Zuberbier / Grattan / Maurer Urticaria and Angioedema

1. Auflage 2010
ISBN: 978-3-540-79048-8
Verlag: Springer Berlin Heidelberg
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 158 Seiten

Urticaria is one of the most common diseases in dermatology and allergy. Unlike many other diseases, the ? eeting nature of the wheals makes ? rst diagnosis by both patients and phy- cians in many cases easy. However, this only refers to the ordinary wheals. The disease itself is highly complex in nature, with variety of clinical manifestations ranging from pinpoi- sized wheals to extensive angiodema. Complexity is also seen in the diversity of possible eliciting factors, the many different clinical subtypes and the therapeutic responsiveness. Only in recent years has a better understanding of the diversity in the different subtypes led to new classi? cations and new evidence-based guidelines for diagnostics and mana- ment of the disease. While mast cells are in the center of most urticaria reactions, it is now clearly understood that the responsible mediators are not only limited to histamines. The current book appears in a series of books by Springer. In 1986, the ? rst monograph was edited by Professor Henz née Chanewsky. Since then, two updates of the book have appeared in the German language with Professor Henz as ? rst editor and T. Zuberbier, J. Grabbe, and E. Monroe as the co-editors of the most recent English version, published in 1998. All these books have been written as a joint effort of Professor Henz together with her team at the Department of Dermatology at the Virchow Clinic, Humboldt University, Berlin.

Autoren/Hrsg.

Zuberbier, Torsten

Grattan, Clive

Maurer, Marcus

Inhaltsverzeichnis

1;Urticaria and Angioedema;2
1.1;Title Page;3
1.2;Copyright page;4
1.3;Preface;5
1.4;Contents;6
1.5;Contributors;8
1.6;Chapter 1;10
1.6.1;History of Urticaria;10
1.6.1.1;1.1 Introduction;11
1.6.1.2;1.2 The Cellular and Molecular Basis of Urticaria: First Steps;11
1.6.1.3;1.3 The Enigma of Chronic “Idiopathic” Urticaria;12
1.6.1.4;1.4 Treatment of Urticaria: Antihistamines;13
1.6.1.5;1.5 Take Home Pearls;14
1.6.1.6;References;15
1.7;Chapter 2;17
1.7.1;Aetiopathogenesis of Urticaria;17
1.7.1.1;2.1 Lessons from Histopathology;18
1.7.1.2;2.2 A Central Role for the Mast Cell;19
1.7.1.2.1;2.2.1 Mast Cell Mediators of Urticaria;20
1.7.1.2.1.1;2.2.1.1 Histamine;20
1.7.1.2.1.2;2.2.1.2 Cysteinyl Leukotrienes;20
1.7.1.3;2.3 Involvement of Other Infl ammatory Cells in Urticaria;21
1.7.1.4;2.4 Urticaria Not Implicating the Mast Cell (Non-histaminergic);22
1.7.1.5;2.5 What Causes Mast Cell Mediator Release in the First Place?;23
1.7.1.5.1;2.5.1 Immunological Stimuli of Mast Cell Secretion;25
1.7.1.5.1.1;2.5.1.1 Allergens;25
1.7.1.5.1.2;2.5.1.2 Autoantibodies;25
1.7.1.5.1.3;2.5.1.3 Complement;26
1.7.1.5.2;2.5.2 Mast Cell Liberators and Pseudoallergens;26
1.7.1.6;2.6 Tests for Autoimmune Urticaria;26
1.7.1.6.1;2.6.1 Laboratory Assays;26
1.7.1.6.2;2.6.2 The Autologous Serum Skin Test;27
1.7.1.7;2.7 A Concept Model for Understanding Chronic Urticaria;27
1.7.1.8;2.8 Clinical Take Home Pearls;29
1.7.1.9;References;29
1.8;Chapter 3;32
1.8.1;Classification of Urticaria;32
1.8.1.1;3.1 Definition;32
1.8.1.2;3.2 Histology;35
1.8.1.3;3.3 Classifi cation of Urticaria on the Basis of Its Symptoms, Duration, Frequency, and Causes;35
1.8.1.4;3.4 Take Home Pearls;38
1.8.1.5;References;38
1.9;Chapter 4;39
1.9.1;Impact of Urticaria: QOL and Performance;39
1.9.1.1;4.1 Take Home Pearls;42
1.9.1.2;References;42
1.10;Chapter 5.1;43
1.10.1;Acute Urticaria;43
1.10.1.1;5.1.1 Definition;43
1.10.1.2;5.1.2 Epidemiology;44
1.10.1.3;5.1.3 Clinical Aspects;44
1.10.1.4;5.1.4 Aetiology;45
1.10.1.5;5.1.5 Natural Course;46
1.10.1.6;5.1.6 Diagnosis;47
1.10.1.7;5.1.7 Treatment;47
1.10.1.8;5.1.8 Take Home Pearls;48
1.10.1.9;References;48
1.11;Chapter 5.2;50
1.11.1;Chronic Urticaria;50
1.11.2;5.2.1 Definition;50
1.11.3;5.2.2 Clinical Picture;52
1.11.4;5.2.3 Epidemiology;52
1.11.5;5.2.4 Pathogenesis;52
1.11.6;5.2.5 Causes and Triggers;53
1.11.6.1;5.2.5.1 CU Due to Autoreactivity;53
1.11.6.2;5.2.5.2 CU Due to Infection;55
1.11.6.3;5.2.5.3 CU Due to Intolerance;55
1.11.6.4;5.2.5.4 CU Due to Other Causes;55
1.11.6.5;5.2.5.5 Triggers and Eliciting Factors;56
1.11.7;5.2.6 Diagnostics;56
1.11.8;5.2.7 Therapy;57
1.11.8.1;5.2.7.1 Removing Underlying Causes, Relevant Triggers and Aggravating Factors;57
1.11.8.2;5.2.7.2 Mast Cell-Targeting Therapies;58
1.11.8.2.1;5.2.7.2.1 Inhibitors of Mast Cell Activation;58
1.11.8.2.2;5.2.7.2.2 Antagonists of Mast Cell Activators;59
1.11.8.3;5.2.7.3 Blocking of Mast Cell Mediators;59
1.11.9;5.2.8 Take Home Pearls;59
1.11.10;References;60
1.12;Chapter 5.3;62
1.12.1;Dermographic and Delayed Pressure Urticaria;62
1.12.1.1;5.3.1 Symptomatic Dermographism (Dermatographism: Urticaria Factitia);62
1.12.1.1.1;5.3.1.1 Making the Diagnosis;62
1.12.1.1.2;5.3.1.2 Taking the History;62
1.12.1.1.3;5.3.1.3 Clinical Findings;63
1.12.1.1.4;5.3.1.4 Confi rming the Diagnosis;63
1.12.1.1.5;5.3.1.5 Diagnostic Implications and Treatment;63
1.12.1.1.6;5.3.1.6 Take Home Pearls;64
1.12.1.2;5.3.2 Delayed Pressure Urticaria;64
1.12.1.2.1;5.3.2.1 Making the Diagnosis;65
1.12.1.2.2;5.3.2.2 Taking the History;65
1.12.1.2.3;5.3.2.3 Clinical Features;65
1.12.1.2.4;5.3.2.4 Diagnostic Implications and Treatment;66
1.12.1.2.5;5.3.2.5 Take Home Pearls;66
1.12.1.3;References;67
1.13;Chapter 5.4;68
1.13.1;Heat and Cold Urticaria;68
1.13.1.1;5.4.1 Introduction: The Disease Spectrum;68
1.13.1.2;5.4.2 Cold and Heat Urticaria;69
1.13.1.2.1;5.4.2.1 Epidemiology;69
1.13.1.2.2;5.4.2.2 Pathogenesis;70
1.13.1.2.3;5.4.2.3 Clinical Features;71
1.13.1.2.4;5.4.2.4 Confi rmation of the Diagnosis;71
1.13.1.2.5;5.4.2.5 Differential Diagnosis;72
1.13.1.2.6;5.4.2.6 Treatment;73
1.13.1.2.6.1;5.4.2.6.1 Pharmacological Treatment;73
1.13.1.2.6.2;5.4.2.6.2 Tolerance Induction;73
1.13.1.2.7;5.4.2.7 Prognosis;74
1.13.1.3;5.4.3 Take Home Pearls;74
1.13.1.4;References;74
1.14;Chapter 5.5;77
1.14.1;Solar Urticaria;77
1.14.1.1;5.5.1 Clinical Features;77
1.14.1.2;5.5.2 Pathogenesis;78
1.14.1.3;5.5.3 Treatment and Prognosis;81
1.14.1.4;5.5.4 Take Home Pearls;82
1.14.1.5;References;82
1.15;Chapter 5.6;85
1.15.1;Cholinergic Urticaria and Exercise-Induced Anaphylaxis;85
1.15.1.1;5.6.1 Introduction: The Disease Spectrum;85
1.15.1.2;5.6.2 Cholinergic Urticaria;86
1.15.1.2.1;5.6.2.1 Epidemiology;86
1.15.1.2.2;5.6.2.2 Pathogenesis;86
1.15.1.2.3;5.6.2.3 Clinical Features;87
1.15.1.2.4;5.6.2.4 Confirmation of the Diagnosis;88
1.15.1.2.5;5.6.2.5 Differential Diagnosis;88
1.15.1.2.6;5.6.2.6 Treatment;89
1.15.1.2.7;5.6.2.7 Prognosis;89
1.15.1.3;5.6.3 Exercise-Induced Anaphylaxis;90
1.15.1.4;5.6.4 Take Home Pearls;91
1.15.1.5;References;91
1.16;Chapter 5.7;94
1.16.1;Contact Urticaria;94
1.16.1.1;5.7.1 Etiology and Pathogenesis;94
1.16.1.2;5.7.2 Clinical Findings;96
1.16.1.3;5.7.3 Diagnostic Approach;97
1.16.1.4;5.7.4 Course and Prognosis;97
1.16.1.5;5.7.5 Therapy;97
1.16.1.6;5.7.6 Take Home Pearls;97
1.16.1.7;References;98
1.17;Chapter 5.8;99
1.17.1;Urticarial Syndromes and Autoinfl ammation;99
1.17.1.1;5.8.1 Distinct Molecular Pathways Underlying Urticarial Syndromes Associated with Autoinflammation;100
1.17.1.2;5.8.2 Urticaria: Inherited or Acquired;100
1.17.1.3;5.8.3 Familial Urticarial Syndromes;100
1.17.1.4;5.8.4 Genotype–Phenotype Disparity in Autoinfl ammatory Disease;104
1.17.1.5;5.8.5 Nonfamilial Autoinfl ammatory Syndromes: Acquired or Polygenic Etiology;106
1.17.1.6;5.8.6 Diagnosis;106
1.17.1.7;5.8.7 Treatment;107
1.17.1.8;5.8.8 Take Home Pearls;107
1.17.1.9;References;108
1.18;Chapter 5.9;111
1.18.1;Urticaria Vasculitis;111
1.18.1.1;5.9.1 Definition;112
1.18.1.2;5.9.2 Epidemiology;112
1.18.1.3;5.9.3 Histopathologic Findings;112
1.18.1.4;5.9.4 Pathophysiology;113
1.18.1.5;5.9.5 Clinical Features;113
1.18.1.6;5.9.6 Systemic Manifestations;114
1.18.1.7;5.9.7 Differential Diagnosis and Investigations;115
1.18.1.8;5.9.8 Prognosis;116
1.18.1.9;5.9.9 Treatment;116
1.18.1.10;5.9.10 Take Home Pearls;116
1.18.1.11;References;118
1.19;Chapter 5.10;119
1.19.1;Angioedema;119
1.19.1.1;5.10.1 Classification of Angioedema;120
1.19.1.2;5.10.2 Pathophysiology of Angioedema;122
1.19.1.3;5.10.3 Clinical Features of Angioedema;122
1.19.1.4;5.10.4 Differential Diagnosis of Angioedema;123
1.19.1.5;5.10.5 Clinical Approach to a Patient with Angioedema;124
1.19.1.6;5.10.6 Recent Advances and Perspectives;125
1.19.1.7;5.10.7 Take Home Pearls;126
1.19.1.8;References;127
1.20;Chapter 6;130
1.20.1;Therapy of Urticaria;130
1.20.1.1;6.1 General Treatment Advice for All Urticaria Subtypes;131
1.20.1.2;6.2 Evidence-Based Treatment of Spontaneous Urticaria;131
1.20.1.2.1;6.2.1 Spontaneous Acute Urticaria;131
1.20.1.2.2;6.2.2 Spontaneous Chronic Urticaria;134
1.20.1.2.2.1;6.2.2.2 Diet;134
1.20.1.2.2.2;6.2.2.3 Non-Sedating H1 Antihistamines;135
1.20.1.2.2.3;6.2.2.4 H2-Antihistamines;135
1.20.1.2.2.4;6.2.2.5 Glucocorticosteroids;135
1.20.1.2.2.5;6.2.2.6 Leukotriene Antagonists;136
1.20.1.2.2.6;6.2.2.7 Cyclosporin A;136
1.20.1.2.2.7;6.2.2.8 Thyroid Hormones;136
1.20.1.2.2.8;6.2.2.9 Other Therapeutic Options;137
1.20.1.3;6.3 Evidence-Based Treatment of Physical Urticaria;137
1.20.1.4;6.4 Evidence-Based Treatment of Special Urticaria Subtypes;138
1.20.1.5;6.5 Take Home Pearls;138
1.20.1.6;References;139
1.21;Chapter 7;141
1.21.1;Standard Operating Procedures: A Practical Approach;141
1.21.1.1;7.1 Assessing Urticaria Activity Score;142
1.21.1.2;7.2 Testing for Autoreactivity;142
1.21.1.3;7.3 Testing for Food Elicited Urticaria Diet;144
1.21.1.4;7.4 Ins and Outs of the Food Labelling Rules;145
1.21.1.5;7.5 Use of Diary Cards;146
1.21.1.6;7.6 Questionnaire;146
1.21.1.7;7.7 Prick Test;149
1.21.1.8;7.8 Take Home Pearls;151
1.21.1.9;References;151
1.22;Appendix;152
1.23;Index;154

Leseproben

"(p. 129-130)


Core Messages

The different urticaria subtypes are common skin diseases persisting often for › years with multifactorial triggering factors and greatly reduced quality of life as well as occupational disability. Therapy can be problematic and is not standardised. Regarding the long duration › of this annoying skin disease, every attempt should be made to identify and avoid speci? c or unspeci? c triggering factors. The treatment goal is to maximise the quality of life, to maintain vigilance and ability to work or to attend school and to minimise drug-related side effects.

Besides antihistamines and the eradication or avoidance of identi? ed triggering › factors, many drugs, most of which are not licensed for urticaria, are administered. The highest grade of recommendation (GoR) according to the criteria of › evidence-based medicine can only be given for second-generation H1 antihistamines. They should be administered in an adequate dose, up to fourfold the normal dose while considering potential side effects. The data on treatment alternatives are totally insuf? cient. Good evidence exists in › severely affected patients for cyclosporin A. Subgroups might bene? t from addition of leukotrienes antagonists. Chloroquine and dapsone may be worthy of further investigation within randomised controlled trials.

The risk–bene? t pro? le of each alternative (off-label use) to second-generation › H1 antihistamines should be carefully considered before treatment. This applies especially to immunosuppressive agents. The clinical pictures of urticaria are of heterogeneous aetiology and therefore subclassi? ed into distinct groups, which can coexist: spontaneous urticaria, physical urticaria and special types. To optimise urticaria treatment, the ? rst strategy should be to correctly classify the respective urticaria subtype. The treatment goal is to maximise the quality of life and ability to work or to attend school and to minimise drug-related side effects.

This is of particular importance regarding the long year duration of many urticaria subtypes. Relevant outcomes of treatment trials include pruritus, weal size, number and frequency, loss of awakening, overall physician and patient assessment and permanent remission of disease. This chapter is based on the results of two recent publications evaluating randomised controlled trials (RCTs) of urticaria therapy (until October 2004) according to the criteria of evidence-based medicine [1, 2 ].

Details of the individual studies, inclusion and exclusion criteria as well as the cited literature are available in the publications [1, 2 ], if not otherwise cited. Additionally, this review includes at least the RCTs published until December 2006 [3–7 ] and also interesting treatment approaches. In the text, the respective GoR according to the criteria of evidence-based medicine of the Scottish Intercollegiate Guidelines Network (SIGN; www.sign.ac.uk, GoR A to D, whereas A represents best evidence) is given in parentheses. Table 6.1 summarises the recommended therapeutic approaches."