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)

Acute myocardial infarction is a potentially fatal complication of SLE. Reported mechanisms include atherosclerosis, arteritis and coronary arterial spasm. The following case report presents a fourth possible cause; intracoronary thrombus with angiographically normal coronary arteries in a patient with active lupus and AMI.
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PMID:Myocardial infarction due to intracoronary thrombi without significant coronary artery disease in systemic lupus erythematosus. 186 45

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Impaired mononuclear leucocyte (MNL) motility can be found both in vascular and autoimmune diseases. Pentoxifylline (PTX) has a well-known therapeutic effect in vascular diseases, which is based on the rearrangement of blood cell cytoskeleton and thus increased microcirculatory flow. Most data on PTX concern red blood cells and granulocytes so now the effect of PTX on previously decreased MNL migration and chemotaxis was investigated in vitro. The results of MNL chemotaxis studies described here suggest that this drug enhances impaired MNL motility in obliterative atherosclerosis and systemic lupus erythematosus and thus may also be introduced in the treatment of certain polysystemic autoimmune diseases with decreased in vitro MNL chemotaxis.
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PMID:Effect of pentoxifylline on decreased in vitro mononuclear leucocyte chemotaxis in vascular and polysystemic autoimmune diseases. 195 Aug 15

Fifty-six patients, 49 females and 7 males, with the confirmed diagnosis of systemic lupus erythematosus were examined by M-mode, 2--D and Doppler echocardiography. Pericardial effusion was found in 15 patients (27%), while pericardial thickening was suspected in 6 additional patients (37.5% altogether). Two patients had the signs of a pericardial tamponade, but both of them were uraemic. Libman-Sacks endocarditis was suspected in 4 patients (7.5%) because of verrucous changes in the aortic or mitral valve and regurgitant jet. Slight to moderate left ventricular hypocontractility was present in 3 patients (5%), while 3 additional patients had borderline values of the left ventricular contractility parameters. Left ventricular hypertrophy, usually mild, was found in 21 patients (37.5%). Echocardiographic signs of pulmonary hypertension were present in 2 patients (3.6%). It has been concluded that pericardial affection is frequent during the course of systemic lupus erystematosus, while a diffuse myocardial involvement is rare, except the consequences of arterial hypertension and accelerated coronary atherosclerosis. Libman-Sacks endocarditis still represents a diagnostic problem. For a more precise definition of cardiac involvement in systemic lupus erythematosus, a comparative analysis of the disease activity and immunosuppressive therapy is needed.
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PMID:[Echocardiographic analysis of changes in the heart in patients with systemic lupus erythematosus]. 207 23

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

Myocardial infarction has rarely been reported in patients with systemic lupus erythematosus but may develop late in the disease usually as a result of severe and accelerated atherosclerosis or coronary arteritis. A 32-year-old man with untreated and unrecognized systemic lupus erythematosus, in the absence of conventional coronary risk factors (except family predisposition) and definite extracardiac manifestations of systemic lupus erythematosus had a silent myocardial infarction early in the course of the disease. A coronary arteriogram revealed multiple stenosis of the left anterior descending artery and critical stenosis of the right coronary artery. It is our belief that lupus vasculitis is a likely contributing factor in the development of obstructive coronary disease in this patient.
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PMID:[Silent myocardial infarct as a main manifestation of systemic lupus erythematosus]. 232 60

Dyslipoproteinemia, a feature of systemic lupus erythematosus may contribute to premature atherosclerosis. In order to develop an experimental model for this dyslipoproteinemia we measured plasma concentrations of lipoproteins in juvenile NZB/W (lupus) and NZB/B (control) mice. Additionally to evaluate the effects of a diet rich in n - 3 fatty acids we measured lipoprotein concentrations in mice on normal or menhaden oil-enriched diets. The lupus mice had elevated triglycerides compared to the controls, similar to that seen in human SLE patients (161 +/- 31 vs 113 +/- 13 mg/dl, P less than 0.003). In contrast, the menhaden oil diet fed NZB/W mice had triglycerides similar to the NZB/B control fed group. In the NZB/W murine SLE model, dyslipoproteinemia is an early sign of disease as has been shown in man, therefore this model will be useful in elucidating the mechanism of dyslipoproteinemia in SLE.
Atherosclerosis 1989 Oct
PMID:Dyslipoproteinemia in murine systemic lupus erythematosus. 259 28

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Serum was examined for a cytotoxic effect on cultured human fibroblasts, using 8 normal controls and 4 patients. Three of the patients had secondary lipidoses associated with monoclonal gammapathies of IgA kappa, IgG kappa and IgG lambda types. The fourth had systemic lupus erythematosus (SLE) with hyperlipidemia. Only serum containing the monoclonal IgG lambda was found to be cytotoxic. This circulating IgG lambda was strongly bound to HDL and behaved like an antilipoprotein antibody. The circulating immune complexes may be the serum factor responsible for the cytotoxicity and the cutaneous plane xanthomas, thus giving another example of 'antibody-dependent' cellular cytotoxicity previously described for endothelial cells in other diseases.
Atherosclerosis 1986 Nov
PMID:Cytotoxic effect of serum on fibroblasts in one case of normolipidemic plane xanthoma and myeloma IgG lambda. 309 2

Factor-VIII-Related antigen (VIII R:Ag) is known to be produced by the blood vessel wall. Noxious stimuli increase endothelial release of VIII R:Ag. It might be expected that the development of vasculitis would be associated with increased levels of VIII R:Ag. To investigate this, eight different groups of subjects were studied: 25 patients with systemic sclerosis, 19 with systemic lupus erythematosus, 15 with rheumatoid arthritis (RA) plus vasculitis, 19 with systemic vasculitis and 14 with atherosclerosis. These groups were compared to 29 patients with primary Raynaud's disease, 15 with RA without vasculitis and 50 controls. Results showed that where there was evidence of vascular disease, then VIII R:Ag was elevated. VIII R:Ag appeared to be a more specific marker for vascular damage than erythrocyte sedimentation rate or C-reactive protein. Longitudinal studies in 11 patients showed good correlation between progression of vascular disease and VIII R:Ag.
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PMID:Vascular damage and factor-VIII-related antigen in the rheumatic diseases. 311 42


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