Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main goal of therapy for lupus nephritis is to achieve remission, as this has a major impact on patient and renal survival. Furthermore, early treatment success has been shown to improve long-term prognosis. This has traditionally been achieved with intravenous cyclophosphamide, but recent data show that mycophenolate mofetil is equally effective and causes fewer adverse effects. Research is ongoing to find new treatment targets. Possible future therapies include monoclonal antibodies against CD20 (rituximab), CD22 (epratuzumab) and CD40, and therapies targeted at cytokine secretion, immunoglobulin secretion, B-cell maturation and T-cell proliferation and differentiation. Rituximab has shown promise in patients with active proliferative lupus nephritis, which suggests that B-cell depletion may be successful. Anti-double-stranded DNA antibodies correlate with flares of lupus nephritis and may represent another therapeutic target. Therapy with LIP 394, which crosslinks anti-double-stranded DNA antibodies in solution or on the B-cell surface, has been shown to reduce flares. Cardiovascular disease is a major cause of mortality in systemic lupus erythematosus, and this must also be addressed if long-term outcomes are to be improved. Many patients with systemic lupus erythematosus have subclinical atherosclerosis quite early in the disease course, and the risk of coronary artery disease at any level of traditional cardiovascular risk factors is higher than in the general population. Specific lupus-associated risk factors include the inflammatory process itself and anticardiolipin antibodies. Possible strategies to reduce the risk include reduction of disease activity to improve endothelial function and reduction of steroid dose whenever possible. Therapy with aspirin or statins may be another possibility. Thus treatment of lupus nephritis is evolving from standardised therapy to individualised therapy based on analysis of organ involvement, risk factors and cytokine, antibody or cell profiles.
Lupus 2007
PMID:Exploring new territory: the move towards individualised treatment. 1743 12

The incidence of cardiovascular disease is significantly increased in the two common autoimmune disorders Systemic Lupus Erythematous (SLE) and Rheumatoid Arthritis (RA). Cardiovascular mortality is a major cause of death in these patients. This has been linked to acceleration of the atherosclerotic process in these disorders. Traditional cardiovascular risk factors alone cannot fully explain the accelerated atherogenesis in these disorders. In addition to the systemic inflammation, additional mechanisms have been put forward that are more specific for the pathophysiology of these autoimmune chronic inflammatory disorders. Further, longitudinal studies are required to define optimal preventive strategies for cardiovascular comorbidity in SLE and RA.
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PMID:Cardiovascular events in systemic lupus erythematosus and rheumatoid arthritis : emerging concepts, early diagnosis and management. 1744 42

The Strategic Research Institute (SRi) hosted the 11th International Inflammation and Immune Diseases Drug Discovery and Development World Summit in San Francisco during 12-13 March 2007. The summit comprised keynote sessions and two parallel tracks and focussed on targeting mechanisms for drug discovery and development, which modulate the immune response and which have anti-inflammatory activity in a number of human diseases. Indications included psoriasis, hepatitis C, allergic dermatitis, systemic lupus erythematosus, rheumatoid arthritis and osteoarthritis, multiple sclnerosis, cardiovascular disease and asthma. Data were presented supporting all stages of drug discovery from target identification and validation through to lead identification and optimisation to both early- and late-stage clinical development.
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PMID:11th annual Inflammatory and Immune Diseases Drug Discovery and Development Summit 12-13 March 2007, San Francisco, USA. 1750 2

With improved therapeutic advances in the care of systemic lupus erythematosus patients, cardiovascular disease has emerged as a leading cause of death. Premature atherosclerosis in lupus patients is probably an interaction between traditional cardiovascular risk factors, inflammatory factors, and factors related to lupus itself. Despite knowledge of this accelerated cardiac risk, evaluation of traditional risk factors has been sub-par. We propose that lupus patients be evaluated by preventive cardiologists and have access to their expertise and resources. In addition to nephrologists and dermatologists, preventive cardiologists should be an integral part of the care of patients with lupus.
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PMID:The role of preventive cardiology in systemic lupus erythematosus. 1750 42

Antiphospholipid syndrome (APS) is a systemic autoimmune disease associated with arterial and venous thrombotic events and recurrent fetal loss. Cardiac manifestations in APS primarily include accelerated atherosclerosis leading to cardiovascular disease. There is increased cardiovascular mortality in APS. Cardiovascular risk is even higher in secondary APS in lupus patients. Several traditional and disease-related, autoimmune-inflammatory risk factors are involved in APS-associated atherosclerosis and its clinical manifestations. Antiphospholipid antibodies (APA), lupus anticoagulant, anti-oxLDL and other antibodies have been implicated in vascular events underlying APS. The primary and secondary prevention of atherosclerosis and CAD in these diseases includes drug treatment, such as the use of statins and aspirin, as well as lifestyle modifications. Apart from atherosclerosis and CVD, other cardiac manifestations may also be present in these patients. Among these conditions, valvular disease including thickening and vegetations is the most common. APA are involved in the pathogenesis of Libman-Sacks endocarditis usually associated with SLE. In addition, ventricular dysfunction, intracardiac thrombi and myxomas, pulmonary hypertension may also exist in APS patients. Early diagnosis of APS, thorough examination of the heart, control of traditional risk factors by lifestyle modifications and pharmacotherapy, probably anti-inflammatory treatment, and close follow-up of APS patients may help to minimize cardiovascular risk in these individuals.
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PMID:Cardiac manifestations in antiphospholipid syndrome. 1753 84

The indications for hormone replacement therapy (HRT) in postmenopausal women is the treatment of climacteric symptoms and the prevention of osteoporosis. Women with systemic lupus erythematosus (SLE) are more likely to have a premature menopause, osteoporosis and cardiovascular disease. HRT can induce SLE flares and cardiovascular or venous thromboembolic events. Therefore it should not be used in women with active disease or those with antiphospholipid (aPL) antibodies. In general, it should be used only for patients without active disease, a history of thrombosis or aPL antibodies. Non-oral administration of estrogen is recommended because of its lesser effect on coagulation. With regard to the progestogen, progesterone or pregnane derivatives are preferred. Otherwise, non-estrogen-based strategies should be used.
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PMID:Systemic lupus erythematosus and hormone replacement therapy. 1754 Jan 36

The recognition that inflammation is a hallmark of atherosclerotic disease and its complications has led to a series of studies reporting high prevalence of atherosclerosis in chronic inflammatory diseases. Indeed, chronic immune diseases, such as systemic lupus erythematosus and rheumatoid arthritis, are associated with proinflammation, accelerated atherosclerosis and increased incidence of cardiovascular disease. Since the susceptibility towards cardiovascular events cannot be explained by classical risk factors, disease-specific pathways have been put forward as additional risk factors, potentially important for future prevention and treatment of atherosclerosis associated with chronic inflammatory diseases.
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PMID:[Atherosclerosis in inflammatory diseases]. 1756 84

Several chronic inflammatory disorders, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and chronic infections that are associated with a chronic inflammatory state, such as human immunodeficiency virus (HIV) infection, are associated with an increased incidence of cardiovascular disease (CVD). Cardiovascular mortality is a major cause of death in patients with these disorders. Direct effects and indirect sequelae of systemic inflammation promote atherothrombotic vascular disease. Pathophysiological processes promoting atherogenesis can initiate years before the diagnosis of a chronic inflammatory disease is made, and since exposure to risk factors in this pre-clinical phase is widespread, early cardiovascular protection in these patients seems warranted.
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PMID:Systemic inflammation as a risk factor for atherothrombosis. 1770 69

Epidemiologic data indicate a large increase in cardiovascular risk in patients with systemic lupus erythematosus (SLE). Non-invasive investigations show increases in intima-media thickness, carotid plaque, and coronary artery calcifications in patients with SLE, compared to controls. Conventional cardiovascular risk factors may fail to fully explain the high cardiovascular risk in SLE patients. Immunological disturbances and inflammation may indirectly contribute to the risk of cardiovascular disease by inducing dyslipidemia and/or insulin resistance. The potential role for glucocorticoid therapy is controversial. Effective control of the disease would be expected to decrease the cardiovascular morbidity and mortality rates. Careful attention should be given to controlling conventional risk factors such as obesity, smoking, and physical inactivity. Hypertension and/or dyslipidemia should be treated optimally. The appropriateness of antiplatelet therapy should be assessed.
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PMID:Atheroma and systemic lupus erythematosus. 1786 65

During recent years it has become evident that atherosclerosis is an inflammatory disease. Furthermore, immune reactions and especially autoimmunity, were demonstrated to modulate atherosclerosis in animal experiments. An interesting example of how autoimmune reactions can influence atherosclerosis and consequences thereafter, is systemic lupus erythematosus (SLE)-associated cardiovascular disease (CVD). Antithrombotic effect exerted by Annexin A5 (ANXA5) is thought to be mediated mainly by forming a mechanical shield over phospholipids (PLs) reducing availability of PLs for coagulation reactions. However, more specific properties of ANXA5 might be of importance for its antithrombotic function. Such examples include downregulation of surface-expressed tissue factor (TF), as well as upregulation of urokinase-type plasminogen activator (uPA) by ANXA5. Also, interaction of ANXA5 with ligands involved in hemostasis, such as sulfatide and heparin, has been demonstrated. We have recently described a novel mechanism potentially contributing to atherothrombosis in SLE, with ANXA5 binding to endothelium decreased in SLE, an effect caused by antiphospholipid antibodies (aPL). It may be hypothesized that ANXA5 can be effective as a treatment to prevent plaque rupture and atherothrombosis not only in SLE, but also in the general population prone to CVD. Antiatherothrombotic potential of ANXA5 deserves further attention and careful studies as the mechanism behind the majority of clinically significant cardiovascular ischemic disease is atherothrombosis, formed on an underlying vulnerable atherosclerotic lesion. It may be hypothesized that ANXA5 can be effective as a treatment to prevent plaque rupture and atherothrombosis not only in SLE, but also in a general population prone to CVD.
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PMID:Annexin A5 as a novel player in prevention of atherothrombosis in SLE and in the general population. 1789 75


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