Med - Urticaria 3rd Yr 08copy

Urticaria & Angioedema JMAbong

Urticaria circumscribed raised areas of erythema and edema involving the superficial portions of the dermis; usually multiple and pruritic

Angioedema - welldemarcated swelling, nonpitting and rarely pruritic resulting from vascular reaction with leakage from post capillary venules; asymmetric edema not in dependent portions

Distribution Urticaria 

occurs on virtually any part of the body

Angioedema 

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involves the face, tongue, extremities, or genitalia do not characteristically occur in dependent areas asymmetrically distributed transient

Clinical Classification of Urticaria 

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Acute Urticaria with known cause idiopathic Chronic Urticaria with known cause idiopathic Physical Urticaria Contact Urticaria Exercise-induced anaphylaxis

Major Causesof Urticaria and Angioedema

• Drug Reactions •Food or food additive •Inhalation, ingestion of, or contact antigen •Transfusion reactions •Infections •Insects •Collagen Vascular disease cutaneous vasculitis serum sickness

Major Causes of Urticaria and Angioedema •Malignancy •Urticarial pigmentosa: systemic mastocytosis •Hereditary diseases Hereditary angioedema Familial cold urticaria Amyloidosis with deafness & urticaria

Causes of Acute Urticaria  

Idiopathic Food: Fruits (strawberry) 

Nuts Seafood Dairy products Spices Tea chocolate

Causes of Acute Urticaria 

Drugs : antibiotics   

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sulfonamide NSAIDs Morphine and codeine

Blood products: Viral infections and febrile illness Radio contrast media Wasp or bee stings

Physical Urticaria       

Cold Urticaria Cholinergic Urticaria Dermographism Pressure urticaria (angioedema) Vibratory angioedema Solar Urticaria Aquagenic urticaria

Chronic Urticaria 

Incidence: 0.1% of population

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More troublesome than acute urticaria

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Defined as occurrence of daily or almost daily widespread itchy wheals for at least six weeks Transient/evanescent

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Chronic urticaria maybe associated with mild Dermographism

Causes of Chronic Urticaria 

Systemic Conditions 

Connective tissue disease

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Systemic Vasculitis/urticarial vasculitis

Immunologic Causes 

Systemic disorders  

Hashimoto’s disease Grave’s disease

Laboratory evaluation  

Antithyroid antibodies Thyroid function tests

Features suggestive of urticarial vasculitis Clinical Duration of wheals >24 hours Wheals painful rather than itchy Residual purpura, bruising, or pigmentary change Prominent systemic features (eg, fever, nephritis, arthralgia) Poor response to antihistamines

Laboratory High erythrocyte sedimentation rate and raised concentrations of acute phase proteins

Features suggestive of urticarial vasculitis Histopathology Venular endothelial cell swelling and disruption Leucocyte invasion of venular endothelium Extravasation of red cells Leucocytoclasia (neutrophil nuclear dust) Fibrin deposition

Causes of Chronic Urticaria 

Infection  

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H pylori? Hepatitis C

Adverse Reaction to Food, Food additives or food dye? 

0.6-0.8% incidence

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However, in 5080% of cases no underlying cause is identified.   

Causes of Chronic Urticaria 

Chronic Idiopathic Urticaria  

50-80% incidence Chronic Autoimmune Urticaria 

30-50% incidence

Autoimmune Chronic Urticaria 

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Associated with presence of circulating histamine releasing factors Presence of IgG1 or IgG3 autoantibodies against FcR1 in 50% of cases Presence of IgG autoantibodies to IgE in 5-10% of cases

Natural History of CAU 

Clinical presentation similar to negative autoantibody urticaria

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Remission and relapse

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Duration? In 50% of cases still present five years later

Natural Course 

Relapse triggers   

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Intercurrent infection Stress Drugs esp aspirin, NSAID, ace inhibitors Menstrual cycle

Treatment of Chronic Urticaria 

Avoidance of precipitating or exacerbating factors     

Food additives, alcohol, Hot environment stress Aspirin, NSAID, codeine, morphine Ace inhibitors if there is angioedema

Treatment of Chronic Urticaria 

Topical treatment   

Tepid shower 1% menthol in aqueous cream 2% ephedrine spray for oral angio-edema

Histamine receptor antagonist 

Mainstay of treatment

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H1 antihistamines with or without H2 antihistamines

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Effective in suppressing pruritus and wheals

Adverse Effects Sedating Antihistamines Associated with their ability to penetrate CNS, antiserotonin and anticholinergic effects:

•sedation •psychomotor/cognitive impairment •confusion •irritability •changes in appetite •dry mouth •urinary retention

Nonsedating & less-sedating antihistamines Have poor penetration of CNS leading to minimal serotonin and anticholinergic blocking activity. Fewer side effects long acting, once or twice a day dosing promote patient compliance

Mechanism of Action H1 receptor antagonist •competitive receptor binding •newer agents may affect components of the inflammatory response: histamine release generation of adhesion molecules influx of inflammatory cells

Combined H1 and H2 blocking agents 

85% H1 receptors in skin

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15% H2 receptors in skin

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H1 and H2 antihistamine combination augments inhibition of histamine induced wheal and flare reaction

Antileukotriene antagonist 

Superior to placebo in wheal and flare inhibition

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No data to support additional efficacy once maximum H1 and H2 blockage is achieved

Corticosteroid 

Highly effective

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Indicated when H1, H2 antihistamine and leukotriene antagonist combination have little response

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Short course corticosteroid if warranted