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)

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

Culture proven bacterial endocarditis occurred in 6 of 571 patients with systemic lupus erythematosus (SLE) admitted to the National Institutes of Health (NIH). Although 4 of the patients had a murmur noted on examination prior to developing endocarditis, only one of the 6 had a recognized valvular abnormality. Bacterial endocarditis followed dental procedures in 2 of the 6 patients; no precipitating events were recorded in the remaining 4. M-mode and 2-D echocardiography of 20 unselected SLE patients did not reveal previously unrecognized cardiac disease. There was an unexpectedly high frequency of bacterial endocarditis among SLE patients relative to all other connective tissue disease patients seen at the NIH.
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PMID:Bacterial endocarditis complicating systemic lupus erythematosus. 662 Feb 68

To evaluate the diagnostic help afforded by immune determinations in feverish valvular patients, we prospectively determined: total hemolytic complement, cryoglobulin, rheumatoid factor, circulating immune complexes and direct skin immunofluorescence. Twenty patients entered the study, twelve with bacterial endocarditis, six without any bacteremia and two septicemic patients without endocarditis. We detected at least one immune abnormality in 10/12 endocarditis patients: - in 7/11 (64 p. cent) circulating immune complexes; - in 3/12 rheumatoid factor; - in 3/12 positive fluorescence in dermal vessels (IgM-C3); - and in one patient an IgG lupus-like band in the membrane basal zone. We also found circulating immune complexes in 3/4 patients without bacteremia and in 1/2 septicemic patients. We conclude that, in our small prospective study, immune abnormalities are frequent in bacterial endocarditis patients but their diagnostic values is rather limited : their absence do not rule out endocarditis and they can be present in many other febrile disorders.
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PMID:[Bacterial endocarditis : lack of diagnostic value of immunological investigations (author's transl)]. 708 72

Mitral annulus calcification (MAC), while a relatively frequent autopsy finding in older patients, is rare in childhood. Such calcification has generally been regarded as a degenerative change and of no clinical significance. Recent studies have shown that MAC may be associated with hemodynamically significant lesions including mitral insufficiency, arrhythmias, heart block, and, rarely, mitral stenosis. We have studied a case of massive calcification in the mitral annulus in a 17-year-old girl with juvenile rheumatoid arthritis and systemic lupus erythematosis. In this case, the MAC was considered secondary to the rheumatoid disease. MAC in younger patients with no history of rheumatic fever or bacterial endocarditis suggests an associated connective tissue disorder.
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PMID:Massive calcification of the mitral annulus in a 17-year-old patient with juvenile rheumatoid arthritis and systemic lupus erythematosis. 724 18

To study the cardiac involvement in systemic lupus erythematosus, the clinical and necroscopy records of 29 patients were analyzed. Of these, 28 were female and 1 was male with a mean age of 28.6 +/- 10.4 years. The mean duration of the disease was 23.8 +/- 20.1 months. Twenty patients had the diagnosis of renal failure, 11 of arterial hypertension and 8 of congestive heart failure. No valvular or coronary arterial disease was diagnosed in any patient. The most frequent cause of death was sepsis, followed by renal failure. Only one patient died of causes directly related to heart disease. At necroscopy, 12 patients had pericarditis and 10 had cardiomegaly. Nonspecific valvular abnormalities were observed in 2 patients, Libman-Sacks' endocarditis in 1 and bacterial endocarditis in 2. Cardiovascular abnormalities were absent in only 8 (7.5%) patients. It was concluded that although frequent and contributing to mortality in some patients, cardiovascular involvement in systemic lupus erythematosus is multifactorial and, usually, nonspecific.
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PMID:[Cardiac involvement in systemic lupus erythematosus: anatomo-pathological study]. 828 Dec

The antiphospholipid syndrome (APS) is defined by the presence of anti-phospholipid antibodies (aPLs) and venous or arterial thrombosis, recurrent pregnancy loss, or thrombocytopenia. The syndrome can be either primary or secondary to an underlying condition, most commonly systemic lupus erythematosus (SLE). Echocardiographic studies have disclosed heart valve abnormalities in about a third of patients with primary APS. SLE patients with aPLs have a higher prevalence of valvular involvement than those without these antibodies. Valvular lesions associated with aPLs occur as valve masses (nonbacterial vegetations) or thickening. These two morphological alterations can be combined and are thought to reflect the same pathological process. Both can be associated with valve dysfunction, although such association is much more common with the latter alteration. The predominant functional abnormality is regurgitation; stenosis is rare. The mitral valve is mainly affected, followed by the aortic valve. Valvular involvement usually does not cause clinical valvular disease. The presence of aPLs seems to further increase the risk for thromboembolic complications, mainly cerebrovascular, posed by valve lesions. Superadded bacterial endocarditis is rare but may be difficult to distinguish from pseudoinfective endocarditis. The current therapeutic guidelines are those for APS in general. Secondary antithrombotic prevention with long-term, high-intensity oral anticoagulation is advised. The efficacy of aspirin, either alone or in combination, is yet to be assessed. Corticosteroids are not beneficial and may even facilitate valve damage. Immunosuppressive agents should only be used for the treatment of an underlying condition. Current data suggest a role for aPLs in the pathogenesis of valvular lesions. aPLs may promote the formation of valve thrombi. These antibodies may also act by another mechanism, as indicated by the finding of subendothelial deposits of immunoglobulins, including anticardiolipin antibodies, and of colocalized complement components in deformed valves from patients with APS.
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PMID:Heart valve involvement (Libman-Sacks endocarditis) in the antiphospholipid syndrome. 860 27

We describe a case of a verrucous non-bacterial endocarditis on the native mitral valve in a patient with polymyositis. This case, to our knowledge, represents the first report in the literature we could get. The case reached our attention after an episode of acute limb ischemia which lead to an echocardiographic examination that showed vegetations on the valve. No cardiac signs or symptoms were evident. We discuss the possible relation between the two disorders. The possibility of autoimmune diseases, other than lupus or lupus-related disorders, to produce this kind of lesions should be confirmed by a systematic echocardiographic study of these patients even if they have no evidence of cardiac involvement.
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PMID:[Verrucous abacterial endocarditis and polymyositis. A possible association?]. 903 27

The objective of this work was to determine markers of endothelial cell activation in valves from patients with antiphospholipid syndrome (APS) and heart valve involvement, in order to establish a role for endothelial cells in the pathogenesis of the valvular disease. Sixteen valves from ten patients with APS, obtained from autopsies or removed during valve replacement, were studied. Two groups of valves were used as controls. One group included seven normal valves from patients who died from non-cardiac diseases. The other group of valves were obtained from patients with bacterial endocarditis during autopsies or valve replacement operations. Immunoperoxidase and immunofluorescence stainings with antibodies to human immunoglobulins, endothelial cells, alpha3beta1 integrin, collagen IV, laminin and fibronectin were employed. Three histopathological patterns were apparent: normal valves, valves with verrucous endocarditis and valves with fibrocalcific changes. In all the valves with verrucous endocarditis the following findings were observed: (1) increased expression of the alpha3beta1 integrin on the endothelial cells, (2) increased amount of collagen IV, laminin and fibronectin, (3) proliferation of blood vessels and (4) linear subendothelial deposition of immunoglobulins and complement. The valves with fibrocalcific changes were deformed and showed a thick layer of collagen IV, laminin and fibronectin, yet in two valves the indothelial cells showed an expression of the alpha3beta1 integrin. The control valves did not express the integrin and had only a thin subendothelial band of collagen IV. In valves from patients with APS, 1 markers of endothelial cell activation are upregulated while the inflammatory exudate is scant. There is also a prominent deposition of immunoglobulins in the valves from patients with APS, suggesting a possible association between the deposition of the antibodies and the activation of the endothelial cells in APS.
Lupus 1999
PMID:Increased endothelial cell expression of alpha3beta1 integrin in cardiac valvulopathy in the primary (Hughes) and secondary antiphospholipid syndrome. 1048 26

We describe a patient with SLE and antiphospholipid syndrome who presented with severe headache and fever. Lumbar puncture analyses indicated meningitis. Kingella kingae was isolated from her blood cultures. A large mobile vegetation was seen on her mitral valve. The association between SLE, Libman-Sacks endocarditis and bacterial endocarditis is discussed.
Lupus 2000
PMID:Kingella endocarditis and meningitis in a patient with SLE and associated antiphospholipid syndrome. 1087 36

The Libman and Sacks non bacterial endocarditis was reported in 1924 in patients with SLE. Its relation to the anti cardiolpin syndrome has only been described as recently as the last decade. In this paper we review the deposition of these antibodies on the valve with complement components initiating the deformation of the valve. The valvulopathy in APS is quite common and may lead to valve replacement. In addition, a diversity of manifestations are detailed. More awareness should be drawn to this new complication of APS.
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PMID:Cardiac valvulopathy in the antiphospholipid syndrome. 1240 16


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