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)

The possible contribution of immunological mechanisms in the development of Libman-Sacks endocarditis was studied in 2 patients with systemic lupus erythematosus who underwent aortic valve replacement. Sections of verrucous lesions, stained with haematoxylin and eosin, showed three apparently distinct zones: an outer exudative zone of fibrin, nuclear debris, and haematoxylin-stained bodies; a middle organizing zone of proliferating capillaries and fibroblasts; and an inner zone of neovascularization which showed distinct, thin-walled junctional vessels. The striking finding was the apparently selective deposition of immunoglobulins and complement identified by direct immunofluorescence, within the walls of the small junctional vessels of the zone of neovascularization. We suggest that the observed immune deposits are immune complexes and that circulating immune complexes may play a critical role in the growth and proliferation of the verrucous lesion.
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PMID:Immunopathogenesis of Libman-Sacks endocarditis. Assessment by light and immunofluorescent microscopy in two patients. 33 50

Clinical and morphologic observations in three patients with systemic lupus erythematosus and severe mitral regurgitation are described. Attention is called to the "healing" of Libman-Sacks endocarditis, an infrequent occurrence in patients with systemic lupus erythematosus in the era before steroid therapy. The mitral regurgitation in our patients appears to have resulted from "healing" of the Libman-Sacks vegetations by scarring and calcification. The healing is attributed to long-term corticosteroid therapy.
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PMID:Systemic lupus erythematosus as a cause of severe mitral regurgitation. New problem in an old disease. 80 40

A patient who developed a multisystem involvement of systemic lupus erythematosus (SLE) after 9 years of procainamide therapy, during which time he ingested enormous amounts of the drug, is described. The patient first suffered from recurrent episodes of pleuritis and arthritis, after which he developed a characteristic SLE nephritis associated with a high level of antinative DNA antibodies and a low level of complement. He finally died from a complication of a nonbacterial endocarditis. Autopsy showed polyserositis and typical deposits of electron-dense material on the glomerular basement membrane, and confirmed the clinical diagnosis of Libman-Sacks endocarditis. The possibility that procainamide-induced SLE might have all the clinical, immunological, and pathological features of spontaneous SLE, especially in patients exposed to large doses of the drug for many years, is discussed.
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PMID:Clinicopathological study of a patient with procainamide-induced systemic lupus erythematosus. 94 76

A patient with systemic lupus erythematosus developed acute mitral regurgitation due to ruptured chordae tendineae, requiring mitral valve replacement. Typical changes of Libman-Sacks endocarditis were observed in the excised mitral valve. Immunofluorescent studies revealed antinuclear antibody and deposits of immunoglobulins and complement within small vessels.
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PMID:Acute mitral regurgitation from ruptured chordae tendineae in systemic lupus erythematosus. 108 31

Libman-Sacks endocarditis caused progressive life-threatening mitral regurgitation necessitating mitral valve replacement in an 18 year old woman with systemic lupus erythematosus (SLE). Although Libman-Sacks endocarditis is frequently seen at autopsy in patients with SLE, hemodynamically significant valvular disease due to that lesion is quite rare. We found no previous reports describing mitral regurgitation in a patient with SLE which has necessitated surgical intervention.
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PMID:Mitral valve disease of systemic lupus erythematosus. A cause of severe congestive heart failure reversed by valve replacement. 113 46

The purpose of this study was to evaluate the spectrum of morphologic and functional cardiac involvement in a selected population of patients with systemic lupus erythematosus (SLE) by means of echocardiography. Thirteen patients (2 male and 11 female) affected by SLE, mean age 41.9 years (range, 21-64), underwent M-Mode, two-dimensional and Doppler echocardiography. Eleven patients had renal disease and 3 of them were undergoing dialysis. One patient had findings of active disease. Six patients had systemic hypertension. None had a history suggestive of rheumatic fever or infective endocarditis. At echocardiographic study nine patients demonstrated findings of valvular involvement. These alterations were defined, according to the echocardiographic features, in two types: vegetation (verrucous Libman-Sacks endocarditis) and thickening. Vegetations were present in 6 patients, involving the mitral valve in all six and the aortic valve in three. The mitral valve vegetations were more frequent on the subannular portion of the posterior leaflet. Seven patients had valvular thickening: involvement of both mitral and aortic valve was present in five, and isolated mitral or aortic valve lesions in the remaining two patients. Combined valvular vegetation and thickening were observed in 4 patients. Eight patients had mild valvular dysfunction on Doppler examination: five isolated mitral regurgitation, two combined mitral and aortic regurgitation and one combined mitral stenosis and regurgitation. In agreement with previous reports, our study shows that valvular involvement in SLE is relatively frequent. Echocardiography can identify additional patterns of valvular lesions different from the known "verrucous Libman-Sacks endocarditis". The degree of valvular dysfunction is not important.
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PMID:[Heart valve involvement in systemic lupus erythematosus: an echocardiographic study]. 129 16

A 39-year-old woman was admitted with abdominal pain and dyspnea, and a diagnosis of systemic lupus erythematosus with renal involvement was established. Laboratory tests revealed highly elevated anticardiolipin antibody, thrombocytopenia and false positive VDRL. Generalized thrombus formation and Libman-Sacks endocarditis were found at postmortem examination. The pancreas showed chronic inflammation with thrombi in pancreatic arteries, but no vasculitic change was observed. Lowering of pancreatic blood flow because of arterial thrombi was a possible cause of pancreatitis in this patient. The spectrum of antiphospholipid antibody associated diseases may be extended to include pancreatitis as a thrombotic complication.
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PMID:Pancreatitis related to antiphospholipid antibody syndrome in a patient with systemic lupus erythematosus. 151 70

We conducted a prospective longitudinal study to determine the nature and prevalence of cardiac abnormalities in systemic lupus erythematosus and to study their natural history and relationship with disease activity. Forty consecutive inpatients with systemic lupus erythematosus were studied during their admission and subsequently 6 to 12 months later. On each occasion a clinical cardiovascular examination was carried out, disease activity was scored using the "Lupus Activity Criteria Count" and a Doppler echocardiographic examination was carried out. 72.5% of patients had an abnormal echocardiogram in the first study while 51.7% were abnormal during the follow-up study. Valvar disease occurred in 37.5% of patients. The mitral valve was most commonly affected. Libman-Sacks endocarditis was rare (2.5%). Pericardial effusions were seen in 36.2% of echocardiograms. The majority (76.0%) of these were associated with hypoalbuminaemia. 80.0% of patients had active disease during the first examination and 41.4% at follow-up. There was no correlation between activity of disease and prevalence of cardiac abnormalities at either examination. We conclude that cardiac disease is common in systemic lupus erythematosus. Prevalence of cardiac abnormality did not correlate with disease activity.
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PMID:Cardiac abnormalities in systemic lupus erythematosus: prevalence and relationship to disease activity. 154 11

A 38-year-old female was admitted to our hospital because she was suffered from severe dyspnea on effort. She had a history of nasal bleeding, endocarditis, fever, proteinuria, and alopecia at the age of 16, and was diagnosed as SLE. She was suffered from recurrent cerebral infarctions at the age of 35 and 38, and then mitral regurgitation was pointed out. Preoperative examination revealed non-active phase of SLE and UCG showed massive mitral regurgitation. Operative findings showed thrombosed verrucca circumferentially on the mitral valve. Mitral valve replacement (B-S #27) was done with using a felt strip in order to reinforce the mitral annular tissues. Histological findings of the verrucca showed Libman-Sacks endocarditis. Postoperative course was uneventful. Surgical treatment for Libman-Sacks endocarditis is extremely rare.
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PMID:[A case of mitral valve replacement for Libman-Sacks endocarditis]. 156 50

Fifty-six patients, 49 females and 7 males, with the confirmed diagnosis of systemic lupus erythematosus were examined by M-mode, 2--D and Doppler echocardiography. Pericardial effusion was found in 15 patients (27%), while pericardial thickening was suspected in 6 additional patients (37.5% altogether). Two patients had the signs of a pericardial tamponade, but both of them were uraemic. Libman-Sacks endocarditis was suspected in 4 patients (7.5%) because of verrucous changes in the aortic or mitral valve and regurgitant jet. Slight to moderate left ventricular hypocontractility was present in 3 patients (5%), while 3 additional patients had borderline values of the left ventricular contractility parameters. Left ventricular hypertrophy, usually mild, was found in 21 patients (37.5%). Echocardiographic signs of pulmonary hypertension were present in 2 patients (3.6%). It has been concluded that pericardial affection is frequent during the course of systemic lupus erystematosus, while a diffuse myocardial involvement is rare, except the consequences of arterial hypertension and accelerated coronary atherosclerosis. Libman-Sacks endocarditis still represents a diagnostic problem. For a more precise definition of cardiac involvement in systemic lupus erythematosus, a comparative analysis of the disease activity and immunosuppressive therapy is needed.
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PMID:[Echocardiographic analysis of changes in the heart in patients with systemic lupus erythematosus]. 207 23


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