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DR A.ESSOP DEPT OF DERMATOLOGY UNIVERSITY OF PRETORIA. Urticaria. Definition:
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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 • 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)
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. Finn AJ, Kaplan A, Fretwell R. J Allergy ClinImmunol 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. • 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)
Lichen Planus • 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 planusPruritic purple polygonal planar papules and plaques (6 p’s)
Lichen Planus • 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 • Treatment options: • Topical steroids • Oral steroids • Antimalarials • Systemic retinoids • PUVA • Cyclosporine Levene & Calnan, Figure 182
Pityriasis Rosea • 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-colouredpatches with fine collarettes of scale at lesion margins. • Lesions follow skin cleavage lines in a “Christmas tree” pattern.
PityriasisRosea • Consider RPR (rapid plasmin reagin) to rule out secondary syphilis. • Treat symptomatically.
Pityriasis Rosea Distribution Herald patch Habif, 3rd Ed., Figures 8-31 and 8-32
Drug ReactionsCutaneous 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. • Exanthematous • Urticaria • Fixed-drug eruption • Phototoxic reactions • Acne • Toxic epidermal necrolysis • Stevens-Johnson syndrome Common Drug Rashes Serious Drug Rashes
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.
TREATMENTHealing occurs over 7 to 10 days after the causative drug is stopped.Topical corticosteroids may help to reduce the intensity of the reaction. DRUGS THAT CAUSE FIXED DRUG ERUPTIONBarbiturates CarbamazepineChlordiazepoxideNSAIDsPhenolphthaleinPhenylbutazoneQuinineSalicylatesTetracyclinesTrimethoprim