DR A.ESSOP DEPT OF DERMATOLOGY UNIVERSITY OF PRETORIA

DR A.ESSOP DEPT OF DERMATOLOGY UNIVERSITY OF PRETORIA

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)

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

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

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

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

Urticaria (hives)

Common- 20-40 year olds Localized mast cell degranulation Pruritic edematous plaques (wheals) Variable duration-hours to months IgE antibody-dependent Triggered by pollens, food, drugs, insect

venom, underlying disease(collagen vascular, lymphoma)

Urticaria

UrticariaErythematous, edematous pruritic circular plaques

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

Management of chronic ordinary urticaria: general principles 2.

Tepid showering and frequent application of 1% menthol in calamine cream if nocturnal pruritus is a problem

Antihistamine 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.

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 Papules

Idiopathic etiology but some suggest association with Hep C Virus

Lichen Planus

Lichen planusPruritic purple polygonal planar papules and plaques (6 p’s)

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

Lichen Planus

Treatment options:

◦ Topical steroids◦ Oral steroids◦ Antimalarials ◦ Systemic retinoids ◦ PUVA ◦ Cyclosporine

Levene & Calnan, Figure 182

Lichen Planus

Lichen Planus

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

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

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

Treat symptomatically.

Pityriasis Rosea

Pityriasis Rosea Distribution

Habif, 3rd 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.

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 Urticaria Fixed-drug eruption Phototoxic reactions Acne

Toxic epidermal necrolysis

Stevens-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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TREATMENTHealing occurs over 7 to 10 days after the causative drug is stopped.Topical corticosteroids may help to reduce the intensity of the reaction.

Thank You