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)

Anti-pyruvate dehydrogenase (PDH) antibodies were determined in 1451 sera of patients with primary biliary cirrhosis (PBC) and several autoimmune rheumatic conditions by ELISA and immunoblotting. They were detected in sera of 93% of the patients with PBC (179 of 192 patients) in 60 of 277 (22%) patients with Sjogren's syndrome (SjS), 34 of 437 (8%) patients with scleroderma, 33 of 191 patients with SLE (17%), and 5 of 55 (10%) patients with rheumatoid arthritis (RA) but in none of the patients with polymyositis or the antiphospholipid syndrome. The ELISA studies were confirmed by immunoblots showing binding of autoimmune rheumatic sera to the same epitope (74 kd) of mitochondria that the PBC sera reacted with. The identical binding characteristics were also confirmed by protein competition assays with purified PDH. In 4 of 53 patients with SjS who were positive for anti-PDH, high titers as in PBC were detected. The anti-PDH antibodies in Sjogren's patients were associated with deranged liver function tests and extraglandular features but did not correlate with any other non-organ-specific antibody. Follow-up studies confirmed the association of the emergence of anti-PDH antibodies with defects in liver function tests. The antibodies were more prevalent in SLE and RA when they were associated with Sjogren's syndrome (30 and 18.8%, respectively). Among patients with different forms of scleroderma, anti-PDH antibodies were noted in subjects with systemic sclerosis, morphea, and Raynaud's phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antimitochondrial (pyruvate dehydrogenase) autoantibodies in autoimmune rheumatic diseases. 140 Sep 1

Our objective was to define the renal involvement in primary antiphospholipid syndrome (APS). We studied 20 patients with primary APS. Fourteen were women, mean age 34.4 years. None met ARA criteria for systemic lupus erythematosus. All patients underwent complete renal function studies. The presence of hypertension was also investigated. Renal disease was found in 5 patients, and was characterized by proteinuria, hypertension and renal failure. Kidney biopsy was performed in these 5 patients, showing thromboses of the microvasculature, mesangiolysis, mesangial interposition, electron lucent subendothelial material and ischemic obsolescence of glomeruli. Arterioles showed luminal narrowing due to medial hypertrophy, mucoid thickening of the intima, thrombosis and fibrosis. We found renal disease in 25% of our patients with primary APS. Biopsy findings were consistent with a thrombotic microangiopathy involving both arterioles and glomerular capillaries.
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PMID:Renal involvement in primary antiphospholipid syndrome. 815 77

A 57-year-old man with no evidence of infection, vasculitis or connective tissue disease died with multiple organ thromboses after an acute illness. He was found to have lupus anticoagulant, IgG anticardiolipin antibody, false positive rapid plasma reagin, prolonged partial thromboplastin time, and thrombocytopenia. Venous and arterial thrombi leading to necrosis were found in his scrotum, testicles, upper and lower extremities, adrenals, kidneys, lungs, and brain. No other explanation could be found for his fatal illness, thus suggesting the primary antiphospholipid syndrome (APS). This is a documented case of primary APS associated with multiorgan arterial and venous thromboses of large and small vessels, presenting as a fulminant and fatal acute illness.
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PMID:Primary antiphospholipid syndrome with multiorgan arterial and venous thromboses. 140 68

A wide spectrum of cardiac involvement including valvular lesions, myocardial infarction and myocardial dysfunction has been reported in patients with antiphospholipid antibodies (aPL), suggesting that cardiac manifestations may be part of the antiphospholipid syndrome (APS). We describe 3 patients (2 with primary APS and one with APS and SLE) who were found to have right atrial masses by echocardiography (transthoracic and/or transesophageal) and/or angiography, which were felt preoperatively to be atrial myxomata. Pathological examination of resected material showed only organized thrombus with calcification. We describe outcome 12 months to 7 years after resection of thrombus and document possible recurrence in one patient after 7 years. Intracardiac mural thrombus may be an additional cardiac manifestation of the APS, and presents considerable diagnostic confusion in its differentiation from atrial myxomata.
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PMID:Intracardiac mural thrombus mimicking atrial myxoma in the antiphospholipid syndrome. 140 69

We report a case of communicating hydrocephalus in a 24-year-old woman with previously undiagnosed systemic lupus erythematosus (SLE) presenting with malignant hypertension, nephritis, serositis, and a seizure disorder of 16 months' duration. The patient demonstrated features of the antiphospholipid antibody syndrome (APS). In proposing cerebral venous thrombosis as a possible, yet unproven, pathophysiologic mechanism for the hydrocephalus in this case we have reviewed and summarized literature relating to SLE, APS, hydrocephalus and pseudotumor cerebri. In cases of unexplained pseudotumor cerebri or hydrocephalus, a search for SLE and APS should be considered.
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PMID:Communicating hydrocephalus in systemic lupus erythematosus with antiphospholipid antibody syndrome. 140 70

In patients with systemic lupus erythematosus (SLE) heart valve lesions are usually discovered at echocardiography; their haemodynamic repercussions are uncommon, and valve replacement is exceptional. We report the case of a woman who had undergone aortic and mitral valve replacement before antiphospholipid antibodies were found associated with 4 ARA criteria of SLE. Histopathological examination confirmed the diagnosis of Libman-Sachs specific endocarditis. The presence of antiphospholipid antibodies leads to a discussion of their role in the physiopathology of the heart valve lesions and vascular accidents that occurred in this patient. The overlap observed between the diagnostic criteria of SLE and those of primary antiphospholipid syndrome is discussed. Heart valve lesions may be one of the modes of access to the antiphospholipid syndrome.
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PMID:[Double heart valve replacement disclosing antiphospholipid syndrome]. 141 Sep 6

Studies of renal involvement in systemic lupus erythematosus continue to dominate the clinical literature. Reports of the prognostic significance of both clinical and histologic parameters at the time of renal biopsy are discussed. The potential impact of anticardiolipin antibodies on the development of renal insufficiency is described. The outcome of renal transplantation in patients with systemic lupus erythematosus is assessed in a study concerned with both allograft survival and recurrence of active nephritis in the transplanted kidney. The incidence and prognosis of various features of neuropsychiatric systemic lupus erythematosus are discussed, while the search for an accurate indicator of lupus involvement of the central nervous system continues. Magnetic resonance imaging and single-photon-emission computed tomography are considered. Abnormalities of pulmonary gas exchange are featured in several reports. Features of the antiphospholipid antibody syndrome are presented, stressing predisposition to thrombosis. The definition and characteristics of systemic lupus erythematosus disease flares is discussed, in relation to several recently developed disease activity indexes. The attempt to distinguish systemic lupus erythematosus activity from infection and preeclampsia is also considered. Finally, the association of systemic lupus erythematosus with the development of cancer is discussed.
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PMID:Clinical manifestations of systemic lupus erythematosus, measures of disease activity, and long-term complications. 141 1

Antiphospholipid syndrome (APLS) is characterized by thrombocytopenia, thromboembolic phenomena and recurrent fetal loss, associated with anti-cardiolipin antibodies (ACA) and/or lupus anticoagulant. The syndrome may be primary or may be associated with other conditions such as systemic lupus erythematosus (SLE). In this study we induced primary APLS following immunization of BALB/c mice with a human monoclonal ACA (H-3). Analysis of the cytokine profile of the mice with experimental APLS indicated low production of IL-2, IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by concanavalin A (Con A)-stimulated splenocytes of H-3 immunized mice. It seems that the low levels of IL-3 and GM-CSF have a potential role in the fetal loss of the APLS. Whatever the mechanism of IL-3 and GM-CSF in preventing fetal loss, these results may have therapeutic bearing on the reproductive outcome in women and other species with APLS.
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PMID:The putative role of cytokines in the induction of primary anti-phospholipid syndrome in mice. 142 85

Antiphospholipid antibody syndromes are primarily manifested as unexplained thrombotic events. Several antiphospholipid antibodies have been identified, the lupus anticoagulant being the most recognized. Considerable confusion surrounds this "anticoagulant," which is highly correlated with an increased risk of thrombosis. Several assays have been designed for the detection of antiphospholipid antibodies. There are limitations on their efficacy and interpretation requires judgment. Treatment strategies for the clinical manifestations of the antiphospholipid antibody syndrome are being developed. The explosive rise in the volume of literature dedicated to this topic will assure new and improved modalities for evaluation and treatment.
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PMID:The lupus anticoagulant and antiphospholipid antibodies. 142 61

Lupus anticoagulants (LA) are acquired inhibitors of coagulation related to the antiphospholipid antibodies. Paradoxically, these anticoagulants do not expose patients to the risk of hemorrhage but, on the contrary, to a thrombotic risk. The association in a patient of an antiphospholipid antibody and a clinical manifestation (thrombosis or equivalent) defines the antiphospholipid syndrome. This syndrome is termed primary or secondary according to whether it appears as an isolated disorder or is associated with an identified disease, frequently autoimmune (systemic lupus erythematous or lupus related syndrome). Clinical complications of LA are arterial or venous thrombosis at various sites. They are frequently recurrent, and deep venous thrombosis of leg, oculo-cerebral ischemic lesions and heart valve complications have all been well documented. Thrombosis of the microcirculation can cause tissue or organ disfunction, the most characteristic effect being repeated abortions. Laboratory demonstration of LA is difficult when the inhibitor is weak, and this should be completed by tests for other antiphospholipid antibodies. Clinical studies are necessary to assess the thrombotic risk of the LA in different clinical conditions and to evaluate the need and type of antithrombotic treatment. The LA are heterogeneous and only a small proportion of patients with LA will develop thrombosis. New tests capable of predicting the thrombotic risk, bases on the physiopathological mechanisms with which LA interfere in vivo, are currently being investigated.
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PMID:[Circulating lupus coagulants. A paradox in vascular pathology]. 143 3


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