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.
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