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

A young man presenting with recurrent deep venous thrombosis was found to have a lupus type coagulation inhibitor. He showed neither clinical nor serological evidence of systemic lupus. The value of the Russell viper venom coagulation time in the detection of the inhibitor is demonstrated. Anticoagulant therapy has not caused any bleeding complication despite the presence of the inhibitor.
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PMID:Recurrent venous thrombosis with a "lupus" coagulation inhibitor in the absence of systemic lupus. 27 Sep 97

Most people who experience venous thrombosis have normal hemostasis. Some people have inherited deficiencies of protein C, protein S, and antithrombin iii. They tend to have deep venous thrombosis which increases their risk for pulmonary emboli. Some acquired disorders which predisposes people to thrombosis include defective fibrinolysis which often occurs after surgery or infection, Trousseau's syndrome (excessive coagulant activity linked with adenocarcinoma), and lupus anticoagulant which is an immunoglobulin G or M antibody directed against negatively charged phospholipids. Hormones and probably not a dilution effect reduces free and bound protein S levels during pregnancy. Functional protein S activity is still 40-50% below normal levels 1-3 days after delivery. This decrease appears to protect against bleeding but does have venous thrombosis and pulmonary emboli during pregnancy as side effects. Non-oral-contraceptive (OC) users have greatly higher protein S levels than do OC users (28.6 mcg/ml vs. 24.3 mcg/ml; p.005) which gives more credence to the belief that hormones are responsible for the fall in protein S activity during pregnancy. OCs reduce free and total protein S levels almost 20%. Smoking may even further reduce these levels in women during pregnancy and who use Ocs. Women who have had venous thrombosis should not use OCs. Physicians should also consider family history especially age of affected family member, severity of thrombotic episodes, and the clinical setting. They should look for an underlying abnormality in patients who develop thrombosis while using OCs. If thrombosis develops during pregnancy, physicians should call for a venogram, venous duplex scanning, and, if required, invasive tests. The most sensible treatment is intravenous heparin for 5-7 days then therapeutic doses of heparin. Heparin therapy should stop before delivery and be reinstituted shortly thereafter and continued throughout the postpartum period. Physicians should take extra precautions when performing surgery on an OC user.
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PMID:Recent advances in understanding clotting and evaluating patients with recurrent thrombosis. 141 44

Lupus anticoagulants (LA) are acquired inhibitors of coagulation related to the antiphospholipid antibodies. Paradoxically, these anticoagulants do not expose patients to the risk of hemorrhage but, on the contrary, to a thrombotic risk. The association in a patient of an antiphospholipid antibody and a clinical manifestation (thrombosis or equivalent) defines the antiphospholipid syndrome. This syndrome is termed primary or secondary according to whether it appears as an isolated disorder or is associated with an identified disease, frequently autoimmune (systemic lupus erythematous or lupus related syndrome). Clinical complications of LA are arterial or venous thrombosis at various sites. They are frequently recurrent, and deep venous thrombosis of leg, oculo-cerebral ischemic lesions and heart valve complications have all been well documented. Thrombosis of the microcirculation can cause tissue or organ disfunction, the most characteristic effect being repeated abortions. Laboratory demonstration of LA is difficult when the inhibitor is weak, and this should be completed by tests for other antiphospholipid antibodies. Clinical studies are necessary to assess the thrombotic risk of the LA in different clinical conditions and to evaluate the need and type of antithrombotic treatment. The LA are heterogeneous and only a small proportion of patients with LA will develop thrombosis. New tests capable of predicting the thrombotic risk, bases on the physiopathological mechanisms with which LA interfere in vivo, are currently being investigated.
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PMID:[Circulating lupus coagulants. A paradox in vascular pathology]. 143 3

Antiphospholipid syndrome (APS) is an entity characterized by recurrent thrombotic events and may occur spontaneously or in the context of systemic lupus erythematosus (SLE). We describe an English Canadian family in whom the propositus, a woman with Graves' disease and SLE, was found to have a lupus anticoagulant and anticardiolipin antibody (aCL). A brother with deep vein thrombosis, pulmonary emboli, bilateral adrenal hemorrhage and thrombocytopenia, circulating anticoagulant and aCL had a positive antinuclear antibody and Coombs' test, but no other features of SLE. Fourteen members of 3 generations of this family underwent clinical assessments, serological testing and HLA typing. The propositus' mother had a family history of autoimmune thyroid disease and the father had aCL, but was asymptomatic. The thyroid disease and the SLE were associated with HLA-B8, DR3 haplotype. The aCL and the anticoagulant were associated with HLA-B60, DR4 haplotype. Both these haplotypes were present in the propositus. Among the other 4 carriers of the haplotype B60, DR4, 3 demonstrated significant titers of aCL. Our findings support the reported association between APS and the HLA haplotype DR4 in patients of English descent with SLE.
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PMID:A family study of the antiphospholipid syndrome associated with other autoimmune diseases. 143 7

An inherited deficiency of protein C, a recognized hypercoagulable state, may cause a clinically significant deep venous thrombosis. Only some persons with a deficiency of protein C experience thrombosis, and almost always the thrombotic event occurs in the venous circulation. Warfarin-induced skin necrosis, a rare event observed in some patients soon after treatment with warfarin is begun, is believed to be another manifestation of this deficiency. We describe a young woman whose basal functional and antigenic levels of protein C were about 45% and who experienced both deep venous thrombosis and warfarin-induced skin necrosis in a clinically severe course. Evidence for lupus anticoagulants was present, with prolonged activated partial thromboplastin time that was corrected when lysed platelets were added, prolonged Russell's viper venom time, anticardiolipin antibodies, and other laboratory evidence. Lupus anticoagulants are associated also with a significant incidence of thrombosis, including arterial thrombosis, and this patient developed concurrently arterial thrombosis. The combined effects of protein C deficiency and lupus anticoagulants, exacerbated by other potentially thrombogenic conditions, are believed responsible for the severe thrombotic events experienced by this patient.
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PMID:Concurrent protein C deficiency and lupus anticoagulants. 156 44

We are reporting a young lady with protracted deep vein thrombosis of her left leg which turned out to be antiphospholipid (anticardiolipin) antibody syndrome of ANA positive systemic lupus erythematosus. Lupus anticoagulant was demonstrated by prolongation of activated partial thromboplastin time and Russell's viper venom time. She had no anti-thrombin III deficiency.
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PMID:Antiphospholipid antibody syndrome of systemic lupus erythematosus presenting as deep vein thrombosis. 829 83

A 25-year-old woman presented with an episode of left calf deep vein thrombosis and pulmonary thrombosis. She was found to have a lupus anticoagulant with anticardiolipin antibodies, some autoimmune antibodies and antibodies for primary Epstein-Barr (EB) virus infection. Six months later, lupus anticoagulant and other autoimmune antibodies were found to be negative and EB virus antibodies were shown to be seroconverted. We suggest that the transient presence of lupus anticoagulant was due to EB virus infection caused by activation of polyclonal B-lymphocytes.
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PMID:Transient lupus anticoagulant induced by Epstein-Barr virus infection. 166 93

We describe a 35-year-old man with a history of previous deep vein thrombosis who presented with hypertension. Renal investigations revealed failure to excrete contrast medium by the right kidney on intravenous pyelography. Digital subtraction angiography showed an 80% stenosis of the left renal artery. He was antinuclear antibody negative, as well as negative for antibodies to double stranded deoxyribonucleic acid and extractable nuclear antigens. The lupus anticoagulant test and antibodies to cardiolipin were positive. He conforms to a diagnosis of "primary" antiphospholipid syndrome.
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PMID:Hypertension, renal artery stenosis and the "primary" antiphospholipid syndrome. 175 47

We present two females with antiphospholipid antibody (APA) syndrome who came with adrenal insufficiency (Addison's disease), recurrent abortions and extensive deep vein thrombosis (DVT). Both cases were positive for lupus anticoagulant (LA), global antiphospholipid test (APA), and IgG, IgA, IgM APA antibodies. Seventeen other cases with documented lupus anticoagulant and various clinical associations were tested for APA IgG, IgA, IgM. Only two were positive for IgA as well as IgG and IgM APA. Thirty volunteer blood donors (24 males and 6 females, aged 19-35 years) were taken as a control group. One person was moderately positive for LA and showed low positivity for IgG APA. These data suggest that the presence of IgA APA may signify a severe disease. Further studies are needed to confirm this observation.
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PMID:IgA antiphospholipid and adrenal insufficiency: is there a link? 180 62

Thromboembolic events occur with a frequency of 3-5% in children with nephrotic syndrome (NS). Although numerous abnormalities in all phases of coagulation have been described in NS, the pathogenesis of clotting abnormalities remains poorly understood in this group of patients. We describe a child with long-standing NS in whom a severe deep venous thrombosis and pulmonary embolism secondary to acquired protein S deficiency and a strong lupus-type circulating anticoagulant developed. In addition, this patient had a markedly decreased plasma level of C4b binding protein. Although acquired protein S deficiency has been described in various clinical disorders including NS, our patient is unusual in having C4bBP deficiency, and his is the only reported pediatric case of NS complicated by thromboembolism in which a circulating anticoagulant has been implicated, to our knowledge.
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PMID:Deep venous thrombosis in a child with nephrotic syndrome associated with a circulating anticoagulant and acquired protein S deficiency. 183 4


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