Case Presentation:

A 52–year–old woman with seropositive (RF,CCP) ANA negative rheumatoid arthritis (RA) diagnosed in 1999, controlled with methotrexate, hydroxychloroquine, and then infliximab (since 2007; last dose 8 weeks prior to admission (PTA)) now admitted with dyspnea, malaise, pleuritic chest pain, nocturnal diaphoresis and arthralgias. History is notable for controlled hypothyroidism and gastric bypass. Symptoms started 1 month PTA with left sided pleurisy and bibasilar infiltrates on CXR; she received moxifloxacin. At that time she had new anemia (Hb 10 g/dL), leukopenia (WBC 3.1 k/uL), lymphopenia (800/uL) and thrombocytopenia (96 k/uL). On current admission, CT scan of the chest showed a moderate pericardial effusion. She had a 10 lb weight loss with night sweats over the past 3 months without anorexia or GI symptoms. She denied Raynaud’s, alopecia, or oral ulcers. She had newly active polyarthritis, new axillary lymphadenopathy and triphasic pericardial friction rub. Echocardiogram revealed small pericardial effusion. Considered diagnoses included RA flare; Felty’s, infectious pericarditis, and RA related lymphoma. CT of abdomen and pelvis was normal. Infectious work–up was negative (cultures, fungal battery, urinary histoplasma antigen, EBV and CMV serologies, TB quantiferon). Immunologic studies: +ANA, dsDNA ab and Crithidiae. Urinalysis, C3 and C4 were normal. In the setting of pericarditis and new–onset cytopenias in patient using TNF inhibitor (TNFi) infliximab it was considered that this was drug–induced SLE. She was started on oral colchicine for pericarditis and prednisone 20 mg for arthritis and constitutional features with symptomatic improvement in her chest pain, dyspnea and arthritis. Methotrexate was resumed and she declined rituximab therapy.

Discussion:

Patients treated with TNFi can develop autoantibodies; but clinically recognized TNFi–induced SLE is infrequent. Due to potentially serious complications associated with this phenomenon, clinicians should consider it if complications arise during treatment with these agents. Since RA can be associated with pericarditis, a positive ANA and even occasional anti–DNA antibodies; Felty’s syndrome can cause neutropenia and thrombocytopenia; and viral, bacterial or fungal infections in the immunosuppressed host can cause pericarditis with constitutional features; drug induced lupus was a diagnosis of exclusion only after thorough evaluation.

Conclusions:

TNFi–induced SLE and other autoimmune syndromes have been described. Clinicians should be aware of this complication and suspect it when a patient with previously controlled inflammatory disease (RA, IBD, psoriasis) experiences an atypical flare or unusual complications.