alexa Infective Versus Libman Sacks Endocarditis In Systemic Lupus Erythematosus
ISSN: 2161-1149

Rheumatology: Current Research
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Case Report

Infective Versus Libman Sacks Endocarditis In Systemic Lupus Erythematosus

Michael Thomas E Salvador* and Sandra V Navarra

Rheumatology and Clinical Immunology, University of Santo Tomas Hospital, Manila Philippines, USA

*Corresponding Author:
Michael Thomas E Salvador
Rheumatology and Clinical Immunology
University of Santo Tomas Hospital
Manila, Philippines, USA
E-mail: [email protected]

Received date: May 22, 2013; Accepted date: June 17, 2013; Published date: June 25, 2013

Citation: Salvador MTE, Navarra SV (2013) Infective Versus Libman Sacks Endocarditis In Systemic Lupus Erythematosus. Rheumatol Curr Res S16:003. doi: 10.4172/2161-1149.S16-003

Copyright: © 2013 Salvador MTE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Background and objective: Libman Sacks endocarditis is a rare cardiac manifestation of Systemic Lupus Erythematosus (SLE). Cardiac valve vegetations may also be due to infective endocarditis especially in patients with risk factors. We report a case of stroke in an SLE patient with positive anti-phospholipid antibodies and echocardiography findings of mitral valve vegetations.

Case: A 33-year old female with stable SLE for 5 years on hydroxychloroquine and prednisone 5 mg/day presented with diplopia and intermittent fever of 2 weeks duration. She has had recurrent throat and gingival infections in the past year treated with antibiotics. Physical exam disclosed right lateral rectus and left medial rectus palsy, grade 3/6 holosystolic apical murmur, and livedo reticularis. Hemoglobin was 9.2 g/dl, and erythrocyte sedimentation rate (ESR) 130 mm/hr, leucocyte and platelet counts, serum complement, urinalysis, renal and liver functions were normal. Lupus anticoagulant and anti-cardiolipin antibody (IgG) were strongly positive. Cranial Magnetic Resonance Imaging (MRI) revealed an infarct at the pontomedullary area, and transesophageal echocardiogram visualized echodense structures on the mitral valve consistent with vegetations. Blood cultures were negative for microorganisms. She was treated with high-dose steroid tapered to prednisone 20 mg/day, tinzaparin later shifted to warfarin and an antibiotic regimen consisting of penicillin and gentamycin administered for 2 weeks; hydroxychloroquine was continued. She was afebrile throughout hospitalization, with gradual resolution of the neurologic manifestations. A repeat cranial MRI 3 weeks later was normal.

Conclusion: This case highlights the challenges in clinically differentiating infective endocarditis from Libman Sacks endocarditis in a patient with risk factors for both conditions. She received empiric treatment for both with favourable outcome.

Funding: Lupus-Inspired Advocacy (LUISA) Project of Rheumatology Educational Trust Fund Inc. (RETFI).

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