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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of systemic lupus erythematosus (SLE) depends on clinical evidence of renal, rheumatologic, cutaneous, and neurologic involvement, supported by serological markers. A previously healthy 14-year-old girl presented with Libman-Sacks endocarditis involving the aortic valve as the first manifestation of SLE. Even though she did not satisfy the American College of Rheumatology criteria for diagnosing SLE, she had anemia, proteinuria, elevated erythrocyte sedimentation rate, low complement 4 (C4) levels, and strongly positive antinuclear antibody titer. A renal biopsy showed stage IV lupus nephritis. Treatment was initiated with immunosuppressants and steroids. This type of presentation may be misdiagnosed as infective endocarditis missing the underlying collagen vascular disease.
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PMID:Occult systemic lupus erythematosus with active lupus nephritis presenting as Libman-Sacks endocarditis. 2252 11

Libman-Sacks endocarditis consists of aseptic valvular abnormalities, associated with systemic lupus erythematosus and antiphospholipid syndrome. Embolic ischaemic stroke is a possible clinical presentation. The authors present the case of a woman in her fourth decade who developed central facial palsy after several transient ischaemic attacks with visual loss. Cerebral imaging revealed multiple small ischaemic lesions in the right hemisphere. The transoesophagic echocardiogram showed mitral vegetations and she tested positive for antiphospholipid antibodies. She underwent mitral valve replacement for a mechanical prosthesis due to extensive valvular damage and started anticoagulation. The valve's microbiological exams were negative establishing the diagnosis of libman-sacks endocarditis. Endocarditis should be suspected with sequential cerebral ischaemia in patients of all ages. Valvular surgery is the mainstay of treatment in recurrent embolic events. Association with antiphospholipid antibodies is common yet a poor-known fact. The patient is currently asymptomatic on warfarin and aspirin, with a normal functioning mitral prosthesis.
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PMID:Cerebral embolism from Libman-Sacks endocarditis. 2269 97

Libman-Sacks endocarditis (LSE) is the most characteristic cardiac manifestation of systemic lupus erythematosus (SLE). It is usually clinically silent but heart failure due to valvular dysfunction, secondary infective endocarditis and embolic phenomena can complicate valvular abnormalities. We present a patient with SLE and blindness due to right central retinal artery occlusion. Echocardiographic examination revealed a verrucous vegetation on the posterior mitral valve leaflet consistent with LSE. Anticoagulation therapy was started. Echocardiographic regression of the vegetation was observed and there has been no recurrence of thromboembolic events to date.
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PMID:Retinal artery embolization complicating Libman-Sacks endocarditis in a systemic lupus erythematosus patient. 2352 93

Cardiac involvement is a well-known complication of systemic lupus erythematosus (SLE), which can involve most cardiac components, including pericardium, conduction system, myocardium, heart valves, and coronary arteries. Libman-Sacks (verrucous) endocarditis is the characteristic cardiac valvular manifestation. Although isolated tricuspid valve involvement is quite rare, we report a patient with SLE who had tricuspid stenosis caused by Libman-Sacks endocarditis. The patient underwent successful commisurotomy and Kay annuloplasty on the tricuspid valve under cardiopulmonary bypass.
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PMID:Isolated tricuspid valve repair for Libman-Sacks endocarditis. 2466 Dec 89

We report a case of severe mitral stenosis caused by Libman-Sacks endocarditis, as an initial manifestation of systemic lupus erythematosus (SLE) in a 20-year-old woman. Cardiac magnetic resonance imaging (MRI) demonstrated a thickening of the mitral valve with basal endocardial thickening exhibiting defect on first-pass perfusion short-axis acquisition and delayed enhancement in keeping with extensive fibrous endocarditis. The patient underwent successful mechanical mitral valve replacement. This case illustrates that MRI is useful in diagnosing this recognised but uncommon cardiac complication of SLE and excluding differential diagnosis such as valve tumour and infective endocarditis with perivalvular abscesses.
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PMID:Severe mitral stenosis as the first manifestation of systemic lupus erythematosus in a 20-year-old woman: the value of magnetic resonance imaging in the diagnosis of Libman-Sacks endocarditis. 2471 38

We present a 54-year-old woman with systemic lupus erythematosus (SLE), fever, pericardial effusion and a mitral valve vegetation. (18)F-Fluorodesoxyglucose positron emission tomography CT ((18)F-FDG-PET-CT) showed very high accumulation of the isotope at the mitral valve. The patient underwent cardiothoracic surgery and pathologic examinations showed characteristic morphology of Libman-Sacks vegetations. All microbiological examinations including blood cultures, microscopy, culture and 16s PCR of the valve were negative and the diagnosis of Libman-Sacks endocarditis was convincing. It is difficult to distinguish Libman-Sacks endocarditis from culture-negative infective endocarditis (IE). Molecular imaging techniques are being used increasingly in cases of suspected IE but no studies have previously reported the use in patients with Libman-Sacks endocarditis. In the present case, (18)F-FDG-PET-CT clearly demonstrated the increased glucose uptake caused by infiltrating white blood cells in the ongoing inflammatory process at the mitral valve. In conclusion, (18)F-FDG-PET-CT cannot be used to distinguish between IE and non-infective Libman-Sacks vegetations.
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PMID:Molecular imaging in Libman-Sacks endocarditis. 2562 44

Libman-Sacks endocarditis is the most widely encountered aseptic endocarditis among patients with systemic lupus erythematosus. Due to the deformed cardiac valves, secondary infective endocarditis should be considered in lupus patients with acute refractory heart failure and fever of unknown origin. The case is reported of a woman with lupus and Libman-Sacks endocarditis who had concurrent coagulase-negative Staphylococcus infective endocarditis that resulted in cerebral septic emboli and acute pulmonary edema. She underwent valve replacement surgery for acute heart failure, and gradually recovered with antibiotic treatment.
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PMID:Coagulase-negative staphylococcus infective endocarditis in a lupus patient with Libman-Sacks endocarditis. 2620 92

Antiphospholipid syndrome is a systemic autoimmune syndrome with cardiac manifestations such as nonbacterial thrombotic endocarditis, also known as Libman-Sacks endocarditis. A 61-year-old female with history of antiphospholipid syndrome presented in acute pulmonary edema. Echocardiography demonstrated mobile vegetations on the free margins of both the anterior and the posterior mitral valve leaflets. Blood cultures and fungal serologies were negative. During mitral valve replacement both the anterior and posterior mitral leaflets were covered with multiple small vegetations with features of nonbacterial thrombotic endocarditis. Though mostly asymptomatic, Libman-Sacks endocarditis may be an indication for valve replacement.
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PMID:Libman-Sacks Endocarditis in a Patient With Antiphospholipid Syndrome. 2734 24

Inflammation of the inner layer of the heart, especially the valvular endothelium, chordae tendinae and mural endocardium was first recognized almost 350 years ago. Over the years it has had many names, but is now generally designated infective endocarditis (IE) and has an associated infectious agent. A sterile vegetative process can also affect the valves and is usually referred to as Libman-Sacks endocarditis. The developments of medical science that allowed for our understanding of this entity included refinement of the autopsy, medical microscopy, microbiology, and in recent years, molecular studies. Some observations were misleading but clarification particularly followed the reports of Morgagni, Osler and Libman. As understanding of the pathobiology of infective endocarditis grew so did the effectiveness of therapy. This paper provides a detailed history of the development of the concept of Infective endocarditis citing many key morphological observations and concludes with brief comments about current concepts of pathogenesis as well as a few remarks about therapy.
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PMID:Infective endocarditis: a history of the development of its understanding. 2858 1

A 47-year-old woman with a medical history of Raynaud's phenomenon presented with fever, cough and shortness of breath. She was found to have left lower lobe consolidation and pleural effusion and was treated as a case of pneumonia. During the hospital course, her respiratory status worsened, and she was intubated on the third hospital day. To investigate the high A-a gradient, a Computerized Tomographic Pulmonary Embolism (CTPE) study was done which identified a large left lower pulmonary artery embolism. She was also found to have a new murmur, and an echocardiogram demonstrated a large lesion on tricuspid valve. However, multiple sets of her blood cultures came back consistently negative. Alternative diagnoses for culture-negative endocarditis were considered, and a full set of rheumatological workup was done. Laboratory tests were suggestive of antiphospholipid syndrome, hence the diagnosis of tricuspid valve Libman-Sacks endocarditis was made.
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PMID:A case of tricuspid valve non-bacterial thrombotic endocarditis presenting as pulmonary embolism in a patient with antiphospholipid antibody syndrome. 2953 97


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