Urticaria-Angioedema-alwi.ppt

7/27/2019 Urticaria-Angioedema-alwi.ppt

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URTICARIA

&

ANGIOEDEMA


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Introduction

As clinical manifestation of

various immunologic &

inflammatory mechanism occurafter :


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IgE-or IgE receptor dependent

reaction.

Assc with abnormalities of the

C sys other plasma effectorsys.

Activation of cellular

arachidonic acid metabolisme

pathway after mast cell deg.


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Epidemiology

1 to 2% have noted, most after

adolescence, with highest

incidence in young.

Adult patients with clinical

problem 50% both urticaria &

angioedema.


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Most common at college

students 15 20%.

50% of patients with urticaria

alone within 1 year, 20%

continue for 20 years.


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In children, urticaria without

angioedema occur in 80%,

both occur in 15%.

50% for more 1 year, with

mean duration of 16 months.


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Classification

Immunologic IgE-and IgE

receptor dependent urticaria /

angioedema.

Urticaria / angioedema

mediated by complementsystem & other plasma effector

system.


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Urticaria / angioedema after

direct mast cell degranulator.

Urticaria / angioedema relating

to abnormalities of

arachidonic acid metabolism.

Idiopathic urticaria /

angioedema.


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The pathogenesis of urticaria

Vasopermeability activities :

Histamine.

Protaglandin D2.

Leukotrine C4.


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Chemotactic factors :

Eosinophil chemotactic

activities.

Netrophil chemotactic

activity.


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Enzymes :

Tryptase.

Chymase.

Carboxypeptidase A.

Catepsin G.


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Cytokines :

Tumor necrosis factor. Interleukin 4,5,6 & 8.

Proteolicans :Heparin.

Chodroitin.

Sulfate E.

Hyaluron.


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Skin chamber model mastcell products appearing.

Identification of mast

cell products in tissuesor biologic fluids


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Scanning laser Droppler

imaging biochemicalmediator in IgE-meadiated

cutaneus reactions.

Intracutaneus injection of

specific antigen role IgE & itsinteraction with the mast cell.


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HLA-DR4, DRB4 53 & HLA-

DQ8, DQA 301 / 12 increased frequency in

patients.


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Clinical manifestations

Lesions are circumscribed

erythematous, pruritic, edema

that involve the superficial

portion of the dermis are

known as urticaria, when intothe deep dermis it is known as

angioedema.


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Both urticaria & angioedema

may occur in any locations

together.

Angioedema commonly effect

the face / an extremity is

painful or pruritic.


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Lesion of urticaria arise

suddenly, rare persist longer

than 24 48 h and may

continue. Episodes less than 6 8 weeks

duration are acute, whereas

those persisting longer are

termed chronic.


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Immunologic IgE-and IgE

receptor-dependent urticaria/ angioedema

Atopic diathesis occuring inindividual with personal / family

history of asthma, rhinitis or

eczema IgE dependent.


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Specific antigen sensitivity

foods (shellfish, nuts &

chocolate), drugs &

therapeutic agents (penicilin),

helminthic infestation.


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Physical urticaria / angioedema

mechanical trauma (elevationin blood histamin level),

prossure (IgE-mediated has not

demonstrated, however

histamine, leukotriene B4, IL6have been detected).


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Temperature IgE,histamine, chemotactic

factors, PGD2, leucotrine

have been documented.


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Light

systemic lupuserythematous, 285 320 nm &

400

500 nm, histamine &chemotactic factors detected

after exposure UVA & UVB, 25 100 kDa.


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Exercise elevation of bloodhistamine, chemotactic

factors, acetylcholine

receptors increased.


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Stress IC injection ofnonadrenalin adrenergic

urticaria. Water blood histamine level

were elevated & mast cell

degranulation was presented.


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Urticaria / angioedema

mediated by the complement

system & other plasmaeffector system

Hereditary & acquired

angioedema there is afungtional deficiency of theinhibitor of the activated of

C1INH & C3b.


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Necrotizing venulitis abnormalities of C1q & IgMcomponent.

Reactions to the administration

of blood product may ariseafter imunization by transfusion

or by plasental tranfer activated IgG & Hageman factor

fragments.


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Infections hepatitis B virusinfection

immune complex-

mediated necrotizing vasculitis

with cryoglobulinemia.

Angiotensin converting enzyme

inhibitors the mechanism notto be immunologic because thelesions occur within hours of

the first dose.


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Laboratory findinds

In all patient :

History & physical

examination.

Provocative test for

physical urticarias.


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In selected patients :

Complete blood count with

differential analysis.

Erytrocyte sedimentation

rate.

Urinalysis.

Blood chemistry pofile.


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Stool examination for ova &

parasites.

Antinuclear factor.

Hepatitis B & C virus surface

Ag & Ab.

Skin test for IgE-mediated

reactions.


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Radioallergosorbent test

(RAST) for specific IgE.

CH50.

Cryoproteins.

Plasma & erythrocyte

protoporphyris.

Skin biopsy.


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Histopathology

Polymorphous perivascular

infiltrate.

Neutrophils. Eosinophils.

Mononuclear cells.

Sparse perivascular

lymphocytes.


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Pathology

Chronic idiopathic urticaria CD4+, CD8+, T lymphocytes,

neu, eusi detected by direct

immunofluorescence, MBP, P-

selectin biopsy. Acut urticaria MBP, ECP.


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Physical urticaria CD4 > CD8,neu, eosi with MBP, E-selectin,

VCAM

by histologic result. Solar urticaria MBP, ECP.

Papular urticaria T lymp,macrophages, eosi, neu.


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Chollergic urticaria MBP,ECP.

Chronic urticaria E-selectin, P-selectin,

intercellular adhesion mol 1,

VCAM.


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Diagnosis &

Differential diagnosis

Urticaria & angioedema

episode & evanescent, seldompersist for > 48 h for several

days.

Several disorder are included in

DD.


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Erythema multiforme edematous, papulovesicular,bullous eruptions with mucosal

involvement, typical iris ortarget.

Lyme borreliosis annuleredematous, urticarial plaques

may expand in diameter.


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Bullous pemphigoid edematous & erythematous

plaques. Urticaria pigmentosa

generalized

red-brown,macular, papular.


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Treatment

The ideal treatment for urticaria /

angioedema is identification &

removal of its cause.


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H1-type antihistamine drugsmainstays.

Newer low-sedating, reducesedative, anticholinergic.

If this drug fails to be effective

combination of 2 agent fromdifferent classes may be used.


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Combination of H1 & H2 may be

beneficial & ketotifen has been

used succesfully

chronicurticaria reported (colchine in

combination with H1to bebenefit) & also cycsporine.


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Systemic glucocorticoid have

no place in regular therapy.

Prednisone in management of

acute urticaria has been

advocated in emergency rooms.


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Oral disodium cromoglycate is

effective food allergy. Terbutaline, a -agonist in

combination with an H1-typehas been reported to be of

benefit idiopathic urticaria failed from conventional

therapy nefidipine.


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Immunoglobulin (IV) was

limited benefit & also trials wasof was of benefit with (SC)

interferon-. Epineprine is widely used

particularly in hospital laryngeal edema, cardivascular

collapse.


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Antihistamine prophylactic physical urticaria.

17--alkylated androgendanazol reduction in exercise

provoked experimental wheals

cholinergic urticaria.


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NSAIDs, cetrizine,

sulfasalazaline & syst.

Glucocorticoid delayedpressure urticaria.

Terbutaline & aminophylline

combination, H1 & H1 comb.cold urticaria.


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Propanolol hydrochlorideadrenergic urticaria.

UVA phototherapy & PUVA

photochemotherapy physical urticaria.


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Urticaria / angioedema may be a

source of frustration to both

physician & patients, most

patients can achieve acceptable

symptomatic control of their

disease without identification of

the cause.


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Urticaria-Angioedema-alwi.ppt

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