Allergic Skin

7/31/2019 Allergic Skin

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Introduction:

Urticaria and Angioedema

Urticaria Angioedema


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Etiology of Urticarial Reactions:

Allergic Triggers

Acute Urticaria

Drugs

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 Urticaria

Physical factors

cold

heat

dermatographic

pressure

solar

Idiopathic


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The Pathogenesis of Chronic Urticaria:

Cellular Mediators


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Histamine as a Mast Cell Mediator


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Role of Mast Cells in Chronic Urticaria:

Lower Threshold for Histamine Release

Release threshold decreased by: Cytokines & chemokines

in the cutaneousmicroenvironment

Antigen exposure Histamine-releasing factor

Autoantibody

Psychological factors

Release threshold increased by: Corticosteroids

Antihistamines

Cromolyn (in vitro)

Cutaneous mass cell


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An Autoimmune Basis for Chronic

Idiopathic Urticaria: Antibodies to IgE


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Initial Workup of Urticaria

Patient history 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, infectiousmononucleosis

Insect stings

Foods

Recent transfusions withblood products (hepatitis)

Recent initiation of drugs

Physical exam Skin

Eyes

Ears

Throat

Lymph nodes

Feet Lungs

Joints

Abdomen


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Laboratory Assessment for

Chronic Urticaria

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

Initial tests CBC with differential

Erythrocyte sedimentation rate

Urinalysis

RAST for specific IgE

Complement studies: CH50

Cryoproteins

Thyroid microsomal antibody

Antithyroglobulin

Thyroid stimulating hormone (TSH)


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Histopathology

Group 2: Polymorphous perivascular infiltrate

Neutrophils

Eosinophils Mononuclear cells

Group 3: Sparse perivascular lymphocyte


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Urticaria Associated With

Other Conditions

Collagen vascular disease (eg, systemic lupus erythematosus)

Complement deficiency, viral infections (including hepatitis Band C), serum sickness, and allergic drug eruptions

Chronic tinea pedis

Pruritic urticarial papules and plaques of pregnancy (PUPPP)

Schnitzlers syndrome


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H1-Receptor Antagonists:

Pros and Cons for Urticaria and Angioedema

First-generation antihistamines (diphenhydramineand hydroxyzine)

Advantages: Rapid onset of action, relatively inexpensive

Disadvantages: Sedating, anticholinergic

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

Advantages: No sedation (except cetirizine); no adverseanticholinergic effects; bid and qd dosing

Disadvantages: Prolongation of QT interval; ventriculartachycardia (astemizole only) in a patient subgroup


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Four-week Treatment Period:

Fexofenadine HCl

Mean Pruritus Scores/Mean Number ofWheals/Mean Total Symptom Scores


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An Approach to the Treatment of

Chronic Urticaria


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Treatment of Urticaria:

Pharmacologic Options

Antihistamines, others First-generation H1

Second-generation H1

Antihistamine/decongestantcombinations

Tricyclic antidepressants(eg, doxepin)

Combined H1 and H2 agents

Beta-adrenergic agonists Epinephrine for acute urticaria

(rapid but short-lived response) Terbutaline

Corticosteroids Severe acute urticaria

avoid long-term use

use alternate-day regimenwhen possible

Avoid in chronic urticaria(lowest dose plus antihistaminesmight be necessary)

Miscellaneous PUVA

Hydroxychloroquine Thyroxine


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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


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Atopic Dermatitis:

Physical Distribution by Age Group


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Immune Response in Atopic Dermatitis

Markedly elevated serum IgE levels

Peripheral blood eosinophilia

Highly complex inflammatory responses > IgE-dependentimmediate hypersensitivity

Multifunctional role of IgE (beyond mediation of specificmast cell or basophil degranulation)

Cell types that express IgE on surface

monocyte/macrophages

Langerhans cells

mast cells

basophils


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Atopic Dermatitis:

Tests to Identify Specific Triggers

Skin prick testing for specific environmentaland/or food allergens

RAST, ELISA, etc, to identify serum IgE directed to specificallergens 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


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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, perioraldermatitis, 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


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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

Allergic Skin

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