1 H. pylori and miRNA: Underlying Mechanisms
24.3.1.1 Modulation of Host Inflammatory Immune Response
24.3.1.2 Promotion of Cell-Cycle Progression
24.3.1.3 Inhibition of Apoptosis and Promotion of Proliferation
24.3.1.4 Promotion of Tumor Invasion and Metastasis
24.4 Conclusions
References
25: Gastric Cancer: H. pylori and Macrophage Migration Inhibitory Factor
25.1 Introduction
25.2 Introduction of Macrophage Migration Inhibitory Factor
25.3 Role of Macrophage Migration Inhibitory Factor in Tumorigenesis and Tumor Progression
25.4 H. pylori and Macrophage Migration Inhibitory Factor
25.5 Potential for Future Studies
25.6 Conclusions
References
26: Gastric Cancer: Epithelial-Mesenchymal Transition
26.1 Introduction
26.2 Three Types of EMT
26.2.1 Type 1: Embryogenesis
26.2.2 Type 2: Tissue Regeneration and Organ Fibrosis
26.2.3 Type 3: Invasiveness and Metastasis of Cancer
26.3 Major Signal Pathways of EMT
26.3.1 TGF-β/Smad Signaling
26.3.1.1 Smad Signaling
26.3.1.2 Non-Smad Signaling
26.3.2 Wnt/β-Catenin Signaling
26.3.3 Notch Signaling
26.4 EMT and Gastric Cancer
26.4.1 Association Between Gastric Cancer and EMT
26.4.1.1 CagA, Cytotoxin-Associated Gene Toxin
26.4.1.2 VacA, Vacuolating Cytotoxin
26.4.2 EMT Factors Related to Gastric Cancer
26.4.2.1 Regulation of E-Cadherin
Functional Loss Through CDH1 Mutation
Repression for the Transcription of CDH1
26.4.2.2 Epigenetic Regulation of EMT via miRNA
26.4.2.3 Other EMT Regulatory Factors
Vimentin
Bone Morphogenetic Protein (BMP)
Claudin
Gastrokine
26.4.3 EMT, Cancer Stem Cells, and H. pylori
26.4.3.1 Promotion of Production of TGF-β- or TNF-α-Inducing Protein
26.4.3.2 Activation of Snail, Twist, or β-Catenin
26.4.3.3 Hypermethylation of CDH1 Promoter
26.4.3.4 Association Between Emergence of Cancer Stem Cells and Chronic H. pylori Infection
26.4.4 Clinical Implications of EMT and Cancer Stem Cells
26.4.4.1 Markers for EMT
26.4.4.2 Prognostic Factors
26.4.4.3 Cancer Stem Cells
26.4.4.4 Targets for the Cancer Treatments
26.5 Conclusions
References
27: Gastric Cancer: ABO Blood Type
27.1 Introduction
27.2 The Association of ABO Blood Group with Different Diseases
27.3 Association Between ABO Blood Groups and H. pylori Infection
27.4 Research Studies Explaining the Interaction Between H. pylori and ABO Antigen, the Results, and Hypotheses
27.4.1 Immune Evasion by Molecular Mimicry
27.4.2 Adhesion Molecules onto Which H. pylori can Attach
27.4.3 Decoy Mechanism by Secretors
27.5 The Association of ABO Blood Group with Gastric Cancer
27.6 The Association of ABO Blood Group with Gastric Cancer by Way of H. pylori Infection
27.7 Conclusions
References
28: Gastric Cancer: First Relatives of Gastric Cancer
28.1 Introduction
28.2 Difference of H. pylori Infection Rate Depending on Family History on Gastric Cancer
28.3 Risk Increment of Gastric Cancer in the Presence of H. pylori Infection and Family History of Gastric Cancer and the Preventive Effect of H. pylori Eradication
28.3.1 Risk Increment of Gastric Cancer in the Presence of H. pylori Infection and Family History of Gastric Cancer
28.3.2 The Preventive Effect of H. pylori Eradication in Subjects with a Family History of Gastric Cancer
28.4 Risk Factors for Gastric Cancer According to the Number of Affected Relatives and According to the Affected Family Member
28.5 Family-Based Exome Sequencing Combined with Linkage Analyses Identifies Rare Susceptibility Variants of MUC4 for Gastric Cancer
28.6 Family History of Gastric Cancer as a Risk Factor for Intestinal Metaplasia
28.7 Prognosis of Gastric Cancer in the Relatives of Gastric Cancer
28.8 Guideline of Gastric Cancer Screening in Case of Family History of Gastric Cancer
28.9 Conclusions
References
29: H. pylori Infection-Negative Gastric Cancer
29.1 Introduction
29.2 Definition of H. pylori Infection-Negative Gastric Cancer
29.3 Incidence
29.4 Clinicopathologic Characteristics
29.5 Molecular Characteristics
29.6 Prognosis
29.7 Conclusions
References
30: Gastroesophageal Reflux Disease
30.1 Introduction
30.2 Epidemiology of GERD in H. pylori-Infected Population
30.3 The Impact of H. pylori Infections on GERD
30.4 Influence of H. pylori Eradication on GERD
30.4.1 Antral-Predominant Gastritis
30.4.2 Corpus-Predominant Gastritis
30.5 Conclusions
References
31: NSAID-Induced Gastropathy and H. pylori Infection
31.1 Introduction
31.2 NSAID-Induced Gastropathy
31.2.1 Mechanisms
31.2.2 Nonselective and Selective NSAIDs
31.3 Association Between NSAID-Induced Gastropathy and H. pylori Infection
31.3.1 Pathophysiology
31.3.2 Diagnosis of H. pylori Infection in NSAID Users
31.3.3 Therapeutic Approach (Table 31.1)
31.3.3.1 H. pylori Infection in Initial NSAID Users
NSAIDs (Excluding Aspirin)
Aspirin
31.3.3.2 H. pylori Infection in Long-Term NSAID Users Without Peptic Ulcer Complications
NSAIDs (Excluding Aspirin)
Aspirin
31.3.3.3 H. pylori Infection in Long-Term NSAID Users with Peptic Ulcer Complications
NSAIDs (Excluding Aspirin)
Aspirin
31.3.3.4 H. pylori Infection in COX-2 Inhibitor Users
31.3.3.5 Meta-analysis Results
31.3.4 Guidelines for Management of H. pylori Infection in NSAID Users
31.3.4.1 Korea
Clinical Guidelines for Drug-Related Peptic Ulcer, 2020 Revised Edition [31]
31.3.4.2 Overseas Countries
Management of H. pylori Infection: The Maastricht VI/Florence Consensus Report [32]
Treatment of H. pylori Infection: ACG Clinical Guideline [33]
Management of H. pylori Infection: Italian Guideline [34]
Evidence-Based Clinical Practice Guidelines for Peptic Ulcer Disease 2020 in Japan [35]
31.4 Conclusions
References
32: Extraintestinal Manifestations of H. pylori Infection: H. pylori-Associated Iron Deficiency Anemia
32.1 Introduction
32.2 Clinical Studies
32.3 Epidemiology
32.4 Mechanisms
32.4.1 Chronic Gastrointestinal Blood Loss Induced by H. pylori Infection
32.4.2 The Effect of Chronic H. pylori Gastritis on Gastric Acid Secretion and Iron Absorption
32.4.3 Increased Iron Consumption by H. pylori
32.4.4 Iron Sequestration in Gastric Mucosa
32.4.5 Higher Hepcidin Levels in H. pylori-Infected Patients with Iron Deficiency Anemia
32.5 Conclusions
References
33: Extraintestinal Manifestations of H. pylori Infection: Idiopathic Thrombocytopenic Purpura
33.1 Introduction
33.2 Idiopathic Thrombocytopenic Purpura (Immune Thrombocytopenic Purpura)
33.3 Association Between Immune Thrombocytopenic Purpura and H. pylori
33.4 Mechanisms
33.5 Conclusions
References
34: Extraintestinal Manifestations of H. pylori Infection: Heart Disease
34.1 Introduction
34.2 H. pylori and Lipid Profile
34.3 H. pylori and Coronary Artery Disease
34.4 H. pylori and Arrhythmia
34.5 Conclusions
References
35: Extraintestinal Manifestations of H. pylori Infection: Asthma and Allergic Disorders
35.1 Introduction
35.2 H. pylori and Allergic Asthma: Epidemiological Evidence
35.3 H. pylori and Allergic Asthma: Proposed Mechanisms Underlying Protective Effects of H. pylori
35.3.1 Basic Concept on the Pathophysiology of Allergic Asthma
35.3.2 Hygiene Hypothesis and Disappearing Microbiota Hypothesis
35.3.3 Theoretical Hypothesis to Explain Protective Effect by H. pylori
35.4 Conclusions
References
36: Extragastric Manifestations of H. pylori Infection: Lower GI Disorders
36.1 Introduction
36.2 Colorectal Cancer or Adenoma
36.2.1 Clinical Studies
36.2.2 Possible Mechanisms for Causal Effects
36.3 Inflammatory Bowel Disease
36.3.1 Clinical Studies
36.3.2 Possible Mechanisms for Causal Effects
36.4 Irritable Bowel Syndrome
36.4.1 Clinical Studies
36.4.2 Possible Mechanisms for Causal Effects
36.5 Conclusions
References
37: Extraintestinal Manifestations of H. pylori Infection: Neurologic Disease
37.1 Introduction
37.2 Pathophysiology
37.2.1 The Microbiota-Gut-Brain Axis
37.2.2 Pathophysiology of H. pylori Infection on the MGBA
37.2.2.1 Route of H. pylori Entering the CNS
37.2.2.2 Neuroinflammation by H. pylori Infection
37.2.2.3 Dysbiosis by H. pylori Infection
37.2.2.4 Effects of H. pylori on Neurotransmitters
37.2.2.5 Microelement Deficiency
37.3 Related Neurologic Diseases
37.3.1 Parkinson’s Disease
37.3.2 Alzheimer’s Disease
37.3.3 Demyelinating Diseases of the CNS; Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders
37.3.4 Guillain–Barré Syndrome
37.3.5 Ischemic Stroke
37.3.6 Migraine
37.4 H. pylori Eradication Effects on Neurologic Diseases
37.4.1 Parkinson’s Disease
37.4.2 Alzheimer’s Disease
37.4.3 Other Diseases
37.5 Conclusions
References
Part VI: Antibiotic Resistance
38: Synopsis of Antimicrobial Resistance
38.1 Introduction
38.2 Mechanisms of Resistance to Antibiotics
38.2.1 Acquisition of Mobile Genetic Elements
38.2.2 Resistance Acquired by Point Mutation
38.2.3 Efflux Pumps and H. pylori Resistance
38.3 Resistance Observed in H. pylori and Its Consequences
38.3.1 Macrolides
38.3.2 Fluoroquinolones
38.3.3 Amoxicillin
38.3.4 Tetracyclines
38.3.5 Rifampin
38.3.6 5-Nitroimidazoles
38.4 Methods to Detect H. pylori Resistance
38.4.1 Phenotypic Methods
38.4.2 Genotypic Methods
38.5 Prevalence of H. pylori Resistance
38.6 Conclusions
References
39: Clarithromycin
39.1 Introduction
39.2 The Antimicrobial Mechanism of Clarithromycin
39.3 The Prevalence and Trends of Clarithromycin Resistance
39.4 Diagnosing Clarithromycin Resistance
39.4.1 Diagnosing Clarithromycin Resistance: Conventional Culture and Susceptibility
39.4.2 Diagnosing Clarithromycin Resistance: Molecular Tests
39.5 Mechanisms of Clarithromycin Resistance
39.6 Current Clarithromycin Resistance Studies and Its Prospection
39.6.1 Current Clarithromycin Resistance Studies
39.6.2 The Prospect About Future Clarithromycin Resistance Studies
39.7 Conclusions
References
40: Amoxicillin
40.1 Introduction
40.2 Prevalence of H. pylori Resistance to Amoxicillin
40.3 The Role and Resistance Mechanism of Amoxicillin in Eradication of H. pylori
40.3.1 Target of ß-Lactam Antibiotics in H. pylori
40.3.2 The Resistance Mechanism of Amoxicillin
40.4 Conclusions
References
41: Fluoroquinolone
41.1 Introduction
41.2 Mechanism of Action of Fluoroquinolone
41.3 Epidemiology of Fluoroquinolone Resistance
41.4 Diagnosis of Fluoroquinolone Resistance
41.5 Mechanism of Fluoroquinolone Resistance
41.5.1 Mechanism of Fluoroquinolone Resistance of H. pylori
41.5.2 Distinct Feature of Genes Responsible for Fluoroquinolone Resistance
41.6 Present Status of the Studies About Fluoroquinolone Resistance
41.7 Perspective and Limitation of Studies About Fluoroquinolone Resistance Mechanism
41.8 Conclusions
References
42: Metronidazole
42.1 Introduction
42.2 Epidemiological Aspects of Metronidazole Resistance
42.2.1 The Resistance Rate
42.2.2 Correlations Between the Resistance and the Eradication Failures
42.3 Principles of Metronidazole Resistance
42.3.1 Mode of Action
42.3.2 Mechanism of Resistance
42.3.2.1 Mutations in rdxA and frxA
42.3.2.2 Structural Alterations in RdxA
42.3.2.3 Other Mechanisms of Resistance
42.4 Conclusions
References
Part VII: Treatment
43: Synopsis of Antibiotic Treatment
43.1 Introduction
43.2 Why Are H. pylori Infections So Difficult to Cure?
43.3 Causes of Treatment Failure
43.4 Evidence-Based Therapy Is Susceptibility-Based Therapy
43.5 General “Rules” for Choosing a Regimen
43.6 H. pylori Therapies
43.6.1 Triple Therapies (Generally Only Used for Susceptibility-Based Therapy)
43.6.2 Four-Drug Therapies
43.6.2.1 Bismuth Quadruple Therapy
43.6.2.2 Bismuth Furazolidone Quadruple Therapy
43.6.3 Non-Bismuth Quadruple Therapies
43.6.3.1 Sequential Therapy (Generally Considered Obsolete Because of Antimicrobial Misuse)
43.6.3.2 Concomitant Therapy (Generally Considered Obsolete Because of Antimicrobial Misuse)
43.6.3.3 Hybrid and Reverse Hybrid Therapy (Generally Considered Obsolete Because of Antimicrobial Misuse)
43.6.4 PPI-Amoxicillin High-Dose Dual Therapy
43.7 Patient Education to Enhance Adherence
43.8 Recommendations
References
44: Triple Therapy
44.1 Introduction
44.2 Current Status of the Eradication Rates of Standard Triple Therapy
44.3 Factors Influencing the Eradication Rate of Standard Triple Therapy
44.3.1 H. pylori Factors
44.3.1.1 Antibiotic Resistance
44.3.1.2 Other H. pylori Factors
44.3.2 Host Factors
44.3.2.1 Medication Adherence
44.3.2.2 Excess Gastric Acid Secretion
44.3.2.3 Treatment Duration
44.3.2.4 Drug Side Effects
44.3.2.5 Underlying Gastroduodenal Disease
44.3.2.6 Gastritis Patterns
44.3.2.7 Smoking
44.3.2.8 Other Factors
44.4 Conclusions
References
45: Quadruple Therapy
45.1 Introduction
45.2 Efficacy of Bismuth Quadruple Therapy as Second-Line Treatment
45.3 Efficacy of Bismuth Quadruple Therapy as First-Line Treatment
45.4 Factors Affecting the Bismuth Quadruple Therapy Eradication Rate: Antimicrobial Resistance
45.5 Conclusions
References
46: Sequential Therapy
46.1 Introduction
46.2 Theoretical Background of Sequential Therapy
46.3 Types of Sequential Therapy
46.4 Outcome of Sequential Therapy
46.4.1 Eradication Rate
46.4.2 Adverse Events
46.5 Limitations of Sequential Therapy
46.5.1 The Complexity of Regimen
46.5.2 Rescue Treatment After Failure
46.5.3 Antimicrobial Resistance
46.5.4 Insufficient Quality of Clinical Trials
46.6 Conclusions
References
47: Concomitant Therapy and Hybrid Therapy
47.1 Introduction
47.2 Theoretical Background of Concomitant and Hybrid Therapies
47.3 Outcome of Concomitant and Hybrid Therapies
47.3.1 Eradication Rate
47.3.2 Adverse Events
47.4 Limitations of Concomitant Therapy
47.4.1 Rescue Therapy After Eradication Failure
47.4.2 Antibiotic Resistance
47.5 Conclusions
References
48: Tailored Therapy Based on Antibiotic Resistance
48.1 Introduction
48.2 The Patient-Specific Therapy: Why Tailored Therapy Is Needed
48.3 Detection of Antibiotic Resistance in H. pylori
48.3.1 Culture-Guided Method for Antibiotic Susceptibility Test in H. pylori
48.3.2 Molecular Methods for Antibiotic Susceptibility Test in H. pylori
48.4 The Efficacy of Tailored Therapy and Guideline for Tailored Therapy Based on Antibiotic Susceptibility Test
48.5 Conclusions
References
49: Fluoroquinolone and Rifabutin-Containing Therapy
49.1 Introduction
49.2 Fluoroquinolone-Containing Triple Therapy
49.2.1 Theoretical Background
49.2.2 Eradication Rate
49.2.3 Adverse Events
49.2.4 Antibiotic Resistance and Limitations
49.3 Rifabutin-Containing Therapy
49.3.1 Theoretical Background
49.3.2 Eradication Rate
49.3.3 Adverse Events
49.3.4 Antibiotic Resistance and Limitations
49.4 Conclusions
References
50: Probiotics
50.1 Introduction
50.2 Mechanism of Action of Probiotics on H. pylori Infection
50.2.1 Immunological Mechanisms
50.2.2 Nonimmunological Mechanisms
50.3 Probiotic Treatment of H. pylori Infection
50.3.1 Studies Using Animals and Cell Line
50.3.2 Human Studies
50.4 Safety
50.5 Conclusions
References
51: Treatment Guidelines
51.1 Introduction
51.2 South Korean Guidelines
51.3 Japanese Guidelines
51.4 European Guidelines (The Maastricht VI/Florence Consensus Report, 2022)
51.5 Conclusions
References
52: Gastric Cancer Screening
52.1 Introduction
52.2 Accuracy of Gastric Cancer Screening Methods
52.2.1 Endoscopic Screening
52.2.2 Radiographic Screening
52.2.3 Comparison of Sensitivity Between Endoscopic and Radiographic Screening
52.3 Effect of Gastric Cancer Screening on Gastric Cancer Mortality
52.3.1 Endoscopic Screening
52.3.2 Radiographic Screening
52.4 Guidelines
52.4.1 Updated Korean Guideline 2015
52.4.2 Further Supporting Evidence After 2015 Guideline
52.4.3 Japanese Guideline
52.5 Serologic Test for Gastric Cancer Screening
52.5.1 Serum Pepsinogen
52.5.2 Serum Trefoil Factor 3
52.5.3 MicroRNAs
52.5.4 Multianalyte Blood Tests
52.6 Conclusion
References
53: Recrudescence and Reinfection After H. pylori Eradication Treatment
53.1 Introduction
53.2 Systematic Review with Meta-Analysis: The Global Recurrence Rate of H. pylori
53.3 Recrudescence After H. pylori Eradication Therapy
53.4 Reinfection After H. pylori Eradication Therapy
53.5 Risk Factors of Reinfection After H. pylori Eradication Therapy
53.6 Conclusions
References
Part VIII: Consequences of H. pylori Eradication
54: Peptic Ulcer Disease
54.1 Introduction
54.2 The Role of H. pylori infection in Peptic Ulcer Disease Pathogenesis
54.3 Impact on Peptic Ulcer Disease Healing
54.4 Impact on Peptic Ulcer Disease Recurrence
54.5 Impact on Peptic Ulcer Disease Complications
54.5.1 Bleeding
54.5.2 Perforation
54.5.3 Obstruction
54.6 Conclusions
References
55: Atrophic Gastritis and Intestinal Metaplasia
55.1 Introduction
55.2 The Effect of H. pylori Eradication on the Atrophic Gastritis and Intestinal Metaplasia
55.2.1 Key Individual Studies
55.2.2 Meta-Analyses
55.2.3 Guidelines
55.2.4 Limitations
55.3 Affecting Factors on the Decrease of Atrophic Gastritis and Intestinal Metaplasia by H. pylori Eradication
55.4 Underlying of Reversibility of Atrophic Gastritis and Intestinal Metaplasia
55.4.1 CDX1 and CDX2
55.4.2 Gastric Stem Cells
55.5 Conclusions
References
56: Primary Prevention of Gastric Cancer
56.1 Introduction
56.2 Key Individual Studies
56.3 Meta-Analyses
56.4 Guidelines
56.5 The Underlying Mechanisms of Chemopreventive Effect of H. pylori Eradication on Gastric Cancer
56.6 Conclusions
References
57: Secondary Prevention of Gastric Cancer After Endoscopic or Surgical Treatment
57.1 Introduction
57.2 Chemoprevention Effect of H. pylori Eradication After Endoscopic Treatments
57.3 Chemoprevention Effect of H. pylori Eradication After Surgery
57.4 Survival Benefits of H. pylori Eradication After Surgery
57.5 Conclusions
References
58: Extraintestinal Manifestations Depending on Sex/Gender and Age: Metabolic Parameters and Glycosylated Hemoglobin A1c
58.1 Introduction
58.2 Metabolic Syndromes and H. pylori Infection
58.2.1 The Effect of H. pylori on the Metabolic Parameters Depending on Age and Sex/Gender
58.2.2 The Underlying Mechanisms of H. pylori on the Metabolic Parameters
58.2.3 The Effect of H. pylori Eradication on the Metabolic Parameters
58.2.3.1 Different Effects of H. pylori Eradication on the Metabolic Parameters
58.2.3.2 The Underlying Mechanisms of Different Effects of Sex on the H. pylori Eradication-Induced Metabolic Parameters
58.3 The Effects of H. pylori and its Eradication on the Insulin Resistance or Hemoglobin A1c Depending on Sex/Gender and Age
58.3.1 The Effects of H. pylori on the Insulin Resistance or Glycosylated Hemoglobin A1c
58.3.2 The Effects of H. pylori Eradication on the Insulin Resistance or Hemoglobin A1c and the Possible Underlying Mechanism
58.3.3 The Effects of H. pylori Eradication on the Hemoglobin A1c Depending on Age and Sex
58.4 Conclusions
References
Part IX: The Effect of H. pylori on the Gastric Microbiota
59: The Effect of H. pylori Infection on the Gastric Microbiota
59.1 Introduction
59.2 The Development of Analysis Methods of Gastric Microbiota
59.3 Various Conditions Affecting the Gastric Microbiota
59.3.1 The Effect of Sampling Site on the Gastric Microbiota Analysis: Mucosa vs. Gastric Fluid
59.3.2 Corpus Biopsy Was More Favorable for the Analysis Regarding a Possible Role of Bacteria Other than H. pylori in the Gastric Carcinogenesis
59.3.3 Influence of Change of pH on the Gastric Microbiota
59.4 The Effect of H. pylori Infection on the Gastric Microbiota
59.4.1 Under the Normal Acidic Condition of a Healthy Stomach Without H. pylori
59.4.2 What Happens When H. pylori Infection Occurs
59.4.3 An Appropriate Cutoff Value for Determining the Colonization of Helicobacter pylori by the Pyrosequencing Method
59.5 Altered Microbiota Composition Related with Disease State
59.5.1 Altered Microbiota Composition in the Gastric Cancer in the Presence of H. pylori
59.5.2 Altered Microbiota Composition in the Gastric Cancer in the Absence of H. pylori
59.6 Link Between Gastric Microbiota and Gastric Cancer
59.6.1 Nitrosating and/or Urease Producing Bacteria
59.6.2 Bacterial Metabolites
59.6.3 Bacterial Genotoxins
59.7 Conclusions
References
60: The Effect of H. pylori Eradication on the Gastric Microbiota
60.1 Introduction
60.2 Gastric Microbiota Changes in the Absence or in the Presence of H. pylori Infection
60.2.1 Gastric Microbiota Changes in the Absence of H. pylori Infection
60.2.2 Gastric Microbiota Changes in the Presence of H. pylori Infection
60.3 The Effect of H. pylori Eradication on the Gastric Microbiota
60.3.1 The Effect of H. pylori Eradication on the Gastric Microbiota Composition and Diversity
60.3.2 The Reversibility of Gastric Microbiota Composition and Diversity to that of H. pylori-Negative Individuals After H. pylori Eradication
60.3.3 The Effect of H. pylori Eradication on the Gastric Microbiota Function
60.4 The Effect of H. pylori Eradication on the Gut Microbiota
60.4.1 The Effect of H. pylori Eradication on the Gut Microbiota Depending on H. pylori Eradication Regimens
60.4.2 The Effect of Probiotics on the H. pylori Eradication-Induced Gut Microbiota Changes
60.4.3 The Effect of Probiotics on the H. pylori Eradication-Induced Gut Microbiota Function
60.4.4 Gastric Microbial Composition Changes in the Persistent H. pylori Infection
60.5 Conclusions
References
Part X: Animal Model
61: Animal Models of H. pylori Infection
61.1 Introduction
61.2 Selection of Animal Models
61.3 Selection of Strains
61.3.1 Characteristic and Morphologic Differences Between H. felis and H. pylori SS1
61.3.2 Pathological Difference Between H. felis and H. pylori SS1
61.4 Differences in Individual Responses
61.5 Transgenic or Knockout Mouse Models
61.5.1 INS-GAS Mice
61.5.2 IFN-γ and TNF-α Knockout Mice
61.5.3 IL-1β Transgenic Mice
61.5.4 IL-10 Knockout Mice
61.5.5 Fas Antigen Transgenic Mice
61.5.6 p27-Deficient Mice
61.5.7 cagA-Transgenic Mice
61.6 Limitations of Mouse Models of Infection
61.7 Conclusions
References
Index