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)

Antiphospholipid antibodies (APA) are present in a variety of autoimmune disorders, including systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). Increasing evidence suggests that a subset of APA can also be detected in patients with atherosclerosis. In this review, we discuss the specificities of the autoantibodies that are present during both APS and atherosclerosis. A critical and unresolved question is whether these APA are specific for epitopes that result from lipid oxidation. Despite the fact that APA are present in patients with systemic autoimmunity and that they may participate in the pathogenesis of APS, recent studies have paradoxically proposed a beneficial role for some APA in atherosclerosis. We review the evidence that some APA specificities may be protective against plaque formation, and we discuss the putative mechanisms by which some APA could be useful in the prevention of atherosclerosis.
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PMID:Antiphospholipid antibodies and atherosclerosis. 1524 Jan 62

Lupus tumidus is a rare sub-type of chronic cutaneous lupus erythematosus characterized by dermal plaques in which excessive mucin accumulates early in disease process. We report a middle aged women having succulent, edematous and persistent plaque over her face for five years that was not responding to various empirical treatments offered to her. Finally, on clinico-pathological basis, it was diagnosed as a case of tumid lupus erythematosus (TLE) and she responded satisfactorily to the treatment regimen including oral steroids, chloroquine and application of sun screen.
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PMID:Lupus tumidus: a variant of cutaneous lupus erythematosus. 1553 Feb 78

Etanercept is a dimeric fusion protein that has been approved for the treatment of rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, active ankylosing spondylitis and moderate to severe plaque psoriasis. It has been reported to be useful in other variants of psoriasis, Still's disease, recurrent aphthous ulcers, and a variety of rare cutaneous conditions. Its cutaneous side effects are rare and include injection site reactions, cutaneous lupus, and cutaneous vasculitis. Its systemic side effects are also rare and include induction or worsening of infections, lupus, multiple sclerosis, and congestive heart failure. Linkage to an increased risk of lymphoma is unclear. In short, etanercept is a promising medication with substantial benefits and use will probably increase in the future. This review surveys off-label uses and side effects of etanercept.
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PMID:The medical uses and side effects of etanercept with a focus on cutaneous disease. 1562 48

There is limited knowledge of potential defects in arterial wall properties in female systemic lupus erythematosus (SLE) patients without manifest cardiovascular disease (CVD) and significant atherosclerotic lesions. The aim of the present study was to investigate the mechanical properties of larger vessels in these patients and to compare them with healthy controls. B-mode ultrasound was used to assess vessel wall structure and to exclude presence of plaque. The ankle/brachial pressure index was measured to exclude occlusive arterial disease. An ultrasound echo-tracking system was used to determine stiffness of the abdominal aorta, common carotid artery (CCA) and popliteal artery (PA) in 39 female patients with SLE and 55 female, healthy controls. SLE had an independent effect on stiffening of the CCA (P = 0.01) and PA (P = 0.005). In addition, larger vessel diameters were observed in the CCA (P = 0.002) after adjustments for the effects of mean arterial pressure and age. Thus, this investigation demonstrated an increased arterial stiffness and signs of premature vascular ageing in the SLE patients without manifest cardiovascular disease and without significant atherosclerotic lesions. The results of this study indicate that other mechanisms besides atherosclerosis might be involved in the pathogenesis of arterial stiffening in SLE patients.
Lupus 2004
PMID:Abnormal mechanical properties of larger arteries in postmenopausal women with systemic lupus erythematosus. 1564 46

The advances in the understanding of the pathogenesis of the autoimmune diseases have led to new treatment targets. Biological agents enhance or replace conventional immunosuppressive therapies in the treatment of autoimmune diseases. TNF-alpha has been validated as a good treatment target but the potential modalities also include the inhibition of the interaction between LFA-3 (lymphocyte function-associated antigen 3) and CD2, the blockade of the IL-1 receptors, the antibodies against the alpha4 integrins, the antibodies against B-cell CD20 and the inhibition of the activation of T-cells. The new treatments have had a major impact on inflammatory symptoms, the radiological damage and the anemia of chronic disease in rheumatoid arthritis and have substantially controlled the signs and symptoms in the spondylarthropathies group and plaque-type psoriasis. The efficacy of the biologic agents in systemic lupus erythematosus warrants further investigation but there have been some promising results in proliferative lupus nephritis. Several small studies have explored their use in the treatment of Sjogren's syndrome, adult onset Still's disease and several vasculitides but the results are still preliminary and warrant confirmation. The efficacy of the biological agents has been impressive. Susceptibility to infections has always been a major concern; a high level of suspicion is necessary and strategies should be implemented for the prevention, the rapid identification and pre-emptive therapy of such infections.
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PMID:Biological therapies of autoimmune diseases. 1572 Feb 35

Chronic inflammatory diseases are associated with premature atherosclerosis; however, it is unknown whether arterial stiffness is increased in this setting, possibly as a manifestation of vascular disease preceding and/or independent of atherosclerosis. Carotid ultrasonography and radial applanation tonometry were performed in 101 patients with systemic lupus erythematosus, 80 patients with rheumatoid arthritis, and 105 healthy control subjects. The 3 groups were comparable in age, gender, and carotid artery absolute and relative wall thickness. Atherosclerotic plaque was more common in lupus (46%) and rheumatoid arthritis (38%) patients than in controls (23%) (P<0.003). Although control subjects had higher central and peripheral blood pressures, arterial stiffness was increased in patient groups compared with controls (lupus, rheumatoid arthritis, controls, respectively: beta: 3.36 versus 3.22 versus 2.60, P<0.001; Young's modulus: 441 versus 452 versus 366 mm Hg/cm, P=0.004; Peterson's elastic modulus: 278 versus 273 versus 216 mm Hg, P<0.001) after adjustment for differences in mean brachial pressure. In multivariate analysis involving the entire population, arterial stiffness was independently related to age, serum glucose, and the presence of chronic inflammatory disease. In multivariate analysis restricted to the patients, arterial stiffness was independently related to age at diagnosis, disease duration, serum cholesterol, and C-reactive protein (and IL-6, when substituted for C-reactive protein). When analyses were repeated in the 186 study subjects without carotid plaque, arterial stiffness remained significantly elevated in patient groups after adjustment for differences in age and mean brachial pressure. In conclusion, arterial stiffness is increased in chronic inflammatory disorders independent of the presence of atherosclerosis and is related to disease duration, cholesterol, and the inflammatory mediator C-reactive protein and the cytokine that stimulates its production, IL-6.
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PMID:Arterial stiffness in chronic inflammatory diseases. 1591 40

A 14-year-old boy presented with a pink firm plaque with well-defined borders in the right infra-orbital skin area. On diascopy, the infiltrate exhibited a typical apple-jelly appearance. No acid-fast bacilli could be demonstrated. A polymerase chain reaction (PCR) assay did not reveal the presence of mycobacteria in a lesional biopsy sample. Culture of biopsied tissue on Loewenstein-Jensen medium was negative. Although the tuberculosis culture and PCR did not confirm tuberculosis, a diagnosis of lupus vulgaris was made considering the clinical and histopathological findings. After a 9-month antituberculous therapy, the lesion disappeared. We believe that a diagnosis of lupus vulgaris still depends more on clinical and histopathological findings than on tuberculosis culture or PCR.
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PMID:A case of lupus vulgaris successfully treated with antituberculous therapy despite negative PCR and culture. 1620 61

The role of the immune system in modulating atherosclerosis has recently been well documented. Studies have revealed that cellular and humoral immunity plays crucial roles in atherogenic plaque formation. This includes macrophages, CD4+ T cells and dendritic cells as well as autoantigens such as oxidized low density lipoprotein (oxLDL), heat shock proteins and beta2-glycoprotein I. Given these recent advances, various modifications of the immune system in experimental models have been proposed as therapeutic strategies, with the potential of inhibiting atherosclerosis progression. These modifications are switching the immune system (CD4+ T cells) from Th1 towards a Th2 anti-inflammatory cytokine secretion, and the induction of protective antibodies both of which may be induced by specific vaccination. Recent identification of specific immunoreactive antigenic epitopes on modified LDL, their successful implementation for immunization and the induction of atheroprotection, supports the idea that active vaccination may emerge as a novel immuno-modulating atheroprotective strategy.
Lupus 2005
PMID:Predictive and protective autoimmunity in cardiovascular diseases: is vaccination therapy a reality? 1621 63

Pericarditis is the most common cardiac abnormality in systemic lupus erythematosus (SLE) patients, but lesions of the valves, myocardium and coronary vessels may all occur. In the past, cardiac manifestations were severe and life threatening, often leading to death. Therefore, they were frequently found in post-mortem examinations. Nowadays cardiac manifestations are often mild and asymptomatic. However, they can be frequently recognized by echocardiography and other noninvasive tests. Echocardiography is a sensitive and specific technique in detecting cardiac abnormalities, particularly mild pericarditis, valvular lesions and myocardial dysfunction. Therefore, echocardiography should be performed periodically in SLE patients. Vascular occlusion, including coronary arteries, may develop due to vasculitis, premature atherosclerosis or antiphospholipid antibodies associated with SLE. Premature atherosclerosis is the most frequent cause of coronary artery disease (CAD) in SLE patients. Efforts should be made to control traditional risk factors as well as all other factors which could contribute to atherosclerotic plaque development.
Lupus 2005
PMID:Cardiac involvement in systemic lupus erythematosus. 1621 67

Recent findings suggest that inflammation plays a key role in atherosclerosis from the earliest stage of lesion initiation, to the ultimate complication of thrombosis. In patients who died because of acute coronary syndromes (ACS), coronary atherosclerotic plaques are characterized by the presence of macrophages, and to a lesser extent T-lymphocytes, at the immediate site of either plaque rupture or superficial erosion. The rupture-related inflammatory cells are activated, indicating ongoing inflammation. ACS patients are also characterized by activated circulating lymphocytes, monocytes and neutrophils, and by increased concentrations of proinflammatory cytokines and of the highly sensitive acute phase reactant C-reactive protein. Interestingly, an unusual subset of T cells, CD4+ CD28null T cells, involved in vascular complication of rheumatoid arthritis because of their functional profile predisposing for vascular injury, are expanded in the peripheral blood and infiltrate the coronary lesions of ACS patients. The presence of activated T lymphocytes implies antigenic stimulation, but the nature of such antigen(s) remains to be investigated. Several autoantigens expressed in the atherosclerotic plaque, including oxidized LDL and heat shock proteins, and infectious agents are able to elicit an immune response. The inflammatory component is not localized to the 'culprit' plaque, but it is diffused to the entire coronary vascular bed, and involves also the myocardium.
Lupus 2005
PMID:T cells and cytokines in atherogenesis. 1621 77


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