Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Changes of blood coagulation in 32 cases of SLE were investigated. Abnormalities frequently found were elevation of blood fibrinogen, FDP, V111R: Ag levels, prolonged or shortened KPTT time, and depressed AT-III value. Half of the patients with SLE showed laboratory changes compatible with the diagnostic criteria of DIC, but acute DIC was encountered clinically only in 2 cases hypercoagulation state or hypercoagulation with lower fibrinolysis, however were frequently seen. Lupus anticoagulant were detected in 6 patients and deep vein thrombosis of lower extremity in 1 patient. Examination of blood coagulation in patients with SLE was, therefore, of clinical importance.
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PMID:[Blood coagulation changes in systemic lupus erythematosus]. 212 40

Lupus anticoagulants have been recognized as significant causes of morbidity in patients for many years. They were originally regarded by physicians and researchers as a nuisance. However, the name is a misnomer that has resisted change over the years. The riddle of the anticoagulant effect in vitro and the apparent procoagulant effect in vivo remains unsolved. Since a lupus anticoagulant can exist in virtually every patient population, it is no longer a topic of interest limited only to the hematologists, but has achieved multidisciplinary attention. The presence of a lupus anticoagulant should be evaluated in any patient who presents with new onset transient ischemic attack or cerebral vascular accident, unexplained deep venous thrombosis, or recurrent fetal wastage.
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PMID:Lupus anticoagulant. 214 Mar 51

Lupus anticoagulant, an immunoglobulin that prolongs the partial thromboplastin time, has been associated with thrombotic events, including deep venous thrombosis, pulmonary emboli, and Budd-Chiari syndrome. In this report, primary sclerosing cholangitis was diagnosed in a man with a 10-year history of multiple thrombotic events related to a circulating lupus anticoagulant. Progressive jaundice and pruritus developed, and sclerosing cholangitis was confirmed by direct cholangiography. Sclerosing cholangitis is the second hepatobiliary disease reported in association with a lupus anticoagulant.
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PMID:Primary sclerosing cholangitis in the presence of a lupus anticoagulant. 309 67

Rapid development of low density bilateral lesions in the brain due to deep venous thrombosis in Systemic Lupus Erythematosis is described. To the best of our knowledge, this type of symmetry, distribution and appearance of brain infarcts in CT due to deep venous thrombosis has not been reported previously.
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PMID:CT demonstration of brain infarcts due to deep venous thrombosis in systemic lupus erythematosus. 317 76

Lupus anticoagulant has been described in association with many autoimmune disorders. Here we describe its occurrence in a patient with ANCA-associated microscopic polyarteritis with medium vessel involvement. A 62-year-old man presented with mononeuritis multiplex and abdominal pain and was demonstrated to have multiple aneurysms on visceral angiography, consistent with the diagnosis of medium vessel vasculitis or classical polyarteritis nodosa. In addition he had active tuberculosis. He developed a deep venous thrombosis at this admission and, on one occasion, had a prolonged APTT but this was not confirmed to be due to a lupus anticoagulant. Two years later when the patient was readmitted with fevers, headaches and nasal discharge, both ANCA and a lupus anticoagulant were demonstrated in his serum, although there was no evidence of a venous thrombosis. Six months later the patient was demonstrated for the first time to have dysmorphic urinary RBC consistent with glomerular bleeding; at the same time he developed a deep venous thrombosis. ANCA was still present, but the lupus anticoagulant could not be detected. The patient was treated with cyclophosphamide and prednisolone and a Greenfield filter inserted into his inferior vena cava.
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PMID:Lupus anticoagulant in anti-neutrophil cytoplasmic antibody-associated polyarteritis. 773 54

Antiphospholipid antibodies (APA) have thought to be implicated in the pathogenesis of both arterial and venous thrombosis. Because of heterogeneity of APA, direct evidence of their involvement in a thrombotic event is not yet available. Development of thrombosis in the antiphospholipid antibody syndrome (APS) may occur because of the presence of additional risk factors. Here we have analysed 60 patients with APA for the presence of the Arg506-->Gln mutation in factor V. Among them 26 suffered from deep venous thrombosis, 13 from arterial thrombosis and 21 had no history of arterial or venous thrombosis. In the first group four patients were found to be heterozygous and one homozygous for the factor V Arg506-->Gln mutation. None of the patients with the factor V mutation was found in the second and third group. The incidence of factor V mutation was significantly elevated in the group of patients with venous thrombosis. These data suggest that in patients with antiphospholipid antibodies the factor V Arg506-->Gln mutation may play a major role in the occurrence of venous thrombosis.
Lupus 1996 Aug
PMID:Factor V Arg506-->Gln mutation in patients with antiphospholipid antibodies. 886 3

Patients with systemic lupus erythematosus (SLE) are at risk of developing deep venous thrombosis (DVT). Should anticardiolipin antibodies (aCL) be detectable, this risk is significantly raised, particularly when these autoanti-bodies are cofactor-dependent. We conducted a cross-sectional study of consecutive unselected outpatients referred for clinical suspicion of DVT, as an attempt to address the following questions: firstly, were aCL antibodies associated with DVT in non-SLE patients? Secondly, was this association related to the cofactor dependence? From March 1992 to February 1994, 208 patients were enrolled in the study. Venography was positive in 110 patients (DVT patients), while the diagnosis of DVT could not be confirmed in the remaining 98 (referred to as disease controls). ACL was measured by ELISA, for IgG and IgM isotypes in two ways: fetal calf serum or bovine serum albumin were used as blocking agents to distinguish between cofactor-dependent and cofactor-independent antibodies. Positive aCL was defined as optical density (OD) values greater than the 95th percentile of OD distribution of 60 healthy controls. We found a high frequency of positive IgG aCL antibodies in both DVT patients and in disease controls (25.5 vs 23.5%). We suggest an association between IgM aCL and DVT. This association was, however, not dependent on the cofactor requirement.
Lupus 1997
PMID:Association between IgM anticardiolipin antibodies and deep venous thrombosis in patients without systemic lupus erythematosus. 922 65


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