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)

Oral contraceptives containing oestrogens and hormone replacement therapy are generally not prescribed for women with systemic lupus erythematosus (SLE). The concern regarding oestrogens is based on the greater incidence of SLE in women, abnormalities of oestrogen metabolism, murine models of lupus, several anecdotes of patients having disease flares while receiving hormones, and one retrospective study in patients with pre-existing renal disease. For healthy women and those with SLE, there are clinical settings in which exogenous oestrogens provide benefit. For pre-menopausal women, these include provision of safe and effective birth control, protection against bone loss, and the consideration of oral contraceptives to preserve fertility in patients taking cyclophosphamide. For post-menopausal women, these include treatment of hot flushes and vaginal dryness, prevention of osteoporosis and, more controversial, prevention of atherosclerosis. Other exogenous hormones (clomiphene citrate, gonadotropins, gonadotropin-releasing hormones) may be used to elevate levels of endogenous oestrogen and stimulate ovulation in patients with diminished fertility. This chapter focuses on three broad categories: birth control, assisted reproduction and hormone replacement.
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PMID:Reproductive health in SLE. 1204 53

Primary anti-phospholipid syndrome (APS) is a thrombophilic state characterized by recurrent arterial and venous thrombosis, recurrent pregnancy loss, and the presence of circulating anti-phospholipid antibodies that may be responsible for thrombophilia and pregnancy morbidity. Ophthalmologic features are present in 15-88% of the patients with primary APS, thus ophthalmologists are one of the first physicians to whom the patient will present. An accurate diagnosis may save the patient from recurrent, potentially life-threatening thrombosis. In the U.S.A., an estimated 35,000 new cases of APS-related venous thrombosis occur each year in a population that is several decades younger than the patient population typically affected by thrombosis. Clinical features, such as chorea, transverse myelitis, cardiac valvular lesions, and accelerated atherosclerosis, are hypothesized to be due to a direct tissue-antibody interaction and cannot be explained purely by thrombosis. The use of recently proposed, well-defined diagnostic criteria, and better standardization of laboratory assays for the anti-phospholipid antibodies should help enable epidemiological surveys to establish the prevalence of these antibodies in patients with thrombosis and in the general population. Diagnosis of APS should be considered in all patients with recurrent systemic or ocular thrombosis in the absence of known risk factors. Several well-designed prospective studies show an increased risk of thrombosis in the presence of medium to high antibody level. With ocular involvement in as many as 88% of APS patients, an ophthalmic assessment should be an integral part of the clinical work-up of any patient with suspected or confirmed APS. The presence of isolated ocular thrombophilia with persistently elevated anti-phospholipid antibodies or lupus coagulant should confirm the diagnosis of APS. Management of these patients must be a multi-disciplinary effort with either a rheumatologist or a hematologist having the overall responsibility for coordinating treatment and monitoring the patient's immune status and anticoagulation. Treatment of isolated ocular thrombophilia in the presence of moderate to high titers of antiphospholipid antibodies should be on the same principles as patients with APS to prevent recurrent ocular or cerebral thrombosis.
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PMID:Primary anti-phospholipid antibody syndrome (APS): current concepts. 1205 9

Immunosuppressive treatment is a critical procedure in dialysis patients, in whom an increased risk of infection is already present. Haemodialytic treatment increases the patient's susceptibility to bacterial infection, mainly by impairing polymorphonuclear leukocyte phagocytosis, but it can also restore the patient's immunological defences by improving the T-cell function, which is reduced by pre-dialysis uraemia. Patients on dialysis usually continue the immunosuppressive treatment that had been established for the illness that caused their renal failure [e.g. systemic lupus erythematosus (SLE) or renal vasculitis]. Less frequently, patients on dialysis need immunosuppression for immunological or inflammatory diseases that appear 'de novo' after initiation of dialysis. SLE and antineutrophil cytoplasmic antibody (ANCA)-related vasculitides are immunological illnesses that frequently cause end-stage renal failure (ESRF). A reduction in serological and/or clinical activity is usually observed in SLE patients after they reach ESRF, but a similar or increased frequency of extrarenal relapse episodes in lupus patients after the beginning of the dialysis, compared with the pre-dialysis period, has also been described. Frequency of relapse episodes in patients on dialysis treatment for ANCA-related vasculitides varies from 10 to 30% per patient/year in different reports, and it is higher than the frequency of relapses after renal transplantation; anti-rejection therapy seems to be the most likely protective factor in these conditions. The treatment of relapse episodes in SLE or ANCA vasculitis in dialysis-dependent patients is usually not different from treatment of relapses in patients with dialysis-independent renal function. However, the risk of severe infection caused by immunosuppressive treatment is relevantly higher in dialysis patients. Furthermore, there is a lack of prospective controlled studies indicating the optimal management of immunosuppressive protocols in dialysis patients. A particularly careful assessment of the patient's risks and benefits is necessary in deciding how long immunosuppressive treatment should last after acute or rapidly progressive renal damage, that should require dialysis treatment, in patients with SLE or ANCA vasculitis. In the above conditions, the risks of prolonging immunosuppressive treatment must be balanced against the relatively good prognosis offered to these patients by dialysis and renal transplantation. In a retrospective review of 24 patients receiving long-term steroid therapy (>3 months) in our dialysis unit in the past 5 years, we found relevant clinical differences in the patients receiving steroid treatment compared with 24 controls. Steroid-treated patients showed less favourable nutritional conditions, with lower serum albumin and body mass index vs non-steroid-treated patients; moreover, C-reactive protein values were persistently higher in the steroid-treated group. Steroid treatment in these patients was usually performed at the beginning of regular dialysis, as a continuation of the treatment that started before the initiation of dialysis. Only two patients, who needed a prolonged low-dose steroidal treatment to control a malnutrition-inflammation-atherosclerosis (MIA) syndrome, started steroids many years after beginning dialysis. Steroid treatment was effective in improving the nutritional condition and inflammatory symptoms in these two patients after all conventional measures had failed.
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PMID:Immunosuppressive treatment in dialysis patients. 1214 70

Blood vessel homeostasis involves a complex interplay between inflammatory signals, hormones, and other mediators. Recent research suggests that although atherosclerosis is primarily a problem of impaired lipid regulation, the very processes of cholesterol and triglyceride metabolism are intrinsically tied to inflammatory and hormonal regulatory signals. Similarities between inflammatory and endocrine disturbances in systemic lupus and the predicted consequences for vascular regulation help explain the high incidence of premature atherosclerosis in lupus. Atherosclerosis in systemic lupus, then, may be a consequence of imbalances in what are intrinsic homeostatic mechanisms, rather than a result of externally superimposed pathologic changes.
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PMID:Regulation of the vasculature: clues from lupus. 1219 45

Cardiovascular diseases secondary to accelerated atherosclerosis are now accepted as a cause of mortality and morbidity in patients suffering from systemic lupus erythematosus and rheumatoid arthritis. More recently, atherosclerosis is emerging as one of the most serious complications in the anti-phospholipid syndrome, although large epidemiological studies, such as those performed in lupus and rheumatoid arthritis patients, have not been performed up to now. Classical risk factors (dislipidemia, hypertension, diabetes, smoking, etc.) and steroid therapy cannot completely explain the high prevalence of cardiovascular complications in systemic autoimmune diseases. Since the modern view defines atherosclerosis as a chronic inflammatory disorder, it has been suggested that systemic inflammation and soluble immune mediators (circulating autoantibodies, immune-complexes, complement activation products) might play a role in accelerating vessel pathology. The main target appears to be the endothelium because of its ability to switch to a pro-adhesive, pro-inflammatory and pro-coagulant surface in response to these mediators. Recent advances in the knowledge of the pharmacology of statins have indicated that these drugs rather than to be simple cholesterol lowering molecules display a pleiotropic effects on several mechanisms involved in the atherosclerotic plaque formation. Their anti-inflammatory activity and particularly their ability to downregulate endothelial cell activation induced by different stimuli strongly suggest their possible use in conditions in which the systemic inflammation and the endothelial activation/damage are thought to represent key pathogenic mechanisms.
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PMID:Anti-inflammatory and immunomodulating properties of statins. An additional tool for the therapeutic approach of systemic autoimmune diseases? 1240 12

Atherosclerosis-mediated coronary artery disease is a significant cause of mortality in lupus patients. Both an activated immune system and hyperlipidemia are implicated in the pathogenesis of the atherosclerotic lesions of lupus. In this study, the increases in anticardiolipin antibodies, total cholesterol, and LDL cholesterol with age were significantly lowered by fish oil and food restriction, either alone or in combination. Food restriction also significantly decreased the elevation in anti-dsDNA antibody production seen with age in ad libitum groups. Interestingly, effects of food restriction and fish oil on both lipid profile and autoantibody production were seen from a young age. Accumulation of leukocytes in the blood vessels and deposition of IgG in the glomerular mesangium also were suppressed by food restriction. Thus, beneficial effects of fish oil and food restriction on lupus nephritis and survival could be, at least in part, due to their selective effect on atherogenic risk factors.
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PMID:Food restriction and fish oil suppress atherogenic risk factors in lupus-prone (NZB x NZW) F1 mice. 1264 57

Atorvastatin and other members of the statin family are widely used for the treatment of hypercholesterolaemia in order to reduce the risk of atherosclerosis and cardiovascular disease. Atorvastatin-induced adverse events are mostly mild and only a few cases of lupus-like syndrome or severe acute hepatitis have been documented. In this case report we describe a patient who developed an atorvastatin-induced severe autoimmune hepatitis. In addition, this patient presented with a concomitant systemic lupus-like syndrome which has been already described for statins but not in association with severe liver disease. Although the drug was immediately withdrawn the disease persisted and even deteriorated to a fulminant disease with evidence of acute hepatic failure. The patient failed to respond to conventional immunosuppression with corticosteroids and azathioprine. Only the introduction of intense immunosuppressive therapy, as used in solid organ transplantation, led to a complete and sustained recovery of the patient. Interestingly, the patient was HLA DR3- and HLA DR4-positive, which are well-known genetic factors associated with autoimmune diseases. This case is the first report of a drug-induced lupus-likesyndrome concomitant with a severe autoimmune hepatitis in a genetically predisposed patient.
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PMID:Drug-induced lupus-like syndrome associated with severe autoimmune hepatitis. 1276 6

Atherosclerosis is the major cause of cardiovascular disease (CVD) and in addition to established risk factors as smoking, hypertension, diabetes and dyslipidemia, inflammation and autoimmune reactions have been much discussed recently. Several lines of evidence indicate that also inflammation and autoimmune reactions are highly relevant in atherosclerosis and CVD. Inflammatory cells and cytokines are present in lesions, already at an early stage; animal experiments suggest that immune reactions, though not necessary for development of atherosclerosis, can modulate disease development and systemic inflammation is associated with an enhanced risk of CVD. The enhanced risk of CVD in a major autoimmune disease, systemic lupus erythematosus (SLE), is therefore highly relevant, and in addition to being an important clinical problem, SLE-related CVD could give insights into the nature of autoimmunity in atherosclerosis and CVD in general. We recently defined traditional and non-traditional risk factors for CVD in SLE. These include increased atherosclerosis (as determined by intima-media thickness of carotid artery); raised oxidized low density lipoprotein (OxLDL) and autoantibodies to OxLDL; dyslipidemia with raised triglycerides and Lp(a) and decreased HDL-cholesterol concentrations; raised systemic inflammation; presence of anti-phospholipid antibodies including lupus anticoagulant, homocysteine-levels and more frequent osteoporosis. Disease duration, smoking, blood pressure or diabetes mellitus did not differ significantly between the groups. Taken together, immune reactions are highly relevant in atherosclerosis, and patients with autoimmune disease like SLE are at high-risk of CVD. If confirmed prospectively, non-traditional risk factors like OxLDL in the circulation, autoantibodies against OxLDL and phospholipids and inflammation could lead to new therapeutic strategies and insight into disease mechanisms.
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PMID:Autoimmunity, oxidized LDL and cardiovascular disease. 1284 1

Systemic Lupus Erythematosus (SLE) is an autoimmune disorder affecting multiple organ systems. Treatment of the disease has contributed dramatically in the long-term survival of the patients and now SLE has become a chronic inflammatory disorder. Present data suggest 5, 10 and 20-year survival rates of 93%, 85% and 68% respectively. Accelerated atherosclerosis and early coronary artery disease have become important causes of death and hospitalisation in SLE patients. Many cardiovascular risk factors can be considered: disease activity (particularly kidney involvement), sedentary life (in nearly 70% of the patients), hyperlipidemia, antiphospholipid antibodies, serum homocysteine and many others. Although traditional risk factors are operative in patients with SLE, the risk for myocardial infarction was increased 8.3 folds after controlling these factors in a study, suggesting that SLE itself was the strongest risk factor for cardiovascular disease. Lipid abnormalities may play a major role in increasing cardiovascular risk in SLE patients who are characterized by elevated triglycerides, very low-density lipoprotein cholesterol (VLDL-C), reduced levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (Apo) A-1. Anticardioli-pin antibodies may influence lipid levels in SLE; in particular SLE patients with IgG anticardiolipin antibodies had significantly lower HDL-C compared with patients with no anticardiolipin antibodies. Elevation of serum homocysteine is observed in 15% of SLE patients and is significantly associated with the development of stroke and arterial thrombotic events. The antiphospholipid syndrome (APS) is an acquired thrombotic disorder characterised by recurrent venous or arterial thrombosis or recurrent miscarriages, or both, associated with the presence in the serum of IgG or IgM anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LAC). APS may occur as a primary disorder (PAPS) or associated with connective tissue diseases, mainly systemic lupus erythematosus (secondary APS). Primary and secondary APS are both associated with a significant increase of cardiovascular risk.
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PMID:[Cardiovascular risk factors in systemic lupus erythematosus and in antiphospholipid syndrome]. 1285 54

Systemic lupus erythematosus (SLE) is a multifactorial polysystemic autoimmune disorder. Although life expectance in SLE has been improved by adequate immune suppressive therapy, the importance of chronic renal failure has not been reduced. Among late complications of the disease accelerated atherosclerosis attempts increasing attention. Dyslipoproteinemia and increased concentration of lipoproteins are important risk factors of atherosclerotic cardiovascular complication in SLE. Serum lipid parameters of 50 patients with lupus were examined in the present work. Thirty patients had histologically proven lupus nephritis (LN+), while the other group did not have renal involvement (LN-). Serum triglyceride, total cholesterol, LDL-C and apolipoprotein B (apoB) concentrations were significantly higher in the lupus nephritis (LN+) group. On the other hand, HDL-C and apoAI levels were also elevated in patients with LN. As a consequence of that, LDL-C/HDL-C and the apoB/apoAI ratios did not differ between patients with or without kidney involvement. This concluded the authors to measure the concentration of lipoprotein (a) in SLE patients, as Lp(a) is known to be an independent risk factor of atherosclerosis. Results indicated a significantly increased Lp(a) concentration in patients with lupus nephritis as compared to the LN- group. All but 2 patients without kidney involvement had lower than 100 mg/L Lp(a) concentration, while 27% of patients with lupus nephritis has an Lp(a) level between 100-300 mg/L. Further more, Lp(a) concentration was higher than 300 mg/L in 13% of the LN+ group. In a good correlation of these observations patients with nephritis suffered more frequently from deep venous thrombosis and ischaemic heart disease. The frequencies of hypertension and non-insulin dependent diabetes mellitus were slightly elevated in patients with nephritis. Present results suggest the importance of elevated lipoprotein (a) concentration in patients with lupus nephritis, further increasing the risk of athero-thrombotic cardiovascular complications.
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PMID:[Lipid profile in patients with systemic lupus erythematosus, with special focus on lipoprotein(a) in lupus nephritis]. 1502 32


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