Urticaria & Angioedema

JMAbong
Urticaria -
circumscribed raised
areas of erythema and
edema involving the
superficial portions of
the dermis; usually
multiple and pruritic
Angioedema - well-
demarcated swelling, non-
pitting and rarely pruritic
resulting from vascular
reaction with leakage from
post capillary venules;
asymmetric edema not in
dependent portions
Distribution
Urticaria Angioedema
 occurs on
 involves the face,
tongue, extremities, or
virtually any part
genitalia
of the body  do not
characteristically occur
in dependent areas
 asymmetrically
distributed
 transient
Clinical Classification of
Urticaria
 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
 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
 More troublesome than acute
urticaria
 Defined as occurrence of daily or
almost daily widespread itchy
wheals for at least six weeks
 Transient/evanescent
Chronic urticaria
maybe
associated
with mild
Dermographism
Causes of Chronic
Urticaria
 Systemic Conditions
 Connective tissue
disease

 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
 H pylori?
 Hepatitis C

 Adverse Reaction to Food, Food

additives or food dye?
 0.6-0.8% incidence

  However, in 50-
80% 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
 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

 Remission and relapse

 Duration? In 50% of cases still

present five years later
Natural Course
 Relapse triggers

 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

 H1 antihistamines with or without

H2 antihistamines

 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

 15% H2 receptors in skin

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

 Superior to placebo in wheal and

flare inhibition

 No data to support additional

efficacy once maximum H1 and
H2 blockage is achieved
Corticosteroid
 Highly effective
 Indicated when H1, H2
antihistamine and leukotriene
antagonist combination have
little response
 Short course corticosteroid if
warranted