Nsaids

Beta Blockers

Lipid-lowering

Oxprenolol

Pravastatin Simvastatin

Griseofulvin Terbinafine Cinnarizine/ Thiethylperazine

Glyburide Taxotere

Interferon beta-1a

Interferon alfa

Etanercept

Phenytoin

Procainamide d-penicillamine

Psoralen-UVA

Insecticides

Drugs. Several drugs are associated with the induction of SCLE lesions (Table 1). Thiazide diuretics (Reed et al. 1985; Fine 1989; Parodi et al. 1989; Brown and Deng 1995), calcium channel blockers (Crowson and Magro 1997; Gubinelli et al. 2003; Marzano et al. 2003a) and angiotensin-converting enzyme (ACE) inhibitors (Patri et al. 1985; Fernandez-Diaz et al. 1995) have most commonly been reported. Others include spironolactone (Leroy et al. 1987), interferon beta-1a (Nousari et al. 1998), procainamide (Sheretz 1988), d-penicillamine (Sontheimer 1989), sulfonylureas (Sontheimer 1989), terbina-fine (Brooke et al. 1998; Callen et al. 2001; Bonsmann et al. 2001), oxprenolol (Gange and Levene 1979), griseofulvin (Miyogawa et al. 1994), naproxen (Parodi et al. 1992), piroxicam (Roura et al. 1991), phenytoin (Ross et al. 2002), etanercept (Bleumink et al. 2001) and PUVA (McGrath et al. 1990). The combination of the antihistamines cinnarizine and thiethylperazine was cited as the cause of annular SCLE lesions in one patient (Toll et al. 1998). Personal anecdotal experience has suggested acid inhibitors such as omeprazole and ranitidine may also be a trigger for SCLE (RDS). Some hypothesize that hormones play a significant enough role in SCLE and that it may be reasonable to recommend that cutaneous LE patients avoid estrogen-containing contraceptives (Tebbe and Orfanos 1997). However, no cases of SCLE have been reported as a result of oral estrogen use. A recent retrospective study showed an association between certain medications and the onset of disease in 15 of 70 patients with Ro positive cutaneous lupus (Srivastava et al. 2003). Antihy-

pertensives were most commonly identified as possible triggers, in addition to statins, interferon alfa, and interferon beta. In that review, clinical disease began between 4 and 20 weeks, and improved 6-12 weeks after discontinuation of the offending drug.

Drug-induced SCLE should be differentiated from classical drug-induced SLE. The former is associated with Ro/SSA autoantibodies and a characteristic photodistributed rash, whereas the latter is dominated by histone autoantibodies and systemic symptoms such as fever, arthritis, myalgias, and serositis (Brogan and Olsen 2003). A lupus-specific skin rash is rarely present in the drug-induced form of SLE, and is much more commonly seen in idiopathic SLE (Rubin 2002). The medications which typically trigger SCLE (Table 1) are distinct from those that trigger classical SLE (e.g., hydralazine, procainamide, isoniazid, minocycline, sulfasalazine, etanercept), with exceptions, probably reflecting different underlying disease mechanisms.

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