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)

Antiphospholipid antibodies such as anticardiolipin antibodies and lupus anticoagulant are frequently detected in sera from patients with systemic lupus erythmatosus and from those with related autoimmune disorders. Thromboembolic manifestations, fetal losses or thrombocytopenia in association with antiphospholipid antibodies, are hallmarks of the antiphospholipid syndrome (APS). Recent studies indicates that anticardiolipin antibodies bind to beta 2-glycoprotein I and that a part of lupus anticoagulant binds to beta 2-glycoprotein I or to prothrombin. Antiphospholipid antibodies might induce thrombosis by altering the function of vascular endothelial cells or by accelerating the progression of atherosclerosis. Warfarin, heparin or low dose aspirin have been recommended to prevent recurrent episodes of thrombosis in patients with the APS.
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PMID:[The antiphospholipid syndrome]. 1042 70

The antiphospholipid syndrome (APS) is now emerging as an important cause of recurrent pregnancy loss. A variety of treatments, including steroids, aspirin, heparin and immunoglobulin, alone or in combination, have been assessed in experimental studies and in clinical trials. Steroids are no longer recommended as first-line therapy for patients with APS without overt lupus, because they are associated with significant foetal and maternal morbidity. Based on data from recent trials, heparin plus low-dose aspirin appears to be the regimen of choice for patients with APS who have a history of thrombosis or pregnancy losses with aspirin alone. Aspirin is safe in pregnancy. Subcutaneous heparin does not cross the placenta and therefore has no adverse effects on the foetus. For the mother, however, potential side effects of heparin treatment include bleeding, thrombocytopenia and osteoporosis. Warfarin must be avoided during the first trimester but may have a role to play subsequently in certain subsets of patients. Some studies have demonstrated that combined therapy with prednisone and aspirin, or with heparin and aspirin, may improve the outcome in women with autoimmune disorders who are undergoing in-vitro fertilization.
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PMID:Is there a role for antithrombotic therapy in the prevention of pregnancy loss? 1062 18

A 26-year-old female presented with an episode of severe mucus membrane bleeding. Investigations revealed prolonged prothrombin time (PT), and partial thromboplastin time (PTT), normal thrombin time (TT) and reptilase time, thrombocytopenia, a positive test for lupus anticoagulant (LA), as well as anti-cardiolipin antibodies (ACL). A toxicology screen for toxic drugs and coumadin was negative. Coagulation factor assays revealed low levels for factor II and XII. Low level inhibitor to factor II was demonstrated. Patient had a negative VDRL test and positive anti-nuclear antibodies (ANA). The diagnosis of acquired hypoprothrombinaemia secondary to circulating inhibitor induced by LA was made, and then the patient was started on prednisone, which led to cessation of the bleeding and normalization of PT and PTT, as well as an increase of factor II and factor XII levels. A few months later, the patient developed arthralgia and alopecia, and antibodies against double-stranded DNA were detected, and the diagnosis of systemic lupus erythematosis (SLE) was confirmed. The patient continued to have mild prolongation of PT and PTT while on a low dose of prednisone, but she had no bleeding symptoms. A computed tomography scan of the brain was carried out for unexplained central nervous system (CNS) symptoms, and it revealed mild hydrocephalus, which was thought to be part of the CNS manifestations of SLE. It was concluded that patients with SLE may present with haemostatic defects that are a result of either platelet-related causes (quantitative or qualitative) or coagulation factor deficiency secondary to circulating inhibitor, or both, in the absence of other features of SLE which may appear later.
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PMID:Systemic lupus erythematosus presenting with haemorrhagic manifestation. 1067 97

Antiphospholipid antibodies (aPL) have been associated with clinical conditions that involve arterial or venous thrombotic events and pregnancy morbidity including fetal loss and preeclampsia. These antibodies are detected by various functional tests for the lupus anticoagulant, the anticardiolipin ELISA, the anti-beta2-glycoprotein I ELISA, or ELISA tests for other aPL. The pathogenic mechanisms are poorly understood. A "2 hit" hypothesis has been entertained in which there is underlying vascular (endothelial) damage, and in the presence of an aPL, a thrombotic complication emerges. Although the role of immunologic processes and autoimmunity appears important, immunosuppressive therapy has not proven very effective. Treatment options are limited to antiplatelet therapy (primarily for arterial events) and anticoagulation (with coumadin, heparin, or low molecular weight heparins) because of lack of understanding of the inciting factors and the pathogenesis of the process.
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PMID:The antiphospholipid syndrome: immunologic and clinical aspects. Clinical spectrum and treatment. 1078 52

1) Antiphospholipid antibody syndrome may be associated with unusual sites of thrombosis. 2) Laboratory evaluation involves testing for antiphospholipid antibodies: lupus anticoagulant and anticardiolipin antibodies. 3) Acute management of thrombosis involves immediate anticoagulation. Low-molecular-weight heparins are as safe and effective as unfractionated heparin in this setting. Arterial events may require emergent thrombolytic therapy. Monitoring of the APTT with unfractionated heparin in the presence of a lupus anticoagulant is ineffective; these patients require monitoring of antifactor Xa levels or the use of LMWH, which does not require monitoring. 4) The pharmacokinetics of LMWH change in pregnancy, resulting in a shorter plasma half-life and larger volume of distribution. Monitoring of antifactor Xa levels is necessary. 5) Chronic anticoagulation is best achieved with warfarin, with significantly decreased rates of recurrent events when the INR is > or = 3.0. Long-term, if not life-long, anticoagulation is often necessary. Warfarin is teratogenic, and individuals desiring pregnancy will need to convert to therapeutic, not prophylactic, doses of either unfractionated heparin or LMWH. 6) As part of optimal management of thrombosis in APS, additional risk factors for thrombosis should be eliminated or reduced. These include comorbid illnesses such as hypertension and hyperlipidemia, as well as smoking. 7) Tamoxifen, raloxifene, oral contraceptives, and hormone replacement therapy are all associated with an increased risk of DVT in the general population. In APS patients receiving therapeutic anticoagulation, the addition of these drugs should not increase thrombosis risk. In APS patients not receiving anticoagulant therapy, these hormonal therapies may increase the thrombosis risk.
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PMID:Management of thrombosis in women with antiphospholipid syndrome. 1121 45

Antiaggregant and anticoagulant drugs are essential in the management of the manifestations due to antiphospholipid syndrome (APS) in patients with primary Hughes' syndrome or systemic lupus erythematosus. Coumadin derivatives (warfarin and acenocumarol), heparin and aspirin are used for secondary thromboprophylaxis and treatment of recurrent miscarriage. The available evidence for each indication is reviewed in this paper. There is still debate regarding the optimal intensity of oral anticoagulation, the best drug combination for pregnancy failure in APS and the management of asymptomatic patients with antiphospholipid antibodies.
Lupus 2001
PMID:Antiaggregant and anticoagulant therapy in systemic lupus erythematosus and Hughes' syndrome. 1131 61

We report the diagnosis and management of a 32-year-old Hungarian male, whose only known risk factor for coronary artery disease was smoking, who presented with an acute thrombotic anterolateral wall myocardial infarction requiring percutaneous transluminal coronary angioplasty (PTCA) stenting of his proximal left anterior descending coronary artery. He arrived to the emergency room with an abnormally prolonged partial thromboplastin time (PTT) that subsequently did not correct by mixing with normal plasma. This was suggestive of an underlying coagulopathy. An extensive coagulopathy work up found him to have the antiphospholipid antibody syndrome with antibodies positive for anticardiolipin, lupus anticoagulant and false-positive VDRL. Genetic typing found him to be homozygous for a mutation in the methylenetetrahydrofolate reductase (MTHFR A1298C) gene, which, in the presence of additional thrombophilic factors, may have increased his risk of myocardial infarction. He was discharged on high dose coumadin.
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PMID:Case report: Acute myocardial infarction in a 32-year-old white male found to have antiphospholipid antibody syndrome and MTHFR mutation homozygosity. 1289 Nov 67

Hypothetical circumstances that may require prophylaxis for a potential antiphospholipid syndrome (primary prophylaxis), or in some instances when there already had been some manifestations ofthe syndrome (secondary prophylaxis), were presented to a panel of experts for their consideration on potential prophylactic intervention. These were subsequently presented to the participants in the First International Consensus on Treatment of the Antiphospholipid Syndrome. In most instances there was consensus in adding low dose aspirin, an exception being aspirin allergy when other antiaggregants could be used in nonpregnant subjects. General measures to prevent thrombosis and other vasoprotective actions should also be provided. Higher risk of fetal loss or thrombosis called for anticoagulation with coumadin in nonpregnant subjects or subcutaneous low molecular weight heparin in pregnant ones. When indicated, prophylaxis of the antiphospholipid syndrome should be provided in systemic lupus erythematosus patients who are being treated for their disease. In no instance should corticosteroids or immunosuppresants be given as prophylactic of an antiphospholipid syndrome.
Lupus 2003
PMID:Prophylaxis of the antiphospholipid syndrome: a consensus report. 1535 30

Antiphospholipid Syndrome (APS) has been widely recognized as a risk factor for the recurrence of both thrombosis and pregnancy losses; however the optimal treatment of patients is debatable. The aim of this paper was to establish a consensus among experts on the treatment of APS in pregnancy. A questionnaire that described possible different clinical situations was sent to the International Advisory Board of the 10th International Congress on Antiphospholipid Antibodies. Sixteen experts from different medical branches and different geographic areas sent their replies. The consensus was that treatment for APS pregnant patients should be low molecular weight heparin (LMWH) and low dose aspirin (LDA). The dosage, and frequency of LMWH depends on different situations, including the body weight and past history. Patients with previous thromboses usually receive two injections per day. Warfarin can also be used from 14 to 34 weeks, for patients with previous stroke or severe arterial thromboses. The use of intravenous immunoglobulin (IVIG) seems to be restricted to patients with pregnancy losses despite conventional treatment. The experts usually advised barrier methods of contraception, intrauterine device (if the patient is not taking corticosteroids) or progestins. Oral contraception with oestrogens was usually avoided.
Lupus 2003
PMID:Treatment of pregnant patients with antiphospholipid syndrome. 1535 30

The antiphospholipid syndrome is characterized by thromboembolic events and/or recurrent miscarriages in the presence of anticardiolipin antibodies and/or a lupus anticoagulant. Anticardiolipin antibodies are detected by ELISA whereas lupus anticoagulant detection includes a variety of coagulometric tests. However, a large number of patients with suspected antiphospholipid syndrome are anticoagulated with either heparin or coumadin when evaluated for the presence of a lupus anticoagulant and false positive test results may ensue, thus making coagulometric testing unreliable in this situation. Modifications of standard coagulometric tests have been suggested in order to circumvent this problem and studies of several patient cohorts have shown that the majority of patients with the antiphospholipid syndrome are anticardiolipin positive. However diagnosis in patients receiving anticoagulation remains a difficult task.
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PMID:[Diagnosis of the antiphospholipid syndrome in anticoagulated patients]. 1560 15


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