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Anaphylaxis and Hypersensitivity Reactions

Mariana C. Castells

 

Verlag Humana Press, 2010

ISBN 9781603279512 , 361 Seiten

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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