Drug-induced subacute cutaneous lupus erythematosus: a paradigm for bedside-to-bench patient-oriented translational clinical investigation
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At least 71 patients have been reported in which their otherwise typical subacute cutaneous lupus erythematosus (SCLE) skin lesions were felt to have been temporally associated with the systemic administration of a drug. The mean age of this cohort of drug-induced SCLE (DI-SCLE) patients was 59 years of age which is somewhat older than the mean age of previously reported idiopathic SCLE patient cohorts. Patients had been taking the suspected triggering drug for weeks to years before the onset of SCLE skin lesions. In addition, it was not unusual for 2–3 months to be required for resolution of the SCLE skin lesions following discontinuation of the triggering drug. A relatively large number of drugs representing different pharmacological classes have been implicated in the induction of SCLE. The drug classes that were more frequently encountered were those used for the treatment of cardiovascular disease, especially hypertension. Calcium channel blockers were especially common in this regard. Elderly individuals being treated for hypertension are often taking multiple classes of drugs that have been implicated in triggering SCLE (thiazide diuretics, calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, beta-blockers). An approach to the management of DI-SCLE is presented. Ro/SS-A autoantibodies tended to remain present in the blood after resolution of drug-induced SCLE skin lesions. A common link between the disparate group of drug structures implicated in triggering SCLE is their tendencies to produce photosensitivity and lichenoid drug reactions. This leads to the speculation that DI-SCLE could represent a photo-induced isomorphic/Köebner response in an immunogenetically predisposed host.
KeywordsDrug-induced subacute cutaneous lupus erythematosus Bedside-to-bench patient-oriented translational clinical investigation
Dr. Sontheimer’s contributions to the preparation of this work was supported by The Richard and Adeline Fleischaker Chair in Dermatology Research at the University of Oklahoma Health Sciences Center.
Conflict of interest
The authors have no potential conflict of interest.
- 3.Costner MI, Provost TT, Sontheimer RD (2004) Lupus erythematosus. Cutaneous manifestations of rheumatic diseases, 2nd edn. Lippincott Williams and Wilkins, PhiladelphiaGoogle Scholar
- 4.Henderson CL, Grau RH, Sontheimer RD (2008) A systematic review of drug-induced subacute cutaneous lupus erythematosus. Br J Dermatol (submitted)Google Scholar
- 9.Litt JZ (2004) Litt’s pocketbook of drug eruptions and interactions, 3rd edn. Parthenon Publishing, Boca RatonGoogle Scholar
- 12.Pellowski DM, Kihslinger JE, Sontheimer RD (2005) Subacute cutaneous lupus erythematosus. In: Hurtl M (ed) Autoimmune diseases of the skin, 2nd edn. Springer-Verlag, WienGoogle Scholar
- 14.Revuz J, Valeyrie-Allanore L (2003) Drug reactions. In: Bolognia JL, Jorrizo JJ, Rapini RP (eds) Dermatology. Mosby, LondonGoogle Scholar
- 15.Rubin RL (2002) Drug-induced lupus. In: Wallace DJ, Hahn BH (eds) Dubois’ lupus erythematosus, 6th edn. Lippincott Williams and Wilkins, PhiladelphiaGoogle Scholar
- 16.Sontheimer RD (2005) Subacute cutaneous lupus erythematosus: 25-year evolution of a prototypic subset (subphenotype) of lupus erythematosus defined by characteristic cutaneous, pathological, immunological, and genetic findings. Autoimmun Rev 4:253–263. doi: 10.1016/j.autrev.2004.10.003 PubMedCrossRefGoogle Scholar
- 19.Wenzel J, Tuting T (2008) An IFN-associated cytotoxic cellular immune response against viral, self-, or tumor antigens is a common pathogenetic feature in “interface dermatitis”. J Invest Dermatol [epub ahead of print]Google Scholar