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)

Antiphospholipid antibody syndrome is characterized by arterial or venous thrombosis associated to the presence of antiphospholipid antibodies. We report a 32 atrial thrombus. Four months later, being with anticoagulant treatment, he had a deep venous thrombosis. A new echocardiogram did not show the atrial thrombus. The laboratory work-up confirmed an antiphospholipid syndrome. Five months later the patient has not presented new thrombotic episodes and is receiving oral anticoagulants and antiplatelet therapy.
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PMID:[Intracardiac thrombosis in a patient with primary antiphospholipid syndrome. Report of a case]. 929 3

During late seventies it became apparent that the appearance of antiphospholipid antibodies is associated with thromboembolic manifestations, such as cerebral or myocardial infarction, pulmonary thromboembolism, deep vein thrombosis, intrauterine fetal losses and thrombocytopenia. The term antiphospholipid syndrome has been used to define this set of pathologic features. Recognition of this syndrome has spread worldwide as its clinical implications have become appreciated. Recent studies showed that cofactor, beta 2-glycoprotein I (beta 2-GPI) is required for binding of anticardiolipin antibodies (aCL) raised in the patients with SLE and related other autoimmune disorders. However, this finding has generated considerable controversy. Four different hypotheses have been proposed to explain the specificity of aCL: (1) CL is directly recognized by aCL; (2) the beta 2-GPI-CL complex is the structure recognized by aCL; (3) the beta 2-GPI is the actual target antigen for aCL but is cryptic in the absence of CL; and (4) the actual epitope for aCL appears on the native structure of beta 2-GPI. We showed that aCL bound to beta 2-GPI interacting with poly-oxygenated plates and in the absence of CL, an interaction which depends on introduction of oxygen atoms on the polystyrene surface. We also showed that the beta 2-GPI bound to CL via a particular region on the fifth domain, namely C281KNKEKKC288, and the tertiary structure of the region is involved in binding to phospholipid. Several mechanisms to explain the vascular injury and thrombosis associated with aCL have been proposed, primarily based on their phospholipid reactivity to activated platelets. Whether aCL-through binding to complex of beta 2-GPI and negatively charged phospholipid in the phospholipid-dependent coagulation reactions of hemostasis contribute to the increased risk of thrombosis in patients with aCL is an important question in need of an answer. We have demonstrated the possibility that not only activated platelets but also oxidized lipoproteins, e.g., low-density lipoprotein (LDL), may be thrombogenic targets of aCL which recognize the altered beta 2-GPI structure.
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PMID:[Autoantibodies and thrombosis]. 936 65

Antiphospholipid antibody syndrome (APS) is now recognized as one of the most important causes of hypercoagulability. The most common site for venous thrombosis in APS is deep venous thrombosis of the lower extremities. Other sites of venous thrombosis include retinal veins, renal veins, and hepatic veins. The authors report a case of splenic vein thrombosis disclosing antiphospholipid syndrome in which also the cytolytic effect of aPL may play a role of "cofactor" in the genesis of thrombosis through the release of thromboplastin from the lysis of red cells, granulocytes and platelets, making them vulnerable to clearance by splenic macrophages. Important considerations are stressed about differential diagnosis, etiopathogenetic factors, therapy and follow-up of the patient.
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PMID:[Splenic vein thrombosis with pancytopenia and fever: antiphospholipid antibody syndrome]. 952

Antiphospholipid antibodies [such as anticardiolipin antibodies (ACLA)] are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with ACLA are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome) or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). Type V patients are those with antiphospholipid antibodies and fetal wastage syndrome. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of ACLA in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through VI) should be defined, if possible, as this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with ACLA, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the activated partial thromboplastin time (aPTT) is unreliable in patients with lupus anticoagulant (prolonged in only about 40 to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests including ELISA for ACLA, the dRVVT for lupus anticoagulant, hexagonal phospholipid neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these are negative, in the appropriate clinical setting, subgroups should also be assessed. Finally, most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, most will fail antiplatelet therapy, thus it is of major importance to make this diagnosis in order that patients can be treated with the most effective therapy for secondary prevention, low-molecular weight heparin (LMWH) or unfractionated heparin (UHF) in most instances.
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PMID:Antiphospholipid syndrome and thrombosis. 1044 63

A 42-year-old woman with the diagnosis of aortic regurgitation was admitted to hospital for surgical treatment. Ten years ago, primary antiphospholipid syndrome had been diagnosed, and she had a history of recurrent spontaneous abortions and deep vein thrombosis. She was suffering from moderate exertional dyspnea and chest pain. Catheter investigation revealed progressive dilatation of the left ventricle and a deterioration of the ejection fraction. The aortic valve was excised and replaced with a mechanical valve. A specimen of the aortic valve showed localized thickening and shrinkage of the midportion and base of each cusp, with vegetation on the surface. These localized, specific findings suggest that another mechanism may be involved in the cardiac valve pathology in patients with primary antiphospholipid syndrome. No hemostatic or thromboembolic problems were encountered after the surgery, and her postoperative course was uneventful.
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PMID:Aortic valve replacement for aortic regurgitation in a patient with primary antiphospholipid syndrome. 1049 90

Antiphospholipid Antibody Syndrome (APS) is defined by arterial and venous thrombosis, recurrent spontaneous abortions and thrombocytopenia associated with persistence of antiphospholipid antibodies. Thrombosis may involve virtually all arterial or venous sites, but deep vein thrombosis of the lower limbs are the most common; however, unusual thrombi that involve the portal vein have been described. We report females with documented portal vein thrombosis and primary APS. The treatment of these patients is difficult because of the risk of bleeding and the recurrent thrombosis if they don't receive appropriate long-term anticoagulant therapy.
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PMID:[Primary antiphospholipid syndrome presented with portal vein thrombosis]. 1050 14

Primary cases of splanchnic vein thrombosis are now less common since a systematic screening for hypercoagulability is performed. In 1996, a sequence variation in the 3'-untranslated region of the prothrombin gene (F.II 20210G/A mutation) has been linked to a threefold increased risk for venous thrombosis. The role of this thrombophilic disorder is not documented in patients with thrombosis of the splanchnic veins. This report presents two patients with a mesenteric ischemia associated with a heterozygous state for the F.II 20210G/A mutation. The first patient developed an ischemic colitis and the second one an ischemic necrosis of the terminal ileum related to a thrombosis of the superior mesenteric vein. In both cases, another thrombotic risk factor was associated: either a general prothrombic state (primary antiphospholipid syndrome) or a focal factor (abnormal hemodynamic conditions related to a liver cirrhosis). It has recently been proposed that several conditions need to be combined for deep vein thrombosis to develop. Screening for the combination of multiple underlying prothrombotic conditions thus appears justified in patients with splanchnic thrombosis. The role of the F.II 20210G/A mutation as a predisposing factor for thrombosis of the digestive vessels should be considered and needs further investigation.
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PMID:Prothrombin 20210G/A mutation in two patients with mesenteric ischemia. 1050 34

Patients with Antiphospholipid syndrome usually present with recurrent deep vein thrombosis, pulmonary thromboembolism and thromboembolic stroke. Recurrent coronary events, though reported, are rare. We describe an unusual case of Antiphospholipid syndrome who presented with recurrent acute ischaemic events in two different coronary territories, who was managed successfully with intracoronary stenting.
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PMID:Recurrent acute coronary events in a patient with primary antiphospholipid syndrome: successful management with intracoronary stenting. 1052 74

Pregnancy has been widely recognized as a predisposing risk factor for deep vein thrombosis (DVT). However, it still remains unclear why pregnant women without a history of familial thrombophilia or antiphospholipid syndrome (APS) have a higher incidence of DVT and pulmonary embolism (PE) during pregnancy and puerperium. We examined the activated protein C (APC) system in healthy pregnant women and in patients with the onset of DVT during puerperium. Sixty unselected Japanese pregnant women without a past or family history of thrombosis or APS and 3 Japanese women with DVT during puerperium were evaluated. Endogenous thrombin potential-ratio (ETP-r) was measured by determination of thrombin-alpha2-macroglobulin complexes in thromboplastin-activated patient plasma. APC sensitivity ratio (APC-sr) was calculated by the determination of ETP-r in patient plasma in the presence and absence of APC (final concentration [conc.] 5.9 nM) to evaluate the functional APC anticoagulant activity. Mean APC-sr was significantly increased at 30 weeks' gestation (2.35 +/- 0.72) and remained high during puerperium compared with the mean APC-sr in nonpregnant women (1.15 +/- 0.63). Mean APC-sr in patients with DVT at the onset was significantly higher (3.57 +/- 0.54) than mean APC-sr during puerperium was, indicating that the sensitivity to APC was reduced in the ETP-based assay. These data suggest a significant reduction in the functional sensitivity to APC associated with an increased risk of venous thrombosis during pregnancy.
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PMID:Detection of decreased response to activated protein C during pregnancy by an endogenous thrombin potential-based assay. 1062 9

A reduction in fibrinolysis has been described in association with thrombosis in the primary antiphospholipid syndrome (PAPS). In this study, we measured anti-tissue-type plasminogen activator (t-PA) antibodies and anti-fibrin-bound t-PA antibodies as possible causes of hypofibrinolysis in 39 patients with PAPS. We also evaluated the differences in anti t-PA antibodies between patients without previous thrombosis (20 patients) and patients with previous episodes of thrombosis (19 patients: deep vein thrombosis in nine, ischaemic stroke in six, arterial leg thrombosis in one, hepatic vein thrombosis in one, thrombophlebitis in one and cerebral venous thrombosis in one). Anti-t-PA antibodies were measured by an enzyme-linked immunosorbent assay (ELISA), and anti-t-PA fibrin-bound antibodies were measured by a solid-phase fibrin immunoassay (SOFIA) in 39 patients with PAPS and in 39 controls matched for gender and age. High levels of IgG anti-t-PA were found in three out of 39 patients with PAPS, and all three patients had a history of thrombosis; four other patients, one of whom had a history of thrombotic events, had high titres of antibodies directed against fibrin-bound t-PA. In addition, patients with ischaemic stroke had significantly higher levels of IgG anti-t-PA than patients without thrombosis (P = 0.029). In conclusion, our data showed that, in patients with PAPS, the highest levels of anti-t-PA antibodies were present in subjects with previous thrombotic events. The discrepancy in the results obtained with two methods of detection of anti-t-PA antibodies, ELISA and SOFIA, indicates a different interaction of the antibodies with the t-PA molecules, which are directly bound to polystyrene plates in ELISA and bound to fibrin as a bridging molecule in SOFIA.
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PMID:Antibodies to tissue-type plasminogen activator in plasma from patients with primary antiphospholipid syndrome. 1079 98


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