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

Candida pericarditis and tamponade developed in a patient with sterile purulent pericarditis secondary to systemic lupus erythematosus. Therapy with amphotericin B and properly timed surgical intervention led to a clinical and microbiological cure. This article emphasizes the importance of differentiating an infected pericardial effusion from the sterile pericarditis of systemic lupus erythematosus and provides suggested guidelines for the management of that complication.
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PMID:Candida pericarditis and tamponade in a patient with systemic lupus erythematosus. 327 74

SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
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PMID:Cardiovascular involvement in systemic lupus erythematosus. 333 84

For 75 patients with systemic lupus erythematosus (SLE), 39 laboratory and clinical characteristics, including HLA-A, B, C and DR typing, were analysed using a cluster analysis technique. Three groups were identified. Group I (46 patients) was characterized by infrequently severe disease, good response to therapy and infrequent multisystem involvement. Group II (24 patients) was characterized by a severe course of disease (although the tendency to remit after therapy was not unusual), and frequently, renal involvement and pericarditis. Group III (5 patients) was characterized by more severe renal disease. Of the 75 patients studied, 38.7% possessed HLA-DR3, compared to 17.4% of controls. Group I patients did not differ from controls but 80% of Group II patients and 4/5 Group III patients had DR3. Cluster analysis identifies subsets of SLE patients who show marked differences in disease course and severity, correlated with possession of the HLA B8, DR3 phenotype.
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PMID:Heterogeneity of systemic lupus erythematosus elucidated by cluster analysis. The influence of HLA. 347 Mar 92

Antinuclear antibodies (ANA) are found in the majority of patients with systemic lupus erythematosus (SLE). We report here the only documented case, out of a series of 38 patients, in which SLE was diagnosed in spite of the fact that we failed to demonstrate any type of autoantibodies. A 25-year-old black woman presented with 6 of the 11 criteria of the American Rheumatism Association for classification of SLE, between August 1984 and April 1985, i.e. malar rash, photosensitivity, arthritis, pleurisy and pericarditis, renal insufficiency and nephrotic syndrome, anemia and leukopenia. Renal biopsy revealed mesangial glomerulonephritis, tubulonephritis and many tubuloreticular inclusions in the capillary endothelium highly suggestive of SLE. Four ANA determinations were performed during the 8 months of observation which were all negative, as were all other antibodies (anti-nDNA, -Sm, -RPN, -Ro, -La). The outcome was very favourable under prednisone and cyclophosphamide. In the rare cases of ANA negative SLE (5-10%) photosensitive dermatitis is the prominent feature and renal or central nervous system involvement is less frequent. Those patients usually have other types of autoantibodies (especially anticytoplasmic) which was not the case in our patient. This indicates that the absence of autoantibodies does not rule out SLE.
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PMID:[Disseminated lupus erythematosus without antinuclear antibodies or other autoantibodies]. 349 6

Antinuclear antibodies are present in most patients receiving procainamide. To ascertain whether IgG antiguanosine antibodies are associated with the development of the symptoms of systemic lupus erythematosus, we compared the levels of these antibodies in the sera of 65 patients receiving procainamide: 18 with procainamide-induced symptoms and 47 asymptomatic patients. Antinuclear antibodies measured by immunofluorescence were present in the 18 patients with drug-induced symptoms but also in 24 asymptomatic patients. Similarly, elevated serum levels of antibodies to single-stranded DNA were found in 15 patients with symptoms and in 20 asymptomatic patients. In contrast, levels of IgG antiguanosine antibodies were elevated in 15 patients with drug-induced symptoms, but in only 3 asymptomatic patients. Antiguanosine antibodies binding to single-stranded DNA were found primarily in patients with arthritis, pleuritis, and pericarditis. These results suggest a strong association between IgG antiguanosine antibodies and major manifestations of procainamide-induced systemic lupus erythematosus.
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PMID:Antiguanosine antibodies: a new marker for procainamide-induced systemic lupus erythematosus. 351 20

I have described a patient in whom cardiac tamponade occurred as the initial clinical manifestation of SLE. Although pericarditis is a common clinical entity in SLE, cardiac tamponade with this disease is rare. If suspected, the diagnosis can be made by the proper selection of tests of serum and pericardial fluid, which should include the search for pericardial LE cells. This report emphasizes the importance of screening for connective tissue disease in patients with pericarditis.
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PMID:Cardiac tamponade in systemic lupus erythematosus: an unusual initial manifestation. 356 85

Pericarditis is a common manifestation of systemic lupus erythematosus (SLE), however, tamponade seems to be extremely rare. A review of the English literature revealed 12 such cases and in 5 the tamponade was the presenting symptom of the disease. We describe an additional patient. She developed pericardial tamponade one week after delivery of a healthy child, and subsequently was diagnosed to have SLE. The effect of pregnancy and the postpartum period on SLE is discussed.
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PMID:Cardiac tamponade in the early postpartum period as the presenting and predominant manifestation of systemic lupus erythematosus. 372 5

Acute myocardial infarction (AMI) is relatively rare in systemic lupus erythematosus (SLE), although other cardiac complications, such as pericarditis and myocarditis, occur frequently in this disease. A 20-year-old woman with documented SLE experienced a transmural anterior AMI due to thrombi in saccular aneurysms of the left main coronary artery and the proximal portion of the left anterior descending coronary artery. There were also saccular and fusiform aneurysms in the right coronary artery, but thrombi were not observed in them. Aorto-coronary bypass surgery was performed to salvage the viable myocardium and to prevent recurrent myocardial infarction and rupture or infection of these coronary aneurysms. Postoperative coronary angiography revealed a new small saccular aneurysm in the mid-portion of the right coronary artery. During this period, there was no immunological evidence of active SLE. It is important to ascertain whether such coronary aneurysms resulted from atherosclerosis or arteritis, because of the choice of the different therapeutic interventions. In this case, however, it was difficult to determine. It was speculated that these coronary aneurysms arose from an arteritic process, because the saccular aneurysm in the mid-portion of the right coronary artery was formed in less than three months, there were no coronary risk factors, and any microscopic evidence of atherosclerosis was not obtained in the aortic specimen during aortocoronary bypass surgery. Serial coronary angiographic studies are necessary for accurately diagnosing coronary artery disease. Anticoagulant therapy and antiinflammatory medication may be necessary to prevent myocardial infarction in patients with SLE, even if there is no immunological evidence of active SLE.
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PMID:[Myocardial infarction due to thrombi in coronary aneurysms in a young woman with systemic lupus erythematosus]. 378 87

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.
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PMID:Cardiovascular manifestations of systemic lupus erythematosus. 390 17

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


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