Role of Anti-Tumor Necrosis Factor-α Blockers in Inducing Lupus Erythematosus Tumidus in “Rhupus Syndrome”

Abstract

To the Editor: We read with interest the case report by Soforo, et al 1 and thoughtful accompanying editorial by Jacob and Jacob2 on anti-tumor necrosis factor (TNF)-induced systemic lupus erythematosus (SLE). They suggest that TNF is proinflammatory in certain disorders and blockade is therapeutically useful, whereas in other disorders, like SLE, it has an immune regulatory role, and blockade can be detrimental2. Anti-TNF treatments are known to induce autoantibodies, particularly antinuclear antibodies (ANA). Hence it is important to check for ANA before initiating anti-TNF treatments. Jacob and Jacob2 have advanced the discussion by mentioning the influence of HLA class II genotype on TNF inducibility. Caucasians possessing HLA-DR3/DR4 have higher levels of TNF in response to activation as compared with subjects who are DR2/DQW1-positive (mostly non-Caucasians) who have lower TNF inducibility3. We describe a patient that developed a rare variant of cutaneous lupus erythematosus several years after anti-TNF therapy for rheumatoid arthritis (RA). Our case reveals the importance of HLA class II genotyping assessment. A 58-year-old woman with a 12-year history of seropositive RA experienced disease progression despite use of triple disease modifying antirheumatic drugs (DMARD) hydroxychloroquine, sulfasalazine, and methotrexate (MTX). In April 2000, she was recruited into a phase IIIB drug trial to assess efficacy and safety of etanercept in RA in a different hospital. She received 177 injections of etanercept 25 mg twice weekly up to November 2001 … Address correspondence to Dr. Chogle; E-mail: archogle{at}vsnl.net