INFLIXIMAB-INDUCED SYSTEMIC LUPUS ERYTHEMATOSUS IN A PATIENT WITH CROHNʼS COLITIS

Abstract

Background: Anti-tumor necrosis factor IgG (Infliximab) therapy offers a promising new strategy in the treatment of rheumatoid arthritis and crohn's disease. Despite good clinical efficacy and tolerance, the occurence of drug-induced autoimmune disorders remains a concern. The induction of antinuclear (ANA), anti-DNA, and anti-histone antibodies has been widely observed in patients on infliximab therapy. However, clinically relevant systemic lupus erythematosus (SLE) is extremely rare with only a few scattered cases reported in the literature. We report a case of infliximab-induced SLE in a patient with crohn's colitis and review the literature. Case Report: A 37-year-old female with crohn's colitis initially presented with a severe flare-up that was refractory to mesalamine, steroid, and mercaptopurine therapy. Infliximab, 5 mg/kg of body weight, was initiated and a complete response was acheived. Shortly after her 5th dose, she became weak and began developing severe arthralgias and myalgias. Her symptoms progressed to the development of pleuritic chest pain and dyspnea. She was admitted to the ICU where and EKG revealed diffuse ST elevations with an echocardiogram showing RV collapse during inspiration. A pericardial window was performed with the fluid analysis for AFB, viral cultures, and cytology all being negative. Serologic evaluation revealed and ESR of 67 mm/hr with antibodies to nuclear antigens (1:640), double-stranded DNA, and antihistone protein. The diagnosis of drug-induced SLE was made and her infliximab therapy was discontinued. The patient's symptoms began to resolve within 8 weeks of the discontinuation of her anti-TNF therapy. Conclusion: The introduction of TNF blockade has been a breakthrough in the management of severe treatment-resistant crohn's disease. An emerging problem with infliximab therapy, however is the development of autoimmunity. Reports show that infliximab treatment is associated with the induction of ANA in 56.8%, ds DNA in 32.5%, and histone in 21% of patients. Despite the high incidence of autoimmunity, clinical relevant SLE is extremely rare. In the six cases reported, clinical SLE was associated with the developments of ANA, ds DNA IgM, histones, and the female sex.