Cardiac Tamponade as a Presenting Manifestation of Infliximab-Induced Lupus in Patient Treated for Crohnʼs Disease: A Case Report and Literature Review

Abstract

Introduction: Crohn's disease (CD) is a chronic inflammatory bowel disease. It has been postulated that TNF-α; a proinflammatory cytokines plays a crucial role in the mucosal inflammation. Infliximab has shown to be associated with increased likelihood of achieving and maintaining remission and improving quality of life in CD. We are presenting an extremely rare case of cardiac tamponade caused by infliximab induced lupus. Case: A 30 year-old female presented to the ED with pleuritic chest pain and dyspnea. Patient denied palpitations, orthopnea, PND, fever and cough. No history of travel or sick contacts. Past medical history was significant for CD, well controlled on infliximab every 8 weeks for the past 1 year. Last dose was 2 months ago. On physical examination Temp: 98.6, HR: 120-130, RR: 41, BP: 100/60 and SaO2: 99%. Chest examination showed muffled heart sounds, raised JVD and equal breath sounds bilaterally. EKG showed sinus tachycardia. Chest X-ray, CT scan and bedside ECHO were consistent with a large pericardial effusion. Patient was taken to the OR for emergent pericardial window and chest tube insertion. Around 800 mL of pericardial fluid was removed. Pericardial fluid and biopsy were sent for further analysis. Biopsy of the pericardium showed fibrinous pericarditis. HIV screen, EBV, CMV, HSV, adenovirus, influenza A&B, Coxsackie B virus were negative. Autoimmune workup was positive for ANA, anti-dsDNA and anti-histone antibodies. A diagnosis of drug induced lupus causing pericardial effusion secondary to infliximab was made. Discussion: The risk of ANA and anti-dsDNA seroconversion with infliximab therapy has been reported to be 41%-62% and 14%-85%, respectively but only 0.2-0.8% patients develop drug induced lupus. More than 100 cases of lupus following treatment with TNF α inhibitors have been reported in literature. Common manifestations include vasculitis, lupus like syndrome and interstitial lung disease. Only few cases of infliximab induced pericarditis and cardiac tamponade has been reported. Exact underlying mechanism is unknown. However, the temporal association between the use of TNFα inhibitors, the development of cardiac tamponade and the resolution of symptoms following the cessation has been a clue to the diagnosis. Conclusion: Early recognition and management of infliximab induced autoimmune complications is necessary. In conclusion, DILE should be considered as differential in cases of pericarditis with cardiac tamponade without a clear cause