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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pericarditis is the most frequent cardiac manifestation of systemic lupus erythematosus (SLE), but pericardial effusion causing tamponade rarely occurs, and it is even less frequent for the pericardial tamponade to be the presenting feature of SLE. We report a case of pericardial tamponade due to SLE with severe hemodynamic involvement as the clinical presentation of the disease. We comment on its clinical course and its rarity in the medical literature.
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PMID:[Cardiac tamponade as a clinical symptom of systemic lupus erythematosus]. 934 Jul 4

A prospective two dimensional and Doppler echocardiographic studies were performed in 41 patients to assess the incidence and spectrum of cardiac abnormalities. All patients included in the study fulfilled the 1982 revised criteria of the American Rheumatism Association for classification of SLE. There were 37 women and 4 men with average age of 38 years. Average duration of SLE was 6.5 years (range 6 months to 20 years). Nineteen patients (46.3%) with SLE had cardiac abnormalities. Valvular abnormalities were found in 14 patients (34.1%). Mitral valve abnormalities were the most common findings-in 7 patients (17.1%). There were 6 patients with aortic (14.6%), and 3 patients with tricuspid valve abnormalities (7.3%). One patient had morphological echocardiographic pattern suggesting noninfective verrucous vegetations affecting the tricuspid valve. Pericardial effusion was identified in 5 patients (12.2%). We found no correlation between the prevalence of cardiac abnormalities and duration, age and disease activity in SLE patients.
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PMID:[Echocardiographic heart assessment in systemic lupus erythematosus]. 948 Jan 81

Two dimensional echocardiography with doppler examination was performed in 54 patients with systemic lupus erythematosus (SLE). Nine (17%) had significant cardiac involvement (four left ventricular hypertrophy, one moderate pericardial effusion, one severe aortic regurgitation, and three ventricular systolic dysfunction). We further studied diastolic function in 45 patients who did not have a major abnormality in echo. SLE was graded as active in 16 patients (SLEDAI > 5) and inactive in 29 patients. Twenty age- and sex-matched subjects acted as controls. The data were compared using one way ANOVA test. Patients with active disease had significant diastolic dysfunction compared to inactive patients and controls as indicated by increased peak A (P < 0.01) and decreased E/A ratio (P < 0.01). There was no linear correlation between disease activity and diastolic dysfunction if SLEDAI was considered as a continuous variable (r=0.29 for E/A). Anticardiolipin antibodies (both IgG and IgM) were elevated in five patients (13 studied). One of them had severe mitral regurgitation, one had trace mitral and aortic regurgitation and one had diastolic dysfunction. We conclude that asymptomatic diastolic dysfunction is present in SLE patients.
Lupus 1998
PMID:Echocardiography in systemic lupus erythematosus. 1034 21

A 57-year-old woman was diagnosed in January 1982 with SLE based on ANA 1:640, positive LE cell preparation, proteinuria (3+), and pericarditis. In 1984, 1994, and 1997, the pericardial effusion was noted to have increased without signs of disease exacerbation or cardiac tamponade, and pericardial drainage was repeated to control the effusion. A massive pericardial effusion developed in August 1997. After tuberculosis, hypothyroidism, neoplasm, and progression of SLE were ruled out, we decided to perform pericardial fenestration. A safe and minimally invasive pericardial fenestration was successfully completed endoscopically. Pathologic study of the specimen revealed chronic pericarditis. We consider endoscopic pericardial fenestration to be useful for at risk patients with pericarditis to control the effusion and establish a differential diagnosis.
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PMID:Endoscopic pericardial fenestration for a patient with sustained lupus pericarditis. 1054 46

Twenty-four children (aged 6-15 years, M:F = 1:11) with systemic lupus erythematosus (SLE), who had respiratory symptoms, were retrospectively reviewed. Chest radiographs obtained from all patients revealed pleural effusion in 13, alveolar infiltration in 9, pericardial effusion and cardiomegaly in 6, interstitial infiltration in 4, hilar adenopathy in 3, lung abscess in 2 and pneumatocele with pneumothorax in 1. Etiologic organisms were identified in 7 cases; (3 cases of nocardia isolated from pleural effusion and sputum, 2 cases of tuberculosis, 1 case with staphylococcus aureus septicemia and 1 case with salmonella septicemia). All except one patient improved with medical treatment. One patient died from pneumonitis. Although pulmonary involvement is increasingly recognized in children with SLE, neither roentgenogram nor clinical findings were specific. The differentiation of pulmonary infiltrates caused by lupus lung disease from pulmonary infection should be carefully evaluated.
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PMID:Pulmonary involvement in childhood systemic lupus erythematosus. 1073 May 34

Two girls with mixed connective tissue disease (MCTD) were treated in our hospital in the past 5 years. Patient 1, a 10-year-old girl presenting with migratory arthralgia, had an initial diagnosis of juvenile rheumatoid arthritis. Muscle weakness with elevated levels of creatine kinase and liver enzymes, sclerodactyly, Raynaud's phenomenon and heliotrope sign developed subsequently in the following 3 years. Patient 2, a 13-year-old girl, had been treated for suspected systemic lupus erythematosus since 9 years of age. She presented with lymphadenopathy, arthralgia, pericardial effusion, and paralytic ileus. The symptoms waxed and waned. Sclerodactyly, Raynaud's phenomenon, proteinuria, and hypertension were also noted. Both patients had high serum titers of antinuclear antibody (speckled pattern, 1:5120) and were seropositive for antiribonuclear protein antibody. Intravenous immunoglobulin, prednisolone, cyclosporine A, and nonsteroidal anti-inflammatory drugs (NSAIDs) were given to patient 1. Patient 2 received cyclosporine A, prednisolone, and methylprednisolone pulse therapy. The disease has been well controlled for 2 years by low-dose immunosuppressants and NSAIDs. MCTD is a rare juvenile rheumatic disease: early identification and appropriate treatment can improve the disease outcome.
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PMID:Childhood mixed connective tissue disease. 1077 31

A 51-year-old woman with overt congestive heart failure with pleural and pericardial effusion was treated with furosemide and nifedipine, leading to improvement in her condition and a decrease in effusions. An echocardiography demonstrated mitral and aortic regurgitation with mitral valve prolapse, which caused the congestive heart failure. Since leukocytopenia and lymphocytopenia with arthralgia could be observed, serological investigations were performed. She was diagnosed as having systemic lupus erythematosus (SLE) with antiphospholipid syndrome, and started on a treatment of prednisolone and aspirin. Based on the treatment, the pleural and pericardial effusion went into complete remission, indicating that the serositis related to SLE had overlapped the heart failure. Since there was no evidence of any other diseases that could be responsible for the valvular lesions, we concluded that they were due to antiphospholipid syndrome. The administration of prednisolone had no significant effect on valvular morphology or function as demonstrated by echocardiography. When patients with valvular disease are seen, a valvulopathy related to antiphospholipid syndrome should be considered as part of the differential diagnosis.
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PMID:Overt congestive heart failure with mitral and aortic regurgitation due to antiphospholipid syndrome in a patient with systemic lupus erythematosus. 1085 59

Many patients with systemic lupus erythematosus (SLE) develop cardiac manifestations during the course of their disease. Pericarditis is most commonly seen, with a reported prevalence of 60%. Myocardial involvement is present in only a minority of patients. In recent years, due to better noninvasive diagnostic techniques, valvular abnormalities can be demonstrated in an increasing number of patients. Depending on the technique used, valvulopathy can be demonstrated in up to 77% of SLE patients. Although most of the valvular lesions will be present without any symptoms, valve incompetence can result in congestive heart failure. Valvular lesions are associated with IgG anticardiolipin antibodies (aCL) and disease duration. We present a patient with SLE and secondary antiphospholipid syndrome (APS) who developed acute congestive heart failure due to pancarditis. Endocarditis, together with left ventricular dysfunction and pericardial effusion, were present. The endocarditis caused hemodynamically significant mitral valve insufficiency due to thickening of the mitral cusps. Just two weeks prior to the occurrence of congestive heart failure echocardiography had been normal. Treatment with high dose corticosteroids resulted in a gradual, almost complete recovery. Literature concerning cardiac manifestations in lupus is reviewed.
Lupus 2000
PMID:Cardiac abnormalities in SLE: pancarditis. 1086 93

The antinuclear antibodies (ANA) test has been a cornerstone of the evaluation of connective tissue disease. The aim of this study was to investigate the diagnostic value of the ANA test in pleural or pericardial effusions of unknown causes. Over a 3-yr period, a total of 126 pleural fluid and 30 pericardial fluid samples were analysed. ANA tests were performed using a commercially available kit. The ANA kit used an indirect immunofluorescent antibody method with a human epithelial (HEP-2) cell line as substrate. Patients with high fluid ANA titre (>1:160) received a second aspiration 2 weeks after the initial aspiration if diagnosis was not confirmed. ANA results were positive in 39 pleural and 10 pericardial fluid samples. All but one of the effusions with positive ANA testing were exudative. Eleven pleural or pericardial effusions due to active systematic lupus erythematosus were identified and all had high ANA titres (1:160) with various staining patterns. Thirty-eight of 145 patients (26%) with effusions of nonlupus aetiologies had positive ANA testing in pleural or pericardial fluid. Thirteen of these 38 patients had high ANA titre. Malignant or paramalignant effusions constituted 11 of the 13 samples. In conclusion, although a negative antinuclear antibodies test makes a diagnosis of lupus serositis unlikely, high antinuclear antibodies titres in pleural or pericardial fluid are not diagnostic of lupus serositis even when as high as 1:5,120. An unexplained high antinuclear antibodies titre in pleural or pericardial effusion warrants search for malignancy.
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PMID:Serial antinuclear antibodies titre in pleural and pericardial fluid. 1088 31

We report on a case of systemic lupus erythematosus associated with superior vena cava syndrome. A 46-year-old woman developed polyarthralgia in December 1994. She was treated with nonsteroidal anti-inflammatory drugs. In February 1995, she was admitted to our hospital with systemic convulsion and disturbance of consciousness (III-300/Japan coma scale). Severe facial edema was also present. Laboratory studies revealed the presence of anti-nuclear antibody, anti-DNA antibody, anti-Sm antibody, and proteinuria. An X-ray film of the chest showed pericardial effusion and bilateral pleural effusions. Computed tomography of the chest showed a severe swelling of mediastinal lymph nodes. A diagnosis of systemic lupus erythematosus was made according to the American Rheumatism Association criteria. Initial treatment with intravenous dexamethasone improved the level of consciousness and decreased the facial edema, mediastinal lymphadenopathy, and the effusions on computed tomography of the chest. We believe that the most likely explanation for the facial edema is superior vena cava syndrome due to severe mediastinal lymphadenopathy.
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PMID:[A case of systemic lupus erythematosus associated with superior vena cava syndrome]. 1091 18


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