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)

The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.
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PMID:[Sneddon syndrome]. 187 23

In order to establish the association between mitral valve prolapse (MVP) and the incidence of thromboembolic disease of the brain we reassessed 36 patients (less than or equal to 50 years old) who were hospitalized during 1983-85 because of cerebrovascular accidents. The patients underwent complete physical and neurological examinations, blood tests including coagulogram and two-dimensional echocardiogram. The control group comprised 117 patients without cerebrovascular events. In the study group, 4 patients (11.1%) had MVP compared with 10 (8.5%) in the control group. Of these four, only one male did not have any risk factor for thromboembolic event; among the other three the risk factors were systemic lupus erythematosus, hyperlipidemia, diabetes, hypertension and pregnancy. We conclude that our results are in accordance with most of the literature that MVP is not a risk factor for thromboembolic disease except in Greek and Italian populations, which are ethnically more homogeneous than other Western societies studied.
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PMID:Mitral valve prolapse in young Israelis with thromboembolic brain disease. 199

The importance of a prothrombotic state as a cause of ischemic stroke in young adults is ill defined. We examined 46 unselected patients under age 50 years with cerebral ischemia for anticardiolipin antibody (aCL) and lupus anticoagulants (LA), over a 3-year-period. Age- and sex-matched patients with other neurologic diseases served as a noncerebral ischemia comparison group to test whether (1) stroke/transient ischemic attacks (TIA) in young people is associated with aCL and/or LA, and (2) their presence is specific to cerebral ischemia. In the stroke/TIA group, 21 patients had aCL or LA and 25 had neither, whereas in the control group, 2 patients had aCL and 24 had neither. Equal numbers of stroke/TIA patients with and without antiphospholipid antibodies (aPL) had other stroke risk factors. Patients with aPL and cerebral ischemia, however, had a more frequent history of multiple events than those without them. These antibodies occur with undue frequency in young patients with stroke/TIA and are not associated with a concurrent diagnosis of systemic lupus in most cases. A coexistent aPL-associated prothrombotic state may be a key determinant of whether patients with atherosclerosis, mitral valve prolapse, or other structural lesions experience recurrent ischemia.
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PMID:Antiphospholipid antibodies and cerebral ischemia in young people. 211 4

Despite a low incidence of clinical manifestations, autopsy data suggest endocardial and myocardial disease in about 50% of patients with systemic lupus erythematosus. To investigate whether mitral valve prolapse can be considered a clinical manifestation of cardiac involvement in systemic lupus erythematosus, we carried out an echocardiographic study in 51 affected subjects and 102 normals matched for age and sex. Prevalence of mitral valve prolapse was 25% in patients with systemic lupus erythematosus and 9% in healthy controls with a statistically significant difference (p less than 0.01). Neither pericardial effusion nor prolonged (more than 12 months) treatment with corticosteroids were associated with higher prevalence of mitral valve prolapse. Libman-Sacks verrucae on the mitral valve apparatus as well as focal myocardial scars affecting the papillary muscles and adjacent myocardium could be responsible for the development of the valvular dysfunction. We suggest that mitral valve prolapse can be considered a manifestation of cardiac involvement in patients with systemic lupus erythematosus.
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PMID:Mitral valve prolapse in systemic lupus erythematosus. 359 66

A prospective clinical and echocardiographic study of 47 patients with systemic lupus erythematosus (SLE) and 46 age- and sex-matched controls showed an increased prevalence of echocardiographic abnormalities in the SLE group. Pericardial abnormalities were identified in ten patients with SLE and in no controls. Excluding mitral valve prolapse, valvular abnormalities were identified in ten patients with SLE (21%) and in three controls (7%). In the patients with SLE, abnormalities included mitral valve leaflet thickening in six, aortic valve thickening in five, and mitral annular calcification in two. The presence of valvular abnormalities correlated with duration but not with severity of SLE. The finding of systolic murmurs in 17 of 47 patients with SLE did not correlate with echocardiographic evidence of valvular disease. In six patients with SLE, valvular abnormalities detected by two-dimensional echocardiography were not seen on M-mode echocardiogram.
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PMID:M-mode and two-dimensional echocardiographic abnormalities in systemic lupus erythematosus. 399 13

In 16 patients with anetoderma, a clinicohistologic entity related to a local dermal defect of elastic tissue, old lesions did not heal, and new lesions often continued to form for many years, despite various forms of treatment. Systemic lupus erythematosus, which occurred in one patient, must be ruled out in patients with anetoderma. Discoid lupus erythematosus occurred later in one patient. Other associated findings, noted in one patient each, included cataract, congenital hip dislocation, congenital fusion of the vertebrae at C2-3, diverticulum of the midesophagus, Addison's disease (before the onset of anetoderma), and mitral valve prolapse. Our results and a review of the literature indicate that patients with anetoderma must be examined for associated eye, bone, heart, pulmonary, digestive tract, and endocrine abnormalities for a better assessment of their skin disorders.
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PMID:Anetoderma. Clinical findings, associations, and long-term follow-up evaluations. 646 9

To assess the nature and distribution of cardiovascular abnormalities associated with mixed connective tissue disease, we studied 38 patients with overlapping clinical manifestations of systemic lupus erythematosus, progressive systemic sclerosis and polymyositis, and circulating antibodies to nuclear ribonucleoprotein. The protocol included taking a medical history and a physical echocardiogram, and pulmonary function tests. Cardiac catheterization was performed on 17 patients. Postmortem examination was performed on four of the five patients who died during follow-up. Acute pericarditis and/or pericardial effusion was detected in 11 patients (29%) and mitral valve prolapse was identified in 10 patients (26%). Marked intimal hyperplasia of coronary arteries was observed in all four hearts that were autopsied and perivascular and myocardial leukocytic aggregates were present in two hearts. Pulmonary vascular resistance was elevated in 11 of the 17 patients who underwent cardiac catheterization. In summary, cardiovascular abnormalities associated with mixed connective tissue disease include acute pericarditis and/or effusion, mitral valve prolapse, intimal hyperplasia of coronary arteries, perivascular and myocardial leukocytic infiltrates, and pulmonary hypertension.
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PMID:Cardiovascular manifestations of mixed connective tissue disease in adults. 664 Aug 71

An echocardiographic study was performed in 60 unselected patients affected with Systemic Lupus Erythematosus (SLE) and in 30 age- and sex-matched control subjects, to evaluate the incidence of cardiac abnormalities and the possible correlation with the presence of antiphospholipid antibodies. 33 patients (55%) had major cardiac abnormalities as valvular stenosis and/or regurgitation (35%), pericardial effusion or thickening (26%), left ventricular hypertrophy (21%), regional or global left ventricular dysfunction (10%). Some patients presented more than one cardiac dysfunction: five patients had one major and one minor lesion, 11 presented with two major lesions, and in five of them a pancarditis was found. Minor cardiac abnormalities as mitral valve prolapse, valvular thickening without valvular dysfunction, calcification of the mitral annulus were demonstrated in nine patients (15%). Increased levels of antiphospholipid antibodies were found in 25 out of 60 patients (41.6%). No clear correlation was evident between endocardial or pericardial involvement and such autoantibodies. In fact, valvular heart diseases were present in 36% of the patients with antiphospholipid antibodies and in 34% of the patients without antiphospholipid antibodies; pericardial involvement was evident in 24% and in 28% of patients with and without them, respectively. On the contrary the demonstration of antiphospholipid antibodies in five out of six patients with regional or global left ventricular dysfunction could suggest a pathogenetic role of these autoantibodies in myocardial hypokinesis. Therefore, antiphospholipid antibodies could represent only one of the pathogenetic factors of the cardiac lesions in SLE patients, together with immunologic and iatrogenic factors. The involvement of other systems as renal, vascular and pulmonary certainly play an important role in predisposing to the development of secondary cardiac manifestations.
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PMID:[Cardiac abnormalities in systemic lupus erythematosus and their association with antiphospholipid antibodies]. 823 32

The aim of this study was to determine the prevalence of cardiac valve disease in systemic lupus erythematosus or in patients with primary antiphospholipid syndrome and to assess the role of the antiphospholipid antibodies as risk factor for endocardial lesions. We studied 39 consecutive patients with systemic lupus erythematosus (mean age 34 +/- 12 years, 38 female and one male), 20 women with primary antiphospholipid syndrome (mean age 32 +/- 4 years) and 20 normal subjects (mean age 35 +/- 8 years, 15 female and five male). All patients with primary antiphospholipid syndrome had increased levels of serum anticardiolipin antibodies and recurrent fetal abortions; some of them also had arterial and/or venous thrombosis and/or thrombocytopenia. M-mode, two-dimensional and Doppler echocardiography were performed in all patients. IgG anticardiolipin antibodies were measured by an enzyme-linked immunosorbent assay. Valvular lesions were observed in 15 patients (38%) with systemic lupus erythematosus. These abnormalities included: mitral valve thickening or vegetation, mitral valve prolapse and aortic valve vegetation; mitral, aortic and tricuspid regurgitation; mitral stenosis. None of the patients with primary antiphospholipid syndrome and of the normal subjects was found to have valvular abnormalities. In systemic lupus erythematosus, high levels of anticardiolipin antibodies were detected in 73% of the patients with valvular lesions and in 67% of the patients without valvular lesions (P > 0.05). We conclude that valvular involvement is frequent in patients with systemic lupus erythematosus but it is apparently unrelated to antiphospholipid autoimmunization.
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PMID:Cardiac valve involvement in systemic lupus erythematosus and primary antiphospholipid syndrome: lack of correlation with antiphospholipid antibodies. 852 6

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


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