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)

Brain magnetic resonance imaging (MRI) was performed in 21 patients with systemic lupus erythematosus (SLE) with and without lupus anticoagulant (LAC), one lupus-like patient and 5 patients with primary antiphospholipid antibody syndrome. Thirteen patients had white matter focal brain lesions on MRI, 10 of whom had LAC (p = 0.03). We found no correlation between these lesions and neurologic manifestations, nor any clinical or serologic indices of activity of SLE. Our MRI lesions were similar to those described in multiple sclerosis and may indicate a similar pathologic process.
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PMID:Lupus anticoagulant: correlation with magnetic resonance imaging of brain lesions. 159 77

Arterial thrombosis is one of the major symptoms of antiphospholipid syndrome (APS). However, thrombosis in a primary branch of the aorta has rarely been reported in APS. We report here a case of APS complicated by thromboses in both the left subclavian artery and the left external iliac vein. A 32-year-old woman was admitted in May, 1990 complaining of no pulse in the left superficial arteries (e.g., left radial artery) for the past 5 years and acute swelling of the left lower extremity. A left ascending phlebography showed an occlusion of the external iliac vein and arteriography revealed obstruction in the left subclavian artery. Collateral circulations were developed at the site of each thrombus. Clotting and immunological studies revealed a prolonged APTT, a high titer of anticardiolipin antibody and lupus anticoagulant positive. We ruled out various diseases and clinical risk factors predisposing to both arterial and venous thromboses. Accordingly, we concluded that both thromboses were based on APS. Following treatment with anticoagulants, aspirin and corticosteroid, the swelling of her left thigh was diminished and the antibody titer was decreased within 3 months.
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PMID:[A case of antiphospholipid syndrome associated with left subclavian artery thrombosis and left external iliac vein thrombosis]. 159 8

The significance of anti-cardiolipin antibodies (ACLA) in patients with a range of autoimmune and infective disorders was investigated in this study. Although lower levels of IgG and IgM ACLA were present in 77 of 400 patients' sera (19%), high antibody levels were found in less than 5% of patients. These latter patients belonged to three clinical categories: patients with connective tissue disease (CTD), infectious mononucleosis or biological false positive serology. An assay was developed to measure lupus anticoagulant (LA) activity in serum: significant LA activity was found in the CTD patients alone (in 6 of 15 tested) and all of these had high titre ACLA. Features of the antiphospholipid syndrome (APS) were present in these six patients but also in three additional CTD patients with normal LA results and high levels of ACLA. In two CTD patients with APS features, the high ACLA were of IgM isotype. These results stress the importance of measuring both ACLA and LA in an investigation of the APS: a high positive ACLA supports the diagnosis of APS, particularly in patients with autoimmune disease, whilst a high positive ACLA in association with LA activity is specific for this syndrome.
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PMID:Selection of patients with the antiphospholipid syndrome by serological measurement of lupus anticoagulant activity in conjunction with anticardiolipin antibodies. 160 Jun 90

Ten percent of 667 consecutive systemic lupus erythematosus (SLE) patients were considered to have definite antiphospholipid syndrome (aPLS) because they had two or more antiphospholipid (aPL)-related clinical manifestations and aPL titers more than 5 SD above the mean of normal controls. Another 14% had either one aPL-related manifestation but high titers of the antibody or two manifestations and low aPL titers (probable aPLS). One fourth of the patients had no manifestations but high titers, one manifestation and low titers, or two or more manifestations and negative aPL titers ("doubtful" aPLS); the other half were considered negative for aPLS. In patients with high-titer aPL, the number of aPL-related manifestations was influenced by disease duration and number of pregnancies, indicating potential mobility of category with time or with risk of recurrent pregnancy loss. Patients with two or more manifestations but variable aPL levels differed in immunosuppressive treatment and in the number of times they had been tested, indicating potential mobility of category with lower treatment and/or further aPL testing. Patients with definite aPLS had increased risk of cutaneous vasculitis, peripheral neuropathy, seizures, psychosis, transient ischemic attacks, and leukopenia. In 11 of 52 SLE patients with definite aPLS the initial manifestation was related to aPL, and in 16 it concurred with an unrelated one. Only two patients fulfilled criteria for aPLS before having other evidence of SLE. The authors conclude that aPLS occurring within SLE is part of the disease rather than an associated condition and propose the use of definite and probable classification categories. These criteria, with appropriate follow-up and clinical and serological exclusion clauses for potential primary conditions, could also be applied to primary aPLS.
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PMID:Preliminary classification criteria for the antiphospholipid syndrome within systemic lupus erythematosus. 160 24

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
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PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84

Sneddon syndrome is know as the association of idiopathic livedo reticularis and cerebrovascular lesions. The most characteristic trait of this syndromes is a non-inflammatory arteriopathy in medium caliber vessels. The pathogenic role of antiphospholipid antibodies in this disease is not clear. Clinical characteristics and etiopathogenic features of eight patients with Sneddon's syndrome are reviewed, specially regarding its relationship with primary antiphospholipid syndrome. A female predominance was found (3:1) as well as a relationship with hypertension (five patients suffered hypertension), but no relation was found with contraceptive use. Three patients showed evidence of antiphospholipid antibodies, present as anticardiolipin antibodies with significative titers in three cases and lupus anticoagulant in one. Digital artery biopsy performed in four patients showed in all of them the pathologic features characteristic of this disease. Seven patients were treated with platelet activity inhibitors and one with oral anticoagulants. Six of them have had a year and half follow-up without showing any new ischemic stroke. The main etiopathogenic factor on Sneddon's syndrome is the presence of a non-inflammatory arteriopathy in medium caliber vessels. Blood hypertension and antiphospholipid antibodies could play a role in the development of cerebrovascular lesions in some cases. No relationship has been found with oral contraceptives in this series of patients. Medium term prognosis with platelet activity inhibitors therapy seems benign.
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PMID:[Sneddon's syndrome: its clinical characteristics and etiopathogenic factors]. 846 57

NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (beta 2-glycoprotein I (beta 2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse beta 2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified beta 2-GPI, aCL from the W/B F1 mice recognized the complex of CL and beta 2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.
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PMID:Anticardiolipin antibodies in NZW x BXSB F1 mice. A model of antiphospholipid syndrome. 163 62

Anticardiolipin antibodies (ACA) frequently appear in patients with autoimmune disorders such as systemic lupus erythematosus, and have also been detected in infections, neoplasia, the primary antiphospholipid syndrome, in association with certain medications and also in those patients without apparent disease. Recently, anticardiolipin antibodies were described in connection with acquired immunodeficiency syndrome (AIDS). 84 human immunodeficiency virus (HIV)-infected patients were examined in order to assess the influence of risk factors for HIV infection and of the stage of HIV-1 infection on the prevalence of IgG-ACA in HIV-seropositive patients. 2 groups were created -- 1 composed of 38 asymptomatic HIV-infected individuals and the other of 46 AIDS patients. A control group of 42 healthy HIV-negative blood donors was also studied. All those in the control group were IgG-ACA-negative. Of the 84 HIV-positive patients, 50 were IgG-ACA positive (59.5%) and 34 IgG-ACA-negative (40.5%). None of the HIV-positive individuals presented any thromboembolic phenomena. There were no significant differences with respect to sex, risk factors, and stage of disease when the presence of IgG-ACA in HIV-positive patients was ascertained. ACA does not appear to be a prognostic marker in HIV-1 infected patients; the presence of IgG-ACA is probably related to HIV-1 infection itself and is indicative of impaired humoral immunity in this group. (author's modified)
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PMID:Anticardiolipin antibodies and acquired immunodeficiency syndrome: prognostic marker or association with HIV infection? 164 88

Since thrombomodulin (TM) is a specific cell surface glycoprotein for vascular endothelial cells, serum TM (s-TM) might be a useful marker of endothelial cell damage. Antiphospholipid antibodies (aPL) frequently detected in systemic lupus erythematosus (SLE) have been associated with vascular occlusive diseases. Therefore we measured the s-TM in 60 patients with SLE, in 23 patients with other diseases including aPL (disease control group) and in 26 healthy subjects, by means of an enzyme immunoassay using monoclonal antibodies to human TM. A significant positive correlation was found between s-TM and serum creatinine levels in SLE patients (r = 0.813, p less than 0.001). When the s-TM level was divided by the serum creatinine level (TM/Cr) to exclude the effect of renal clearance, the TM/Cr ratios were significantly increased in SLE patients with active lupus nephritis (LN) compared to those without LN (p less than 0.05). The ratios did not correlate with the presence of aPL or antiphospholipid antibody syndrome (APLS) in SLE patients or in the disease control group, although a weak correlation between the TM/Cr ratios and IgG-anticardiolipin antibody titers was found in the SLE patients without LN (r = 0.449, p less than 0.01). The present results suggest that elevated TM/Cr ratios reflect renal and possibly extra-renal endothelial cell damage in SLE patients with active LN, but that s-TM levels do not associate with the presence of aPL or a history of APLS.
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PMID:Serum thrombomodulin and anticardiolipin antibodies in patients with systemic lupus erythematosus. 165 8

Twenty-three patients with the 'primary' antiphospholipid syndrome were studied over 2-6 years. Twenty-two (96%) had antiphospholipid antibodies detected by ELISA (87% had antibodies to thromboplastin and 70% to cardiolipin), and 18 out of the 21 tested patients (86%) had lupus anticoagulant activity by coagulative assays. Mean age of the cohort was 29.9 years and the sex ratio (female:male) 4.75:1. Eleven patients presented 18 venous and/or arterial thrombosis and 13 had 25 foetal losses (84% occurred during the second and third trimester). Other clinical features were migraine, livedo reticularis, and epilepsy. Three patients had relatives with systemic lupus erythematosus. Thrombocytopaenia was seen in 33%, antinuclear antibodies in low or moderate titre in 30%, and haemolytic anaemia in 13%. During the follow-up, two patients presented recurrent thrombosis despite anticoagulant therapy, one of them dying because of recurrent pulmonary thromboembolism. Four patients achieved successful term pregnancies after treatment with aspirin and a further patient after treatment with aspirin and low dose prednisolone. No patient developed systemic lupus erythematosus or any other definable connective tissue disease. The 'primary' antiphospholipid syndrome may exist as a distinct clinical entity and all younger patients presenting with thrombotic events, foetal losses and/or thrombocytopaenia, without any evidence of a well defined disease, should be tested for antiphospholipid antibodies in order to rule out this syndrome.
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PMID:The 'primary' antiphospholipid syndrome: antiphospholipid antibody pattern and clinical features of a series of 23 patients. 166 49


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