Abstract
We present a case of a 21-year-old African-American female with no significant medical history, who presented to the emergency department with a one-week history of blurry and double vision. Ophthalmology evaluation revealed bilateral retinal artery occlusion. Further workup with imaging of the brain was consistent with an ischemic stroke. Hereditary hypercoagulable workup was unremarkable and initial testing for antiphospholipid syndrome was positive. She underwent transesophageal echocardiogram (TEE), which showed severe mitral regurgitation and thickening of mitral valve leaflets consistent with Libman-Sacks endocarditis. Autoimmune workup was positive for IF-ANA, anti-RNP, and anti-Smith antibody. She fulfilled 4/11 of the ACR criteria and met 5 of the SLICC (Systemic Lupus International Collaborating Clinics) criteria for lupus (nonscaring alopecia, thrombocytopenia, positive ANA, and positive anti-Smith and positive anti-phospholipid antibodies). This case highlights the importance of early recognition of underlying connective tissue diseases and timely management of these diseases in young patients with no previous manifestations of diseases.
Highlights
We present a case of a 21-year-old African-American female with no significant medical history, who presented to the emergency department with a one-week history of blurry and double vision
Hereditary hypercoagulable workup was unremarkable and initial testing for antiphospholipid syndrome was positive. She underwent transesophageal echocardiogram (TEE), which showed severe mitral regurgitation and thickening of mitral valve leaflets consistent with Libman-Sacks endocarditis
In view of the unremarkable extensive infectious workup, hereditary coagulopathy workup, and clinical presentation accompanied by a positive lupus anticoagulant and lupus serology, coupled with TEE images, she was diagnosed with Libman-Sacks endocarditis attributed to Antiphospholipid syndrome (aPS) and SLE
Summary
A previously healthy 21-year-old African-American female was transferred to our hospital for escalation of treatment. In view of the unremarkable extensive infectious workup, hereditary coagulopathy workup, and clinical presentation accompanied by a positive lupus anticoagulant and lupus serology, coupled with TEE images, she was diagnosed with Libman-Sacks endocarditis attributed to aPS and SLE. She was started on intravenous heparin, which was bridged with oral warfarin to achieve an INR goal of 2-3. She was started on 20 mg of oral prednisone daily in view of her symptoms related to her diagnosis of SLE Her condition was stable throughout her hospital course except for elevated blood pressure. Her diagnosis of aPS was confirmed by repeating antiphospholipid antibodies on follow-up visit 16 weeks apart
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