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 Lupus Anticoagulant (LA) is an immunoglobulin directed towards the phospholipid portion of the prothrombin activator complex. This immunoglobulin because first identified in the plasma of patients with Systemic Lupus Erythematodes, was named as Lupus Anticoagulant. Although initially described in patients with SLE, it was subsequently observed in other diseases and also in patients without any manifest disease. SLE or similar diseases are present in 35% of LA (+) patients. The LA prevalence in SLE patients has been found as 34% whereas ACA prevalence was found as 44%. While searching for the presence of LA and the levels of APA in cases having unexplained recurrent fetal losses, a family (a mother and 3 daughters) was discovered, whose each member has been diagnosed as SLE at different times and with different symptoms. Data suggesting the presence of LA and high APA levels were determined in all the members of the family and also it was realised that cause who had recurrent fetal losses had the highest APA levels. In addition to immunoassay methods to detect APA, examination of coagulation tests in patients with unexplained thrombosis and/or fetal losses, would be of great help.
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PMID:[Lupus anticoagulant and antiphospholipid antibody values in a family with systemic lupus erythematosus]. 141 67

Anticardiolipin antibody (ACA) levels were determined in 17 Asian female SLE patients with autoimmune haemolytic anaemia (AIHA) and 29 Asian female SLE inpatients without AIHA (control patients). Both IgG and IgM isotypes were measured by ELISA. Elevated IgM APA titres (greater than 5 SD of normal health controls) were seen in 11 (64.7%) of 17 AIHA patients and six (20.7%) of 29 control patients (P less than 0.01). There was no significant difference in IgG ACA titres between the two groups. Thrombocytopenia was present in 11 (64.7%) of the AIHA patients and nine (31%) of the control patients (P less than 0.05). None of the control SLE patients with thrombocytopenia had raised IgM ACA levels and only one had an elevated IgG ACA titre. Autoimmune haemolytic anaemia occurring in the context of SLE frequently associated with the concomitant presence of thrombocytopenia (Evan's syndrome) and with the presence of ACA.
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PMID:Anticardiolipin antibodies, haemolytic anaemia and thrombocytopenia in systemic lupus erythematosus. 162 67

Autoantibodies to phospholipids (APA) occur frequently in systemic lupus erythematosus (SLE) and other autoimmune disorders and predispose to intravascular thromboses. Major histocompatibility complex (MHC) class II alleles (HLA-DR and DQ) were determined by restriction fragment length polymorphisms (RFLP) in 20 patients with APA (lupus anticoagulant). HLA-DQw7 (DQB1*0301), linked to HLA-DR5 and -DR4 haplotypes, occurred in 70% and was significantly increased compared to 139 race-matched normal controls (P = 0.002, P corrected [pc] = 0.05, odds ratio [OR] = 5.1). Moreover, the frequency of HLA-DQw7 was significantly higher in SLE patients with APA as compared with patients without APA but with other autoantibodies, including anti-Ro and La (P = 0.0001, pc = 0.002, OR = 10.7), anti-Ro alone (P = 0.001, pc = 0.02, OR = 11.2), anti-dsDNA (P = 0.001, pc = 0.02, OR = 7.1), and possibly anti-Sm (P = 0.04, pc = NS, OR = 6.8) and anti-nRNP (U1-RNP) (P = 0.01, pc = NS, OR = 7.8). The DQB1*0301 allele of DQw7 showed the strongest association, while the frequencies of the DQA1*0301 (45%) and DQA1*0501 (50%) alleles did not differ from the controls. Among the HLA-DQB1*0301 (DQw7) negative patients, all possessed HLA-DQw8 (DQB1*0302) and/or HLA-DQw6 (DQB1*0602 or DQB1*0603) alleles. The HLA-DQB1*0301 chain shares an identical seven amino acid sequence with DQB1*0302, *0602, and *0603 chains in the third hypervariable region of the HLA-DQ molecule. This candidate "epitope" may play a role in mediating an autoimmune response to APA.
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PMID:Molecular analysis of major histocompatibility complex alleles associated with the lupus anticoagulant. 167 88

An enzyme-linked immunospot assay was used to quantitate the number of autoantibody-secreting B cells in the peripheral blood of 67 patients with systemic lupus erythematosus. These patients had 1.5-4-fold more lymphocytes secreting IgG and IgM per million peripheral blood lymphocytes than did normal controls. There was a concomitant increase in the number of B cells secreting antibodies reactive with a diverse panel of foreign and self antigens (including actin, myosin, tri-nitrophenylated keyhole limpet hemocyanin, ovalbumin, and retroviral gp160). By comparison, the number of B cells producing anti-DNA antibodies was increased disproportionately. The magnitude of this anti-DNA response correlated significantly with disease activity. Thus, B cell activation in human systemic lupus erythematosus had characteristics of both generalized (polyclonal) B cell activation and (auto)antigen-specific immune stimulation.
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PMID:Quantitation of IgM- and IgG-secreting B cells in the peripheral blood of patients with systemic lupus erythematosus. 171 87

Antibodies against negatively charged phospholipids, such as those to cardiolipin, can often be detected in the serum of patients with autoimmune related conditions, chronic infections and in patients treated with phenothiazines. In the present study, peripheral blood lymphocytes from nine healthy controls and eight patients with phenothiazine-induced IgM anticardiolipin antibodies (ACA) and the lupus anticoagulant were placed in vitro. Culture supernatants were assayed for ACA by measurement of optical densities using an ELISA. A significant difference (p less than 0.05) was demonstrated between the mean concentration of culture supernatant ACA from the patients as compared to healthy controls. The concentration of ACA in culture supernatants strongly correlated (r = 0.85) with that from the serum. There was a weak correlation between serum and culture supernatant ACA concentration and the lupus anticoagulant activity as measured by prolongation of the partial thromboplastin time. This technique uses readily accessible peripheral blood lymphocytes and should permit dissection of cytokine and cellular immune pathways regulating APA production.
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PMID:Production of anticardiolipin antibodies by cultured human lymphocytes. 196 31

The objective of this work was to determine whether HIV-1 and HIV-2 could be involved in the pathogenesis of systemic lupus erythematosus (SLE). Seventy-five consecutive Caucasian patients with SLE presenting at one institution over a 2-year period were studied. Serum samples were surveyed for anti-HIV-1 antibodies by a commercial ELISA coated with HIV-1-p24. For confirmation, conventional immunoblots were performed with the following antigens: HIV-1-gp41, p31, p24 and p17 (recombinant) and HIV-2-gp36 (synthetic peptide). Additionally, Western blots with HIV-1-gp160, gp120, gp41, p65, p51, p24 and p18 bands were applied. Seventeen (23%) patients exhibited reactivity with HIV-1-p24 in the ELISA, but in the immunoblots and Western blots these sera samples were negative. Patients with SLE may exhibit a reactivity with HIV-1-p24 in the ELISA for HIV infection screening but not in the confirmatory blots. This false-positive reactivity is probably due to molecular mimicry between autoantigens and retroviruses or a contaminant or artefacts in the antigen preparation procedure.
Lupus 1995 Feb
PMID:Lack of relationship between human immunodeficiency virus infection and systemic lupus erythematosus. 776 39

Antiphospholipid antibodies (aPL) are heterogeneous and are now accepted to be mainly phospholipid-protein-dependent antibodies. Although these antibodies are classically associated with thrombosis, their clinical relevance remains to be established. The subgroups of antibodies characterized by their proteic targets were reported to be more appropriate thrombotic markers. We analysed the prevalence of a large panel of antiphospholipid-related antibodies (aPLR), comprising antibodies directed to phospholipid-protein complexes and to different protein cofactors (beta2GPI, prothrombin, annexin V and protein S), in 122 consecutive unselected patients who had experienced at least one venous thrombotic event. The presence of lupus anticoagulants was assessed with an integrated assay using hexagonal phase phospholipids. Two types of aPL (APA and anti-beta2GPI-PL) were measured using a mixture of phospholipids containing cardiolipin and goat serum or human beta2GPI, respectively, as a source of protein cofactor. Our results show a similar prevalence, close to 15%, of lupus anticoagulants, APA and anti-beta2GPI-PL. In contrast, antibodies to beta2GPI were detected in only 8% of the patients, and very few patients had antibodies directed to other proteins. Of the 35 patients having at least one positive aPLR, 17 were classified as severe, because they had recurrent or early onset of thrombosis (< 35 years). The distribution of aPLR between severe and mild cases was not significantly different except for lupus anticoagulants. Our results clearly indicate that lupus anticoagulant is the only aPLR test to be strongly associated with the severity of thrombosis.
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PMID:Prevalence of antiphospholipid-related antibodies in unselected patients with history of venous thrombosis. 971 91

The aim of the study was the assessment of the prevalence of antiphospholipid syndrome (APS) in patients with systemic lupus erythematosus (SLE). 72 patients with SLE had been investigated, 66 females and six males, aged 17 to 70 years, average 37.03. The presence of APA was determined using both ELISA assay for antiphospholipid antibodies, ASSERACHROM APA by Diagnostica Stago and clotting tests for lupus anticoagulant: activated partial thromboplastin time (aPTT), tissue thromboplastin inhibition test (TTI) and dilute Russell viper venom time (dRVVT). Antiphospholipid antibodies have been found in 24 patients (33.44%), 10 of them were with positive lupus anticoagulant tests, 6 of them were with positive ELISA test, while 8 of them had positive coagulation and immunological tests. Clinical manifestations that could be related to antiphospholipid syndrome were present in 22 patients (30.5%). The most common were thrombotic complications in 16 patients (22.25), recurrent spontaneous abortions in 7 patients (9.7%) and thrombocytopenia in 1 patient (1.39%). Presence of antiphospholipid syndrome was determined in 15 patients (20.83%). We can conclude that there is a significant correlation between presence of antiphospholipid antibodies and both thrombotic events and recurrent spontaneous abortions in SLE patients. Occurrence of thrombotic complications is in direct correlation with the level of antiphospholipid antibodies.
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PMID:Antiphospholipid syndrome accompanying systemic lupus erythematosus. 1207 Sep 37

Antiphospholipid antibodies (APLA) present very heterogeneous groups of antibodies which can significantly and in various ways influence processes on different levels of coagulation cascade. Their presence can be accompanied with repetitive venous and arterial thromboses, recurrent loses of foetus, and thrombocytopenia. Incidence of these thrombotic disorders was monitored in a group of 46 patients with systemic lupus erythematodes (SLE). Positive lupus anticoagulant (LA), antiphospholipid antibodies complex, and thrombocyte counts were assessed. Thrombotic disorders were assessed in a retrospective analysis. In the LA+ group 62% of patients had history of venous thromboses, 31% had history of arterial thromboses, and 18% had history of spontaneous abortions. In a group without positive LA 18% of venous thromboses (p = 0.0006) and 6% of arterial thromboses (p = 0.03) were indicated. In the assessment of spontaneous abortions no statistically significant difference was found. An average value of thrombocytes in LA+ group was 152 +/- 66 x 10(5)/l, in LA- group 223 +/- 86 x 10(5)/l, which is statistically significant difference (p < 0.05). In the assessment of thrombotic disorders in a group with combination LA+ and APA+ statistical significance was indicated only in venous thromboses (p = 0.004). We can state from the results that in thrombotic disorders which can be seen in the framework of systemic tissue disorders positive LA and APA and a range of other factors such as activity of a basic disease, associated diseases, and treatment which can aggravate thrombotic disorders of individual patients can participate.
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PMID:[Incidence of selected antiphospholipid antibodies in a group of patients with systemic lupus erythematosus]. 1521 92

Amendments to the Sapporo criteria for the diagnosis of the antiphospholipid syndrome (APS) have recently be published and include testing for the presence of IgG and IgM beta2-glycoprotein I (beta(2)GPI) antibodies. The Asserachrom Antiphospholipid antibodies line (Diagnostica Stago) with a monoclonal based standardisation, was evaluated in a Lupus anticoagulant (LAC) positive (n = 138) and a LAC negative (n = 134) populations. The ELISA line consists of the Asserachrom APA Screen, the Asserachrom APA IgG,M and the Asserachrom anti-beta(2)GPI IgG and IgM. Anti-prothrombin antibodies (APT), not being included in the updated laboratory criteria, have been tested by the Asserachrom anti-prothrombin IgG,M. Imprecision characteristics showed coefficients of variation (CV) ranging from 4.9% to 13.9%. Cut-off values were calculated with the 99 percentile. The Asserachrom APA Screen showed 1,5% false positive and 0,7% false negative results in correlation with the Asserachrom APA IgG,M. 14.7% of the patients were positive for beta2GPI antibodies, 30,0% of them showed a negative Asserachrom APA Screen. beta(2)GPI antibodies may be the only test positive in a minority of patients, so the Asserachrom APA Screen and the Asserachrom anti-beta(2)GPI IgG and IgM should be performed in parallel when APS is suspected. LAC and APA assays, however, remain essential in the laboratory diagnosis of APS.
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PMID:Evaluation of new commercial enzyme-linked immunosorbent assay kits in the laboratory diagnosis of antiphospholipid syndrome in view of the revised classification criteria of the antiphospholipid syndrome. 1710 52


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