Introduction:

Urticaria and Angioedema

Urticaria Angioedema

Etiology of Urticarial Reactions:

Allergic Triggers

Acute UrticariaDrugs

Foods

Food additives

Viral infections–hepatitis A, B, C–Epstein-Barr virus

Insect bites and stings

Contactants and inhalants (includes animal dander and latex)

Chronic UrticariaPhysical factors–cold–heat–dermatographic–pressure–solar

Idiopathic

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

Release threshold decreased by:Cytokines & chemokines

in the cutaneous microenvironment

Antigen exposureHistamine-releasing factorAutoantibodyPsychological factors

Release threshold increased by:CorticosteroidsAntihistaminesCromolyn (in vitro)

Cutaneous mass cell

An Autoimmune Basis for Chronic

Idiopathic Urticaria: Antibodies to IgE

Initial Workup of Urticaria

Patient historySinusitisArthritisThyroid diseaseCutaneous fungal infectionsUrinary tract symptomsUpper respiratory tract infection

(particularly important in children)Travel history (parasitic infection)Sore throatEpstein-Barr virus, infectious

mononucleosisInsect stingsFoodsRecent transfusions with

blood products (hepatitis)Recent initiation of drugs

Physical examSkinEyesEarsThroatLymph nodesFeetLungsJointsAbdomen

Laboratory Assessment for

Chronic Urticaria

Possible tests for selected patientsStool examination for ova

and parasitesBlood chemistry profileAntinuclear antibody titer (ANA)Hepatitis B and CSkin tests for IgE-mediated

reactions

Initial testsCBC with differentialErythrocyte sedimentation rateUrinalysis

RAST for specific IgEComplement studies: CH50

CryoproteinsThyroid microsomal antibodyAntithyroglobulinThyroid stimulating hormone (TSH)

Histopathology

Group 2:Polymorphous perivascular infiltrateNeutrophilsEosinophilsMononuclear 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)

Schnitzler’s 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, othersFirst-generation H1

Second-generation H1

Antihistamine/decongestant combinations

Tricyclic antidepressants (eg, doxepin)

Combined H1 and H2 agents

Beta-adrenergic agonistsEpinephrine for acute urticaria

(rapid but short-lived response)Terbutaline

CorticosteroidsSevere acute urticaria–avoid long-term use–use alternate-day regimen

when possibleAvoid in chronic urticaria

(lowest dose plus antihistamines might be necessary)

MiscellaneousPUVAHydroxychloroquineThyroxine

Atopic Dermatitis: Acute, Subacute,

and Chronic Lesions

Acute Cutaneous LesionsErythematous, intensely pruritic papules and vesiclesConfined to areas of predilection–cheeks in infants–antecubital–popliteal

Subacute Cutaneous LesionsErythema excoriation, scalingBleeding and oozing lesions

Chronic LesionsExcoriations with crustingThickened lichenified lesionsPostinflammatory hyperpigmentationNodular 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

Gram’s 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 TreatmentOral antihistamines to relieve itchingMoisturizer to minimize dry skin Topical corticosteroids

Hard-to-manage DiseaseAntibioticsCoal tar preparations (antipruritic and anti-inflammatory)Wet dressings and occlusionSystemic corticosteroidsUV light therapyHospitalization