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)

This is the case of a 27 years-old woman with signs and symptoms of severe untreatable congestive heart failure, anemia, gingival mucosa ulcers, photosensitivity and alopecia. The electrocardiographic, echocardiographic, angiographic and hemodynamic data oriented the diagnosis of restrictive cardiomyopathy, mitral insufficiency secondary to mitral prolapse and bi-atrial dilation. The histologic study of the endomyocardial biopsy, performed during catheterization, showed signs of endomyocardial fibrosis, and immunological analysis was compatible with systemic lupus erythematosus. As far as we know, this is the first case of endomyocardial fibrosis (Davies disease) associated with systemic lupus erythematosus published in the medical literature. The etiology of Davies disease remains unrevealed and its association with systemic lupus erythematosus suggest a probable autoimmune origin.
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PMID:Endomyocardial fibrosis (Davies disease) coincidental with systemic lupus erythematosus. 1085 12

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 first case was of a 27-year-old female, who was diagnosed as having mitral valve stenosis with regurgitation, systemic lupus erythematosus and antiphospholipid syndrome at her previous pregnancy. We performed mitral valve plasty, which included open mitral commissurotomy and Kay's annulo plasty. The second case was of a 53-year-old female, who was diagnosed as old myocardial infarction, mitral regurgitation, systemic lupus erythematosus and antiphospholipid syndrome. She underwent mitral valve plasty and coronary artery bypass grafting. Both cases were treated by administration of methylpredonisolone and heparin perioperatively to avoid thrombosis and aggravation of systemic lupus erythematosus. Both patients showed good postoperative outcome without complications. We consider that it is important to perform the plasty as far as possible, and to administer effective anticoagulation treatment to prevent complications for patients in the setting of systemic lupus erythematosus and antiphospholipid syndrome.
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PMID:Mitral valve plasty in systemic lupus erythematosus in the setting of antiphospholipid syndrome. 1093 34

Since its description in 1965, Sneddon syndrome (SNS) is usually characterized by the association of an ischemic cerebrovascular disease and a widespread livedo reticularis. The presence of many other manifestations suggests that it is a systemic syndrome. The prevalence of anti-phospholipid antibodies (aPL) is highly variable, 41% in our experience. Comparison of patients with or without aPL showed that the fishnet of the livedo was clearly larger in aPL-negative patients who nevertheless, did not develop thrombocytopenia. Seizures and clinically audible mitral regurgitation were more frequently observed in aPL-positive patients. These data lead to consider that SNS is not a unique entity. As patients with primary anti-phospholipid syndrome (APS) and SNS did not differ from those with livedo reticularis, ischemic cerebral events and APS within systemic lupus erythematosus (SLE), there is no reason today to exclude patients with SLE. On one hand, SNS might cover a continuum spectrum joining diverse clinico-biological entities ranging from aPL-negative to SLE-related cases, with primary APS-SNS standing amidst. On the other hand, one might speculate that SNS should be regarded as a nearly similar clinical expression of two distinct disorders, i.e. a peculiar form of APS characterized by preferential arteriolar involvement or on the opposite a primary non-aPL related small artery disease mainly involving brain and skin vessels.
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PMID:The mystery of Sneddon syndrome: relationship with antiphospholipid syndrome and systemic lupus erythematosus. 1096

We presented a patient of cerebral embolism caused by Libman-Sacks endocarditis with systemic lupus erythematosus (SLE). This 35-year-old housewife with SLE suffered from abrupt visual disturbance in December 1998. Angiography revealed the occlusion of her right posterior cerebral artery. Transesophageal echocardiography showed the mitral regurgitation and hyperplasia of the anterior mitral valve leaflet without vegetation. In April 1999, she again suffered from sudden onset of transient left hemiparesis and dysphasia. Angiographic findings were unchanged. Transesophageal echocardiographic examination detected vegetation on the anterior mitral valve leaflet and aggravation of the mitral regurgitation. Laboratory examination revealed inactivity of SLE. No bacteria was recovered from repeated blood cultures. We diagnosed that Libman-Sacks vegetation caused cerebral embolism.
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PMID:[Cerebral embolism in systemic lupus erythematosus with Libman-Sacks endocarditis: a case report]. 1118 9

We report a case of 52-year-old woman with primary antiphospholipid syndrome who developed mitral insufficiency and chronic renal failure. Continuous ambulatory peritoneal dialysis was started preoperatively due to thrombocytopenia that was aggravated by hemodialysis. Mitral annuloplasty was performed since the mitral valve was not severely damaged. Her postoperative hemodynamics were stable, and anticoagulant therapy was controlled easily. She recovered from severe thrombocytopenia while on continuous ambulatory peritoneal dialysis. Valvular heart disease is a well known feature of primary antiphospholipid syndrome, and there have been several reports about valve replacement in patients who had antiphospholipid syndrome with or without systemic lupus erythematosus. However, valve repair has been reported in only a few such patients. We believe that valve repair is better than valve replacement in patients with antiphospholipid syndrome because of its hypercoagulable tendency. In addition, it seems that continuous ambulatory peritoneal dialysis is a suitable method for the perioperative management of patients with antiphospholipid syndrome who suffer from chronic renal failure as well as thrombocytopenia, and require cardiac surgery under cardiopulmonary bypass.
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PMID:Mitral insufficiency associated with primary antiphospholipid syndrome and chronic renal failure. 1130 57

A 48-year-old woman admitted with progressive dyspnea had previously been diagnosed with systemic lupus erythematosus, antiphospholipid syndrome, and chronic renal failure, and had undergone mitral valve replacement with a Carpentier-Edwards pericardial bioprosthesis for mitral insufficiency 9 years before. She suffered a cerebral infarction 5 years earlier, despite appropriate anticoagulant therapy. On admission, echocardiography showed severe bioprosthetic stenosis. Repeat mitral valve replacement was conducted using a Mosaic bioprosthesis. On postoperative day 2, when heparinization was commenced, she suddenly had an epileptic fit. She also developed ischemic necrosis of the fingers and toes, considered secondary to microthrombosis. Aspirin was administered and heparin replaced by warfarin sodium. Necrosis gradually disappeared, and she was discharged 3 months after surgery. The original bioprosthesis showed degenerative changes with significant thrombus formation on cusps, thought to be mainly due to her hypercoagulable state. Considering the thrombophilic tendency in patients with antiphospholipid syndrome, strict management of anticoagulant therapy is required.
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PMID:Secondary mitral valve replacement in antiphospholipid syndrome and chronic renal failure. 1180 97

Libman-Sacks endocarditis complicating systemic lupus erythematosus has rarely been reported to cause hemodynamically significant valvular lesions. This report presents a case of severe aortic stenosis combined with severe mitral regurgitation associated with systemic lupus erythematosus in a young woman who died while on the quota list for surgery.
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PMID:Severe aortic stenosis and mitral regurgitation in a woman with systemic lupus erythematosus. 1200 79

We report an illustrative case of a 60-year-old man with Streptococcus viridans subacute bacterial endocarditis (SBE) and positive antineutrophil cytoplasmic autoantibodies (c-ANCA). C-ANCA positivity has been associated with a variety of rheumatic and infectious disease areas, but has been rarely associated with SBE. The patient had mitral valve prolapse with mitral regurgitation, and S viridans SBE developed after a dental procedure. Laboratory abnormalities included anemia, elevated erythrocyte sedimentation rate, positive rheumatoid factor, positive anticardiolipin antibody, positive lupus anticoagulant, and highly elevated c-ANCA level. We believe this is only the ninth reported case of S viridans SBE with a positive c-ANCA, and the third with mitral valve prolapse and vegetations.
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PMID:Streptococcal viridans subacute bacterial endocarditis associated with antineutrophil cytoplasmic autoantibodies (ANCA). 1273 37

Valvular involvement is the most encountered form of heart disease in systemic lupus erythematosus (SLE). Immunoglobulin and complement deposition in the valvular structure will subsequently lead to Libman-Sacks vegetations, valve thickening, and valve regurgitation. Valvular stenosis is rarely seen. Involvement of the mitral valve is most frequently encountered. Valve disease for most patients is mild and asymptomatic, but patients in whom severe mitral regurgitation develops will present with symptoms of congestive heart failure. A heart murmur will be heard in almost all patients with moderate or severe regurgitation. Transesophageal echocardiography is the most sensitive method to detect the valvular involvement. The valvular changes, the hemodynamic status, or the symptomatology have been shown to progress, remain stable, or sometimes improve. Severe regurgitation, infective endocarditis, and thromboembolic events (mostly stroke or transitory ischemic attacks) are complications of valvular involvement in SLE. In treatment of these patients, prophylaxis of infectious endocarditis, selective antiaggregant and anticoagulant medication, and valve replacement are currently offered. The role of corticosteroid treatment is still unclear in the outcome of SLE valvulopathy.
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PMID:Valvular heart disease and systemic lupus erythematosus: therapeutic implications. 1450 33


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