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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed the causes of death in 50 patients treated for systemic lupus erythematosus at the University of Mississippi Medical Center between 1973 and 1985. Two groups of patients could be distinguished based on the age at onset but not on the duration of disease. Younger patients more often died of active renal disease an infectious complications, while older patients died of other organ involvement, inactive renal disease, and miscellaneous causes. Common causes of infection were gram-positive cocci and gram-negative bacilli. Atherosclerotic cardiovascular disease was an infrequent cause of death, and no patients died of malignancy. Patients who died had more multisystemic involvement, with serositis and renal, central nervous system, and hematologic manifestations than patients who were alive at last follow-up.
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PMID:Cause of death in systemic lupus erythematosus: a pattern based on age at onset. 366 41

One of the most compelling clinical challenges in the management of systemic lupus erythematosus (SLE) is the high incidence of atherosclerotic cardiovascular disease (ASCVD). Potential mechanisms for accelerated atherosclerosis in SLE include chronic inflammation, excess of traditional risk factors, and corticosteroid therapy. Given the high prevalence of atherosclerosis in SLE patients relative to young women in the general population, we propose that the presence of SLE constitutes a sufficiently potent risk factor for ASCVD to warrant more aggressive goals for risk factor reduction and strategies to reduce inflammation.
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PMID:Accelerated atherosclerosis in systemic lupus erythematosus: implications for patient management. 1160 86

Systemic lupus erythematosus (SLE) patients have increased cardiovascular morbidity and mortality. QT-interval parameters are presumed markers of cardiovascular risk and have not been previously evaluated in SLE. Standard 12-lead ECGs were obtained from 140 female SLE outpatients and 37 age and body mass index-matched controls. QT interval was measured in each lead and heart rate-corrected maximum QT-interval duration (QTcmax) and QT-interval dispersion (QTd) were calculated. Risk factors for cardiovascular disease and lupus clinical features, disease treatment, disease activity and damage index were recorded. SLE patients have increased QT-interval parameters when compared to controls (QTcmax: 427.91 +/- 31.53 ms(1/2) versus 410.05 +/- 15.45 ms(1/2), P < 0.001; QTd: 52.38 +/- 22.21 ms versus 37.12 +/- 12.88 ms, P < 0.001). These differences persisted after excluding those patients with arterial hypertension, diabetes and with ECG abnormalities (QTcmax: 419.90 +/- 28.78 ms(1/2) versus 409.15 +/- 15.85 ms(1/2), P = 0.041; QTd: 54.74 +/- 26.00 ms versus 37.96 +/- 13.05 ms, P = 0.001). Multivariate linear regression for factors associated with QTcmax selected the presence of electrocardiographic left ventricular hypertrophy (ECG-LVH) (P = 0.003), nonspecific ST-T-wave abnormalities (P = 0.022) and left atrial enlargement (P = 0.044). Multivariate associates with QTd were age (P = 0.018), ECG-LVH (P = 0.022) and ST-T abnormalities (P = 0.031). In conclusion, SLE patients have increased QT interval parameters when compared to controls. This prolongation may lead to an increased cardiovascular risk. This finding might be due to subclinical atherosclerotic cardiovascular disease.
Lupus 2005
PMID:QT-interval parameters are increased in systemic lupus erythematosus patients. 1630 81

Accelerated atherosclerotic cardiovascular disease is increasingly recognized as a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Cardiac manifestations of SLE are frequent and can involve almost all components of the heart. Pulmonary hypertension often develops during the course of SLE. The high incidence of cardiovascular complications may justify a screening of SLE patients in order to ensure early diagnosis and therapy. Results of diagnostic procedures that detect coronary insufficiency, surrogates of atherosclerotic burden and echocardiographic findings are often abnormal in SLE. However, evidence to support a routine screening for cardiovascular disease is currently not available. Therefore, based on the recommendations that have been proposed for other conditions associated with cardiovascular disease, we suggest assessment of risk factors and the performance of echocardiography at least annually in asymptomatic SLE patients. If two or more risk factors are present, an exercise ECG is recommended. The benefit, however, of screening SLE patients for cardiovascular disease has to be confirmed in prospective studies.
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PMID:[Cardiovascular monitoring of patients with systemic lupus erythematosus]. 1632 62

Mounting evidence from a growing body of epidemiologic studies demonstrates that patients with systemic lupus erythematosus (SLE) are at increased risk for the development of premature cardiovascular disease (CVD). However, awareness of accelerated atherosclerosis in young SLE patients, albeit growing, is still limited, as documented by the brief case presented. Inflammation is thought to play an important role in both the pathogenesis of SLE, as well as atherosclerotic vascular disease. Inflammatory processes that are shared by SLE and atherosclerotic disease include immune complex deposition and fixation, autoantibody binding, complement activation and CD40-CD40 ligand interaction. By examining the inflammatory mechanisms in common between SLE and atherosclerotic disease, we can come to a better understanding of the pathophysiology of the accelerated atherosclerotic process seen in patients with SLE and can gain insights into developing and instituting preventative and treatment strategies. In this article, we present a case of a young woman with SLE who presents with chest pain, followed by a review of inflammation-based pathogenic mechanisms that are shared by SLE and atherosclerotic cardiovascular disease.
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PMID:Premature atherosclerotic disease in systemic lupus erythematosus--role of inflammatory mechanisms. 1643 36

Cardiovascular and cerebrovascular events, the third leading cause of death in patients with systemic lupus erythematosus (SLE), are disproportionately common by age and gender. Risk factors for atherosclerotic cardiovascular disease (ASCVD) cannot reliably predict subsets of patients at risk for events. Coronary electron beam computed tomography (EBCT), a noninvasive imaging technique that quantifies ASCVD by measuring calcium deposition in the walls of coronary arteries, has been demonstrated to be a marker of ASCVD in traditional populations. A pilot group of 13 SLE patients (ages, 33-48 years) with two or more traditional risk factors for cardiovascular disease were studied by EBCT. Five of these SLE patients had calcification scores in the 70th percentile or higher, as compared with age-matched women without known coronary artery disease, and three had scores in the 90th percentile. Four of these five patients had antiphospholipid antibodies currently or in the past. These data suggest that EBCT may be able to detect premature ASCVD in SLE patients and may be a useful noninvasive tool as more attention is directed to ASCVD as a major complication of SLE.
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PMID:Coronary electron beam computed tomography in 13 patients with systemic lupus erythematosus and two or more cardiovascular risk factors. 1704

Patients with systemic lupus erythematosus (SLE) and those with rheumatoid arthritis (RA) have increased risk for atherosclerotic cardiovascular disease. The aims of this study were to compare the presence of coronary artery calcium (CAC) in age- and race-matched women with SLE, those with RA, and healthy controls without diabetes mellitus or history of myocardial infarction, angina pectoris, or stroke and to investigate its relation with traditional risk factors, inflammation, and endothelial activation. Study subjects completed cardiovascular risk factor assessment and electron-beam computed tomography that measured CAC. The 2 patient groups had similar prevalence and extent of CAC as well as significantly increased odds of having any CAC (odds ratio 1.87, 95% confidence interval 1.09 to 3.21) and more extensive CAC (odds ratio 4.04, 95% confidence interval 1.42 to 11.56 for CAC score >100) compared with healthy controls. After controlling for differences in cardiovascular risk factors, including insulin resistance and hypertension, the results remained statistically significant. After adjustment for differences in levels of C-reactive protein and/or soluble intercellular adhesion molecule-1, however, women with chronic inflammatory diseases no longer had significantly increased odds of having any CAC or more extensive CAC compared with controls. In conclusion, asymptomatic and nondiabetic women with chronic inflammatory diseases had significantly increased odds of having CAC and more extensive CAC compared with age- and race-matched healthy controls. The increased odds for CAC may in part result from higher levels of inflammation and endothelial activation in these patients.
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PMID:C-reactive protein and coronary artery calcium in asymptomatic women with systemic lupus erythematosus or rheumatoid arthritis. 1877 2

Cardiovascular morbidity and mortality in SLE is increased in patient with established disease, and SLE itself has been determined to be an independent risk factor for cardiovascular events. Autopsy studies have demonstrated that the coronary vessels of SLE patients have atherosclerotic plaque, and most cardiovascular events are not attributable to active vasculitis. It is believed that patients with inflammatory disease, including SLE, are more likely to have vulnerable plaque rupture, accounting for more frequent events. Elevated homocysteine levels have been associated with the presence and progression of atherosclerotic plaque. Enzyme polymorphisms involved in the folatehomocysteine pathway do not seem to contribute to differences in homocysteine concentration or atherosclerotic plaque. Recently, endothelial dysfunction has been identified as an early abnormality in ASCVD, and has been demonstrated in the vessels of SLE patients. Premature cardiovascular disease in SLE patients is likely attributable to the consequences of inflammation. There is preliminary evidence that type I interferons maybe the initial stimulation of the cascade of atherosclerotic development, starting with endothelial damage, and abnormal vascular repair.
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PMID:Premature atherosclerotic cardiovascular disease and systemic lupus erythematosus from bedside to bench. 1893 29

Hydroxychloroquine has been suggested to exert lipid lowering effects. The purpose of this study was to determine the effect of hydroxychloroquine on total cholesterol and on other lipoproteins in a controlled trial involving patients with systemic lupus erythematosus (SLE). Seventeen female patients with SLE were enrolled in a double-blind, randomized, placebo-controlled, multiple-dose pilot study comparing placebo with hydroxychloroquine at daily doses of 400 and 800 mg. The primary endpoint was alteration in total cholesterol. Patients were evaluated at two screening visits pretreatment and at three monthly follow-up visits. At all visits, a fasting panel of lipoproteins, disease activity, and adverse drug effects were assessed. There were no significant alterations in lipoproteins in patients receiving placebo. Treatment with 400 mg/day of hydroxychloroquine resulted in a significant decrease in total cholesterol (mean decrease of 11.6 mg/dL). Treatment with 800 mg/day of hydroxychloroquine resulted in a significant decreases in total cholesterol (mean decrease of 13.4 mg/dL), triglycerides, very low density lipoproteins, cholesterol, and the ratios of total cholesterol/high density lipoprotein cholesterol and low density lipoprotein/high density lipoprotein cholesterol. More adverse effects were noted among patients receiving the high dose (800 mg/day). Hydroxychloroquine affects a significant reduction in total cholesterol in patients with SLE. The findings of this double-blind, placebo-controlled, pilot trial support the conclusions of earlier open trials. This lipid-lowering effect may be an added benefit of hydroxychloroquine treatment in these patients with a high prevalence of atherosclerotic cardiovascular disease.
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PMID:Hydroxychloroquine Effects on Lipoprotein Profiles (the HELP trial): A Double-Blind, Randomized, Placebo-Controlled, Pilot Study In Patients With Systemic Lupus Erythematosus. 1907 10

Premature atherosclerotic cardiovascular disease (ASCVD) is a common and devastating complication of systemic lupus erythematosus (SLE). It is likely that immunologic derangements contribute to premature ASCVD in these patients, possibly by disrupting homeostatic mechanisms that orchestrate cholesterol balance in monocytes/macrophages in the artery wall. CD36, a macrophage scavenger receptor responsible for recognition and internalization of oxidized lipids, is a major participant in atherosclerotic foam cell formation. We hypothesized that lupus plasma would affect CD36 expression in a pro-atherogenic manner in THP-1 human monocytes and differentiated macrophages. SLE patient plasma markedly stimulated expression of CD36 message in a dose-dependent fashion in THP-1 human monocytes. A 50% volume/volume concentration of plasma derived from SLE patients increased CD36 mRNA by 71 +/- 8% (n = 3, P < 0.001) above 50% normal human plasma. 50% SLE patient plasma increased CD36 mRNA expression to 290 +/- 12% of no-plasma control (n = 3, P < 0.001), compared with only 118 +/- 3.7% of control in the presence of 50% normal human plasma (n = 3, not significant). 50% lupus plasma also upregulated CD36 protein expression by 482.3 +/- 76.2% (n = 4, P < 0.05), whereas the presence of 50% normal human plasma increased the CD36 protein level by only 239.8 +/- 61.9% (n = 4, P < 0.05). To our knowledge, this is the first demonstration that CD36 expression is enhanced by plasma from patients with an autoimmune disorder. Premature atherosclerosis is common in SLE patients. Upregulation of CD36 may contribute to this pathological process by increasing vulnerability to cholesterol overload. Demonstration of disrupted cholesterol homeostasis in this select group of patients provides further evidence of the involvement of the immune system in atherogenesis and may inform us of the role of CD36 in the general atherogenic process. CD36 may provide a novel therapeutic target in the treatment of ASCVD in SLE patients.
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PMID:Enhanced CD36 scavenger receptor expression in THP-1 human monocytes in the presence of lupus plasma: linking autoimmunity and atherosclerosis. 1914 74


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