Yellow skin discoloration induced by quinacrine in a patient with cutaneous lupus erythematosus.

To the Editor: We report the case of a 67-year-old woman who presented with quinacrine-induced skin toxicity. At 32 years of age, the patient was diagnosed with systemic lupus erythematosus with both cutaneous and pleural manifestations, for which she was treated for many years with prednisone and chloroquine. Several years ago she was diagnosed with peripheral chorioretinal atrophy (retinitis pigmentosa) and chloroquine treatment was suspended. One year ago, upon reducing the prednisone dose from 30 to 15 mg/day, the patient experienced an outbreak of erythematous lesions that affected the face (Fig. 1), trunk, and extremities. A skin biopsy revealed orthokeratotic hyperkeratosis, epidermal atrophy, vacuolar degeneration of the basal membrane, loss of skin appendages, and chronic inflammatory interstitial and perivascular infiltrate. Analyses revealed an anti-nuclear antibody titre of 1/160 with a speckled pattern, anti-Ro/SS-A antibodies (124 U/mL), and anti-DNA antibodies (5 U/mL). Other examinations revealed no relevant findings and the patient was diagnosed with an outbreak of cutaneous lupus erythematosus. Topical tacrolimus (0.1%) was administered, but was not tolerated, and after analyzing serum levels of thiopurine methyltransferase the patient was treated with azathioprine at 50 mg/day. After 4 months, azathioprine treatment was stopped due to general malaise and abnormal test results: erythrocyte sedimentation rate, 86 mm/h; aspartate aminotransferase, 41 U/L; alanine aminotransferase, 59 U/L; gamma-glutamyl transferase, 1006 U/L; alkaline phosphatase, 240 U/L. The cutaneous lupus erythematosus persisted with no improvement, and as the patient did not wish to take more immunosuppressants, quinacrine for compassionate use was obtained from the hospital pharmacy service. After providing informed consent the patient began treatment with quinacrine (100 mg/day) and prednisone (50 mg/day). Two months later the lupus erythematosus lesions had completely resolved with no residual scarring, allowing a reduction in the dose of prednisone. Five months after starting quinacrine treatment the prednisone dose had been reduced to 15 mg/day, but the patient began to experience yellow discoloration of the skin and sclera (Fig. 2). As liver function and bilirubin levels were normal, quinacrine treatment was suspended. In the following months the skin regained its normal color and methotrexate was administered to prevent lupus erythematosus relapse. Currently the patient remains free of lupus erythematosus lesions and is being treated with prednisone (2.5 mg/day) and methotrexate (5 mg/week) (Fig. 3).