Introduction: Urticaria and Angioedema

Urticaria

Angioedema

Etiology of Urticarial Reactions: Allergic Triggers

Acute Urticaria

Drugs Foods

Chronic Urticaria

Food additives
Viral infections hepatitis A, B, C Epstein-Barr virus

Physical factors cold heat dermatographic pressure solar

Idiopathic

Insect bites and stings

Contactants and inhalants (includes animal dander and latex)

The Pathogenesis of Chronic Urticaria: Cellular Mediators

Histamine as a Mast Cell Mediator

Role of Mast Cells in Chronic Urticaria: Lower Threshold for Histamine Release

Cutaneous mass cell

Release threshold decreased by:
Cytokines & chemokines in the cutaneous microenvironment Antigen exposure Histamine-releasing factor Autoantibody Psychological factors

Release threshold increased by:

Corticosteroids Antihistamines Cromolyn (in vitro)

An Autoimmune Basis for Chronic Idiopathic Urticaria: Antibodies to IgE

Initial Workup of Urticaria

Patient history

Physical exam

Sinusitis Arthritis Thyroid disease Cutaneous fungal infections Urinary tract symptoms Upper respiratory tract infection (particularly important in children) Travel history (parasitic infection) Sore throat Epstein-Barr virus, infectious mononucleosis Insect stings Foods Recent transfusions with blood products (hepatitis) Recent initiation of drugs

Skin Eyes Ears Throat Lymph nodes Feet Lungs Joints Abdomen

Laboratory Assessment for Chronic Urticaria

Initial tests
CBC with differential Erythrocyte sedimentation rate Urinalysis

Possible tests for selected patients

Stool examination for ova and parasites Blood chemistry profile Antinuclear antibody titer (ANA) Hepatitis B and C Skin tests for IgE-mediated reactions

RAST for specific IgE Complement studies: CH50 Cryoproteins Thyroid microsomal antibody Antithyroglobulin Thyroid stimulating hormone (TSH)

Histopathology

Group 2:
Polymorphous perivascular infiltrate Neutrophils Eosinophils Mononuclear cells

Group 3:

Sparse perivascular lymphocytes

Urticaria Associated With Other Conditions

Collagen vascular disease (eg, systemic lupus erythematosus) Complement deficiency, viral infections (including hepatitis B and C), serum sickness, and allergic drug eruptions Chronic tinea pedis Pruritic urticarial papules and plaques of pregnancy (PUPPP) Schnitzlers syndrome

H1-Receptor Antagonists: Pros and Cons for Urticaria and Angioedema

First-generation antihistamines (diphenhydramine and hydroxyzine)

Advantages: Rapid onset of action, relatively inexpensive Disadvantages: Sedating, anticholinergic

Second-generation antihistamines (astemizole, cetirizine, fexofenadine, loratadine)

Advantages: No sedation (except cetirizine); no adverse anticholinergic effects; bid and qd dosing Disadvantages: Prolongation of QT interval; ventricular tachycardia (astemizole only) in a patient subgroup

Four-week Treatment Period: Fexofenadine HCl

Mean Pruritus Scores/Mean Number of Wheals/Mean Total Symptom Scores

An Approach to the Treatment of Chronic Urticaria

Treatment of Urticaria: Pharmacologic Options

Antihistamines, others
First-generation H1 Second-generation H1 Antihistamine/decongestant combinations Tricyclic antidepressants (eg, doxepin) Combined H1 and H2 agents

Corticosteroids
Severe acute urticaria avoid long-term use use alternate-day regimen when possible Avoid in chronic urticaria (lowest dose plus antihistamines might be necessary)

Beta-adrenergic agonists
Epinephrine for acute urticaria (rapid but short-lived response) Terbutaline

Miscellaneous
PUVA Hydroxychloroquine Thyroxine

Atopic Dermatitis: Acute, Subacute, and Chronic Lesions

Acute Cutaneous Lesions
Erythematous, intensely pruritic papules and vesicles Confined to areas of predilection cheeks in infants antecubital popliteal

Subacute Cutaneous Lesions

Erythema excoriation, scaling Bleeding and oozing lesions

Chronic Lesions
Excoriations with crusting Thickened lichenified lesions Postinflammatory hyperpigmentation Nodular prurigo

Atopic Dermatitis: Physical Distribution by Age Group

Immune Response in Atopic Dermatitis

Markedly elevated serum IgE levels

Peripheral blood eosinophilia

Highly complex inflammatory responses > IgE-dependent immediate hypersensitivity Multifunctional role of IgE (beyond mediation of specific mast cell or basophil degranulation) Cell types that express IgE on surface monocyte/macrophages Langerhans cells mast cells basophils

Atopic Dermatitis: Tests to Identify Specific Triggers

Skin prick testing for specific environmental and/or food allergens RAST, ELISA, etc, to identify serum IgE directed to specific allergens in patients with extensive cutaneous involvement Tzanck smear for herpes simplex

KOH preparation for dermatophytosis

Grams stain for bacterial infections Culture for antibiotic sensitivity for staphylococcal infection; supplement with bacterial cultures

Cultures to support tests bacterial, viral, or fungal

Topical Corticosteroids

Ranked from high to low potency in 7 classes Group 1 (most potent): betamethasone dipropionate 0.05% Group 4 (intermediate potency): hydrocortisone valerate 0.2% Group 7 (least potent): hydrocortisone hydrochloride 1% Local side effects: Development of striae and atrophy of the skin, perioral dermatitis, rosacea Systemic effects: Depend on potency, site of application, occlusiveness, percentage of body covered, length of use May cause adrenal suppression in infants and small children if used long term

Antihistamines and Other Treatments

Standard Treatment
Oral antihistamines to relieve itching Moisturizer to minimize dry skin Topical corticosteroids

Hard-to-manage Disease
Antibiotics Coal tar preparations (antipruritic and anti-inflammatory) Wet dressings and occlusion Systemic corticosteroids UV light therapy Hospitalization