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A Rare Case of Mitral Valve Libman-Sachs Endocarditis Caused by Antiphospholipid Antibody Syndrome Leading to Diffuse Alveolar Hemorrhage

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A3051 - A Rare Case of Mitral Valve Libman-Sachs Endocarditis Caused by Antiphospholipid Antibody Syndrome Leading to Diffuse Alveolar Hemorrhage
Author Block: R. Hyde1, M. C. Runnstrom2, A. Anderson1, G. Graves3, H. M. Alnuaimat4, A. Ataya5; 1Department of Medicine, University of Florida, Gainesville, FL, United States, 2Medicine, University of Florida, Gainesville, FL, United States, 3PCCM, University of Florida, Gainesville, FL, United States, 4Univ of Florida, Gainesville, FL, United States, 5University of Florida, Gainesville, FL, United States.
Background:Diffuse Alveolar Hemorrhage (DAH) is associated with a high rate of morbidity and mortality. The association of DAH with autoimmune disease is well established and is frequently seen in vasculitides and other rheumatological disorders.
Case presentation:A 26 year old female presented to our institution for a complaint of recurrent blood tinged sputum for the past year and recent development of frank hemoptysis along with respiratory insufficiency three days prior to admission. DAH was confirmed on admission with serial lavages. The patient had no history of autoimmune disease, vascular thrombosis or pregnancy morbidity including miscarriages or pre-eclampsia. High dose steroids were initiated along with noninvasive ventilatory support. Transthoracic echocardiogram ordered for acute severe mitral regurgitation showed a vegetation on the mitral valve and transesophageal echocardiogram (TEE) determined the lesion highly suggestive of Libman-Sachs endocarditis. Blood cultures were all negative. Immunological evaluation established that the patient was negative for anti-nuclear antibody (ANA), anti-double-stranded DNA antibody (anti-dsDNA Ab), rheumatoid factor, anti-smith antibody and anti-cyclic citrullinated peptide, anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibodies. Further evaluation revealed that the patient did have elevated levels of anticardiolipin immunoglobulin G and anti-beta 2 glycoprotein immunoglobulin G, which continued to increase for months after the patient was initially hospitalized. She was diagnosed with DAH secondary to acute mitral regurgitation caused by Libman-Sachs endocarditis due to antiphospholipid antibody syndrome.
Discussion:Diffuse alveolar hemorrhage is an important disease to understand and consider given its high mortality rate. To date there have been few case reports relating the presence of Libman-Sachs endocarditis induced by antiphospholipid antibody syndrome leading to DAH. What is unique in this case is the absence of rheumatologic markers. Because this patient had no findings associated with autoimmune vasculitides, rheumatological disorders (with the exception of Libman-Sachs endocarditis on TEE) or clotting disorder this patient's diagnosis could have been overlooked. This case further illustrates the importance of evaluating DAH without a known inciting factor. Identifying the cause of DAH in this patient changed future management, as evidenced in this case by the need for lifelong anticoagulation.
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