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)

We conducted this study to investigate whether antioxidized low-density lipoprotein (a-oxLDL) is an antibody to cryptic and/or neo-antigen on beta2-glycoprotein I (GPI), which is introduced by binding to anionic phospholipid, similar to that of GPI-dependent anticardiolipin antibody (aCL) employing a-oxLDL ELISA. We found that no significant optical density differences existed among systemic lupus erythematosus patients, including cases with aCL and/or lupus anticoagulant positivity, before and after the addition of GPI. Our results suggest that a-oxLDL is not an antibody to denatured GPI, but rather to oxLDL.
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PMID:Negligible synergistic effect of beta2-glycoprotein I on the reactivity of antioxidized low-density lipoprotein antibody to oxidized low-density lipoprotein. 863 31

The aim of this study was to analyse the prevalence and isotype distribution of antibodies to endothelial cells (aEC) and to beta 2-glycoprotein I (a beta 2GPI) in the antiphospholipid syndrome (APS). Fifteen patients with an APS [nine associated with systemic lupus erythematosus (SLE) and six "primary'] and 15 with SLE without an APS were prospectively studied. The aEC were determined by an enzyme-linked immunosorbent assay (ELISA) using endothelial cells derived from human umbilical vein and the a beta 2GPI by ELISA using highly purified beta 2GPI. A positive titre of aEC was detected in 20 out of 30 patients (67%), but in none of the control group. Ten patients had both IgG and IgM isotypes, five had IgG only and five had only IgM. Thirteen patients with the APS (87%) were found to have a positive titre of aEC, while only seven with SLE but without a history of APS (47%) had aEC (P < 0.05). Nine patients with the APS (60%) had a positive titre of a beta 2GPI (four had both IgG and IgM isotypes, one had IgG only and four had only IgM), while none of the patients without an APS (0%) had these antibodies (P < 0.001). A significant association was also found between the presence of aPL and aEC (P < 0.05), as well as between aPL and a beta 2GPI (P < 0.001). Both aEC and a beta 2GPI can be found in the APS. This reinforces the theory that APS represents a complex autoimmune disorder in which several autoantibodies co-exist with aPL.
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PMID:Antibodies to endothelial cells and to beta 2-glycoprotein I in the antiphospholipid syndrome: prevalence and isotype distribution. 867 May 71

There is accumulating evidence that anti-phospholipid (aPL) antibodies in the sera of patients with autoimmune diseases bind to a complex of anionic phospholipids and plasma phospholipid-binding proteins, namely beta 2-glycoprotein I (beta 2-GPI) and prothrombin. It has been suggested that a conformational change in beta 2-GPI, induced by binding either to anionic phospholipids or to the oxygen molecules on the irradiated microtiter plate, reveals cryptic antigenic epitope(s) in the native protein. We used an enzyme-linked immunoassay for measuring antibodies against two phospholipid-binding proteins, i.e., beta 2-GPI and prothrombin, absorbed to an irradiated plate in an unselected series of 139 patients with systemic lupus erythematosus (SLE). Elevated levels of antibodies against beta 2-GPI were found in 49% of patients and antibodies against prothrombin in 34% of patients. Both antibodies were significantly associated with deep venous thrombosis in patients with SLE (P = 0.009 for both antibodies). Accordingly, testing of these antibodies seems to be clinically useful in evaluating the risk of thrombosis.
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PMID:Antibodies to phospholipid-binding plasma proteins and occurrence of thrombosis in patients with systemic lupus erythematosus. 867 35

Since the recognition of the antiphospholipid syndrome, a great number of cardiac manifestations have been reported in association with these antibodies: valvular disease, coronary artery disease, cardiomyopathy and intracardiac thrombosis. However this association raises numerous questions related to the pathogenic role of antiphospholipids, their prognostic significance and their frequency in a non-selected population with a definite cardiac manifestation. In view of the literature and our personal experience, it seems necessary to distinguish two kinds of situations. During systemic lupus and primary antiphospholipid syndrome (which must be systematically looked for in patients with history of thrombo-embolic disease), antiphospholipids antibodies certainly play a role in the occurrence of cardiac manifestations, but the precise place of thrombosis has to be best defined along with immunologic/inflammatory mechanisms. On the other hand, in a non-selected population, antiphospholipids antibodies may just be the consequence of the cardiac lesion and do not seem to have prognostic implications. This distinction, actually hypothetical, should be supported on the basis of distinct specificities of antiphospholipids antibodies and especially their dependence on beta 2-glycoprotein I, which would help to distinguish the harmful antibodies from those which probably just appear as an epiphenomenon.
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PMID:[The heart and antiphospholipid antibodies. Personal experience and review of the literature]. 867 84

A portion of anticardiolipin antibodies is defined as phospholipid-dependent anti-beta 2-glycoprotein I (beta 2-GPI) antibodies and recognizes the conformationally altered beta 2 GPI which interacts with anionic phospholipids. We studied the clinical significance of IgG phospholipid-dependent anti-beta 2-GPI antibodies in patients with antiphospholipid syndrome (APS). The subjects consisted of 60 APS patients. IgG phospholipid-dependent anti-beta 2-GPI antibodies were detected by ELISA in 32 of the 60 patients (53%). Significantly higher incidences of prolonged APTT and lupus anticoagulants were found in patients with these anti-beta 2-GPI antibodies. Moreover, significantly lower incidences of malar rash, serositis, LE cell preparation and anti-Sm antibodies were found in patients with these anti-beta 2-GPI antibodies. It was found that 88% of the patients with these anti-beta 2-GPI antibodies satisfied less than five of the revised criteria items for the classification of SLE. These findings indicate the clinical characteristics of APS patients with IgG phospholipid-dependent anti-beta 2-GPI antibodies.
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PMID:Phospholipid-dependent anti-beta 2-glycoprotein I (beta 2-GPI) antibodies and antiphospholipid syndrome. 868 96

We measured serum antiphospholipid antibodies (aPL) in patients with multiple sclerosis (MS) using enzyme linked immunosorbent assay (ELISA) and examined the correlations between these antibodies and MS. This study included thirty-two patients with clinically definite MS, thirteen patients with other autoimmune neurological diseases excluding collagen diseases (disease control A), eight patients with collagen vascular diseases (disease control B) and twenty-six healthy persons (normal control). In MS group IgG antibody against cardiolipin (CL) was detected in 3 (9%); among them, cofactor (beta 2-glycoprotein I) dependency was shown in 2 but one was cofactor independent. IgM antibody was elevated in 14 of 32 patients (44%) with MS, but cofactor dependency was not determined. However, this was significantly higher in frequency than that of the disease control A (p < 0.01) and normal control (p < 0.01). Results of antibodies against phosphatidylserine were found similar to CL, but antibodies against phosphatidylcholine were in most cases negative. Each of anti-CL IgG antibody purified from four patients with diverse immunological disorders (primary antiphospholipid antibody syndrome, MS, polyarteritis nodosa and systemic lupus erythematosus) had different reactivities against DNA. In addition, the aPL positive group in MS possessed the autoantibodies such as antinuclear antibody at higher rate than the negative group. However, clinically two groups of MS were indistinguishable. The higher incidence of aPL may imply that a broad spectrum of autoantibodies might be produced in MS; some antibodies presumably related directly to MS pathogenesis are yet to be identified.
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PMID:Characterization of serum anti-phospholipid antibodies in patients with multiple sclerosis. 872 2

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.
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PMID:Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis. 873 42

Antiphospholipid antibodies were originally thought to bind negatively-charged (anionic) phospholipids. Current evidence suggest that the target antigen is considerably more complex and includes beta 2-glycoprotein I, a phospholipid-binding plasma protein. Our understanding of the pathophysiology of the antiphospholipid syndrome has increased exponentially with a number of studies into the interactions of antiphospholipid antibodies and beta 2-glycoprotein I.
Lupus 1996 Apr
PMID:The role of beta 2-glycoprotein I in the antiphospholipid syndrome. 874 29

'Antiphospholipid' (aPL) antibodies are of clinical importance because of their strong association with vascular thrombosis, recurrent pregnancy loss, thrombocytopenia and other clinical manifestations like livedo reticularis, chorea and cardiac valvular disease. While aPL antibodies have traditionally been thought to be directed against negatively-charged (anionic) phospholipids current evidence suggests that these autoantibodies recognise protein-phospholipid complexes or the proteins themselves. A number of candidate proteins have been investigated with the two most extensively researched being beta 2-glycoprotein I and prothrombin.
Lupus 1996 Apr
PMID:Immunology of antiphospholipid antibodies and their interaction with plasma proteins. 874 30

Systemic lupus erythematosus is a complex immunological and rheumatological disease that has numerous complications. Central to the pathogenesis of systemic lupus erythematosus is immune complex formation and deposition in blood vessels and end organs. This is a case report of an autopsy of a patient with systemic lupus erythematosus, end stage renal disease, peripheral vascular occlusive disease, pancreatitis, and aortitis. The aortitis was found to be immune complex mediated with deposition of IgG, C3, as well as fibrinogen in the wall of the aorta as shown by immunofluorescence. The hypercoagulable state of the patient is discussed with particular emphasis on the role of anticardiolipin antibodies, antiphospholipid antibodies, and anti-beta-2-glycoprotein I in the pathogenesis. This case is unique in that the immune complex mediated aortitis has not been described in the literature over the past 25 years. We recommend that the diagnosis of immune complex mediated aortitis be considered in the differential diagnosis of aortitis, particularly in the background of a patient with systemic lupus erythematosus.
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PMID:Lupus aortitis: a case report and review of the literature. 874 62


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