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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite recent advances, patients with systemic lupus erythematosus (SLE) still experience considerable morbidity and mortality. To try and improve their prognosis, varied novel biological interventions and immune manipulations are being developed. They may hold promise in particular for patients whose disease is organ-threatening and refractory to conventional treatment. In addition, awareness of the tendency of lupus patients to develop accelerated atherosclerosis as well as newly gained insights into the underlying mechanisms, may lead to better control of risk factors, earlier diagnosis of prevalent cardiovascular disease and more effective treatment. Infections also remain a significant threat that may be amenable to improved preventive measures. Evidence related to a better management of lupus patients by specialists, the need to address the impact of commonly associated stress and depression and other significant developments are also presented and discussed.
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PMID:The future of the treatment of systemic lupus erythematosus. 1589 1

Chronic inflammatory diseases are associated with premature atherosclerosis; however, it is unknown whether arterial stiffness is increased in this setting, possibly as a manifestation of vascular disease preceding and/or independent of atherosclerosis. Carotid ultrasonography and radial applanation tonometry were performed in 101 patients with systemic lupus erythematosus, 80 patients with rheumatoid arthritis, and 105 healthy control subjects. The 3 groups were comparable in age, gender, and carotid artery absolute and relative wall thickness. Atherosclerotic plaque was more common in lupus (46%) and rheumatoid arthritis (38%) patients than in controls (23%) (P<0.003). Although control subjects had higher central and peripheral blood pressures, arterial stiffness was increased in patient groups compared with controls (lupus, rheumatoid arthritis, controls, respectively: beta: 3.36 versus 3.22 versus 2.60, P<0.001; Young's modulus: 441 versus 452 versus 366 mm Hg/cm, P=0.004; Peterson's elastic modulus: 278 versus 273 versus 216 mm Hg, P<0.001) after adjustment for differences in mean brachial pressure. In multivariate analysis involving the entire population, arterial stiffness was independently related to age, serum glucose, and the presence of chronic inflammatory disease. In multivariate analysis restricted to the patients, arterial stiffness was independently related to age at diagnosis, disease duration, serum cholesterol, and C-reactive protein (and IL-6, when substituted for C-reactive protein). When analyses were repeated in the 186 study subjects without carotid plaque, arterial stiffness remained significantly elevated in patient groups after adjustment for differences in age and mean brachial pressure. In conclusion, arterial stiffness is increased in chronic inflammatory disorders independent of the presence of atherosclerosis and is related to disease duration, cholesterol, and the inflammatory mediator C-reactive protein and the cytokine that stimulates its production, IL-6.
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PMID:Arterial stiffness in chronic inflammatory diseases. 1591 40

Previous studies have shown an increased risk of retinal vein occlusion (RVO) in patients with hypertension, hypercholesterolemia and diabetes mellitus. Literature on the association between thrombophilic factors and RVO consists of small studies and case reports. The objective was to determine the relationship between thrombophilic risk factors and RVO. Thrombophilic risk factors analyzed were hyperhomocysteinemia, MTHFR gene mutation, factor V Leiden mutation, protein C and S deficiency, antithrombin deficiency, prothrombin gene mutation, anticardiolipin antibodies and lupus anticoagulant. For all currently known thrombophilic risk factors odds ratios for RVO were calculated as estimates of relative risk. The odds ratios were 8.9 (95% CI 5.7 - 13.7) for hyperhomocysteinemia, 3.9 (95% CI 2.3 - 6.7) for anticardiolipin antibodies, 1.2 (95% CI 0.9 - 1.6) for MTHFR, 1.5 (95% CI 1.0 - 2.2) for factor V Leiden mutation and 1.6 (95% CI 0.8 - 3.2) for prothrombin gene mutation. In conclusion, regarding thrombophilic risk factors and RVO there is only evidence for an association with hyperhomocysteinemia and anticardiolipin antibodies, factors that are known as risk factors for venous thrombosis as well as for arterial vascular disease. The minor effect of factor V Leiden mutation and the protrombin gene mutation (risk factors for venous thrombosis only) suggests that atherosclerosis might be an important factor in the development of CRVO.
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PMID:Retinal vein occlusion: a form of venous thrombosis or a complication of atherosclerosis? A meta-analysis of thrombophilic factors. 1596 81

Antibodies against oxidized low-density lipoproteins (anti-oxLDL antibodies) are involved in the development of atherosclerosis in animal models, but their role in humans is not clear. The aim of this study was to explore the relationship between the presence of anti-oxLDL antibodies and the presence of anti-beta2glycoprotein I (beta2gpI) antibodies, anticardiolipin antibodies and lupus anticoagulant. We also analyzed the relationship between the appearance of anti-oxLDL antibodies and clinical signs of antiphospholipid syndrome. This study included three groups of patients: 27 patients with primary antiphospholipid syndrome, 20 with secondary antiphospholipid syndrome associated with systemic lupus erythematosus and 13 patients with systemic lupus erythematosus. Levels of anti-oxLDL, anticardiolipin and anti-beta2gpI antibodies were detected by ELISA. The presence of lupus anticoagulant was detected by coagulation tests. We found that the presence of anti-oxLDL antibodies was associated with a history of arterial thromboses in patients with secondary antiphospholipid syndrome (chi2 = 8.89, p < 0.01) and in patients with primary antiphospholipid syndrome (chi2 = 4.64, p < 0.05). Also, the appearance of anti-oxLDL antibodies was associated with the presence of anti-beta2gpI antibodies (chi2 = 4.25, p < 0.05), which was not dependent on diagnosis. These preliminary observations have to be confirmed in a larger study.
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PMID:Anti-oxLDL antibodies--marker for arterial thromboses in antiphospholipid syndrome? 1599 1

The objective of the study was to determine the clinical differences at diagnosis and during follow-up between male and female patients with primary antiphospholipid syndrome (PAPS). We analysed 68 patients, 30 males and 38 females diagnosed and followed between 1990 and 2003. Patients with antiphospholipid syndrome associated with systemic lupus erythematosus at onset and during follow-up were excluded. The mean age at diagnosis was 31.4 +/- 11 years in males and 35.7 +/- 11 years in females (NS). The follow-up after diagnosis was 8.7 +/- 3.1 years in males and 9.2 +/- 2.9 years in females (NS). We did not find significant differences between the two groups with respect to venous and arterial thrombosis. However, in female patients, stroke was more prevalent than in male patients (12/38 versus 3/30, P = 0.03). In contrast, we found a significant prevalence of severe gastrointestinal complications in male compared to female patients (7/30 versus 1/38, P = 0.009). One male patient died due to catastrophic antiphospholipid syndrome. This study suggests that clinical course in patients with PAPS may be different with significant prevalence of central nervous system involvement in females and gastrointestinal involvement in males. Factors such as accelerated atherosclerosis, hormones, related to gender could be the explanation of these findings.
Lupus 2005
PMID:The impact of gender on clinical manifestations of primary antiphospholipid syndrome. 1617 32

Heart damage, mediated by different autoantibodies can involve several anatomical heart structures: valves, arteries, conduction tissue. Verrucous endocarditis is frequently reported in patients with antiphospholipid syndrome (APS) with or without systemic lupus erythematosus (SLE), particularly if they suffer from central nervous system involvement. Antiphospholipid antibodies (aPL) were shown deposited at subendothelial level of the affected valves. According to several in vitro and in vivo experimental models, aPL, anti-oxidized LDL (oxLDL), anti-heat shock protein 65 (HSP65) and anti-endothelial cells antibodies (AECA) seem to be involved in the pathogenesis of the atherosclerosis phenomena described in systemic autoimmune disease and vasculitis. However, the observation of the association of the same antibodies with clinical and subclinical atherosclerosis in patients is still controversial. The children of anti-Ro/SSA positive mothers can be affected by the congenital heart block. Anti Ro/SS-A antibodies play a major pathogenic role in affecting the heart conduction tissue in this rare condition.
Lupus 2005
PMID:Nonorgan specific autoantibodies and heart damage. 1621 61

The role of the immune system in modulating atherosclerosis has recently been well documented. Studies have revealed that cellular and humoral immunity plays crucial roles in atherogenic plaque formation. This includes macrophages, CD4+ T cells and dendritic cells as well as autoantigens such as oxidized low density lipoprotein (oxLDL), heat shock proteins and beta2-glycoprotein I. Given these recent advances, various modifications of the immune system in experimental models have been proposed as therapeutic strategies, with the potential of inhibiting atherosclerosis progression. These modifications are switching the immune system (CD4+ T cells) from Th1 towards a Th2 anti-inflammatory cytokine secretion, and the induction of protective antibodies both of which may be induced by specific vaccination. Recent identification of specific immunoreactive antigenic epitopes on modified LDL, their successful implementation for immunization and the induction of atheroprotection, supports the idea that active vaccination may emerge as a novel immuno-modulating atheroprotective strategy.
Lupus 2005
PMID:Predictive and protective autoimmunity in cardiovascular diseases: is vaccination therapy a reality? 1621 63

Systemic inflammatory/autoimmune rheumatic diseases are associated with a significantly increased rate of atherosclerosis and cardiovascular disease. Several mechanisms of accelerated atherosclerosis have been proposed, including abnormal lipid and lipoprotein profiles, oxidative stress, enhanced apoptosis, thrombophilia, immune complexes and increased mononuclear cell infiltration of atherosclerotic lesions, local generation of cytokines and female estrogen deficiency. However, the widely shared enthusiasm about the cardioprotective potential of hormone replacement therapy (HRT) with estrogens, has come to an abrupt halt since very recent randomized trials failed to show a cardiovascular risk reduction in postmenopausal women. Several factors might play a role in these discrepancies, in particular, parts of the striking discrepancy between observational and randomized data have been attributed to an estrogen-mediated adverse effect on inflammation (enhancement, possibly dose-related). In fact, estrogens potentially increase the inflammatory/immune response in autoimmune rheumatic diseases. New roles for estrogen peripheral metabolites (hydroxylated) and their increased formation in inflammatory sites, might partially introduce some explanations for several apparently contrasting evidences.
Lupus 2005
PMID:Estrogens, autoimmunity and the heart. 1621 65

Cardiovascular (CV) disease morbidity and mortality are increased in patients with rheumatoid arthritis (RA) and much of the excess CV disease morbidity appears to be due to atherosclerosis. The pathogenesis of atherosclerosis (ATS) in RA is complex and there is increasing evidence that many factors including novel and traditional cardiovascular risk factors, RA treatments and the RA inflammatory disease process are involved in the development of CV disease in these patients. Of particular interest are the effects of chronic inflammation and immune dysregulation associated with RA. These have been shown to be associated with endothelial dysfunction, which is an early, potentially reversible, functional abnormality of the arterial wall. However, as several CV disease risk factors and drug prescribing are also influenced by RA disease severity it is very difficult to separate out the effects of the inflammatory disease burden on the cardiovascular system in RA.
Lupus 2005
PMID:Cardiovascular involvement in rheumatoid arthritis. 1621 66

Pericarditis is the most common cardiac abnormality in systemic lupus erythematosus (SLE) patients, but lesions of the valves, myocardium and coronary vessels may all occur. In the past, cardiac manifestations were severe and life threatening, often leading to death. Therefore, they were frequently found in post-mortem examinations. Nowadays cardiac manifestations are often mild and asymptomatic. However, they can be frequently recognized by echocardiography and other noninvasive tests. Echocardiography is a sensitive and specific technique in detecting cardiac abnormalities, particularly mild pericarditis, valvular lesions and myocardial dysfunction. Therefore, echocardiography should be performed periodically in SLE patients. Vascular occlusion, including coronary arteries, may develop due to vasculitis, premature atherosclerosis or antiphospholipid antibodies associated with SLE. Premature atherosclerosis is the most frequent cause of coronary artery disease (CAD) in SLE patients. Efforts should be made to control traditional risk factors as well as all other factors which could contribute to atherosclerotic plaque development.
Lupus 2005
PMID:Cardiac involvement in systemic lupus erythematosus. 1621 67


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