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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With improved treatment modalities and survival rates, patients with systemic lupus erythematosus live longer and their co-morbidities have become more apparent. Of great concern is cardiovascular disease, which has become a leading cause of death. Lupus patients prematurely develop atherosclerosis, which likely arises from an interaction among traditional cardiovascular risk factors, factors specific to lupus itself and inflammatory mediators. Despite these findings, lupus patients are not always adequately evaluated for traditional risk factors, many of which are treatable and reversible. We propose that lupus patients be assessed and managed regarding cardiovascular risk factors in the same manner as patients with known cardiovascular disease. As a result, preventive cardiology should be considered an essential component of the care for patients with lupus.
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PMID:Cardiovascular risk assessment and treatment in systemic lupus erythematosus. 1959 79

Cardiac disease is common among patients with Systemic Lupus Erythematosus (SLE). Pericardial, myocardial, valvular, and coronary artery involvement have been extensively reported. The three major coronary abnormalities associated with myocardial injury in SLE are premature atherosclerosis, coronary arteritis and, less frequently, coronary aneurysms. A 26-year-old black male patient with a 5-year history of anti-phospholipid syndrome sustained a lateral wall myocardial infarct associated to angiographic evidences of multiple, diffuse, saccular coronary aneurysms without evidence of atherosclerotic occlusive disease in all three coronary arteries. Serologic studies were consistent with active SLE. Lupus-associated nephritis was also present. Radiographic studies showed no evidence of brain or thoracic aneurysms. A transthoracic echocardiogram showed an estimated ejection fraction of 35% and a moderate pericardial effusion. High dose i.v. steroids were started along with systemic anticoagulation. The patient had an uneventful clinical course and was discharged by the fourteenth day on high doses of oral steroids (60 mg daily), statins, oral anticoagulation (warfarin 5 mg), antihypertensives and aspirin. The patient was lost to follow-up and developed steroid-induced hyperglycemia, 20 pound weight gain and warfarin intoxication. A three-month follow up coronary angiography showed complete resolution of the aneurysms and serologic studies showed no active autoimmune disorder at that time. Coronary artery aneurysms have previously been reported in 15 cases of patients with SLE. An extensive Medline search of the literature revealed no previous reports of diffuse saccular coronary aneurysms involving all three coronary arteries associated with active SLE. This case highlights the unusual presentation of acute SLE in a young patient complicated by multiple aneurysms and acute myocardial infarction. In this case, we believe that a direct causal association exists between acute SLE-associated aneurysms and myocardial ischemic injury. Early recognition and prompt treatment with large doses of corticosteroids may decrease the mortality and morbidity associated with this condition.
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PMID:An unusual presentation of chest pain. 1961 May 65

The research projects of the European Forum on Antiphospholipid Antibodies are representative of how dynamic is this area of investigation. The present review is focused on the most recent projects of the Forum on the aetiopathogenic aspects of the antiphospholipid syndrome (APS). Studies on the genetic background of the APS are ongoing in order to better define the proximity between APS and full-blown systemic lupus erythematosus. However, the analysis of the polymorphisms of genes coding for inflammatory mediators may offer new information on the role of inflammatory processes in triggering thrombotic events as well as the whole susceptibility for developing the vascular manifestations. A systematic and wide detection of serological markers of infectious processes will give new insight on the role of infectious agents in favouring autoimmunity in APS. Owing to the well-known role of vitamin D(3) defect in autoimmune disease, the detection of vitamin plasma levels in APS patients will offer the rationale for a possible therapeutic supplementation. Additional projects are aimed to better characterize the diagnostic/prognostic value of antiphospholipid antibodies (aPL) by defining their epitope specificity and binding avidity. Pregnancy complications represent the obstetric side of APS. Research projects are focussed on the role of complement activation in placenta damage and on the potential ability of aPL to affect the fertility. Finally, a study has been planned in order to draw definitive conclusions on the associations between aPL and atherosclerosis.
Lupus 2009 Sep
PMID:European Forum on Antiphospholipid Antibodies: research in progress. 1967 94

Cardiovascular disease risk is increased in individuals suffering from systemic lupus erythematosus. Understanding the mechanism(s) of systemic lupus erythematosus-accelerated atherosclerosis is critical for the development of effective therapies. Our laboratory previously demonstrated that radiation chimeras of systemic lupus erythematosus-susceptible B6.Sle1.2.3 and low density lipoprotein receptor (LDLr)(-/-) mice have augmented atherosclerosis, which is associated with increased T-cell burden and activation in the lesion. The goals of this study were to further define specific immune mechanisms that mediate accelerated atherosclerosis and to determine whether the gene interval Sle3, which is linked to lupus-associated T-cell dysregulation, was sufficient to modulate atherogenesis. We transferred B6.Sle3 or C57Bl/6-derived bone marrow cells into lethally irradiated LDLr( -/-) mice (hereafter referred to as LDLr.Sle3 and LDLr.B6, respectively). Sixteen weeks after transplantation, the mice were placed on a western-type diet for 8 weeks. Our analyses revealed that LDLr.Sle3 mice had increased auto-antibody production against double-stranded DNA and cardiolipin compared with LDLr.B6 controls. We also found an increase in atherosclerosis-associated oxLDL antibodies. Antibody isotypes and serum cytokine analysis suggested that the humoral immune response in LDLr.Sle3 mice was skewed toward a Th2 phenotype. This finding is consistent with lupus-associated immune dysregulation. Additionally, LDLr.Sle3 mice had decreased serum cholesterol and triglyceride levels. However, there was no difference in lesion area or cellular composition of lesions between the two groups. These data demonstrate that, despite no change in lesion area, transfer of Sle3-associated T-cell dysregulation alone to LDLr-deficient mice is sufficient to decrease serum cholesterol and to exacerbate humoral immune responses that are frequently associated with atherosclerosis.
Lupus 2010 Jan
PMID:The lupus susceptibility locus Sle3 is not sufficient to accelerate atherosclerosis in lupus-susceptible low density lipoprotein receptor-deficient mice. 1985 Jun 56

Racial differences are known to account for a higher incidence of systemic lupus erythematosus (SLE), as well as increased disease severity and mortality. The purpose of this study was to determine whether there are any race-specific risk factors that affect measures of subclinical atherosclerosis in SLE patients. Traditional and SLE-related cardiovascular disease (CVD) risk factors were assessed in 106 female SLE patients. Carotid medial intimal medial thickness (mIMT) and coronary artery calcification (CAC) were measured on all subjects. Differences were evaluated between races for all clinical, serologic, and CVD risk factors and the racial interactions with all covariables. Outcomes included mIMT and CAC. There were no significant differences between races with regard to mIMT or CAC. Significant covariables in the final model for mIMT included age, triglycerides, glucose, and race-age and race-smoking interactions. A prediction model with fixed significant covariables demonstrated that Black subjects with a smoking history had a significantly higher mIMT than Blacks who had never smoked, an effect not seen in Whites. There were no differences between having CAC or with the CAC scores between the races. In the final model for CAC, age and SLE disease duration were significant covariables impacting CAC. When controlling for other significant CVD covariables and interactions, Black women, but not White, with SLE with a history of smoking have higher mIMT measurements than those who have never smoked. This is the first report documenting the race-specific effect of smoking on subclinical measures of CVD in SLE.
Lupus 2009 Dec
PMID:The relationship between race, cigarette smoking and carotid intimal medial thickness in systemic lupus erythematosus. 1986 42

Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe(+/ --) ldlr(+/--) mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis.
Lupus 2009 Nov
PMID:Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis. 1988 May 62

Atherosclerosis is an inflammatory disease, leading to the formation of pro-inflammatory and pro-oxidative lipids that generate an immune response. Several antigens have been shown to activate the immune response and affect the development of atherogenesis. Systemic lupus erythematosus is an autoimmune and inflammatory disease strongly associated with premature development of atherosclerotic plaques. Modulation of the immune system could represent a useful approach to prevent and/or treat atherosclerosis. A vaccination-based approach might be a useful, effective tool in the modern arsenal of cardiovascular therapies and could be used on a large scale at a low cost. In non-systemic lupus erythematosus populations, vaccines against oxidized low-density lipoprotein, beta-2-glycoprotein I, heat shock proteins, lipoproteins, cholesterol, molecules involved in cholesterol metabolism, and other molecules (CD99, vascular endothelial growth factor-receptor, and interleukin-2) have been tested, with promising results. However, there are no studies of vaccination against atherosclerosis in systemic lupus erythematosus.
Lupus 2009 Nov
PMID:Vaccination, atherosclerosis and systemic lupus erythematosus. 1988 May 70

We tested the hypothesis that carotid atherosclerosis in systemic lupus erythematosus (SLE) is associated with poor health-related quality of life (HRQOL), which is independent of any association with traditional risk factors (TRFs), lifestyle and socioeconomic factors. Women with SLE completed the RAND Medical Outcome Study 36-Item Short-Form Health Survey version 1 (MOS SF-36). B-mode Doppler examination of the carotid arteries determined the presence of atherosclerotic plaque. The association between carotid plaque and HRQOL domains was analysed using logistic regression models with sequential adjustments for age, TRFs, education level and employment status. We studied 181 women, 47 (26%) of whom had carotid plaque. Carotid plaque was significantly associated with lower levels of physical functioning (p = 0.047), vitality (p = 0.04), role emotional (p = 0.04) and mental health subscales (p = 0.01) and lower mental component summary score (MCS) (p = 0.03). These associations were no longer significant after adjustment for age and TRFs, especially smoking. Smokers had lower physical functioning, vitality and mental health and more bodily pain. The association between carotid plaque and HRQOL was not independent of TRFs and smoking was a key mediator of the associations found. Poor HRQOL in smokers will need addressing as part of any smoking cessation strategies in SLE patients.
Lupus 2010 Mar
PMID:Health-related quality of life, smoking and carotid atherosclerosis in white British women with systemic lupus erythematosus. 2000 14

Patients with systemic lupus erythematosus (SLE) have an impairment in phenotype and function of endothelial progenitor cells (EPCs) which is mediated by interferon alpha (IFN-alpha). We assessed whether murine lupus models also exhibit vasculogenesis abnormalities and their potential association with endothelial dysfunction. Phenotype and function of EPCs and type I IFN gene signatures in EPC compartments were assessed in female New Zealand Black/New Zealand White F(1) (NZB/W), B6.MRL-Fas(lpr)/J (B6/lpr) and control mice. Thoracic aorta endothelial and smooth muscle function were measured in response to acetylcholine or sodium nitropruside, respectively. NZB/W mice displayed reduced numbers, increased apoptosis and impaired function of EPCs. These abnormalities correlated with significant decreases in endothelium-dependent vasomotor responses and with increased type I IFN signatures in EPC compartments. In contrast, B6/lpr mice showed improvement in endothelium-dependent and endothelial-independent responses, no abnormalities in EPC phenotype or function and downregulation of type I IFN signatures in EPC compartments. These results indicate that NZB/W mice represent a good model to study the mechanisms leading to endothelial dysfunction and abnormal vasculogenesis in lupus. These results further support the hypothesis that type I IFNs may play an important role in premature vascular damage and, potentially, atherosclerosis development in SLE.
Lupus 2010 Mar
PMID:Lupus-prone New Zealand Black/New Zealand White F1 mice display endothelial dysfunction and abnormal phenotype and function of endothelial progenitor cells. 2006 18

The objective of this study was to determine the frequency of Metabolic Syndrome (MetS) in patients with SLE and to analyze the association of MetS with traditional risk factors for CHD and lupus characteristics. In this cross-sectional study the frequency of MetS was determined according to the National Cholesterol Education Program Adult Treatment Panel III in patients with SLE. The association of MetS with the traditional risk factors for CHD not included in the syndrome definition, and with lupus characteristics was examined. The mean age (sd) of the 162 females patients was 38.8(11.2) years. The frequency of MetS was 32.1%. Abdominal obesity and hypertension were the two most common components of the syndrome (86.5% each) followed by low levels of HDL-cholesterol (84.6%), hypertriglyceridemia (69.2%) and hyperglycemia (15.4%). MetS was significantly associated with older age, family history of CHD, obesity, postmenopausal status, LDL-c > or =100mg/dl, and higher Framingham risk score. Lupus characteristics associated with MetS were history of nephrotic proteinuria during follow-up and current cyclophosphamide use, higher modified SLEDAI-2k, higher damage index score (SLICC/ACR), and older age at lupus diagnosis. In the logistic regression analysis, obesity, LDL-c > or =100mg/dl, older age at lupus diagnosis, higher damage index and nephrotic proteinuria were independently associated with MetS. We conclude that MetS diagnosis was frequent in patients with lupus. The syndrome was associated not only with traditional risk factors for CHD, confirming the clustering of those risk factors, but also with lupus characteristics. Some of those factors, especially LDL-c > or =100mg/dl and age at lupus diagnosis, have been associated with atherosclerosis in lupus patients. Lupus (2010) 19, 803-809.
Lupus 2010 Jun
PMID:Metabolic syndrome in patients with systemic lupus erythematosus: association with traditional risk factors for coronary heart disease and lupus characteristics. 2011 59


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