Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA). Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group < 50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hyper-cholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI. Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.
Lupus 1995 Aug
PMID:The presence of antiphospholipid antibodies in acute myocardial infarction. 852 29

A young woman had a history of spontaneous venous thromboembolic disease which recurred on several occasions after cessation of treatment with oral anticoagulants. The presence of antiphospholipid antibodies (lupus anticoagulant and a high titre of lgG class anticardiolipin antibodies) in the absence of other clinical and serological features of systemic lupus erythematosus (SLE) confirmed a diagnosis of primary antiphospholipid syndrome (PAPS). Antinuclear antibodies (ANA) were positive (1:1280; speckled pattern). Twelve years after the first thrombotic episode she fulfilled criteria for the classification of SLE (antinuclear antibodies, platelet count < 100 x 10(9)/l, anti-dsDNA antibodies, Coombs' positive haemolytic anaemia). She suffered a myocardial infarction while adequately anticoagulated and developed polyarthritis and immune complex-mediated nephritis over the next 3 years. This case history supports suggestions made by others that a strongly positive ANA test in a patient diagnosed with PAPS may be a harbinger for the development of SLE. Such evolution can take place over more than 10 years.
Lupus 1996 Feb
PMID:Primary antiphospholipid syndrome evolving into systemic lupus erythematosus. 864 24

NZW x BXSB F1 mice develop a systemic autoimmune syndrome with various lupus-like manifestations. Male animals develop a degenerative coronary disease with myocardial infarction, resulting in death before 6 mo of age. The presence in these mice of anti-phospholipid Abs reacting with beta2-glycoprotein I may contribute to the pathogenesis of the cardiovascular lesions. beta2-glycoprotein I, a plasma protein implicated in various aspects of the coagulation pathway, is also the target of autoantibodies in humans with the anti-phospholipid syndrome. We obtained several mAbs from NZW x BXSB F1 mice that were selected for binding to cardiolipin. Two mAbs are specific for beta2-glycoprotein I and display a species-dependent pattern with preferential reactivity to mouse beta2-glycoprotein I. The other mAbs display charge-mediated interactions with anionic phospholipids in the absence of beta2-glycoprotein I. The analysis of the V region sequences of the mAbs suggests that cationic residues in the H chain complementarity-determining region 3 are important for their phospholipid reactivity. The structural features of the V(H)-D-J(H) junctions of these mAbs further support the view that an increased frequency of unusual V(D)J rearrangements directly contributes to the development of murine autoimmunity.
 ...
PMID:Monoclonal antibodies from NZW x BXSB F1 mice to beta2 glycoprotein I and cardiolipin. Species specificity and charge-dependent binding. 878 29

The family of antiphospholipid antibodies includes antibodies binding to cardiolipin in serological test for syphilis, antibodies prolonging the clotting time in lupus anticoagulant test, antibodies reacting with plasma phospholipid-binding proteins, such as beta 2-glycoprotein I and prothrombin, and antibodies binding to oxidized low-density lipoprotein (LDL). Antiphospholipid antibodies are traditionally associated with arterial and venous thrombosis in patients with primary or secondary antiphospholipid syndrome. The recent studies, especially those on patients with myocardial infarction, extend the concept of antiphospholipid antibodies, and suggest that they play a role also in atherosclerosis. Based on the clinical studies and immunological findings, it seems that the differences in the specificity of antiphospholipid antibodies may reflect to their pathogenetic mechanisms and, finally, to their clinical consequences. The present review suggests that antibodies to oxidized LDL may not interfere directly with blood coagulation, but seem to have importance in the inflammation of the vessel wall in atherosclerosis and in vasculitis. Instead, antibodies to beta 2-glycoprotein I and to prothrombin show a closer association with thrombosis. It is possible that in the atherosclerotic plaque, the plasma proteins, such as beta 2-glycoprotein I or prothrombin, are bound to the endothelial surface and antibodies to cryptic epitopes revealed in these proteins are induced. These antibodies may contribute to the formation of atherosclerotic thrombosis by changing the balance of haemostasis toward hypercoagulative state.
Lupus 1996 Oct
PMID:Antiphospholipid antibodies and atherosclerosis. 890 78

The authors ascertained cardiovascular events (myocardial infarction and angina pectoris) in 498 women with systemic lupus erythematosus seen at the University of Pittsburgh Medical Center from 1980 to 1993 (3,522 person-years). Subjects were stratified by age, and cardiovascular event incidence rates were determined. The authors compared these rates with cardiovascular event rates were determined. The authors compared these rates with cardiovascular event rates occurring over the same time period in 2,208 women of similar age participating in the Framingham Offspring Study (17,519 person-years). Age-specific rate ratios were computed to determine whether the cardiovascular events in the lupus cohort were greater than expected. The risk factors associated with cardiovascular events in women with lupus were determined. There were 33 first events (11 myocardial infarction, 10 angina pectoris, and 12 both angina pectoris and myocardial infarction) after the diagnosis of lupus: two thirds were under the age of 55 years at the time of event. Women with lupus in the 35- to 44-year age group were over 50 times more likely to have a myocardial infarction than were women of similar age in the Framingham Offspring Study (rate ratio = 52.43, 95% confidence interval 21.6-98.5). Older age at lupus diagnosis, longer lupus disease duration, longer duration of corticosteroid use, hypercholesterolemia, and postmenopausal status were more common in the women with lupus who had a cardiovascular event than in those who did not have an event. Premature cardiovascular disease is much more common in young premenopausal women with lupus than in a population sample. With the increased life expectancy of lupus patients due to improved therapy, cardiovascular disease has emerged as a significant threat to the health of these women. The impact of this problem has been underrecognized, with little focus placed on aggressive management of hypercholesterolemia and other possible risk factors.
 ...
PMID:Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. 904 14

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.
 ...
PMID:[Prevalence of thrombosis in secondary antiphospholipid-protein syndrome]. 927 2

Atherosclerosis may represent a significant cause of death and morbidity in patients with systemic lupus erythematosus. Coronary involvement is more premature in lupus patients. We present the case of a young woman diagnosed with SLE at the age of 20 years who had a myocardial infarction at age 29 years. We review the mechanisms of atherosclerosis, the interrelations between atherosclerosis and autoimmunity, and between atherosclerosis and SLE. We also review the risk factors, influence of disease and treatment and the guidelines for management of accelerated atherosclerosis in lupus patients.
Lupus 1997
PMID:Accelerated atherosclerosis and coronary disease in SLE. 930 60

Circulating anticoagulants are a major risk factor for thrombotic problems (eg, myocardial infarction, stroke) and pregnancy complications. The authors present a retrospective survey of anticardiolipin antibody and lupus anticoagulant in 200 consecutive patients presenting to their office.
 ...
PMID:Should circulating anticoagulant [AKA anti-phospholipid] assays be a routine component of well-patient assessment? 940 33

A patient with a history of recurrent late fetal loss associated with multiple placental infarcts and cerebrovascular ischemia at the age of 36, followed a year later by a myocardial infarction, was referred for further investigation. Coronary angiography was normal. Antinuclear factor, lupus anticoagulant, anticardiolipin antibodies, and other thrombophilia parameters were negative, but there was moderate hyperthyroidism with positive thyroid peroxidase antibodies. Platelet numbers and von Willebrand factor (vWF) were normal. Her platelets showed spontaneous aggregation that disappeared with aspirin intake. However, aggregation still was induced by low levels of ristocetin (0.3 to 0.5 mg/mL). The low-dose ristocetin aggregation in patient platelet-rich plasma (PRP) was completely blocked by neutralizing antiglycoprotein Ib (GPIb) and anti-vWF antibodies. The monoclonal anti-Fc gamma RII receptor antibody IV.3 inhibited partly, which suggests that PRP aggregation by low-dose ristocetin was elicited by vWF-immunoglobulin (Ig) complexes. Upon addition to washed human platelets, with vWF (10 micrograms/mL), purified patient Igs dose-dependently enhanced ristocetin (0.15 mg/mL)-induced aggregation between 0 and 500 micrograms/mL, an effect that disappeared again above 1 mg/mL. Aggregation was dependent on the vWF concentration and was blocked by IV.3 or neutralizing anti-GPIb or anti-vWF antibodies. The spontaneous aggregation of normal platelets resuspended in patient plasma could be inhibited totally by IV.3 and partially by neutralizing anti-GPIb or anti-vWF antibodies. Perfusion with normal anticoagulated blood, enriched with 10% of control or patient plasma, over surfaces coated with vWF showed increased platelet adhesion and activation in the presence of patient antibodies. Treatment of the patient with the antithyroid drug thiamazol and temporary corticosteroids, aspirin, and ticlopidine did not correct the platelet hypersensitivity to ristocetin. These observations suggest that some autoantibodies to vWF may both enhance vWF binding to platelets and cause platelet activation through binding to the Fc gamma RII receptor, and thereby may be responsible for a new form of antibody-mediated thrombosis.
 ...
PMID:Recurrent arterial thrombosis linked to autoimmune antibodies enhancing von Willebrand factor binding to platelets and inducing Fc gamma RII receptor-mediated platelet activation. 953 91

Patients with subacute cutaneous lupus erythematosus (SCLE) have circulating antibodies to Ro/SSA directed to two antigenically distinct ribonucleoproteins of 60 kDa and 52 kDa. Three laboratory tests may be used to detect anti-Ro/SSA antibodies: counterimmunoelectrophoresis (CIE), enzyme-linked immunosorbent assay (ELISA) and immunoblotting (IB). Their relative efficacy and clinical correlations were ascertained. We determined anti-Ro/SSA antibodies with CIE, with two different ELISA methods (ELISA 1 and 2) and with IB in 29 SCLE patients. Anti-52 kDa and -60 kDa Ro/SSA antibodies were also assayed with IB. In addition, we determined antinuclear antibodies with indirect immunofluorescence, anti-Sm, anti-RNP, anti-La/SSB and anti-Ro/SSA antibodies with CIE and ELISA, and anti-nDNA and cardiolipin antibodies using an ELISA method. CIE detected anti-Ro/SSA antibodies in 22 patients while ELISA 1 and 2 did so in 17 and 18 patients, respectively. In five patients, IB revealed a reactivity to 60 kDa polypeptides and in two, a reactivity to 52 kDa polypeptides. Of these seven patients, four had a myocardial infarction. Of these, two reacted to the 52 kDa antigen and two to the 60 kDa antigen. A combination of techniques was often needed to detect all specificities. ELISA proved to be very specific and sensitive. The IB technique detected a group of patients with myocardial infarction. A case-control study is needed to confirm the data of cardiac involvement.
 ...
PMID:Counterimmunoelectrophoresis, ELISA and immunoblotting detection of anti-Ro/SSA antibodies in subacute cutaneous lupus erythematosus. A comparative study. 953 32


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>