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Anaphylaxis and Hypersensitivity Reactions
Mariana C. Castells
Verlag Humana Press, 2010
ISBN 9781603279512 , 361 Seiten
Format PDF
Kopierschutz Wasserzeichen
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