DR - PowerPoint Presentation

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DR A.ESSOP DEPT OF DERMATOLOGY UNIVERSITY OF PRETORIA

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Urticaria

Definition:

A wheal and flare reaction initiated at the level of the small venules of the skin in response to substances that cause vasodilatation, increase vascular permeability, and for histamine, stimulate type C unmyelinated afferent cutaneous neurons to release neuropeptides (axon reflex)

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Definition of urticaria (also called hives, nettle rash) and epidemiology

Urticaria

affects up to 2% of the population at some time in a lifetime

Transitory (individual episodes < 24h duration) red skin swellings with itching

No desquamation, rarely affects mucous membranes

Associated with

angioedema

in about 40% of cases

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Pathophysiology of urticaria

Most types of urticaria are due to promiscuous activation of dermal mast cells, although basophils may also be involved

Release of histamine and other mediators (including eicosanoids, proteases, cytokines) causes local vasodilation, vasopermeability, fibrin deposition, perivascular infiltration by lymphocytes, neutrophils, and eosinophils, and pruritus

There is minimal endothelial swelling and no leukocytoclasis

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Classification of urticaria into acute and chronic

“

Urticaria

” is an umbrella term inclusive of diverse clinical entities

Conventionally

it

is broadly divided into

acute

and

chronic

Chronic

urticaria

is conventionally defined as “daily or almost daily

urticarial

eruptions occurring for 6 weeks or more”

Chronic

urticaria

is further

subclassified

into several distinct entities

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Physical urticarias: classification

Common

:

Symptomatic dermographism (also called factitious urticaria)

Delayed pressure urticaria

Cholinergic urticaria

Less common

:

Cold contact urticaria

Rare

:

Solar urticaria

Heat contact urticaria

Aquagenic urticaria

Vibratory angioedema

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Urticaria (hives)

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Common- 20-40 year oldsLocalized mast cell degranulationPruritic edematous plaques (wheals)Variable duration-hours to monthsIgE antibody-dependentTriggered by pollens, food, drugs, insect venom, underlying disease (collagen vascular, lymphoma)

Urticaria

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Urticaria

Erythematous, edematous pruritic circular plaques

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Management of chronic ordinary urticaria: general principles 1.

Avoidance of

:

NSAIDS, alcohol, spicy foods

Overtiredness and stress

Wearing of tightly fitting garments, footwear

Strenuous physical exercise

Overheated ambient temperature

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Management of chronic ordinary urticaria: general principles 2.

Tepid showering and frequent application of 1% menthol in calamine cream if nocturnal pruritus is a problemAntihistamine treatment: Low sedation antihistamines taken regularly - not on an “as required” basis (desloratidine 5mg daily; levocetirizine 5mg daily; fexofenadine 120-180mg daily) Sedative antihistamine such as hydroxyzine 25mg taken before sleep if nocturnal pruritus is a problem (warn about impairment of cognitive function the following morning)

Finn AJ, Kaplan A,

Fretwell

R. J Allergy

Clin

Immunol

103:1071-1078, 1999.

Nelson H, Reynolds R, Mason J. Annals Allergy Asthma

Immunol

84:517-522, 2000.

LaRosa

M,

Leonardi

S,

Marchese

G, et. al. Annals Allergy Asthma

Immunol

87:48-53, 2001.

Clough B,

Boutsiouki

P, Church M. Allergy 56:985-988, 2001.

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An acute (and sometimes chronic) inflammatory dermatosis involving skin, hair, nails and mucous membranes.The classic “five P’s” of Purple (violaceous) Polygonal Planar (flat-topped) Pruritic PapulesIdiopathic etiology but some suggest association with Hep C Virus

Lichen Planus

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Lichen planus

Pruritic purple polygonal planar papules and plaques (6 p

’

s)

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Lesions typically found on flexor wrists, lumbar area, glans penis and genitalia, shins, buccal mucosa, and nails.Oral lesions resemble lacy white reticulated pattern (Wickham’s striae).May persist months to years.

Lichen Planus

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Lichen Planus

Treatment options:Topical steroidsOral steroidsAntimalarials Systemic retinoids PUVA Cyclosporine

Levene & Calnan, Figure 182

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Lichen Planus

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Lichen Planus

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An acute exanthematous eruption with a distinctive pattern and self-limited course.A single “herald” lesion (patch or plaque) develops on the trunk, followed in 1-2 weeks by a generalized secondary eruption.Lesions spontaneously regress in ~6 weeks.

Pityriasis Rosea

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Etiology suspected to be HHV7 (human herpes virus) Typically occurs in young people in spring and fall.Salmon-coloured patches with fine collarettes of scale at lesion margins.Lesions follow skin cleavage lines in a “Christmas tree” pattern.

Pityriasis Rosea

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Consider RPR (rapid plasmin reagin) to rule out secondary syphilis.Treat symptomatically.

Pityriasis

Rosea

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Pityriasis Rosea Distribution

Habif, 3

rd

Ed., Figures 8-31 and 8-32

Herald patch

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Drug Reactions

Cutaneous drug reactions may be

classified

with respect to

pathogenesis and clinical morphology.

They may be mediated by immunologic and

nonimmunologic

mechanisms.

Immunologic reactions require host immune response and may result from

IgE

-dependent, immune complex-initiated,

cytotoxic

, or cellular immune mechanisms.

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Nonimmunologic reactions may result from nonimmunologic activation of effector pathways, overdosage, cumulative toxicity, side effects, ecologic disturbance, interactions between drugs, metabolic alterations, or exacerbation of preexisting dermatologic conditions.

Common Drug Rashes

Serious Drug Rashes

Exanthematous UrticariaFixed-drug eruptionPhototoxic reactionsAcne

Toxic epidermal necrolysisStevens-Johnson syndrome

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FIXED DRUG ERUPTION:The site of eruption is fixed, when the individual takes the causative drug again the eruption recurs within at the same site as was previously affected. PATHOGENESISFDEs are caused by the activation of cytotoxic T lymphocytes in the basal layer by drugs. Common causative drugs are NSAIDs, tetracyclines and sulfa drugs.SYMPTOMSThe sites mainly affected are the hands, feet and perianal areas. It consists of erytematous round or oval lesions of a dusky brown colour sometimes featuring blisters or vesicles.

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DRUGS THAT CAUSE FIXED DRUG ERUPTION Barbiturates Carbamazepine ChlordiazepoxideNSAIDsPhenolphthaleinPhenylbutazoneQuinineSalicylatesTetracyclinesTrimethoprim

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TREATMENT

Healing occurs over 7 to 10 days after the causative drug is stopped.

Topical corticosteroids may help to reduce the intensity of the reaction.

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Thank You