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lfamethoxazole/trimethoprim Exanthemas Differential diagnosis (DDx) Viral eruption ? Presentation: Wheals or angioedema. My be part of a more severe anaphylactic reactons with bronchospasm, laryngospasm, or hypotension ? Types: 1. Nonimmunologic – Aspirin and NSADS are the most mon cause. – They alter prostaglandin metabolism, enhancing degranulation of mast cells. 2. Immunologic – Most monly associated with penicillin and related betalactam antibiotics – Skin test: penicillin exposure – Cross reaction with cephalosporins Urticaria DDx Papular urticaria urticaria ?Known plication of the use of ACE inhibitors ?Effect is dose dependent and may resolve with decreased dose. ?ACE users with one episode of angioedema have a 10x risk of a second episode which may be more severe. ?Mechanism :Blocking of kininase II by ACE inhibitors may increase tissue kinin levels? Angioedema Fixed drug eruption ?Unknown pathogenesis ?Variant: Nonpigmented fixed drug eruption –It is characterized by large, tender, often symmetrical erythematous plaques that resolve pletely within weeks, only to recur on reingestion of offending drug –Pseudoephedrine by far most mon. –Baboon syndrome !! ?Unknown pathogenesis ?Present anywhere on body (50% occur on oral and genital mucosa) ?Presentation: –Six or less lesions occur, typically one. –Clinically begin as a red patch that soon evolves to an iris or target lesion identical to EM. –Eventually may blister and erode. 187。Lesions of oral mucosa and genitalia usually present as erosions. –Postinflammatory hyperpigmentation results. ?Topical corticosteroids may induce allergic contact dermatitis . –Consider this plication in any pt with an eczematous dermatitis who bees worse or is refractory to topical steroid tx. –Systemic corticosteroid administra