Introduction: Urticaria and Angioedema

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IntroductionUrticaria and Angioedema

• Urticaria

Angioedema
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Etiology of Urticarial ReactionsAllergic
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 UrticariaCellular
Mediators
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Histamine as a Mast Cell Mediator
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Role of Mast Cells in Chronic UrticariaLower
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)

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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, 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

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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)

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Histopathology

• Group 2
• Polymorphous perivascular infiltrate
• Neutrophils
• Eosinophils
• Mononuclear cells

• Group 3
• Sparse perivascular lymphocytes

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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)
• Schnitzlers syndrome

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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

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Four-week Treatment PeriodFexofenadine HCl
Mean Pruritus Scores/Mean Number of Wheals/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/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

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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 gt
  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

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Atopic DermatitisTests 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
• 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, 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

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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