Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30 year old man presenting with a 10 year history of delayed pressure urticaria had a secondary lupus-induced double mitral and aortic regurgitation which necessitated double valve replacement within 2 years. The anatomical appearances of the valvular lesions were very unusual and suggest a new anatomo-clinical form of the classical Libman-Sacks endocarditis. In addition to infective endocarditis, systemic lupus erythematosus may also lead to valvular lesions necessitating valve replacement. The association of S.L.E. and delayed urticaria is rare, and also merits publication.
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PMID:[Double valve replacement in a 30-year-old man with acute systemic lupus erythematosus]. 357 90

This is a report of abnormal endocardial structures on the left ventricular wall as visualized by two-dimensional echocardiography (2-D echo) in patients with systemic lupus erythematosus. Abnormal endocardial structures, arising from the left ventricular endocardium and appearing to proliferate into the cavity, were found in 11 (20%) of 54 patients. The most frequently involved site was posterobasal left ventricular wall in the parasternal long-axis view, and the posterolateral segment of the left ventricle including the anterior and posterior papillary muscles in the parasternal short-axis view. M-mode echocardiograms, simultaneously recorded with 2-D echo, revealed abnormal structures of increased intensity adjacent to the endocardium with thicknesses of 4 approximately 7 mm. Most of the abnormal endocardial structures were observed in patients in the active phase by 2-D echo, and they appeared to regress with steroid therapy. In one autopsy case, fibrous endocardial thickening suggesting healed endocarditis was present in the anterior papillary muscle as observed by 2-D echo. Their location and response to steroid therapy suggests that these abnormal echoes could represent Libman-Sacks endocarditis.
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PMID:[Abnormal left ventricular endocardial structures detected by two-dimensional echocardiography in systemic lupus erythematosus]. 384 91

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A case of aortic infective endocarditis due to Hemophilus paraphrophilus in a patient with previous Libman-Sacks endocarditis is presented. Suggestions regarding antibiotic prophylaxis are made concerning patients with systemic lupus erythematosus.
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PMID:Clinical considerations regarding infective Libman-Sacks endocarditis. 398 75

The authors report a case of Libman-Sacks endocarditis of the posterior mitral leaflet in a child treated for disseminated lupus erythematosus for 8 years. Mitral valve replacement was performed. Libman-Sacks vegetations are hardly ever recognised in vivo and have never been previously reported in a child. The incidence of this cardiac complication of lupus erythematosus is probably higher than indicated in the literature. Attentive cardiac examination and systematic echocardiography should be part of routine follow-up of patients with disseminated lupus erythematosus.
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PMID:[Mitral valve replacement in an infant with disseminated lupus erythematosus and Libman-Sacks endocarditis]. 641 Oct 38

Hemodynamically significant valvular lesions have been rarely reported sequelae of Libman-Sacks endocarditis complicating systemic lupus erythematosus (SLE). Furthermore, embolic phenomena associated with these vegetations have not been clearly documented. We present a report of critical aortic stenosis associated with SLE in a patient who had received corticosteroid treatment for several years. An embolus, histologically identical with the aortic valve vegetation, was found in the left anterior descending artery at necropsy. There was no evidence of rheumatic heart disease, bacterial endocarditis or a bicuspid aortic valve. Recent reports suggest an increased incidence of significant valvular dysfunction in patients with SLE who have received long-term corticosteroid treatment.
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PMID:Aortic stenosis associated with systemic lupus erythematosus. 646 59

Immunopathologic studies were performed on cardiac tissue obtained at autopsy in 10 patients with severe systemic lupus erythematosus (SLE). The immunopathologic findings were correlated with histopathologic and clinical evidence of cardiac injury, and with clinical and serologic features of SLE. Immune reactants were demonstrated by direct immunofluorescence in nine patients in a granular deposition pattern suggesting immune complex aggregates. Histologic and gross anatomic findings of inflammation were generally more focal than was the distribution of immune reactants. Most of the immune deposits were present in the walls of the blood vessels of myocardium (eight of 10) or pericardium (two of three). In one patient with Libman-Sacks endocarditis, immunoglobulin and complement components were present in the valve stroma and the vegetations. The immune deposits around epicardial nerve fibers in two patients with severe neurologic manifestations contained immunoglobulin E(IgE). In general, the most intense and widespread immune deposits were observed in patients with persistently increased serologic and clinical evidence of activity of their systemic disease. These results suggest a role for immune complex deposition in the pathogenesis of the cardiac lesions of SLE.
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PMID:Immunopathology of cardiac lesions in fatal systemic lupus erythematosus. 700 81

Left homonymous hemianopia, hemiparesis, left-body clonic seizures, and progressive deterioration of consciousness complicated the clinical course of a 57-year-old woman with systemic lupus erythematosus (SLE). Autopsy documented the presence of multiple brain infarcts and cerebral arterial emboli that originated from the verrucae of Libman-Sacks endocarditis. Clinicians and pathologists should consider this unusual vascular mechanism of cerebral injury in patients with SLE who develop strokes.
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PMID:Cerebral embolism in Libman-Sacks endocarditis. 718 54

We conducted an echocardiographic study to determine the incidence and spectrum of morphologic and functional cardiac abnormalities in systemic lupus erythematosus (SLE) and to relate these findings to the disease activity and duration, and the presence of antiphospholipid (APL) antibodies. Thirty consecutive patients with LES (5 male and 25 female, mean age 37 +/- 11 years) were studied with a clinical cardiovascular examination and M-mode, 2-D Doppler echocardiogram. All patients fulfilled the American Rheumatism Association criteria for diagnosis of SLE. Disease activity was scored using the "Lupus Activity Criteria Count". The duration of the disease was less than 1 year in 5 patients (16.7%), between 1 and 5 years in 7 (23.3%), and superior to 5 years in 18 (60%). No patient had a history of rheumatic fever or infective endocarditis. All patients had received steroid therapy. In 26.7% of patients the disease was active, and in 33.3% APL antibodies were present. Patients were matched by number, age and sex with the control group. In 73.3% of the patients the echocardiogram resulted abnormal; valvular disease occurred in 30% and the echocardiographic features were of diffuse thickening, with 4 mitral and 2 aortic regurgitations. No valvular dysfunctions were significant, nor was Libman-Sacks endocarditis present. Pericardial disease, effusion or thickening was detected in 33.3% of the echocardiograms. Furthermore, there was one patient with left ventricular mild hypertrophy; 2 with a mild enlargement of the left ventricle with no segmental abnormalities of wall motion and no systolic disfunction; 8 patients (26.7%) were normal. Compared with the control group, patients with SLE had an increased prevalence of echocardiographic abnormalities, especially pericardial (p < 0.001) and valvular (p < 0.01). No association was found between activity, duration of the disease and prevalence of cardiac abnormalities. On the contrary, an association between the presence of APL antibodies and cardiac abnormalities at the echocardiographic examination was evident (p < 0.05).
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PMID:[Cardiac anomalies in systemic lupus erythematosus: their prevalence and relation to duration, disease activity and the presence of antiphospholipid antibodies]. 816 2

Recurrent thrombosis and pregnancy loss are well-recognized features of the antiphospholipid syndrome. Uncertainty exists, however, as to whether other reported features of the antiphospholipid syndrome such as cardiac valvular vegetations are truly part of this disorder or more reflective of associated systemic lupus erythematosus (SLE). Several recent studies have concluded that patients with antiphospholipid antibodies have a higher risk of developing Libman-Sacks endocarditis. This study was performed to determine whether antiphospholipid antibodies are the only risk factors for cardiac valvular disease in patients with primary antiphospholipid syndrome (PAPS) or SLE. Ten patients with PAPS were matched with 20 patients with SLE and 20 healthy control subjects by sex. All participants were tested for anticardiolipin (aCL) antibodies by means of a standardized enzyme-linked immunosorbent assay technique, and all underwent two-dimensional and color-flow Doppler echocardiography. The echocardiograms were interpreted by two cardiologists blinded to the patients' underlying disease. Sixty percent of the PAPS group had cardiac valvular involvement compared with 40% of the SLE group (p = NS). We conclude that cardiac valvular vegetations are common both in aCL-negative patients with SLE and in patients with PAPS. This suggests that aCL antibodies either play no causative role or are not the only risk factors in the development of cardiac valvular vegetations.
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PMID:A comparison of cardiac valvular involvement in the primary antiphospholipid syndrome versus anticardiolipin-negative systemic lupus erythematosus. 846 38


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