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 authors report a thirty-seven-year-old woman with systemic lupus erythematosus (SLE), a coronary aneurysm, and myocardial infarction. SLE was diagnosed at twenty-three years of age and treated with prednisolone. Seven years later, she developed inferior myocardial infarction, and coronary angiography showed an aneurysm in the proximal right coronary artery without associated stenosis. At the age of thirty-seven years, she died from cerebral infarction and sepsis. Autopsy revealed an aneurysm (6 mm in diameter) in the proximal right coronary artery and an old inferior myocardial infarction. Histologic examination showed recanalization and fibrosis in the media of the aneurysm wall. This case suggests that coronary aneurysm may cause myocardial infarction in SLE and that aneurysm formation may be a sequela of arteritis.
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PMID:Myocardial infarction secondary to coronary aneurysm in systemic lupus erythematosus. An autopsy case. 778 96

An 8-year-old black girl with a 5 month history of systemic lupus erythematosus (SLE) and secondary antiphospholipid syndrome (APS) developed Raynaud's phenomenon, marked hemolytic anemia, and a fatal myocardial infarction (MI). Pathologic evaluation of the heart demonstrated a transmural acute MI associated with a recent thrombus of the circumflex coronary artery, thrombosis of small intramural arteries, and a coronary arteriopathy resembling fibromuscular dysplasia. Inflammatory or atherosclerotic changes of the coronary arteries were distinctly absent. This case represents the youngest reported patient with SLE, MI, and pathologic confirmation of nonatheromatous coronary artery disease. The observed coronary pathological findings may have accentuated the thrombogenic potential of the APS, resulting in coronary thrombosis. Cardiac lesions in SLE and APS are reviewed, and pathogenetic considerations for the coronary vasculopathy are discussed.
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PMID:Fatal myocardial infarction in an 8-year-old girl with systemic lupus erythematosus, Raynaud's phenomenon, and secondary antiphospholipid antibody syndrome. 779 Nov 80

We report a patient with Takayasu's arteritis associated with antiphospholipid antibodies. An 84-year-old woman gradually developed gait and visual disturbances, dementia, myocardial infarction, and gangrene in all four limbs during a period of 8 years. Persistent inflammatory signs also continued for at least 8 years. Positive reaction for lupus anticoagulant by the diluted Russel viper venous time and positive reactions for cardiolipin antibodies were confirmed. However, she did not develop SLE. MR angiography revealed multiple and extensive occlusive changes in large vessels such as the aorta and its major branches. We believe antiphospholipid antibodies may have been related to severe occlusive vasculopathy in this patient.
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PMID:[An elderly patient with Takayasu's arteritis associated with antiphospholipid antibodies]. 782 7

The occurrence of cardiac manifestations and their relationship with the lupus anticoagulant (LA) in SLE was studied in 74 patients who were followed up for 22 years (median), of which 16 years were after the initial LA testing. Pericarditis was the most common cardiac event occurring in 16 (22%) patients but it did not correlate with LA. Valvular heart disease, coronary artery disease, left ventricular failure and/or cor pulmonale were observed in 16 (22%) patients. Taken together, their occurrence was associated with a history of leg ulcers (odds 3.8, P = 0.028) but not with LA or other common clinical manifestations of the antiphospholipid syndrome. Valvular heart disease in five patients was significantly associated with LA (P = 0.05). Cor pulmonale due to chronic pulmonary embolism was present in two patients with LA. Myocardial infarctions in five patients occurred late in the course of disease but in relatively young patients (mean 43 years). Fatal myocardial infarction in the absence of atherosclerosis in two LA-positive patients supports a pathogenetic role for LA in these cases. In conclusion, of the various cardiac complications in SLE, valvular heart disease and cor pulmonale appear to be connected with the antiphospholipid syndrome. Both conditions should be actively sought in patients with LA to decrease possible adverse events (arterial emboli and right ventricular failure) affecting the patients' prognosis.
Lupus 1994 Jun
PMID:Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus. 795 2

In (NZW x BXSB) F1 (W/B F1) male mice, systemic lupus-like disease, thrombocytopenia and coronary vascular disease with myocardial infarction occur, due to the presence of platelet-associated antibodies, anti-platelet antibodies and anti-cardiolipin antibodies (aCL). We developed monoclonal aCL and analysed the specificity of aCL. In the W/B F1 mice, there are aCL with pathogenic properties, which have an IgG isotype and reveal a cofactor-dependent binding to CL, binding activity to platelets, and lupus anti-coagulant (LA) activity. Here, we analysed the usage of VH and V kappa genes of six aCL, including two pathogenic aCL, from W/B F1 mice, in an attempt to address the question of whether or not aCL with pathogenic properties use restricted Ig V genes. Sequence analysis of VH and V kappa genes of aCL showed that the pathogenic aCL had VHJ558 and V kappa 21 or V kappa 23 genes, whereas the other aCL without pathogenic features used mainly the 7183 VH family and the random V kappa gene group. However, two pathogenic aCL showed a 86.6% homology with the IgV region, each other, indicating that they were not closely related clones. Thus, these findings suggest the possibility that usage of Ig VH genes in pathogenic aCL is not random, but that there may exist a few epitopes of antigen recognized by the pathogenic aCL.
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PMID:V gene analysis of anti-cardiolipin antibodies from (NZW x BXSB) F1 mice. 795 86

In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma predictors of ischemic complications of atherosclerosis: open issues. 806 Dec 44

Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease (CVD) with myocardial infarction. To determine whether this murine lupus-associated CVD can be prevented by the reduction of dietary calories, male W/BF1 mice were separated into five experimental groups and fed either ad libitum (designated group A, n = 50), fed 32% fewer calories of an otherwise comparable diet (designated group B6, n = 20), or initially fed ad libitum and then switched to reduced calorie intake (RCI) feeding at ages 14, 17, or 22 weeks (designated B14, n = 10; B17, n = 20; or B22, n = 20). Occlusive CVD was prevented by RCI. Life-span was significantly extended among the early onset RCI cohorts, B6 and B14 (P = 0.0001 and P = 0.005), compared to group A mice. Mean anti-cardiolipin autoantibody titers and mean levels of circulating immune complexes were also lowered in RCI mice when all RCI mice were compared to ad libitum fed group A mice. Histological grades of both coronary vascular and glomerular lesions were significantly less than those of group A mice (P < 0.001). Immunoprecipitates indicative of immunoglobulin deposition within coronary or glomerular vascular walls were also substantially less than those of group A mice. These findings indicate a possible causal role for anti-cardiolipin autoantibody in development of autoimmune CVD in W/BF1 mice and suggest that regulating dietary calories can influence the mechanism involved in pathogenesis of autoimmune-associated CVD development.
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PMID:Calorie restriction prevents the occlusive coronary vascular disease of autoimmune (NZW x BXSB)F1 mice. 818 20

Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease with myocardial infarction (CVD). To determine whether this murine lupus-associated CVD could be transferred to otherwise autoimmune-resistant (C57BL/6 x C3H/He)F1 (B6C3F1) mice via W/BF1 T-cell-depleted marrow (TCDM) transplants, or conversely whether the CVD of W/BF1 mice could be prevented by the reciprocal transplant, reciprocal haploidentical transplants of TCDM were performed. CVD developed only in mice with systemic autoimmunity. Mice that developed lupus had glomerulonephritis and thrombocytopenia and also had elevated titres of autoantibodies to double-strand DNA, cardiolipin, and platelets and elevated levels of circulating immune complexes. Of control W/BF1 mice, 80% developed lupus, and of these, 81% developed CVD with a mean grade of 2.5 +/- 0.8. Engraftment of W/BF1 mice with B6C3F1 marrow protected 90% of the recipients from the development of lupus, and none developed CVD. Engraftment of B6C3F1 mice with W/BF1 marrow induced lupus in 60% of the recipients, and of those, 33% developed CVD with a mean grade of 1.3 +/- 0.3. The B6C3F1 recipients of W/BF1 marrow which developed CVD had significantly higher titres of autoantibodies to cardiolipin (aCL; P < .01). These findings show that genetic abnormalities present in the W/BF1 hematopoietic stem cells contribute to autoantibody development, including aCL, and suggest that thrombogenic mechanisms induced by aCL may contribute to the development of CVD in this form of murine lupus erythematosus.
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PMID:Prevention and induction of occlusive coronary vascular disease in autoimmune (W/B)F1 mice by haploidentical bone marrow transplantation: possible role for anticardiolipin autoantibodies. 821

Patients with nephrotic syndrome (NS) are believed to be at increased risk of atherosclerosis and coronary heart disease (CHD), although existing evidence for this association has not been persuasive. The risk of CHD among 142 persons with NS documented by protein-uria > or = 3.5 g daily was compared with that among 142 matched controls randomly selected from the membership of a large Northern California health plan. Controls were matched for sex, year of birth, and presence in the health plan when the referent case was diagnosed. No diabetics were included in this study. Mean follow-up for nonfatal CHD events was 5.6 years for NS subjects and 11.2 years for controls. Among the NS subjects myocardial infarction (MI) developed in 11, and there were 58 deaths, seven because of CHD. Among the controls, there were four MIs and 10 deaths, three because of CHD. In matched-pair analysis, there were 11 MIs among NS subjects and none among controls [P = 0.001, lower bound of 95% confidence interval for relative risk (CI), 2.8]. In an unmatched analysis adjusted for hypertension and smoking at diagnosis of NS, the relative risk of MI was 5.5 (95% CI 1.6 to 18.3) and the relative risk of coronary death was 2.8 (95% CI 0.7 to 11.3). Omitting data of NS subjects with minimal change disease and systemic lupus erythematosus yielded similar results. These data suggest that persons with NS are at increased risk of CHD.
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PMID:The increased risk of coronary heart disease associated with nephrotic syndrome. 823 Oct 39

Six patients under 50 with confirmed systemic lupus erythematosus (SLE) developed myocardial infarction at different intervals from the disease onset (1-21 years). Five of them had chronic disease, one suffered from acute SLE. The analysis of clinical findings identified myocardial infarction risk factors in SLE (chronic course of the disease, long-term glucocorticosteroid treatment, hypercholesterolemia, persistent nephrotic syndrome, arterial hypertension, vasculitis, hypercoagulation, antiphospholipid antigens) and provided a basis for prevention of this severe SLE complication.
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PMID:[Myocardial infarction in systemic lupus erythematosus]. 824 13


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