Download Urticaria and Angioedema - Hatzalah of Miami-Dade

Introduction:
Urticaria and Angioedema
Urticaria
Angioedema
Etiology of Urticarial Reactions:
Allergic Triggers
Acute Urticaria
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Drugs
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Foods
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Food additives
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Viral infections
– hepatitis A, B, C
– Epstein-Barr virus
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Insect bites and stings
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Contactants and inhalants
(includes animal dander and latex)
Chronic Urticaria
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Physical factors
– cold
– heat
– dermatographic
– pressure
– solar
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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
Cutaneous mass cell
Release threshold decreased by:
Cytokines & chemokines
in the cutaneous
microenvironment
 Antigen exposure
 Histamine-releasing factor
 Autoantibody
 Psychological factors
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Release threshold increased by:
Corticosteroids
 Antihistamines
 Cromolyn (in vitro)
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An Autoimmune Basis for Chronic
Idiopathic Urticaria: Antibodies to IgE
Initial Workup of Urticaria
Patient history
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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
Physical exam
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Skin
Eyes
Ears
Throat
Lymph nodes
Feet
Lungs
Joints
Abdomen
Laboratory Assessment for
Chronic Urticaria
Initial tests
CBC with differential
 Erythrocyte sedimentation rate
 Urinalysis
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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
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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
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Group 3:
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Sparse perivascular lymphocytes
Urticaria Associated With
Other Conditions
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Collagen vascular disease (eg, systemic lupus erythematosus)
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Complement deficiency, viral infections (including hepatitis B
and C), serum sickness, and allergic drug eruptions
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Chronic tinea pedis
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Pruritic urticarial papules and plaques of pregnancy (PUPPP)
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Schnitzler’s syndrome
H1-Receptor Antagonists:
Pros and Cons for Urticaria and Angioedema
First-generation antihistamines (diphenhydramine
and hydroxyzine)
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Advantages: Rapid onset of action, relatively inexpensive
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Disadvantages: Sedating, anticholinergic
Second-generation antihistamines (astemizole,
cetirizine, fexofenadine, loratadine)
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Advantages: No sedation (except cetirizine); no adverse
anticholinergic effects; bid and qd dosing
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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
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Beta-adrenergic agonists
Epinephrine for acute urticaria
(rapid but short-lived response)
 Terbutaline
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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)
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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
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Subacute Cutaneous Lesions
Erythema excoriation, scaling
 Bleeding and oozing lesions
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Chronic Lesions
Excoriations with crusting
 Thickened lichenified lesions
 Postinflammatory hyperpigmentation
 Nodular prurigo
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Atopic Dermatitis:
Physical Distribution by Age Group
Immune Response in Atopic Dermatitis
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Markedly elevated serum IgE levels
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Peripheral blood eosinophilia
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Highly complex inflammatory responses > IgE-dependent
immediate hypersensitivity
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Multifunctional role of IgE (beyond mediation of specific
mast cell or basophil degranulation)
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Cell types that express IgE on surface
– monocyte/macrophages
– Langerhans’ cells
– mast cells
– basophils
Atopic Dermatitis:
Tests to Identify Specific Triggers
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Skin prick testing for specific environmental
and/or food allergens
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RAST, ELISA, etc, to identify serum IgE directed to specific
allergens in patients with extensive cutaneous involvement
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Tzanck smear for herpes simplex
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KOH preparation for dermatophytosis
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Gram’s stain for bacterial infections
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Culture for antibiotic sensitivity for staphylococcal infection;
supplement with bacterial cultures
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Cultures to support tests bacterial, viral, or fungal
Topical Corticosteroids
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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%
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Local side effects:
Development of striae and atrophy of the skin, perioral
dermatitis, rosacea
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Systemic effects:
Depend on potency, site of application, occlusiveness,
percentage of body covered, length of use
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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
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Hard-to-manage Disease
Antibiotics
 Coal tar preparations (antipruritic and anti-inflammatory)
 Wet dressings and occlusion
 Systemic corticosteroids
 UV light therapy
 Hospitalization
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