Department of Rheumatology, Gartnavel General Hospital and 1Department of Dermatology, Western Infirmary, Glasgow, UK
Correspondence to: G. McKellar, Department of Rheumatol-ogy, Gartnavel General Hospital, Glasgow G12 0YN, UK. E-mail: gayle_mckellar{at}hotmail.com
SIR, In the dermatology literature, terbinafine has been reported as causing cutaneous lupus erythematosus (LE) de novo and exacerbating pre-existing LE, but this association has not previously been reported in the rheumatology literature. We report the case of a 35-yr-old male who presented with probable systemic lupus erythematosus in 1998. He presented with fever, type 1 respiratory failure associated with patchy interstitial lung disease, but no prior cutaneous lupus. Immunology showed him to be seropositive for antinuclear antibodies (ANA) (1:2560), double-stranded DNA (298 IU/ml, positive >50 IU/ml) and anti-Ro (SS-A) antibodies. Serum complement assays demonstrated low C3 (1.25 g/l) and C4 (0.18 g/l). He was seronegative for anticardiolipin antibodies and lupus anticoagulant assays were negative. Pulmonary thromboembolic disease was excluded by pulmonary angiography, and a full sepsis screen was negative. He was treated with oral prednisolone and azathioprine. Over the next 34 yr his immunosuppression was tapered and stopped in April 2003.
In July 2002, oral terbinafine at the dose of 250 mg daily, was commenced for suspected onychomycosis; no cultures were obtained prior to commencement. Two months later, he presented with a severe maculopapular rash affecting his trunk and limbs, tender erythema of his palms and soles and a small erosion on his glans penis; his mucous membranes were otherwise intact. ANA and antihistone antibodies were negative, but he remained anti-Ro (SS-A)-positive and complement levels were reduced (C3 0.83 g/l, C4 0.09 g/l). A skin biopsy demonstrated patchy interface vacuolar alteration and focal exocytosis of inflammatory cells in the overlying epidermis. Skin immunofluorescence was positive, with linear granular staining at the dermal/epidermal junction for immunoglobulin (Ig) A, IgG, IgM and C3, consistent with the diagnosis of cutaneous lupus erythematosus. The terbinafine was stopped and he was treated with topical steroids [clobetasol propionate to the body, clobetasone butyrate to the face and Trimovate (clobetasone butyrate plus antimicrobial agents)] to the groin, with complete recovery.
Terbinafine is very widely used and is the drug of choice in mycologically proven onychomycosis. A large postmarketing surveillance programme of 25 000 patients on this drug showed a frequency of cutaneous side-effects in the region of 2.5% [1]. There have been five previous reports of cutaneous lupus in patients receiving terbinafine therapy in the dermatology literature [26]. Gupta et al. [7] reported a series of different cutaneous manifestations of the adverse effects of terbinafine, including erythema multiforme, erythroderma, worsening of psoriasis and pityriasis rosea. Contrary to the report of Bonsmann et al. [6], our patient was negative for ANA and anti-histone antibodies. Our patient was anti-Ro (SS-A) positive, and it has previously been noted that this antibody pattern is commonly seen in drug-induced cutaneous lupus [8]. It is notable that there is no reference to cutaneous lupus being a potential adverse effect in the data sheet for terbinafine, and terbinafine is not listed as a potential cause of drug-induced lupus in major rheumatology texts or electronic texts such as UpToDate. We conclude that terbinafine should only be used with caution, if at all, in patients with lupus, especially those who are anti-Ro (SS-A)-positive and then only if nail-clipping mycology is positive.
The authors have declared no conflicts of interest.
References