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

The haemostatic balance can basically be described as the equilibrium between fibrin formation (coagulation) and fibrin lysis (fibrinolysis). The status of this balance may therefore be reflected by the products of these two processes. Until recently, the tests for assessment of fibrin(ogen) degradation products were performed in serum since they were based on polyclonal antibodies, which cross-react with fibrinogen. However, the use of serum introduces many artefacts so the utility of these serum tests is limited. New assays have now become available, which can be divided into quantitative enzyme immunoassays (EIAs) and semi-quantitative latex agglutination assays. The new assays can be carried out in plasma since they use highly specific monoclonal antibodies, the majority of which do not cross-react with fibrinogen. This makes it possible to avoid the serum artefacts. Furthermore, these plasma assays can discriminate between degradation products of fibrin and those of fibrinogen (FbDPs and FgDPs, respectively). The possible clinical utility of the new assays is discussed on the basis of literature data on the following clinical states: deep venous thrombosis (DVT) and pulmonary embolism, liver disease and liver transplantation, sickle cell disease, renal diseases, pregnancy and preeclampsia, disseminated intravascular coagulation (DIC), malignancy, coronary artery disease and thrombolytic therapy. Fibrinolysis appears to be accompanied by fibrinogenolysis. Detection of fibrin(ogen) derivatives may be used to rule out DVT and to monitor efficacy of anticoagulant treatment for DVT or DIC, and reflects severity of renal disease but not renal function. High levels of FgDPs were found during orthotopic liver transplantation and thrombolytic therapy. Fibrin(ogen) degradation products cannot be used to predict reperfusion following thrombolytic therapy. The fibrinolytic system remained active during normal and complicated pregnancy and in patients with malignancies. The new assays provide valuable information on fibrin(ogen)olysis in several diseases. More information on the haemostatic balance may be obtained by using these new assays for fibrin(ogen)olysis products in combination with assays for coagulation products.
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PMID:Monoclonal antibody-based plasma assays for fibrin(ogen) and derivatives, and their clinical relevance. 210 91

An attempt was made to define the correlation between the clinical features of systemic lupus erythematosus and levels of circulating antihistone antibodies of the IgG, IgA, and IgM isotypes. Serum antibody levels were determined by enzyme linked immunosorbent assay (ELISA) on serial blood samples (n = 4) from 25 patients, representing five subgroups: (a) renal disease; (b) central nervous system disorders; (c) skin and joint disease only; (d) serositis; and (e) deep venous thrombosis with or without spontaneous abortion. The levels of antihistone antibodies of each isotype varied widely from patient to patient, but antibody levels in the four samples from each patient correlated closely. A close correlation between levels of IgG and IgA antihistone antibodies was found but there was no correlation between these isotypes and IgM antihistone antibodies. In individual patients no simple correlation between disease activity and antihistone antibody levels was established, but levels of antihistone antibodies of the IgG and IgA isotypes were significantly higher in those patients in whom the disease was consistently more active.
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PMID:Correlation between clinical features of systemic lupus erythematosus and levels of antihistone antibodies of the IgG, IgA, and IgM isotypes. 238 77

Clinical and serological features in SLE patients with arterial or venous thrombosis were studied. The subjects consisted of 140 patients with SLE who met the revised criteria for the classification of SLE by the American Rheumatism Association. Forty patients (29%) had arterial or venous thrombosis. Arterial thrombosis such as stroke was found in 30 patients, and venous thrombosis such as deep vein thrombosis was seen in 24 patients. Average age at the disease onset was 34.5 +/- 12.5 years old. Renal disorder was found as a clinical feature, and IgG anticardiolipin antibodies (aCL), IgG phospholipid-dependent anti-beta 2-glycoprotein I (beta 2-GPI) antibodies and IgG anti-Annexin V antibodies were identified as serological features in SLE patients with thrombosis. These patients were diagnosed as having antiphospholipid syndrome. It was necessary to perform primary prevention therapy as well as secondary prevention therapy. Multiple thrombotic events in the past history and sustained positive reactions of IgG aCL were suggested as predictors of recurrent thrombosis. These data indicated the clinical and serological characteristics in SLE patients with arterial or venous thrombosis.
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PMID:[Thrombosis in patients with SLE and antiphospholipid syndrome]. 778 37

Patients who have end-stage renal disease have an acquired platelet dysfunction that leads to prolonged bleeding time and that may put them at risk for bleeding. This platelet dysfunction is manifest in reduced platelet adhesion and impaired platelet aggregation. As a result, a bleeding tendency exists in end-stage renal disease, and understandably deep vein thrombosis is vanishingly rare in patients with this condition. We present three end-stage renal disease patients undergoing maintenance hemodialysis who developed deep vein thrombosis. These cases illustrate that in some patients with end-stage renal disease, the pro thrombotic forces may be so profound that they overwhelm the bleeding tendency.
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PMID:Deep vein thrombosis in end-stage renal disease. 818 84

Thrombin generation is a key event in the pathophysiology of coronary syndromes and provides the rationale for treatment with anticoagulants. Unlike standard heparin, low-molecular-weight heparin (LMWH) has little effect on activated partial thromboplastin time. LMWH treatment has been monitored by measurement of anti-Factor Xa activity, but this may not accurately reflect the anticoagulant action because LMWHs also inhibit Factor II. The Heptest is a clotting assay that is sensitive to both anti-Xa and anti-IIa activity, as well as inhibition of the extrinsic pathway by LMWH-stimulated release of tissue factor pathway inhibitor. The plasma thrombin neutralization assay has also been used to measure LMWH and to detect low concentrations to which chromogenic assays are insensitive. In the clinical setting, monitoring the anti-Xa activity in patients treated with LMWH after acute deep vein thrombosis offered no advantages over a standard weight-adjusted dose. Moreover, in acute coronary syndromes there is no increase in major hemorrhage rates with weight-adjusted LMWH. Monitoring of LMWH concentrations may be advisable in the presence of comorbid conditions carrying an increased risk of hemorrhage, such as renal disease, advanced age, severe over- or underweight, or a history of previous bleeding episodes.
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PMID:Monitoring of low-molecular-weight heparins in cardiovascular disease. 973 79

We report the results of a detailed examination of clinical events associated with the antiphospholipid antibody (aPL) syndrome in 96 consecutive patients with systemic lupus erythematosus (SLE) who underwent renal transplantation between January 1, 1984, and September 1, 1996. Because of the retrospective nature of our study, we developed strict definitions of clinical events considered to be associated with the aPL syndrome. We reviewed all available hospital, clinic, and outside records of the patients with SLE who underwent transplantation at our center during this time period and noted the results of three standard serological tests for aPLs, when available. Mean follow-up of the 96 patients was 62.6 months. Eighty-five of the 96 patients (88.5%) had at least one test for aPLs performed, and 25 patients (29.4%) had at least one abnormal test result. Among these 25 patients, 15 patients (60%) had clinical events associated with aPL syndrome. Ten patients (10.4%) either died of the aPL syndrome or had an aPL-associated clinical event within 3 months of transplantation. Other morbidity from the aPL syndrome in these 15 patients included: thrombotic arteriolar microangiopathy (2 patients), stroke (4 patients), ocular ischemia (7 patients), deep vein thrombosis or pulmonary embolism (6 patients), renal artery or vein thrombosis (4 patients), peripheral ischemia (1 patient), and fetal wastage (3 patients). By comparison, among the 60 patients with normal aPL test results, only 5 patients had clinical events compatible with the aPL syndrome (P < 0.0001 by chi-squared test). aPLs may be associated with significant morbidity and mortality in patients with SLE undergoing renal transplantation. This study is the first attempt to quantify the impact of aPLs on renal transplantation in a large population of patients with SLE. Further investigation of aPLs in SLE patients with end-stage renal disease is required to clarify the risks, benefits, and optimal clinical management of renal transplantation for these patients.
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PMID:Antiphospholipid antibody syndrome in renal transplantation: occurrence of clinical events in 96 consecutive patients with systemic lupus erythematosus. 1058 13

A hypercoagulable state and the risk of thromboembolism in both arterial and venous circulation is a relatively frequent and serious feature of nephrotic syndrome (NS) in children and adults. The aim of this study was to evaluate the coagulation states of children with NS before and after corticosteroid (CS) therapy and to compare the results with a healthy control group. The first group consisted of 49 nephrotic children (30 boys and 19 girls) with a mean age of 6. 5+/-4.9 years (range 1-16 years). The control group included 17 healthy children (9 boys and 8 girls). At the time of admission, all patients were evaluated for the presence of clinical thromboembolism, hematological and biochemical indicators of a hypercoagulative state, and renal disease. This was repeated after CS treatment. Deep vein thrombosis was observed in 2 nephrotic patients who had very low plasma antithrombin III (AT III) levels and fibrinogen levels above 750 mg/dl. Thus, the prevalence of thromboembolism was 4% in our pediatric nephrotic population. The mean AT III level of the study group was 68.2+/-23.4% at the onset of the disease, which was significantly lower than the level of the control group (84.0+/-7. 6%). Plasma AT III levels increased to 74.4+/-15.3% after CS treatment, which correlated with the serum albumin levels. However, there was no correlation with urinary protein excretion. Protein C levels were higher than controls during all stages of the disease in both steroid-responsive and -unresponsive patients. The mean protein S level was similar in both groups. Plasma fibrinogen and cholesterol levels were significantly higher in the study group but decreased to within normal limits with remission. Our study suggests that thromboembolic complications are not infrequent in children with NS, and may be related to low plasma AT III and albumin and high fibrinogen and cholesterol levels.
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PMID:Hemostatic problems and thromboembolic complications in nephrotic children. 1119 16

Skin ulceration is a well-characterized thrombotic complication of the heparin-induced thrombocytopenia (HIT) syndrome. We present the case of a 73-year-old diabetic woman nearing end-stage renal failure who developed extensive upper thigh, abdominal and buttock ulceration following initiation of subcutaneous heparin for prophylaxis against deep vein thrombosis. A preliminary diagnosis of calciphylaxis was made based on the classical distribution and macroscopic appearance of the ulceration in a patient with end-stage renal failure and secondary hyperparathyroidism. However skin biopsy showed complete absence of calcium deposits in the dermal microvasculature. The presence of extensive microthrombi within dermal vessels prompted serologic testing to detect a prothrombotic state. We identified the combined presence of heparin-dependent platelet activating (HIT) antibodies and functional protein S deficiency. To our knowledge this is the first reported case of a dialysis patient presenting with skin ulceration induced by heparin and protein S deficiency. This case highlights the importance of a skin biopsy and testing for a hypercoaguable state in patients with end-stage renal disease and skin ulceration. We suggest that HIT antibodies should be requested in all dialysis patients presenting with skin ulceration.
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PMID:Heparin-induced skin necrosis in a patient with end-stage renal failure and functional protein S deficiency. 1150

Renal allograft recipients with thrombophilic (hypercoagulable) states are at higher risk for early allograft loss. Presumably, the combination of endothelial injury at surgery and thrombophilia predisposes to arterial or venous thrombosis. Of 270 consecutive renal transplants at our center one allograft failed secondary to renovascular thrombosis. At exploration the iliac and renal veins were thrombosed. Thrombectomy and re-implantation were attempted, but unsuccessful. Also noted at surgery was extensive clot in the femoral vein that could not be removed by embolectomy catheters. Post-operatively, a Doppler ultrasound confirmed the presence of extensive deep venous thrombosis (DVT) in the femoral and popliteal veins. The adherent nature of this clot, the extent of clot found less than 12 h after renal transplantation and the absence of leg edema suggested that the DVT existed prior to surgery. This case demonstrates that a pre-existing, asymptomatic DVT can precipitate allograft thrombosis and highlights the importance of diagnosing thrombophilia in patients undergoing renal transplantation. Current practices in our unit have evolved to include screening for thrombophilia in all patients with a suggestive history. As thrombophilic states are increasingly appreciated in the end-stage renal disease population, effective management of these patients while on hemodialysis and at the time of renal transplantation presents an ongoing challenge.
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PMID:Renal allograft loss due to proximal extension of ileofemoral deep venous thrombosis. 1209 90

Although renal failure has classically been associated with a bleeding tendency, thrombotic events are common among patients with end-stage renal disease (ESRD). A variety of thrombosis-favoring hematologic alterations have been demonstrated in these patients. In addition, "nontraditional" risk factors for thrombosis, such as hyperhomocysteinemia, endothelial dysfunction, inflammation, and malnutrition, are present in a significant proportion of chronic dialysis patients. Hemodialysis (HD) vascular access thrombosis, ischemic heart disease, and renal allograft thrombosis are well-recognized complications in these patients. Deep venous thrombosis and pulmonary embolism are viewed as rare in chronic dialysis patients, but recent studies suggest that this perception should be reconsidered. Several ESRD treatment factors such as recombinant erythropoietin (EPO) administration, dialyzer bioincompatibility, and calcineurin inhibitor administration may have prothrombotic effects. In this article we review the pathogenesis and clinical manifestations of thrombosis in ESRD and evaluate the evidence that chronic renal failure or its management predisposes to thrombotic events.
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PMID:Thrombosis in end-stage renal disease. 1471 19


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