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)

We identified a group of 24 young (less than 50 years of age) women with isolated, premature atherosclerotic aortoiliac occlusive disease and attempted to identify distinguishing hemostatic characteristics. Most of these patients (62%) presented with acute thromboembolic events (blue toe syndrome, n = 6; macroemboli, n = 6; or aortoiliac thrombosis, n = 3). Aortoiliac reconstruction (aortoiliac endarterectomy, n = 10, aortobifurcation bypass grafts, n = 6; and percutaneous angioplasty, n = 4) was complicated by early thrombosis in 6 of 20 cases (30%), (1 of 10 endarterectomies, 4 of 6 bypass grafts, and 1 of 4 angioplasties). Fresh thrombus overlying an atherosclerotic plaque was a common finding at surgery. This observation and the relatively high incidence of thromboembolic events led us to hypothesize that a characteristic hemostatic profile might underlie the remarkably similar clinical presentations of these women. Levels of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant), plasminogen activator inhibitor-1, fibrinogen, antithrombin III, protein C, protein S, plasminogen, prothrombin fragment F1 + 2, and D-dimer were determined for these young women and for 21 age-matched white female control subjects without vascular disease and nine white male patients with aortoiliac occlusive disease (mean 61 years, range 43 to 74 years). The incidence of anticardiolipin antibodies was 42% (8 of 19) in the female patients, which was significantly elevated (p = 0.028). The female (62.5%) and male (100%) patients had significantly elevated D-dimer levels (p < 0.001). Deficiencies of antithrombin III, protein C, and protein S were rare. A unique pattern of premature aortoiliac atherosclerosis exists in some young women. Intra-arterial thromboembolic events are common at presentation and complicate surgical management. The role of antiphospholipid antibodies remains uncertain.
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PMID:Young women with advanced aortoiliac occlusive disease: new insights. 898 71

Aortoiliac occlusion due to atherosclerosis is known to occur in elderly people. Two unique cases are documented here in which aortoiliac occlusion was observed in young men. These patients had no identifiable risk factors for developing atherosclerotic thrombosis except for the lupus anticoagulant, an immunoglobulin associated with thromboembolic episodes. Although previously the lupus anticoagulant has been reported to cause thrombosis only in relatively small-sized arteries or veins, it may also be associated with aortoiliac atheromatous occlusion in young men.
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PMID:Aortoiliac occlusion associated with the lupus anticoagulant. Report of two cases. 911 85

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.
Lupus 1997
PMID:SLE mortality in an oriental population. 911 15

Reactive oxygen species (ROS) are cytotoxic, causing inflammatory disease, including tissue necrosis, organ failure, atherosclerosis, infertility, birth defects, premature aging, mutations and malignancy. ROS are produced in the metabolism of drugs and industrial chemicals by (i) one-electron peroxidase oxidations to form cation radicals, (ii) cytochrome P450 metabolism to free radical products, (iii) stabilisation of the ROS-generator, CYP2E1, and (iv) futile cycling of other cytochromes P450. ROS production initiates inflammation which unless quenched may result in chronic inflammatory disease states, e.g. hepatitis, nephritis, myositis, scleroderma, lupus erythematosus, multiple system organ failure. Quenching of ROS is affected by the redox buffer, glutathione (GSH), and the antioxidants, ascorbic acid, tocopherols, retinoids, in conjunction with the redox enzymes, GSH reductase, GSH peroxidase, catalase and superoxide dismutase. Many industrial workers with symptoms of systemic inflammation, resulting from exposure to toxic chemicals, are diagnosed as having rheumatoid arthritis, virus infections, or other microbial lesions, largely because many physicians are unaware that exposure to certain chemicals can initiate inflammatory disease states.
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PMID:Chemical toxicity and reactive oxygen species. 911 92

This report traces the development of our knowledge about immune-complex arteritis from the early 20th Century to the present time. The emphasis is on the work which began with the seminal observations of serum sickness by Longcope, MacKenzie, and Rich, to the pathogenetic studies of serum sickness arteritis in rabbits by several groups including the outstanding contributions by Dixon and coworkers concerning the role of circulating immune complexes. This work was followed by investigations of the relationship to atherosclerosis revealed by the sustained studies by Minick et al. on serum sickness arteritis in hypercholesterolemic rabbits. This pioneering research work has more recently been of pivotal value in understanding the arteritis observed in certain primate species such as the cynomolgus and the nemestrina, in human lupus erythematosus, and in organ transplantation arteritis. More recently it has become apparent that one of the microscopic hallmarks of this type of immune complex injury is the concentic micro-architecture of the inflammatory arterial lesions, for which, when they are also lipid containing, we have coined the term artheroarteritis. The contributions of the neoantigens from glycosylated LDL and oxidized LDL to the development of this type of atheroarteritis are considered. New frontiers in this area of research are being opened by the PDAY study which offers new opportunities to link circulating immune complexes and new antigens to arheroarteritis with its accelerated stenotic arterial lesion development.
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PMID:Atheroarteritis: a combined immunological and lipid imbalance. 911 26

We studied the initial manifestations and late features in our lupus patients. The clinical data of patients fulfilling the American College of Rheumatology criteria for systemic lupus erythematosus (SLE) were entered prospectively for newly diagnosed patients and cumulatively for those with at least 10 years of disease duration. Ninety-seven Group A (newly diagnosed; 86 females and 11 males; mean age 31 years; 83 Chinese, 11 Malays, and 3 Indians) and 58 Group B (more than 10 years disease duration; 56 females and 2 males; mean age 41 years; 50 Chinese, 5 Malays, and 3 Indians) lupus patients were studied. The commonest clinical features in Group A were: haematological (73%), arthritis (57%), malar rash (43%), renal disorder (31%) and photosensitivity (30%). Group B patients had haematological (78%), malar rash (73%), arthritis (69%), renal disorder (59%) and photosensitivity (33%). Renal disorder was significantly increased over the years (P < 0.001). Hypertension was present in 18% (Group A) and 59% (Group B) (P < 0.00001), diabetes mellitus in 5% (Group A) and 10% (Group B) (P = ns), atherosclerosis in 2% (Group A) and 7% (Group B) (P = ns). Cataract formation was not present in Group A patients but was present in 10% of Group B patients. Renal disorders and morbidity factors like hypertension and cataracts increased significantly over the years. Optimum treatment of lupus patients should therefore include close attention to these factors.
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PMID:Systemic lupus erythematosus: initial manifestations and clinical features after 10 years of disease. 928 16

Atherosclerosis may represent a significant cause of death and morbidity in patients with systemic lupus erythematosus. Coronary involvement is more premature in lupus patients. We present the case of a young woman diagnosed with SLE at the age of 20 years who had a myocardial infarction at age 29 years. We review the mechanisms of atherosclerosis, the interrelations between atherosclerosis and autoimmunity, and between atherosclerosis and SLE. We also review the risk factors, influence of disease and treatment and the guidelines for management of accelerated atherosclerosis in lupus patients.
Lupus 1997
PMID:Accelerated atherosclerosis and coronary disease in SLE. 930 60

Atherosclerosis is a process initiated by accumulation of macrophages in distinct areas of endothelial cell damage and uptake of large amounts of lipids. Recently, it has been shown that the immune system plays an active part in the progression of the atherosclerotic plaque although its precise role has not yet been elucidated. Anticardiolipin antibodies (aCL) are generally found in the sera of patients with the antiphospholipid syndrome (APS) and are associated with a prothrombotic state. Several authors have demonstrated that aCL can activate platelets and endothelial cells as well as increase oxidized low density lipoprotein (LDL) uptake by macrophages. In the present study we sought to assess the effect of immunization with aCL (Ab1, leading to the production of mouse aCL-Ab3) on the progression of atherosclerosis. Two groups of 8-weeks old female LDL-receptor knockout mice (n = 13 per group) were immunized with IgG purified from the serum of an APS patient or with normal human IgG, respectively. The aCL immunized mice developed high titres of 'self' aCL (detected using the standard aCL ELISA) as compared with the normal human IgG immunized mice, whereas no differences were noted between both study groups with respect to the serum lipid levels. The extent of fatty streak formation was significantly higher in the aCL immunized mice in comparison with the human IgG injected mice (mean aortic lesion size of 5308 +/- 471 microns2 vs 1027 +/- 184 microns2, respectively, P < 0.01). The immunohistochemical analysis of the atherosclerotic plaques from both mouse groups did not display differences in cellular composition. The results of the study show that mouse aCL induced by immunization with human aCL from an APS patient enhance atherogenesis in LDL-RKO mice and imply that these antibodies may play a role in atherosclerosis development in patients with the APS.
Lupus 1997
PMID:Atherosclerosis in LDL-receptor knockout mice is accelerated by immunization with anticardiolipin antibodies. 941 88

Antiphospholipid syndrome (APLS), is defined as the presence of antiphospholipid antibodies (APLA) associated with clinical phenomena of arterial or venous thrombosis, recurrent spontaneous abortions and thrombocytopenia. APLA represent the family of antibodies of different specificity. They are mostly directed to various anionic phospholipids (cardiolipin, phosphatidylcholine, phosphatidylserine, phosphatidyl acid and phosphatidyl ethanolamine). The part of APLA is directed towards epitope at the structurally changed beta-2-GPI, the so-called anti beta-2-GPI antibodies and the hypothesis was established that the subgroup of APLA was directed towards complex of beta-2-GPI with the phospholipids and oxidized lipoproteins of high and very low density. This could explain the clinically observed association of mutual onset of thrombosis and atherosclerosis. The most frequent target tissues for APLA are endothelial cells, thrombocytes, monocytes, natural anticoagulant system and placenta. APLA can be detected in a serum with one of the following assays: testing of lupus anticoagulant presence, determination of anticardiolipin antibodies (ACLA) concentration by ELISA and by testing the false positivity of VDRL test (standard test for syphilis). The pathological base for so-called vasculopathy in APLS are arterial and venous thrombosis. Clinical manifestations of APLS are mainly the result of blood vessels' occlusion but the thrombotic mass deposition on the surface of the heart valves may also occur. Clinically APLS can be divided into primary and secondary one, and manifestations of the secondary APLS are mainly expressed in the patients with SLE. Some clinical and serological variants of primary APLS were also described. The tendency for thrombotic process as a crucial characteristic of the syndrome and the lack of inflammation, imposes the choice of antithrombotic and anticoagulant therapy.
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PMID:[The antiphospholipid syndrome--yesterday, today, tomorrow]. 962 52

In examining reasons for premature atherosclerosis in systemic lupus erythematosus (SLE), we previously reported low levels of the cholesterol transport protein apolipoprotein A1 (apoA1) in these patients, and specific antibodies to purified apoA1 were identified in the sera of 5 out of 30 lupus patients. The current study was initiated to determine whether these antibodies are common in lupus patients. 520 serum samples from 175 patients with SLE or primary antiphospholipid syndrome (PAPS) were tested for antibodies to purified apoA1. Positive sera were retested for binding to apolipoprotein incorporated into reconstructed nascent or mature high-density lipoprotein (HDL). Autoantibodies to apoA1 were found in 32.5% of patients with SLE and 22.9% of patients with PAPS, associated with the presence of aPL (anti-beta2 glycoprotein-1, anti-beta2 GP1) antibodies. When reconstructed, nascent and mature HDL molecules were compared as antigen-containing environments, positive sera reacted best to apoA1 embedded in mature HDL molecules. This report confirms the high prevalence of antibodies to apoA1 in patients with systemic lupus and suggests a high affinity of these antibodies for mature HDL.
Lupus 1998
PMID:Frequency of antibodies to the cholesterol transport protein apolipoprotein A1 in patients with SLE. 969 40


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