Allergic Skin
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Transcript of 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