Significance of Drugs and Hormones

SCLE has been linked to a variety of drugs, although it seems that thiazides are the most commonly reported agents (Callen 2001, Reed et al. 1985). Other drug classes frequently associated with the development of LE are calcium channel blockers and angiotensin-converting enzyme inhibitors (Crowson and Magro 1997, Fernandez-Diaz et al. 1995). More recently, terbinafine was mentioned as a causative agent for SCLE (Bonsmann et al. 2001). Several case reports mention a variety of drugs responsible for the induction of SCLE, including griseofulvin, interferon beta-1a, cimeti-dine, cinnarizine, thiethylperazine, and eternacept (Bleumink et al. 2001, Davidson et al. 1982, Miyagawa et al. 1989, Nousari et al. 1998, Toll et al. 1998). In most reported cases drug-induced SCLE had a good prognosis and skin lesions resolved after discontinuation of the responsible drug.

Because CLE clearly shows a female predominance, with disease onset mainly during the childbearing years, it has to be considered that hormones are a triggering factor for the disease or influence its course in genetically determined susceptible women. Empiric observations are that premenstrual flares occur in 20% of 57 women (Yell and Burge 1992). Perimenopausal flares occur in 35% of patients with CLE, whereas postmenopausal disease manifestations are rare (Yell and Burge 1992). SCLE-like disease can be induced by estrogen-containing contraceptives (Furukawa et al. 1991). Females taking postmenopausal estrogen replacement therapy for 2 or more years had a significantly increased risk of developing DLE (Meier et al. 1998).

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