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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of intestinal amoebiasis with subsequent development of antiphospholipid syndrome, manifested by deep vein thrombosis and pulmonary emboli. Anticardiolipin antibodies (aCL) of IgM type at medium titer and aCL IgG antibody at low titer were determined during the days after the onset of infection. To our knowledge this is the first case of antiphospholipid syndrome associated with amoebiasis to be presented in the literature.
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PMID:Antiphospholipid syndrome associated with intestinal amoebiasis. 1186 73

We describe a patient with antiphospholipid antibody syndrome (APS) who died because of relentless inferior vena cava (IVC) tumor thrombosis due to an unsuspected leiomyosarcoma. Laboratory confirmation for APS was provided by functional identification of a lupus anticoagulant and anticardiolipin IgG and anti-beta2-glycoprotein I IgM antibodies. Although sensitive for detecting vascular obstruction, radiocontrast venography and magnetic resonance imaging and angiography detected the IVC thrombosis but failed to distinguish its malignant nature. Concomitant refractory thrombocytopenia prevented further invasive diagnostic and therapeutic maneuvers for progressive, severe IVC thrombosis unresponsive to aggressive treatment of APS. Deep venous thrombosis refractory to anticoagulant and immunomodulatory therapies in a patient with APS may be due to a concomitant underlying malignancy, such as a leiomyosarcoma, causing vascular obstruction.
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PMID:Fatal tumor thrombosis due to an inferior vena cava leiomyosarcoma in a patient with antiphospholipid antibody syndrome. 1205 32

The purpose of this study was to check whether antiphospholipid antibodies (aPL) could be an independent risk factor for atherosclerosis. Eighty-five subjects were studied: 45 with primitive antiphospholipid antibody syndrome and 40 controls affected by deep vein thrombosis secondary to known causes. The two groups were homogeneous for age, sex, and risk factors for atherosclerosis. All the subjects submitted to echo-color doppler of the carotid arteries, femoral arteries, and abdominal aorta. The cases were then subdivided into three subgroups on the basis of the positivity to the three subpopulations of aPL. Results demonstrate that there is no correlation between aPL and atherosclerosis. The different positivity to aPL does not modify this conclusion.
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PMID:Are antiphospholipid antibodies an independent risk factor for atherosclerosis? 1212 Oct 50

Antiphospholipid antibodies are a heterogeneous group of immunoglobulins with specificity for a number of phospholipids, phospholipid-binding proteins and phospholipid-protein complexes. The association between antiphospholipid antibodies and a variety of pathologic disorders, such as arterial and venous thrombosis and recurrent pregnancy loss is recognized as Antiphospholipid Syndrome. The immunoassay currently used to detect antiphospholipid antibodies is the anticardiolipin test. Anticardiolipin antibodies are believed to be polyspecific antibodies that cross-react with all the anionic phospholipids. Therefore, testing only for anticardiolipin antibodies does not always permit detection of all antiphospholipid antibodies, specially when only IgG are evaluated. In a selected population of 74 idiopathic and secondary deep venous thrombosis patients, IgG anticardiolipin, antiphosphatidylinositol and antiphosphatidylserine antibodies were detected by solid-phase immunoassays. Our results show that by testing for each antiphospholipid family, many patients, not evidenced by the standard anticardiolipin assay, were found to be antiphospholipid-positive. The anticardiolipin positive patients have always low, moderate or high levels of antiphospholipid antibodies, suggesting that the antiphospholipid positivity is predictive of anticardiolipin positivity. It should be noted that the patients with only antiphosphatidylinositol positive antibody have a story of nervous system pathology. The meaning of these results is at present under discussion.
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PMID:Antiphosphatidylinositol antibody in deep venous thrombosis patients. 1257 33

Antiphospholipid antibodies are associated strongly with thrombosis and are the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, numerous theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACLAs 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). Patients with type V disease are those with antiphospholipid antibodies and RMS. 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 ACLAs in association with arterial and venous thrombosis strongly suggests that they 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-VI) should be defined, if possible, because this identification may dictate both the type and the duration of immediate and long-term anticoagulant therapy. Unlike those patients with ACLAs, patients with primary LA-thrombosis syndrome usually have venous thrombosis. Because the aPTT is unreliable in patients with LA (prolonged in only approximately 40%-50% of patients) and usually is not prolonged in patients with ACLAs, definitive tests, including ELISA for ACLA, the dilute Russell's viper venom time for LA, hexagonal phospholipid-neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be ordered immediately when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these test results are negative, subgroups also should be assessedin the appropriate clinical setting. Most patients with antiphospholipid thrombosis syndrome will fail to respond to warfarin therapy, and except for retinal vascular thrombosis, may fail some types of antiplatelet therapy, so it is of major importance to make this diagnosis so patients can be treated with the most effective therapy for secondary prevention-LMWH or unfractionated heparin in most instances and clopidogrel in some instances.
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PMID:Antiphospholipid thrombosis syndromes. 1262 66

Antithrombotic therapy is often used during pregnancy for the treatment and prevention of venous thromboembolism, the prevention of systemic embolism in patients with heart valve prostheses and the prevention of foetal loss in patients with antiphospholipid syndrome. Low-molecular-weight heparins (LMWHs), including nadroparin, have largely replaced unfractionated heparin as the anticoagulant of choice. The use of the LMWH nadroparin in pregnant women at an increased risk of thromboembolism or foetal loss is discussed in this review. Deep vein thrombosis can be effectively treated or prevented with nadroparin without any serious adverse events. Nadroparin 0.1 ml/10 kg s.c. once daily prevents thromboembolic complications in pregnant women with heart valve prostheses. Nadroparin is also effective in preventing foetal loss, through contributing to normal placental development and in decreasing the risk of premature delivery in pregnant women with antiphospholipid syndrome or women with herpes and antiphospholipid syndrome. These results demonstrate nadroparin is effective, easy to administer and associated with a low incidence of foetal and maternal complications. The use of nadroparin at a prophylactic dose of 0.3 ml (2850 IU AXa, 95 IU/kg) (for high-risk patients, 0.3-0.6 ml) s.c. once daily, and a therapeutic dose of 0.1 ml/10 kg (95 IU/kg) s.c. twice daily, is in line with the latest international guidelines of the American College of Chest Physicans.
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PMID:Use of the low-molecular-weight heparin nadroparin during pregnancy. A review. 1266 74

Thromboangiitis obliterans (TAO) and antiphospholipid syndrome (APS) share the clinical characteristics of arterial thrombosis and recurrent thrombophlebitis. Although the association of anticardiolipin antibodies (aCLa) and TAO has been previously recognized, the prevalence and the clinical impact of this association remains unclear. aCLa were measured by double ELISA in patients with TAO (n = 47), premature atherosclerosis (pASO) (n=48) and otherwise healthy individuals (n = 48). Antibody status was then compared to clinical presentation and outcomes in patients meeting the diagnostic criteria for TAO. The prevalence of aCLa was significantly higher in patients with TAO (36%) compared to either pASO (8%; p = 0.01) or healthy individuals (2%; p < 0.001). Patients with TAO and a high antibody titer tended to be younger and suffer a significantly higher rate of major amputations compared to those without the antibody (100% versus 17%; p = 0.003). Clinical features of TAO not significantly altered by the presence of aCLa included upper limb involvement, digital necrosis, superficial thrombophlebitis (or deep venous thrombosis). Protein C, protein S, and anti-thrombin III were normal in all individuals. TAO is associated with an increased prevalence of aCLa. The presence of a high antibody titer in these patients is associated with increased morbidity, including major limb amputation. In patients meeting the diagnostic criteria for TAO, screening for aCLa should be considered. Although attractive, the efficacy of chronic anticoagulation in this setting remains to be proven.
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PMID:Antiphospholipid antibodies in thromboangiitis obliterans. 1271 Aug 39

The antiphospholipid antibody syndrome (APS) may present with serious cardiovascular complications which should be recognised by the cardiologist. The authors report a series of 6 cases of APS diagnosed after thrombotic events and the finding of antiphospholipid antibodies. The APS was primary in 5 cases and associated with tuberculous lymphadenitis in 1 case. There was cardiac involvement in 5 patients with pericardial effusion in 3 cases, complicated by tamponade as the presenting sign of primary APS in the other 2, valvular disease in one case (moderate mitral stenosis with aortic valve disease) and pulmonary embolism in one case. Five patients developed recurrent deep vein thrombosis of the legs. One patient had a transient ischaemic cerebral attack.
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PMID:[Cardiovascular abnormalities of the antiphospholipid antibody syndrome]. 1274 9

Purple toes syndrome is an extremely uncommon, nonhemorrhagic, cutaneous complication associated with warfarin therapy. It is characterized by the sudden appearance of bilateral, painful, purple lesions on the toes and sides of the feet that blanch with pressure. The syndrome usually develops 3-8 weeks after the start of warfarin therapy. A 47-year-old man with a history of purple toes syndrome that resolved after discontinuing warfarin--prescribed for a deep vein thrombosis (DVT) in his right lower leg--experienced an acute, proximal DVT in his other leg. Warfarin again was prescribed; 1 week later, purple toes syndrome developed in that extremity. Warfarin therapy again was discontinued, and intravenous unfractionated heparin was started; the patient's clinical picture indicated a possible pulmonary embolism, and laboratory analysis suggested antiphospholipid syndrome. The patient's toe pain resolved, but the purple discoloration persisted. Follow-up laboratory analysis confirmed antiphospholipid syndrome, and warfarin was restarted with close monitoring. No further complications occurred with long-term therapy. Although a rare complication of therapy, clinicians should monitor for the development of purple toes syndrome in patients taking warfarin.
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PMID:Purple toes syndrome associated with warfarin therapy in a patient with antiphospholipid syndrome. 1274 43

The classical clinical picture of the antiphospholipid syndrome (APS) is characterized by venous and arterial thromboses, fetal losses and thrombocytopenia, in the presence of antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), anticardiolipin antibodies (aCL), or antibodies to the protein "cofactor" b2 glycoprotein I. Single vessel involvement or multiple vascular occlusions may give rise to a wide variety of presentations. Any combination of vascular occlusive events may occur in the same individual and the time interval between them also varies considerably from weeks to months or even years. Deep vein thrombosis, sometimes accompanied by pulmonary embolism, is the most frequently reported manifestation in this syndrome. Cerebrovascular accidents-either stroke or transient ischemic attacks-are the most common arterial thrombotic manifestations. Early and late fetal losses, premature births and pre-eclampsia are the most frequent fetal and obstetric manifestations. Additionally, several other clinical features are relatively common in these patients, i.e., thrombocytopenia, livedo reticularis, heart valve lesions, hemolytic anemia, epilepsy, myocardial infarction, leg ulcers, and amaurosis fugax. However, a large variety of other clinical manifestations have been less frequently described in patients with the APS, with prevalences lower than 5%. These include, among others, large peripheral or aortic artery occlusions, Sneddon's syndrome, chorea, transverse myelopathy, intracardiac thrombus, adult respiratory distress syndrome, renal thrombotic microangiopathy, Addison's syndrome, Budd-Chiari syndrome, nodular regenerative hyperplasia of the liver, avascular necrosis of the bone, cutaneous necrosis or subungual splinter hemorrhages. In this article, some of these "unusual" manifestations are reviewed.
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PMID:Unusual manifestations of the antiphospholipid syndrome. 1279 62


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