LAUSR

Multiple drugs as inducing or exacerbating agents in subacute cutaneous lupus erythematosus Dear Editor, Drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) was first described in five patients taking hydrochlorothiazide (HCTZ) by Reed et al. in 1985. More than three decades later, over 100 agents have been linked to this distinct subtype of cutaneous lupus erythematosus, with approximately 20% of newly diagnosed cases of SCLE thought to be drug-induced or drug-exacerbated. SCLE presents clinically as annular plaques or papulosquamous lesions in a photodistribution, and most patients have anti-Ro/SSA antibodies. With the exception of cross-reactivity of proton pump inhibitors, SCLE recurrence following exposure to drugs of different classes has rarely been reported. We describe two patients with multiple drugs as inducing or exacerbating factors in SCLE. To our knowledge, one of the implicated drugs (abatacept) has only been reported twice in the literature in association with DISCLE. A woman in her mid-70s with a history of hypertension, rheumatoid arthritis, parkinsonism, gastroesophageal reflux disease, and anxiety/depression first developed DI-SCLE in 2001 presumably due to hydrochlorothiazide. In 2009, she again developed DI-SCLE due to golimumab, and in 2017 her disease was re-awakened by esomeprazole. In late 2019, amlodipine was prescribed in place of losartan, and within 3 months, she developed pruritic, erythematous, and scaly patches on the lateral arms (Fig. 1). A punch biopsy was performed, which revealed interface dermatitis. Amlodipine was identified as the fourth agent to trigger an episode of SCLE in this patient. Approximately 1 month after discontinuing the drug, her lesions had improved in appearance. A woman in her mid-70s with a history of rheumatoid arthritis, Sj€ ogren’s syndrome, and biopsy-proven SCLE diagnosed in 2004 presented with pruritic, erythematous, polycyclic, psoriasiform plaques on the dorsal hands, forearms (Fig. 2), and upper arms that had gradually worsened in severity over the course of several months. She had a prior exacerbation of her disease due to leflunomide in 2010. Temporally, her rash started approximately 1 month after her first abatacept infusion and worsened with each subsequent monthly infusion. She had been applying triamcinolone 0.025% cream to both arms and was taking oral hydroxychloroquine 400 mg daily without improvement. Her serologic testing was notable for an ANA titer greater than 1:640 and SSA IgG and SSB IgG greater than 8.0 antibody index units (AI). Abatacept was determined to be the cause of her SCLE exacerbation, and she was ultimately switched to tocilizumab infusions for her rheumatoid arthritis. Her rash has since resolved, approximately 6 months after her last treatment with abatacept. SCLE associated with a single drug is a well-described phenomenon. The present case series serves to extend the literature by highlighting multiple drugs from distinct pharmacologic classes utilized in the same patient as exacerbating agents in SCLE. The first patient had a history of DI-SCLE attributed to HCTZ, golimumab, and esomeprazole prior to