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A3440 - A Rare Case of Loffler's Endocarditis After Initiation of Adalimumab
Author Block: P. Patel1, J. Q. Yin2, R. M. Davis1, O. I. Ikladios3; 1Pulmonary Critical Care Fellowship, University of Illinois College of Medicine Peoria, Peoria, IL, United States, 2Internal Medicine, University of Illinois College of Medicine Peoria, Peoria, IL, United States, 3Pulmonary Medicine, Illinois Lung Institute, Peoria, IL, United States.
Tumor necrosis factor antagonists (anti-TNF) are increasingly prescribed as maintenance therapy for a variety of autoimmune conditions. Therefore, frequent monitoring and awareness of side effects are of the utmost importance. Adalimumab is known to cause peripheral eosinophilia, but there are few reports of more severe adverse events. Loeffler’s endocarditis is a rare and fatal disease characterized by eosinophilic infiltration of the endomyocardium leading to fibrosis and restrictive cardiomyopathy. Herein we describe a patient recently started on adalimumab therapy presenting with Loeffler’s endocarditis.
Our patient is a 72 year-old female with rheumatoid arthritis treated with adalimumab for the past two years. She presented with a three week history of progressive dyspnea on exertion and intermittent low-grade fevers that did not resolve after an outpatient course of antibiotics for community acquired pneumonia. Her last dose of adalimumab was two weeks prior to onset of symptoms. Initial chest x-ray showed right middle and basilar lower lobe consolidation accompanied by a small right sided pleural effusion. Initial blood work revealed leukocytosis with profound eosinophilia. She was treated with broad spectrum antibiotics. Her troponin I trended up slightly. This prompted an echocardiogram which revealed a normal ejection fraction with no wall motion abnormalities, but a small pericardial effusion. She continued to worsen on appropriate therapy, and a CT scan of the chest was obtained. This showed moderate to large right pleural effusion with right basilar atelectasis and findings consistent with a laminar thrombus within the left ventricular apex. A repeat echocardiogram showed a filling defect in the apex, confirming left ventricular thrombus and findings suspicious for eosinophilic heart disease. She underwent thoracentesis and pleural fluid studies showed significant eosinophilia and an exudative effusion. A bronchoscopy with bronchoalveolar lavage revealed 88% eosinophilia without signs of infection. She was started on therapeutic heparin and high-dose prednisone for treatment of her thrombus and eosinophilic heart disease respectively. Fungal, parasitic, bacterial, and autoimmune workup were all negative. After a negative bone marrow biopsy and flow cytometry, she was diagnosed with adalimumab-induced eosinophilia leading to Loeffler’s endocarditis.
Due to the high mortality of Loeffler’s endocarditis, most cases are only diagnosed on autopsy. This case represents a rare case of Loeffler’s endocarditis diagnosed rapidly and without myocardial biopsy. As early intervention is crucial in the prevention of permanent fibrosis and mortality in Loeffler’s endocarditis, this case demonstrates the need for close monitoring and early recognition in patients on anti-TNF therapy.