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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared the concordance and predictive powers of activated partial thromboplastin time (APTT) and of IgG and IgM antibody to cardiolipin (aCL), for predicting fetal death in 50 pregnant women with systemic lupus erythematosus (SLE) and/or lupus anticoagulant. Overall concordance of any abnormal determination of aCL during pregnancy with any abnormal determination of APTT was 76% (0.05 less than p less than 0.10). Fetal death occurred in 6/12 (50%) of patients with high APTT compared to 5/20 (16%) of patients with low APTT; fetal death occurred in 10/13 (77%) of patients with abnormal aCL and in 2/37 (5%) of patients with normal aCL. Sensitivity for predicting fetal death was .55 for APTT and .85 for aCL; specificity was .81 for APTT and .92 for aCL. Abnormalities of APTT and aCL are sufficiently frequently discordant to prevent equation of the 2 assays. ACL is the better assay for predicting fetal death.
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PMID:Antibody to cardiolipin, lupus anticoagulant, and fetal death. 311 Apr 18

Up to 44% of patients with systemic lupus erythematosus have antiphospholipid antibodies, which in some patients have been associated with thrombocytopenia, in vitro coagulation abnormalities, and a thrombotic tendency. Patients with lupus nephritis who reach end-stage renal disease may continue to have anticardiolipin antibodies (ACL-Ab) at the time of renal transplantation despite a lack of clinical or serologic activity of systemic lupus. The risk of thrombotic and other complications has not been previously reported in these patients. To evaluate the effect of ACL-Ab on the course of renal transplantation, the clinical course of eight ACL-Ab-positive lupus patients transplanted in the period from January 1990 to June 1992 were compared with five ACL-Ab-negative lupus patients transplanted during the same period. All patients had lupus nephritis as the cause of renal failure. There were four thrombotic episodes in the patients who were ACL-Ab-positive but none in the control group. Neither of the two groups differed in the number of rejection episodes, the rate of graft loss, or renal function at last follow-up. Patients with systemic lupus erythematosus who are ACL-Ab-positive can be successfully transplanted. However, these patients require attention to possible thrombotic events with a potential role for prophylactic anticoagulation.
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PMID:Renal transplantation in anticardiolipin antibody-positive lupus erythematosus patients. 831 Oct 89

Antiphospholipid antibodies (APL) are associated with venous and arterial thrombosis in SLE patients. Various thrombotic and non-thrombotic neurological manifestations have been reported in SLE but whether or not they are related to the presence of APL antibodies remains uncertain. To assess the possible association between neurological involvement in SLE and APL antibodies, IgG anticardiolipin antibodies (IgG ACL) were looked for using an ELISA technique in 92 consecutive SLE patients seen over a one-year period. Other APL determinations included VDRL and lupus anticoagulant (LAC) testing using APTT and the diluted thromboplastin time. Twenty-four SLE patients presented with neurological manifestations (40 episodes): 15/24 (62.5%) were found positive for APL antibodies (11 VDRL, 8 LAC, 7 ACL antibodies) versus 22/68 patients (32%) without neurological symptoms (p < 0.01). APL antibodies antedated neurological symptoms in 13/16 cases. Neurological manifestations were subsequently divided into 3 groups: thrombotic (n = 14), psychosis and convulsions (n = 15), miscellaneous (n = 10). No correlation was found between APL antibodies and any of the 3 subgroups. Among patients with neurological SLE, APL antibodies were present in two with valvular heart disease, as well as in seven with a history of either deep vein thrombosis, livedo reticularis or miscarriage. Among 7 patients with thrombocytopenia and neurological symptoms, 6 had APL antibodies. These data suggest that APL syndrome is associated with neuro-ophthalmological manifestations of SLE regardless of whether or not the mechanism of neurological involvement is thrombotic. SLE patients with APL antibodies may be at risk for future neurological manifestations. However, it is still questionable that APL positivity has definite therapeutic consequences.
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PMID:Neurological manifestations of systemic lupus erythematosus: role of antiphospholipid antibodies. 840 81

We describe the design of a quantitative test for lupus anticoagulants (LA), based on the Activated Partial Thromboplastin Time (APTT) and the Russell Viper Venom Time (RVVT). In this assay system, test plasmas mixed 1:1 with a pooled normal plasma (NP) are tested at a low as well as a high cephalin concentration, using an ACL 3000 automated clot timer. The ratio of these two clotting times, divided by the corresponding ratio for the NP, was defined as the Lupus Ratio (LR) and calculated by means of a computer program. The frequency distribution of the LR in a reference population of 150 healthy individuals was determined, and the 97.5 percentile was defined as the upper reference limit and allocated the value one Lupus Anticoagulant Unit (LA-U). Using dilutions of one strong LA positive plasma, standard curves for LA-U determination were constructed for the APTT as well as the RVVT based test, and fitted with a log-logit computer model. The sensitivity of the tests was comparable to that of the Kaolin Clotting Time (KCT). Plasma samples from warfarin treated patients were uniformly negative, while most heparin-containing plasmas were positive in both tests. Plasmas deficient in Factors V, VIII and IX were negative, whereas one Factor VIII-inhibitor containing plasma was positive in the APTT and negative in the RVVT. The present work shows that it is possible to adapt the APPT as well as the RVVT for LA quantification. With an automated clot timer and computer based calculation of results, the assays are simple and reproducible and have a high sensitivity and specificity.
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PMID:A quantitative, semi-automated and computer-assisted test for lupus anticoagulant. 844 53

Clinical analysis was performed on anti-cardiolipin x beta2 glycoprotein 1 (ACL x beta2 GP1) antibody positive patients with collagen vascular diseases. Nine patients out of 89 showed positive aCL x beta2 GP1 antibody which was a relatively lower percentage compared to that of othoffanti-phospholipid antibodies, such as anti-cardiolipin antibody (23 out of 58), lupus anti-coagulant (15 out of 51) or biological false positive (BFP) test for syphilis (10 out of 50). However, 8 patients out of 9 with positive aCL x beta2 GP1 antibody showed thrombotic lesions, a relatively higher frequency compared to that seen in aCL x beta2 GP1 negative patients. Among these cutaneous manifestations, livedo reticularis and palmar nodules with histopathological evidence of thrombosis were the most characteristic features. All but one patient with palmar nodules showed positive aCL x beta2 GP1 antibody, anti-cardiolipin antibody and lupus anticoagulant.
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PMID:Clinical analysis of anti-cardiolipin.beta 2 glycoprotein 1 antibody positive patients in anti-phospholipid syndrome. 866 20

We have evaluated the technical performance of the MDA-180 automated coagulation analyser in a working diagnostic hemostasis laboratory environment. The analyser has been on site now for over 18 months, and has undergone considerable testing. More than 22,000 samples have been processed, with over 90% of these via the MDA-180's cap-piercing facility. The instrument has been primarily assessed for its technical ease of use and continued reliability, as well as its analytical performance. The instrument has also been successfully interfaced to, and used with, our Laboratory information (CERNER PATHNET) system. A major feature of our evaluation has been an assessment of the MDA-180's ability to perform assays currently performed using alternative methodology or instrumentation (eg; ELISA methodology or the Coagamate-X2 and ACL-300R instruments), as well as its potential to streamline the technical performance of some of these assays. We have co-evaluated the following assays: PT/INR, APTT, TT, Fibrinogen, Protein C, ATIII, Factors II, V, VII, VIII, IX, X, XI, and XII, Lupus anticoagulant (dRVVT), and heparin (alpha Xa). In addition, a number of different reagents (particularly for PT and APTT assays) have been tested on the instrument. Intra-assay and inter-assay variation appears to be remarkably low (five different plasmas tested: PT: 0.6 to 1.3% and 0.5 to 1.3% respectively; APTT: 0.7 to 3.2% and 0.6 to 3.6% respectively; single day analysis). Other comparative assessment data typically showed good correlation to existing test assay systems. A review of other features which may enhance or detract from the instrument's worth in a given hemostasis laboratory is also presented. In summary however, we conclude that the instrument is reliable, easy to use and capable of fast sample through-put.
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PMID:The MDA-180 coagulation analyser: a laboratory evaluation. 921 38

A functional clotting assay was recently reported to detect the factor V-Leiden mutation (R506Q) in patients receiving oral anticoagulants and in patients with Lupus Anticoagulant inhibitor. The original assay (Dahlback) to detect resistance to activated protein C (aPC-resistance) frequently gave unreliable findings in these patients. The change in the method is the use of bovine thromboplastin in a PT-derived assay, with a 1:10 sample dilution. In these conditions a reference normal plasma gives a prolongation of more than 35 seconds, while samples with a heterozygous or homozygous mutation give a prolongation respectively of 10-18 seconds or less 2 seconds. The test is easily automated and quickly performed on ACL/3000, and the reproducibility is good.
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PMID:An improved test to identify aPC-resistant factor V-Leiden. 921 26

Patients with systemic lupus erythematosus (SLE) are at risk of developing deep venous thrombosis (DVT). Should anticardiolipin antibodies (aCL) be detectable, this risk is significantly raised, particularly when these autoanti-bodies are cofactor-dependent. We conducted a cross-sectional study of consecutive unselected outpatients referred for clinical suspicion of DVT, as an attempt to address the following questions: firstly, were aCL antibodies associated with DVT in non-SLE patients? Secondly, was this association related to the cofactor dependence? From March 1992 to February 1994, 208 patients were enrolled in the study. Venography was positive in 110 patients (DVT patients), while the diagnosis of DVT could not be confirmed in the remaining 98 (referred to as disease controls). ACL was measured by ELISA, for IgG and IgM isotypes in two ways: fetal calf serum or bovine serum albumin were used as blocking agents to distinguish between cofactor-dependent and cofactor-independent antibodies. Positive aCL was defined as optical density (OD) values greater than the 95th percentile of OD distribution of 60 healthy controls. We found a high frequency of positive IgG aCL antibodies in both DVT patients and in disease controls (25.5 vs 23.5%). We suggest an association between IgM aCL and DVT. This association was, however, not dependent on the cofactor requirement.
Lupus 1997
PMID:Association between IgM anticardiolipin antibodies and deep venous thrombosis in patients without systemic lupus erythematosus. 922 65

Antiphospholipid-protein syndrome (APS) comprises venous and arterial thrombosis, spontaneous abortion and thrombocytopenia in patients with antiphospholipid-protein antibodies (APA). Such antibodies are detected by immunoenzymatic (ELISA) methods (e.g. anticardiolipin antibodies-ACL) or coagulation assays (lupus anticoagulant-LA). APS in patients showing other symptoms of autoimmune disease is called secondary antiphospholipid-protein syndrome. The aim of the study was to find relation between history of thrombosis and APA in a group of patients with lupus erythematosus and lupus-like disease. Lupus anticoagulant was detected by a three step procedure using phospholipid dependent clotting assays and anticardiolipin antibodies were measured by ELISA. We studied 95 subjects (91 women, 4 men) suffering from lupus erythematosus (67 patients) and lupus-like-disease (28 patients). Lupus anticoagulant was found in 26, anticardiolipin antibodies IgG in 34 and IgM in 27 subjects. In a retrospective study 40 thrombotic events were detected in 36 patients; deep vein thrombosis in 19, pulmonary embolism in 7, ischaemic CNS events in 13 and myocardial infarction in one. Thrombosis was present more often in subjects with LA (61%) and ACL IgG (52%) than in subjects without these antibodies (24%) (p = 0.004 and 0.015, respectively). ACL IgM antibodies were not related to thrombotic episodes. The ACL IgG antibodies and LA are helpful in identifying subjects at risk factors of venous and arterial thrombosis among patients suffering from lupus erythematosus and lupus-like disease.
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PMID:[Prevalence of thrombosis in secondary antiphospholipid-protein syndrome]. 927 2

In 27 of 47 patients with Sneddon's syndrome (33 females, 14 males age 40 years) enzyme immunoassay has detected IgG-antibodies to prothrombin (aPT)--one of cofactor proteins responsible for binding of antiphospholipid antibodies (aPL) to phospholipids. Other aPL were also found: antibodies to cardiolipin (aCL), lupus anticoagulant (LA) in 14 and 27 patients, respectively. 37 (79%) patients had at least one of the studied aPL suggesting that such patients belong to patients with primary antiphospholipid syndrome. A correlation exists between aPT and LA: LA is detectable in 67% of aPT-positive patients compared to 45% of aPT-negative patients (p < 0.05). This is in agreement with the fact that prothrombin is a cofactor for most aPL registered as LA. Comparison of two subgroups of aPL patients different by dominant antigenic specificity (18 patients with aPT but free of ACL and 6 patients with aCP but free of aPT) demonstrated that the latter developed disorders of cerebral circulation, head ache, dementia and renal syndrome less frequently. aPT in Sneddon's syndrome seems to be a marker of comparatively low risk of thrombosis and less severe course of the disease.
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PMID:[Sneddon syndrome new clinical and immunological data]. 969 98


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