1. Introduction: Urticaria and Angioedema1

2. 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

3. The Pathogenesis of Chronic Urticaria: Cellular Mediators

4. Histamine as a Mast Cell Mediator

5. 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)

6. An Autoimmune Basis for Chronic Idiopathic Urticaria: Antibodies to IgE

7. 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, infectious mononucleosis
Insect stings
Foods
Recent transfusions with blood products (hepatitis)
Recent initiation of drugs
Physical exam
Skin
Eyes
Ears
Throat
Lymph nodes
Feet
Lungs
Joints
Abdomen

8. 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)

9. Histopathology Group 2: Group 3: Polymorphous perivascular infiltrate
Neutrophils
Eosinophils
Mononuclear cells
Group 3:
Sparse perivascular lymphocytes

10. 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

11. 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

12. Four-week Treatment Period: Fexofenadine HCl
Mean Pruritus Scores/Mean Number of Wheals/Mean Total Symptom Scores

13. An Approach to the Treatment of Chronic Urticaria

14. 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
Beta-adrenergic agonists
Epinephrine for acute urticaria (rapid but short-lived response)
Terbutaline
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)
Miscellaneous
PUVA
Hydroxychloroquine
Thyroxine

15. 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

16. Atopic Dermatitis: Physical Distribution by Age Group

17. 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

18. 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

19. 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

20. 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