Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic Lupus International Collaborating Clinics (SLICC) comprises 27 centres from 11 countries. An inception cohort of 918 SLE patients has been assembled according to a standardized protocol between 2000 and 2006. Clinical features, classic coronary artery disease (CAD) risk factors, as well as other potential risk factors were collected. Of the 918 patients 89% were females, and of multi racial origin. Less than half the patients were living in a permanent relationship, 58% had post secondary education and 51% were employed. Eight percent had family history of SLE. At enrolment, with at mean age of diagnosis of 34.5 years, a significant number of patients already had CAD risk factors, such as hypertension (33%) and hypercholesterolemia (36%). Only 15% of the patients were postmenopausal, 16% were current smokers and 3.6% had diabetes at entry to the SLICC-RAS (Registry for Atherosclerosis). A number of patients in this multi-racial, multi-ethnic inception cohort of lupus patients have classic CAD risk factors within a mean of 5.4 months from diagnosis. This cohort will be increased to 1500 patients to be followed yearly for 10 years. This will provide a unique opportunity to evaluate risk factors for accelerated atherosclerosis in SLE.
Lupus 2007
PMID:Clinical manifestations and coronary artery disease risk factors at diagnosis of systemic lupus erythematosus: data from an international inception cohort. 1772 67

C-reactive protein CRP is an acute-phase protein known as a biomarker for inflammation. As such CRP levels have been traditionally used to detect and predict the outcome of infections inflammatory and necrotic processes and to monitor the efficacy of treatment in these conditions. With the development of high sensitivity assays CRP has resurfaced as a very strong predictor in cardiovascular disease and as a mediator of atherosclerosis. The Centers for Disease Control and American Heart Association have elaborated guidelines for the use of CRP in the primary prevention setting and in patients with stable coronary disease or acute coronary syndromes. CRP has been used for differentiation between Systemic Lupus Erythematosus activity and infection in individuals without serositis. More recently CRP has also elicited interest as a therapeutic option in lupus. Murine lupus models treated with CRP have been reported to present delayed Lupus onset decreased antibody levels enhanced survival and reversal of ongoing proteinuria. In this paper we reviewed the multiple roles of CRP particularly in lupus.
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PMID:C-Reactive protein and its implications in systemic lupus erythematosus. 1815 97

Lupus treatment has evolved considerably with spectacular advances that can be summarized in 10 points. Hydroxychloroquine and cyclophosphamide are still standard drugs, provided their use is optimized. Contraception and postmenopausal hormone replacement therapy have finally been tested in randomized studies with fairly reassuring results, although prudence remains essential in patients with severe lupus and above all in those with thrombotic complications (antiphospholipid syndrome). Mycophenolic acid has been shown to be useful in the treatment of lupus nephropathies, but its specific place in the therapeutic strategy remains to be defined. Other drugs (sirolimus, abatacept) are currently being evaluated. Anti-lymphocyte B therapies are growing in popularity. Rituximab and other drugs (anti-BAFF, TACI-Fc) are also being evaluated and their results appear very interesting. Interferon alpha (type I) inhibition is an attractive therapeutic approach in lupus but its use in humans is still premature. Peptide vaccination with fragments of autoantibodies or autoantigens is an elegant strategy, and preliminary results justify further studies. Anti-TNF molecules may be beneficial in lupus. Complement inhibition can be useful in lupus and antiphospholipid syndrome but drugs usable in humans (anti-C5) must be developed. Atheromatosis in lupus is the principal cause of morbidity and mortality and must be managed. Smoking cessation is essential, but other approaches (statins) should also be discussed. Many futuristic types of immune manipulation may be envisioned (proteasome inhibition, modulation of Fc gammaRIIB, and modulation of cell signaling (PI3kgamma)). Hence the perspectives are numerous. We will soon be able to optimize the treatment of our patients. Nevertheless, rigorous evaluation of the risk/benefit ratio of new drugs and of their most appropriate place in the therapeutic strategy against systemic lupus is indispensable.
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PMID:[Systemic lupus erythematosus: news and therapeutic perspectives]. 1824 45

To determine the frequency of carotid plaque and intima-media thickness (IMT) in patients with systemic lupus erythematosus (SLE) and their association with risk factors in a Brazilian university setting. Carotid plaque and IMT were identified and measured by ultrasonography. Traditional risk factors and lupus-related factors were analysed. One hundred and seventy-two patients (women = 96%, age = 38 +/- 11 years) were evaluated. The frequency of carotid plaque was 9.3%. The median (IR) IMT was 0.60 mm (0.54-0.71 mm). Age, family history (FH) of premature coronary disease, low-density cholesterol (LDL-c) >100 mg/dL, hypertriglyceridemia, diabetes, hypertension, smoking, postmenopause, number of risk factors, Framingham risk score, age at diagnosis, duration of lupus, mucocutaneous manifestations and duration of prednisone use were associated with plaque (P < 0.05), univariate analysis. Nephritis, immunosuppressive therapy, intravenous methylprednisolone and a higher average daily dose of prednisone were associated with the absence of plaque. Independent predictors of plaque were smoking (P = 0.004), LDL-c >100 mg/dL (P = 0.044), Framingham score (P = 0.006) and absence of immunosuppressive therapy (P = 0.032). There was an independent correlation between IMT and age (P < 0.001) and duration of prednisone use (P = 0.020). Subclinical atherosclerosis was associated with traditional risk and SLE-related factors, especially the absence of immunosuppressive therapy. The present study suggests that the levels of LDL-c should be kept under 100mg/dL in lupus.
Lupus 2008 Feb
PMID:Carotid atherosclerotic alterations in systemic lupus erythematosus patients treated at a Brazilian university setting. 1825 Jan 33

It has been reported that IgG to oxidized LDL/beta2-glycoprotein I (oxLDL/beta2GPI) complexes are associated with arterial thromboembolism (TE) in patients with antiphospholipid syndrome (APS). How these antibodies behave in arterial as compared to venous TE in APS is unknown. The aim of the present study was to evaluate the association of IgG anti-oxLDL/beta2GPI with clinical manifestations in category I APS patients. Fifty-seven APS patients with triple positivity (Lupus Anticoagulant (LAC), anti cardiolipin (aCL) and anti-beta2-glycoprotein I (abeta2GPI) antibodies), 28 with arterial and 29 with venous thromboembolism, were included in the study. There were no differences in the dRVVT ratio, IgG/IgM aCL and IgG/IgM abeta2GPI titers in the two patient groups. There were no differences in the IgG (78.5 U+/-59.8 vs. 112.2 U+/-92.3) and IgM (16.3 U+/-15.9 vs. 21.1 U+/-14.3) anti-oxLDL/beta2GPI mean values. A significant correlation was found between IgG anti-oxLDL/beta2GPI and IgG anti-beta2GPI titers in the whole group of APS patients. Patients in the arterial group were older and had more risk factors for atherosclerosis. Data from this study do not support the hypothesis that IgG anti-oxLDL/beta2GPI are specifically associated to arterial TE in Category I APS patients.
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PMID:Antibodies to oxidized LDL/beta2-glycoprotein I in antiphospholipid syndrome patients with venous and arterial thromboembolism. 1832 38

Over recent decades short- and medium-term survival has greatly improved in patients affected with systemic lupus erythematosus, but long-term prognosis still remains poor mainly due to complications of the disease and/or its treatment. To improve long-term prognosis in systemic lupus erythematosus, we should try to adopt, early in the disease course, strategies that can contribute to reducing long-term complications, including screening for and prophylaxis against infections, control of risk factors for atherosclerosis, and cancer surveillance. However, in patients with systemic lupus erythematosus all these preventive strategies are often not sufficient. Indeed, two important systemic lupus erythematosus-related factors play a relevant role in all these complications: severe disease manifestations, such as glomerulonephritis and central nervous system involvement, and corticosteroid and cyclophosphamide use. Therefore, to prevent long-term complications, we should try to control disease activity and severity using the lowest effective dosage of these drugs. Moreover, strategies directed at preventing clinical manifestations in asymptomatic antinuclear antibody-positive individuals or in antiphospholipid antibody-positive systemic lupus erythematosus patients, as well as at preventing severe manifestations in patients with mild systemic lupus erythematosus at the time of the diagnosis should be considered.
Lupus 2008 Mar
PMID:Lupus: improving long-term prognosis. 1837 55

A premature atherosclerosis has been presumed in patients with antiphospholipid syndrome. The potential role of antiphospholipid antibodies in the development of atheroma is rather controversial. In this study, we tested the hypothesis that antiphospholipid antibodies could induce atherosclerosis via vascular functional changes. CD1 mice received one single injection of antiphospholipid monoclonal antibodies derived from male (BXSB x NZW) F1 mice with a lupus-like disease associated with an antiphospholipid syndrome and coronary artery disease. One week later, first-order mesenteric arteries (diameter 220-260 microm) were isolated and mounted on a small-vessel myograph for the measurement of the relaxation responses to acetylcholine or the NO donor nitroprusside after precontraction by phenylephrine. Five out of eight antiphospholipid monoclonal antibodies reduced the response to acetylcholine compared with control mice, and this effect was especially marked with one of them. No change in the response to nitroprusside was observed. The impairment was maintained after 3 weeks of treatment and appeared related to a moderate decrease in NO-mediated responses and a marked decrease in prostanoid-mediated relaxations. These vascular functional changes could be prevented by chronic treatment with statins or aspirin. These data could constitute additional elements supporting a direct pathogenic role of antiphospholipid antibodies. We suggest that a sub-population of these autoantibodies could be responsible for the endothelial dysfunction observed in antiphospholipid syndrome.
Lupus 2008 Mar
PMID:Antiphospholipid antibodies induce vascular functional changes in mice: a mechanism of vascular lesions in antiphospholipid syndrome? 1837 58

Atherosclerosis is an inflammatory disease characterised by presence of activated immune competent cells in middle-sized and large arteries and is the major cause of cardiovascular disease (CVD). The risk of CVD is very high in systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are, therefore, important clinical problems but may in addition also have implications for the role of immune reactions in CVD in general. Others and we have recently demonstrated that risk factors for CVD in SLE are both traditional and non-traditional acting in concert. Traditional risk factors implicated in SLE include, for example, dyslipidemia (especially high triglycerides), hypertension, renal disease, non-traditional as inflammation, antiphospholipid antibodies (aPL) and low-density lipoprotein (LDL) oxidation are also associated with CVD in SLE. Atherothrombosis is likely to be a major underlying mechanism and is not only an increased risk of thrombosis per se. It is possible that factors like proinflammatory reactions or prothrombotic factors, such as aPL, make atherosclerotic lesions in SLE more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients is presently not clear. Treatment of patients with SLE should include a close monitoring of traditional risk factors and also the above-mentioned non-traditional for CVD.
Lupus 2008 May
PMID:Systemic lupus erythematosus and cardiovascular disease. 1849 Apr 8

The accelerated atherosclerosis that occurs in some patients with systemic lupus erythematosus (SLE) has a complex pathogenesis, including alterations in lipids, inflammation and the immune system. In this article, we review the evidence that peroxidase-related alteration of normal, protective high-density lipoprotein (HDL) converts them to pro-inflammatory HDL (piHDL), characterized by lower content of the cholesterol transport lipoprotein ApoA1 and impaired function of the antioxidant enzyme paroxonase, which prevents oxidation of low-density lipoprotein (LDL). Forty-five per cent of women with SLE have piHDL compared with 20% of patients with rheumatoid arthritis and 4% of healthy controls. The presence of piHDL increases risk for coronary artery events and carotid artery plaque. Another result of lipid oxidation in patients with SLE is generation of highly oxidized LDL and phospholipids (PL), probably stimulating antibodies to OxPL phospholipids. These antibodies along with promoting thrombosis also interfere with deposits of Annexin V onto endothelial cells, which probably promote increased instability of atherosclerotic plaque. Thus, piHDL and anti-OxPL promote plaque formation, plaque instability and thrombosis, accounting for some of the large increase in atherosclerosis and coronary artery events in SLE.
Lupus 2008 May
PMID:Atherosclerosis and systemic lupus erythematosus: the role of altered lipids and of autoantibodies. 1849 Apr 9

Moyamoya disease is a rare, progressive cerebrovascular disorder that is characterized by a stenosis or occlusion of the bilateral internal carotid arteries and the development of collateral vessels. Transient ischemic attacks or seizures are the usual presentation of moyamoya disease in children, whereas cerebral hemorrhage is the most common symptom in adults. We report an 18-year-old female patient with active lupus nephritis who presented with the sudden onset of left hemiparesis. Brain magnetic resonance imaging showed acute infarctions in the right basal ganglia and subcortical white matter of the right frontal lobe. Cerebral angiography showed the stenosis of the bilateral internal carotid arteries with rich basal collateral vessels (moyamoya vessels). There was no evidence of atherosclerosis or antiphospholipid syndrome. Glucocorticoid therapy was used to control the systemic lupus erythematosus. Prophylactic bypass surgery was performed to prevent recurrent ischemic attacks. This case report shows that an underlying cerebrovascular lesion of moyamoya vessels in a patient with systemic lupus erythematosus is susceptible to cerebrovascular accidents.
Lupus 2008 Jul
PMID:Moyamoya syndrome associated with systemic lupus erythematosus. 1862 42


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