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)

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 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

In order to assess the prevalence of cardiac involvement in the primary antiphospholipid syndrome (PAS), a syndrome which associates thromboembolism, recurrent abortion, the presence of antiphospholipid antibodies and thrombocytopenia, transthoracic (TTE) and trans-esophageal echocardiography (TEE) was performed in 15 patients, 10 women and 5 men with a mean age of 38.8 +/- 11 years, with the PAS but without systemic lupus erythematosus. The presentation of the PAS was a thrombotic event (6 arterial and 7 venous) in 13 cases, and recurrent abortion in 3 cases. Twelve patients had high anticardiolipin antibody levels (> or = 15 U GPL) and 12 had a raised anti-prothrombinase antibody title. Valvular heart disease was detected in 9 patients (60%) as a valve thickening (> or = 5 mm for the mitral and > or = 3 mm for the aortic valve) or nodule. Mitral regurgitation was observed in 4 cases both on TTE and TEE and was mild in 3 cases and severe in 1 case. Aortic regurgitation was diagnosed in 6 patients, in 3 cases by TTE and in 6 cases by TEE. It was mild in 5 cases and moderate in the other cases. Pericardial effusion was observed in 3 patients (20%), alone in 1 case and associated with valvular disease in the other two cases. No abnormality of left ventricular systolic or diastolic function could be demonstrated. In conclusion, cardiac involvement seems to be common in the PAS, and TEE is a sensitive and accurate method for describing the valvular, especially aortic valve, abnormalities.
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PMID:[Prevalence and description of cardiac involvements in primary antiphospholipid syndrome]. 130 23

Anticardiolipin antibodies (acLa) are associated with a thrombotic tendency (often involving cerebral ischemic events), are frequently present with systemic lupus erythematosus and have been found together with cardiac valve abnormalities. Previous studies evaluated patients characterized by the presence of acLa or lupus, precluding assessment of the frequency of acLa in those with valvular disease. This study aims to establish the prevalence of acLa in patients with valve disease in the absence of lupus and, furthermore, to determine the influence of acLa on the risk of cerebral events in valve disease. Eighty-seven consecutive patients with mitral or aortic regurgitation, or both, prospectively underwent enzyme-linked immunosorbent assay testing for immunoglobulin G (IgG) and M acLa, as did 24 normal subjects. AcLa values greater than or equal to 3 SD above the normal mean were considered "positive." Prior cerebral events were defined retrospectively. Of 87 patients with valvular disease, 26 had positive IgG acLa levels compared with 0 of 24 normal subjects (p less than 0.01). AcLa values did not vary with valve disease etiology. Focal cerebral events had occurred in 8 patients and were embolic or probably embolic in 7, including 7 of 26 IgG acLa-positive and 1 of 60 IgG acLa-negative patients (p less than 0.001). In the absence of lupus, IgG acLa is highly prevalent among patients with aortic or mitral regurgitation, or both; this association may indicate a relatively high risk for cerebral emboli.
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PMID:Prevalence of anticardiolipin antibody in isolated mitral or aortic regurgitation, or both, and possible relation to cerebral ischemic events. 152 45

Clinical tricuspid stenosis has not previously been reported in patients with systemic lupus erythematosus (SLE). A 25 year old woman with active SLE presented with signs of severe right ventricular failure. Cardiac catheterisation confirmed the diagnosis of tricuspid stenosis and regurgitation together with mitral regurgitation. This patient underwent successful tricuspid and mitral valve replacement.
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PMID:Systemic lupus erythematosus complicated by tricuspid stenosis and regurgitation: successful treatment by valve transplantation. 154 16

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

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
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PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84

To evaluate cardiac involvement in primary antiphospholipid syndrome, two-dimensional and Doppler echocardiographic studies were performed in 34 consecutive patients with this syndrome. All patients had an increased level of serum anticardiolipin antibodies with no evidence of malignancy or systemic lupus erythematosus. The clinical manifestations of primary antiphospholipid syndrome were arterial thrombosis in 14 patients, venous thrombosis in 6 and recurrent fetal loss in 14. Valvular lesions were observed on two-dimensional echocardiography in 11 patients (32%) (9 women and 2 men), aged 24 to 57 years (mean +/- 1 SD 36 +/- 10). Abnormal echocardiographic findings were observed in 9 (64%) of 14 patients with arterial thrombosis versus 1 (17%) of 6 patients with venous thrombosis and 1 (7%) of 14 patients with recurrent fetal loss. The most common echocardiographic abnormality was mitral leaflet thickening, found in five patients; this was associated with mitral regurgitation in three and with combined mild mitral stenosis and regurgitation in one patient. Localized subvalvular mitral thickening was observed in one patient and calcification of the anulus in another. Aortic valve thickening was observed in two patients, one of whom also had a moderate degree of aortic regurgitation. Vegetation-like lesions on the mitral or aortic valve were found in two patients. It is concluded that valvular lesions are commonly found in primary antiphospholipid syndrome, particularly when the syndrome is manifested by peripheral arterial thrombosis. The location and appearance of valvular lesions in this syndrome are heterogeneous. Most patients have no clinically significant valvular disease. Two-dimensional and Doppler echocardiographic studies are often informative in these patients.
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PMID:Cardiac involvement in patients with primary antiphospholipid syndrome. 189 66


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