Anaphylaxis and Hypersensitivity Reactions (eBook)

Anaphylaxis and HypersensitivityReactions 3
Preface 5
Foreword 7
Contents 9
Contributors 11
Chapter 1: Definition and Criteria for the Diagnoses of Anaphylaxis 15
1.1 Introduction 15
1.2 History 16
1.3 Issues Surrounding the Definition Today 17
1.4 The Basis for the Definition of and Criteria for the Diagnosis of Anaphylaxis 19
1.5 Less Common Presentations of Anaphylaxis 20
1.6 Conditions with Similar Manifestations: The Differential Diagnosis of Anaphylaxis 21
1.7 The Need for a Biomarker 23
1.7.1 Tryptase 23
1.7.2 Plasma Histamine and Urinary Histamine 23
1.7.3 Carboxypeptidase A 24
1.7.4 Platelet-Activating Factor 24
1.8 Conclusions 24
References 25
Chapter 2: An Epidemiological Approach to Reducing the Risk of Fatal Anaphylaxis 27
2.1 Introduction 27
2.2 Prevalence and Incidence of Anaphylaxis 29
2.3 Epidemiological Studies of Nonfatal Anaphylaxis 29
2.4 Factors Determining the Severity of Acute Allergic Reactions 31
2.5 Epidemiology of Fatal Anaphylaxis 33
2.6 Fatal Anaphylaxis Around the World 33
2.7 The UK Fatal Anaphylaxis Register 34
2.7.1 What Has Triggered Fatal Reactions? 35
2.7.2 Who Died from Anaphylaxis? 36
2.7.3 When Did They Die? 37
2.7.4 How Did They Die? 37
2.8 Fatal First Reactions: Why Was Rescue Treatment Unsuccessful? 38
2.9 Fatal Recurrent Reactions 39
2.9.1 Reducing the Likelihood of a Severe Recurrence 39
2.9.2 Why Did Avoidance Fail? 39
2.10 Self-injectible Epinephrine 40
2.11 Conclusion 42
References 42
Chapter 3: Pathophysiology and Organ Damage in Anaphylaxis 46
3.1 Background 46
3.2 Proposed Immunopathologic Mechanisms 47
3.3 Non-immunologic Anaphylaxis 49
3.4 Chemical Mediators of Anaphylaxis 50
3.4.1 Histamine and Tryptase 50
3.4.2 Arachidonic Acid Metabolites 51
3.4.3 Nitric Oxide in Anaphylaxis 51
3.4.4 Other Inflammatory Pathways Are Probably Important 52
3.5 Shock Organs in Anaphylaxis 52
3.6 The Heart as Shock Organ in Anaphylaxis 53
3.6.1 Non-pharmacologic Myocardial Ischemia in Anaphylaxis 54
3.6.2 Bradycardia During Anaphylaxis 54
3.7 Respiratory Effects of Anaphylaxis 55
3.8 Autopsy Findings in Fatal Anaphylaxis 55
3.9 Anaerobic Metabolism Complicates Anaphylaxis 55
3.10 Conclusion 56
References 56
Chapter 4: Mast Cells: Effector Cells of Anaphylaxis 60
4.1 Introduction 60
4.2 The Basic Biology of Mast Cells 61
4.3 Approaches to Assess Mast-Cell Functions 62
4.4 Mouse Models of Anaphylaxis 64
4.5 IgE-Dependent Passive Systemic Anaphylaxis 64
4.6 IgE- or IgG1-Dependent Passive Local Anaphylaxis 68
4.7 Active Systemic or Local Anaphylaxis 69
4.8 Mast Cells in Peanut Allergy 71
4.9 Mast Cells in Intestinal Anaphylaxis 71
4.10 Roles of Mast Cells in Other Immune or Nonimmune Mechanisms of Anaphylaxis 72
4.11 Manipulation of Mast-Cell Effector Function 73
4.12 Conclusions 74
References 75
Chapter 5: Basophils in Anaphylaxis 82
5.1 Introduction 82
5.2 Review of Basophil Biology 83
5.2.1 Ontogeny 83
5.2.2 Morphology and Biochemistry 83
5.2.3 Life Span 84
5.2.4 Extravasation 84
5.2.5 Activation 84
5.2.6 Signal Transduction: Fce(epsilon)RI-Mediated Signal Transduction in Human Basophils 86
5.2.6.1 Lyn Kinase and Syk Kinase 86
5.2.6.2 Fyn Kinase 86
5.2.6.3 Phosphatidyl Inositol 3¢ Kinase (PI3K) 86
5.2.6.4 SH-2-Containing 5¢ Inositol Phosphatase-1 (SHIP-1) 87
5.2.6.5 MAP Kinase Pathway 87
5.2.6.6 Dynamics and Variability of Syk Expression 87
5.2.6.7 Regulation of Syk Expression 88
5.2.6.8 Variability of SHIP-1 Expression 88
5.2.6.9 Nuclear Factor of Activated T Cells (NFAT) 89
5.2.7 Effects of IL-3 89
5.2.7.1 Effects on Basophil Mediator Secretion 89
5.2.7.2 Effects on Basophil Survival 90
5.3 Evidence of Basophil Involvement in Anaphylaxis 91
5.3.1 Basophil Mediators 91
5.3.1.1 Histamine 91
5.3.1.2 Leukotriene C4 91
5.3.1.3 Platelet-Activating Factor 91
5.3.1.4 IL-4 92
5.3.2 Basophil Receptors 92
5.3.3 Location of Basophils 92
5.3.3.1 Circulation in Peripheral Blood 92
5.3.3.2 Migration into Tissues Involved in Allergic Reactions 93
5.4 Evidence for Basophil Activity in Human Anaphylaxis 93
5.5 Evidence for Basophil Activity in Murine Models of Anaphylaxis 93
5.6 Conclusion 96
References 96
Chapter 6: Protease Mediators of Anaphylaxis 101
6.1 Introduction 101
6.2 Chymase-like Peptidases 102
6.2.1 General Considerations 102
6.2.2 Rat Chymases 102
6.2.3 Mouse Chymases as Biomarkers 104
6.2.4 Human Chymase as a Biomarker 105
6.2.5 Chymases in Basophils 105
6.2.6 Cathepsin G 106
6.3 Tryptase-like Peptidases 106
6.3.1 Mast Cell Tryptases in Rats and Mice 106
6.3.2 Mast Cell Tryptases in Humans: Roles in Anaphylaxis 107
6.3.3 Human Mast Cell Tryptases: Variation of Form and Function 109
6.3.4 Human Soluble Tryptases: Significance of Genetic Variation and Disequilibrium 110
6.3.5 Tryptase Expression in Human Basophils 110
6.4 Carboxypeptidase A3 111
6.5 Dipeptidylpeptidase I (DPPI)/Cathepsin C 111
References 112
Chapter 7: Aspirin and NSAID Reactions: Diagnosis, Pathophysiology, and Management 118
7.1 Introduction 118
7.2 Aspirin-Exacerbated Respiratory Disease 119
7.3 Characteristics of AERD 120
7.3.1 Acetaminophen and AERD 120
7.3.2 COX-2 and AERD 121
7.4 AERD: An Aggressive Airway Disease 121
7.5 AERD in Children 121
7.6 Mediators Involved in AERD 122
7.7 AERD and Diagnostics 124
7.8 Routes of Challenge: Inhaled, Intranasal, and Intravenous 124
7.9 AERD and Desensitization 125
7.10 Side Effects 126
7.11 ASA Desensitization Specifics 126
7.12 Leukotriene-Modifying Drugs (LTMDs) in AERD and During Desensitization 127
7.13 Local Nasal Desensitization 128
7.14 Desensitization Events 128
7.15 Cutaneous Reactions 128
7.16 Desensitization 129
7.17 Isolated NSAID Reactions 129
7.18 Desensitization 131
7.19 COX-2 Isolated Reactions 131
References 131
Chapter 8: IgE-Dependent and Independent Effector Mechanisms in Human and Murine Anaphylaxis 137
8.1 Introduction 138
8.2 Definition of Anaphylaxis 138
8.3 Murine Models of Anaphylaxis 138
8.3.1 Advantages and Disadvantages 138
8.3.2 Murine IgE-Mediated Anaphylaxis 140
8.3.3 Murine IgG-Mediated Anaphylaxis 141
8.3.4 The Multiple Roles of Basophils in Anaphylaxis 143
8.3.5 Complement-Dependent Anaphylaxis 144
8.3.6 IgE–IgG Interactions in Murine Anaphylaxis 144
8.3.7 Fcg(gamma)RIIb-Dependent Inhibition of IgE-MediatedAnaphylaxis by IgG 145
8.3.8 Controversial and Confusing Issues in Murine Anaphylaxis 145
8.4 Human Anaphylaxis 146
8.4.1 Human IgE-Mediated Anaphylaxis 146
8.4.2 IgE-Independent Human Anaphylaxis 147
8.4.3 IgG-Dependent Human Anaphylaxis 147
8.4.4 Complement-Dependent Human Anaphylaxis 148
8.4.5 Other Mechanisms of Human Anaphylaxis 148
8.5 Conclusions and Clinical Implications 149
References 150
Chapter 9: Food-Induced Anaphylaxis 155
9.1 Introduction 155
9.2 Epidemiology 156
9.3 Food Allergens and Route of Exposure 157
9.4 Pathophysiology of Food-Induced Anaphylaxis 158
9.4.1 Murine Models 158
9.4.2 Intestinal Antigen Uptake 158
9.4.3 Allergenicity of Food Antigens 159
9.5 Clinical Presentation 160
9.5.1 Onset of Symptoms 160
9.5.2 Patterns of Anaphylaxis 161
9.5.3 Differential Diagnosis 161
9.6 Risk Factors for Food-Induced Anaphylaxis 161
9.7 Pediatric Considerations 162
9.7.1 Clinical Presentation 162
9.7.2 Risk Factors 162
9.7.3 Anaphylaxis in Infants 162
9.8 Biphasic Reactions 163
9.9 Fatal Food-Induced Anaphylaxis 164
9.10 Treatment of a Food-Induced Anaphylactic Reaction 165
9.11 Diagnosis of Food-Induced Anaphylaxis 165
9.12 Prevention, Education and Emergency Treatment Plan 167
9.13 Natural History 168
9.14 Future Therapies 168
9.14.1 Non-Allergen-Specific Therapy 168
9.14.1.1 Humanized Monoclonal Anti-IgE 168
9.14.1.2 Traditional Chinese Medicine (TCM) 169
9.14.2 Allergen-Specific Immunotherapy 169
9.14.2.1 Subcutaneous Peanut Immunotherapy 169
9.14.2.2 Oral Immunotherapy 170
Mechanism of OIT 171
Safety of OIT Home Dosing 171
9.14.2.3 Sublingual Immunotherapy 172
9.14.2.4 Immunotherapy with Recombinant Engineered Food Proteins 173
9.14.2.5 Other Approaches 174
9.15 Conclusion 174
References 175
Chapter 10: Antibiotic-Induced Anaphylaxis 180
10.1 Introduction 180
10.2 Drug Allergy Workup 181
10.2.1 Clinical History 181
10.2.2 Skin Tests 182
10.2.3 Provocation Tests 182
10.2.4 Biological Tests 182
10.2.5 Standard Operating Procedures and Preventive Measures 183
10.3 Antibiotic Anaphylaxis Diagnosis 184
10.3.1 ß(beta)-Lactams 184
10.3.2 Quinolones 187
10.3.3 Macrolides 187
10.3.4 Other Antibiotics 188
References 188
Chapter 11: Anaphylaxis During Radiological Procedures and in the Peri-operative Setting 192
11.1 Introduction 192
11.2 Definition 193
11.3 Epidemiology 195
11.3.1 Immediate Reactions Following Iodinated Contrast Agents 195
11.3.1.1 Hyperosmolar Ionic Iodinated Contrast Media 195
11.3.1.2 Comparison Between Ionic and Non-ionic Contrast Media 195
11.3.2 Immediate Reactions to Gadolinium-Containing Contrast Agents 196
11.3.3 Immediate Reactions in the Perioperative Setting 197
11.4 How to Diagnose Anaphylaxis 197
11.4.1 The Clinical History Should Always Be Known for an Appropriate Diagnosis 198
11.4.2 Predictive Criteria of Anaphylaxis Severity 200
11.4.3 Are There Any Clinical Differences Between Anaphylaxis Occurring During the Perioperative and the Radiological Setting 200
11.4.3.1 In the Perioperative Setting 200
11.4.3.2 In the Radiological Setting 201
11.4.4 Which Tools to Prove the Diagnosis? 201
11.4.4.1 Biological Assessment Is a Contributive Tool to the Appropriate Diagnosis 202
In vivo Biochemical Tests 202
In vitro Biochemical Tests 203
11.4.4.2 Skin Testing Is Essential to Prove the Diagnosis and Prevent Further Recurrences 203
General Considerations: How to Perform Skin Testing? 204
Skin Testing with Drugs or Agent Used During the Perioperative Setting? 204
Skin Testing with Contrast Agents 207
11.4.4.3 The Allergenic Determinant Is Not Iodine for Iodinated Contrast Agents 207
11.5 Management of Anaphylaxis 208
11.5.1 Epinephrine: When and How? 208
11.5.2 Fluid Therapy: When and How? 208
11.5.3 Bronchospasm 208
11.5.4 Additional Therapy 209
11.5.5 Anaphylaxis and Catecholamine Failure 209
11.6 Premedication 209
11.6.1 Anesthetic Drugs 209
11.6.2 Iodinated Contrast Agents 209
11.7 Conclusion 212
References 212
Chapter 12: Hymenoptera-Induced Hypersensitivity Reactions and Anaphylaxis 218
12.1 Introduction 218
12.2 Taxonomy of Hymenoptera Insects 219
12.3 Epidemiology of Hymenoptera Venom Allergy 220
12.4 Reactions to Hymenoptera Venom Stings 220
12.4.1 Fatalities from Anaphylaxis to Hymenoptera Stings 221
12.5 Diagnosis of Venom Hypersensitivity 221
12.5.1 Patients with Positive Allergy Tests to Both Honeybee and Wasp Venom 222
12.6 Anaphylaxis in Patients with Negative Allergy Tests 223
12.7 Treatment of Venom Hypersensitivity 223
12.7.1 Venom Immunotherapy 223
12.7.2 Selection of Patients Requiring Venom Immunotherapy 223
12.7.3 Contraindications for VIT 224
12.7.4 Selection of Venom To Be Used in Immunotherapy 224
12.7.5 Treatment Protocols 225
12.7.6 Duration of Venom Immunotherapy 226
12.7.7 Safety of Venom Immunotherapy 226
12.7.8 Efficacy of Venom Immunotherapy 227
12.8 Anaphylaxis After Hymenoptera Sting and Mastocytosis 228
References 228
Chapter 13: Idiopathic Anaphylaxis 232
13.1 Introduction 232
13.2 Pathogenesis 233
13.3 Differential Diagnosis 235
13.4 Classification of Idiopathic Anaphylaxis 238
13.5 Treatment 238
References 240
Chapter 14: Exercise-Induced Anaphylaxis and Food-Dependent Exercise-Induced Anaphylaxis 244
14.1 Introduction and Definition 244
14.2 Clinical Manifestations 245
14.2.1 Triggering Activities 245
14.2.2 Signs and Symptoms 245
14.2.3 Co-triggers 246
14.2.4 Causative Foods in FD-EIAn 246
14.3 Prevalence 247
14.4 Pathophysiology 247
14.5 Evaluation and Diagnosis 247
14.6 Differential Diagnosis 248
14.7 Management 248
14.8 Prognosis 250
14.9 Summary 250
References 251
Chapter 15: Mastocytosis and Mast Cell Activation Syndromes Presenting as Anaphylaxis* 253
15.1 Introduction 253
15.2 Mechanisms of Mast Cell Activation 254
15.3 Clinical Manifestations of Mast Cell Activation 255
15.3.1 Skin and Soft Tissues 255
15.3.2 Respiratory 256
15.3.3 Cardiovascular 257
15.3.4 Gastrointestinal 257
15.3.5 Musculoskeletal 257
15.3.6 Urinary 258
15.3.7 Hematopoietic and Immune Systems 258
15.3.8 Constitutional 258
15.4 Disorders of MC Activation 258
15.5 Systemic Mastocytosis 259
15.6 Monoclonal Mast Cell Activation Syndrome 260
15.7 Mast Cell Activation Syndrome 260
15.8 Diagnostic Approach to Mast Cell Activation Disorders 261
References 262
Chapter 16: Anaphylaxis in Mastocytosis* 265
16.1 Introduction 265
16.2 Mastocytosis 266
16.3 Allergy in Mastocytosis 267
16.4 Anaphylaxis in Mastocytosis 267
16.4.1 Idiopathic Anaphylaxis and Triggers for Anaphylaxis in Mastocytosis 269
16.4.2 Hymenoptera Venom Anaphylaxis in Mastocytosis 269
16.4.3 Anaphylaxis and Venom Immunotherapy in Mastocytosis 270
16.4.4 Anaphylaxis During Surgical Procedures and General Anesthesia 270
16.4.5 Treatment of Patients with Mastocytosis Associated to Anaphylaxis 271
16.4.5.1 General Considerations 271
16.4.5.2 Anesthesia 271
16.4.5.3 Systemic Therapy 272
16.4.6 Treatment of Refractory Cases 272
16.4.6.1 Interferon Alpha 272
16.4.6.2 Cladribine 272
16.4.6.3 Omalizumab 273
16.5 Concluding Remarks 273
References 273
Chapter 17: Flushing and Urticarial Syndromes Presenting as Anaphylaxis 278
17.1 Flushing and Urticaria 278
17.1.1 Introduction 278
17.1.2 Signs, Symptoms, and Pathophysiology of Flushing 279
17.1.3 Flushing in Anaphylaxis and Disorders with Non-IgE Anaphylaxis Features 279
17.1.4 Specific Flushing Syndromes with Anaphylaxis Features 280
17.1.4.1 Carcinoid Syndrome 280
17.1.4.2 Systemic Mastocytosis 281
17.1.4.3 Mast Cell Activation Disorder 283
17.1.4.4 Pheochromocytomas 283
17.1.4.5 Medullary Carcinoma of the Thyroid 283
17.1.4.6 Scombrotoxism 284
17.1.4.7 Medications 284
17.2 Urticarial Syndromes Presenting as Anaphylaxis 284
17.2.1 Introduction 284
17.2.2 Anaphylaxis Symptoms Associated with Specific Urticarial Syndromes 285
17.2.3 Physical Urticarias 285
17.2.3.1 Cholinergic Urticaria 285
17.2.4 Cold Urticaria Syndromes 285
17.2.5 Urticaria and Angioedema in Systemic Reactions to Allergens, Vaccines, and Drugs 286
17.2.5.1 Vespids 286
17.2.5.2 Vaccines 286
17.2.5.3 Drugs 286
17.3 Summary 287
References 287
Chapter 18: Pharmacologic Management of Acute Anaphylaxis 292
18.1 General Approach: Recognition of Anaphylaxis and Pharmacologic Management 292
18.2 Pharmacologic Management 294
18.2.1 Epinephrine 294
18.2.1.1 Indications and Toxicity 295
18.2.1.2 Route of Administration of Epinephrine 296
18.2.1.3 Epinephrine Dosing 296
18.2.2 Oxygen 298
18.2.3 Fluid Management 298
18.2.4 Antihistamines 299
18.2.5 Systemic Corticosteroids 299
18.3 Other Agents 299
18.3.1 Inhaled Albuterol 299
18.3.2 Glucagon 299
18.3.3 Other Vasopressors 300
18.4 Persistent Anaphylaxis Unresponsive to Epinephrine 300
18.5 Cardiac Arrest 300
18.6 Prevention of Anaphylaxis 301
References 301
Chapter 19: Drug Desensitizations in the Management of Allergy and Anaphylaxis to Chemotherapeutic Agents and Monoclonal Antibodies 303
19.1 Introduction 303
19.2 Mechanism of Drug Desensitization 304
19.3 Skin Testing for Drug Hypersensitivity 304
19.4 Drug Desensitization Procedures 305
19.5 Hypersensitivity and Drug Desensitization to Carboplatin and Cisplatin 308
19.6 Hypersensitivity and Drug Desensitization to Oxaliplatin 310
19.7 Hypersensitivity and Drug Desensitization to Taxanes 310
19.8 Hypersensitivity to Monoclonal Antibodies – General Considerations 311
19.9 Hypersensitivity to Monoclonal Antibodies – Clinical Observations 312
19.10 Desensitization to Monoclonal Antibodies 313
19.10.1 Cetuximab – An Unexpected Mechanism for Hypersensitivity 313
19.11 Summary 314
References 315
Chapter 20: Rapid Desensitizations for Antibiotic-Induced Hypersensitivity Reactions and Anaphylaxis 318
20.1 Introduction 318
20.2 Definition of Rapid Intravenous Desensitization 319
20.3 Indications for Desensitization 319
20.3.1 Inclusion Criteria for Desensitization 319
20.3.2 Type I HSRs (IgE-Mediated) 319
20.3.3 HSRs – Non-IgE-Mediated 320
20.3.4 Adverse Reactions Not Amenable to Desensitization 320
20.3.4.1 Cellular and Molecular Targets 321
20.3.4.2 Principles and Protocols of Rapid Desensitization 321
20.3.4.3 Symptoms During the Desensitization and Their Management 321
20.3.4.4 Safety Measures 322
20.3.4.5 Beta-Lactams 322
20.3.4.6 Glycopeptides 326
20.3.4.7 Quinolones 327
20.3.4.8 Aminoglycosides 327
20.3.4.9 Macrolides 327
20.3.4.10 Linezolid 328
20.3.4.11 Antivirals (Including Antiretroviral Agents) 329
20.3.4.12 Antitubercular Drugs 330
20.3.4.13 Sulfonamides 330
20.3.4.14 Antifungals 331
20.4 Conclusions 333
References 333
Chapter 21: Induction of Tolerance for Food-Induced Anaphylaxis 337
21.1 Introduction 337
21.2 Immunology and Oral Tolerance 338
21.3 Antigen Processing in the Gastrointestinal Tract 339
21.4 Mechanisms of Oral Tolerance 339
21.5 Factors Influencing Development of Tolerance 342
21.6 Potential Therapeutic Strategies 343
21.7 Conclusions 346
References 346
Chapter 22: Management of Anaphylaxis: Relevance of Causes and Future Trends in Treatment 349
22.1 Introduction 349
22.2 Relevance of Causes 350
22.2.1 Established Causes and Their Treatment 350
22.2.2 Novel Causes of Anaphylaxis 351
22.2.2.1 Overview of Cross Reactive Carbohydrate Determinants 351
22.2.2.2 Implications for Recombinant Therapeutics 353
22.3 Future Trends in Treatment: Anti-IgE 353
22.3.1 Mechanism of Action 353
22.3.2 Evidence for a (Broader) Role in Allergic Diseases 355
22.3.3 Safety and Efficacy 355
22.4 Conclusion 355
References 356
Index 359