Progress in the understanding of the pathology and pathogenesis of cutaneous drug eruptions - Implications for management

被引:45
作者
Crowson, AN
Brown, TJ
Magro, CM
机构
[1] Reg Med Labs, St Johns Med ctr, Tulsa, OK 74104 USA
[2] Univ Oklahoma, Tulsa, OK 74136 USA
[3] Univ Oklahoma, Oklahoma City, OK USA
[4] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA
关键词
D O I
10.2165/00128071-200304060-00005
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 [皮肤病与性病学];
摘要
Cutaneous drug eruptions are among the. most common adverse reactions to drug therapy. The etiology may reflect immunologic or nonimmunologic mechanisms, the former encompassing all of the classic Gell and Combs immune mechanisms. Cumulative and synergistic effects of drugs include those interactions of pharmacokinetic and pharmacodynamic factors reflecting the alteration by one drug of the effective serum concentration of another and the functions of drugs and their metabolites that interact to evoke cutaneous and systemic adverse reactions. Recent observations include the role of concurrent infection with lymphotropic viruses and drug effects that, through the enhancement of lymphoid blast transformation and/or lymphocyte survival and the contribution of intercurrent systemic connective tissue disease syndromes, promote enhanced lymphocyte longevity and the acquisition of progressively broadening autoantibody specificities. The latter are particularly apposite to drug-induced lupus erythematosus and to drug reactions in the setting of HIV infection. Specific common types of cutaneous drug eruptions will be discussed in this review. Successful management of cutaneous drug eruptions relies upon the prompt discontinuation of the causative medication; most drug eruptions have a good prognosis after this is accomplished. Oral or topical corticosteroids can be administered to aid in the resolution of some types of eruptions. Antihistamines or anti-inflammatory agents may also be administered for some eruptions.
引用
收藏
页码:407 / 428
页数:22
相关论文
共 176 条
[1]
Phenytoin-induced linear IgA bullous disease [J].
Acostamadiedo, JM ;
Perniciaro, C ;
Rogers, RS .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1998, 38 (02) :352-356
[2]
Agnew K L, 2001, Australas J Dermatol, V42, P200, DOI 10.1046/j.1440-0960.2001.00516.x
[3]
Anticonvulsant hypersensitivity syndrome associated with reactivation of cytomegalovirus [J].
Aihara, M ;
Sugita, Y ;
Takahashi, S ;
Nagatani, T ;
Arata, S ;
Takeuchi, K ;
Ikezawa, Z .
BRITISH JOURNAL OF DERMATOLOGY, 2001, 144 (06) :1231-1234
[4]
Al-Khenaizan S, 1999, J Cutan Med Surg, V3, P162
[5]
Nonpigmented fixed drug eruption from pseudoephedrine [J].
Alanko, K ;
Kanerva, L ;
MohellTalolahti, B ;
Jolanki, R ;
Estlander, T .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1996, 35 (04) :647-648
[6]
BULLOUS PEMPHIGOID MIMICKING BULLOUS ERYTHEMA MULTIFORME - AN UNTOWARD SIDE-EFFECT OF PENICILLINS [J].
ALCALAY, J ;
DAVID, M ;
INGBER, A ;
HAZAZ, B ;
SANDBANK, M .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1988, 18 (02) :345-349
[7]
Linear IgA disease: a report of two dermal binding sera which recognize a pepsin-sensitive epitope (?NC-1 domain) of collagen type VII [J].
Allen, J ;
Zhou, S ;
Wakelin, SH ;
Collier, PM ;
Wojnarowska, F .
BRITISH JOURNAL OF DERMATOLOGY, 1997, 137 (04) :526-533
[8]
RATES OF CUTANEOUS REACTIONS TO DRUGS - REPORT FROM BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM [J].
ARNDT, KA ;
JICK, H .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1976, 235 (09) :918-923
[9]
Role of delayed cellular hypersensitivity and adhesion molecules in amoxicillin-induced morbilliform rashes [J].
Barbaud, AM ;
Bene, MC ;
Schmutz, JL ;
Ehlinger, A ;
Weber, M ;
Faure, GC .
ARCHIVES OF DERMATOLOGY, 1997, 133 (04) :481-486
[10]
Clinically significant drug interactions in dermatology [J].
Barranco, VP .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1998, 38 (04) :599-612