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

Deep venous thrombosis is a multicausal disease, i.e. more than one risk factor needs to be present to cause the disease. Oral contraceptive use increases the risk of venous thrombosis but since not all women using oral contraceptives develop thrombosis, the presence of additional risk factors in patients is likely. The aim of this study was to assess the joint effect of oral contraceptive use and the levels of procoagulant factors (F)(FII, FV, FVII, FVIII, FIX, FX, FXI, FXII, FXIII and fibrinogen). Data of premenopausal women were re-analyzed in the Leiden Thrombophilia Study. The highest relative risks were observed for the combination of oral contraceptive use and high levels (>90th percentile) of FII (Odds Ratio [OR]OC+FII 10.1; 95% confidence interval [CI] 3.5-29.0), FV (OROC+FV 12.6; 95% CI 3.8-41.5), and FXI (OROC+FXI 11.9; 95% CI 3.6-39.2) and low levels (< 10th percentile) of FXII (OROC+FXII 12.3; 95% CI 2.4-63.0). No interaction was observed between oral contraceptive use and high levels of the other coagulation factors, i.e. the joint effect of these risk factors did not exceed the sum of the separate effects. The results of this study indicate that the risk for the joint effects of oral contraceptive use and coagulation factor levels are minor compared with the joint effect of oral contraceptive use and the FV Leiden mutation (RR > 30).
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PMID:Interaction between oral contraceptive use and coagulation factor levels in deep venous thrombosis. 1452 3

Factor VIII (FVIII) is key component of the fluid phase of the blood coagulation system. Recent evidence suggests a direct relationship between high plasma levels of FVIII and an increased risk for arterial and venous thrombosis. Thus material reviews the most important clinical and epidemiological evidence about this prothrombotic association. Main function of FVIII is to activate FX functioning as a cofactor for activated FIX in the presence of phospholipids and calcium. Since its deficiency has been historically associated with a hemorrhagic disease (namely hemophilia A), it was never studied its role in thrombosis. In order to explain the association FVIII and thrombosis, defects in its synthesis that increase its plasma concentration as well as postranslational modifications that allow a higher activity, have been proposed. Since 1977 it was suggested that increased plasma concentrations of FVIII and thrombosis may be associated. Shortly after, several other studies confirmed this association. Indeed, patients with stroke of acute myocardial infarction having high plasma levels of FVIII have a shorter survival. On the other hand, deep venous thrombosis is more frequent in patients with high plasma levels of FVIII. This rise in plasma FVIII concentration is also associated with recurrent venous thrombosis. The increment of plasma FVIII concentration is not due to an acute phase reaction. Plasma concentrations of FVIII above 100-150 IU/dL increase 3-fold the risk of thrombosis while concentrations above 150 IU/dL increase the the same risk 6-fold. While it is established the real importance of FVIII as a cause of thrombosis, every patient at risk of thrombosis must have a quantification of this factor. Evaluation of plasma FVIII concentration must be performed in patients with suspected thrombophilia since there is evidence that shows that high plasma FVIII levels is an independent thrombophilic risk factor. There are not effective therapeutic interventions able to normalize the high concentrations of FVIII. Therefore, appropriate prophylaxis during high thrombosis risk clinical episodes is the best alternative for the patient.
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PMID:[A new thrombophilia risk factor: the increase of plasma factor VIII]. 1463 11

This study was purposed to investigate the correlation of deep vein thrombosis (DVT) with C-reactive protein (CRP), fibrinogen (Fg), coagulation factor VIII (FVIII:C), coagulation factor IX (FIX:C) and to explore the effect of inflammation and coagulation as well as their interaction in DVT and its mechanism. 59 patients with DVT undergoing selective venous ultrasonography and 26 healthy individuals as controls were enrolled in this study. The plasma level of CRP was detected by immunoturbidimetry, FVIII:C, FIX:C levels were determined by a one-stage assay and fibrinogen level was measured by full-automatic biochemical apparatus. The results showed that the mean levels of plasma CRP, Fg, FVIII:C and FIX:C were significantly higher in deep vein thrombosis group than that in controls [CRP (2.67 +/- 0.91) vs (0.14 +/- 0.08) mg/dl; Fg (4.73 +/- 1.36) vs (2.79 +/- 0.66)g/L; FVIII:C (126.71 +/- 28.10) vs (81.35 +/- 20.77)%; FIX:C (81.01 +/- 23.60) vs (70.71 +/- 11.3)%] (p < 0.01), and the level of plasma CRP was strongly correlated with Fg, FVIII:C and FIX:C (r(s) = 0.432, 0.571 and 0.544, p < 0.01). It is concluded that the DVT and inflammation are closely related, increased level of plasma CRP may be a predictor of DVT. Increased plasma levels of Fg, FVIII:C and FIX:C all are important risk factors to DVT. Interaction between inflammation and coagulation promote the incidence of DVT, which may be one of DVT pathogenesis.
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PMID:[Correlation of inflammatory marker and coagulation factors with deep vein thrombosis]. 2056 44

Pulmonary embolism is a complication of deep vein thrombosis. It occurs in the population with a normal clotting mechanism, but it may also occur in patients with congenital bleeding conditions. Here, we report on all cases of pulmonary embolism in congenital hemorrhagic disorders. All reported cases of pulmonary embolism in congenital coagulation disorders have been gathered by a time-unlimited PubMed search. Cross-checking of the references listed at the end of the single papers was carried out to avoid omissions. Seventy-two patients had an objectively demonstrated pulmonary embolism. The event occurred in patients with fibrinogen, factor V, factor VIII (FVII), FVIII, FIX, and FXI deficiency, and in those with von Willebrand's disease. No embolism was reported in FII, factor X, and FXIII deficiency. Thirty were women and 28 were men, whereas in the remaining 14 cases, sex was not reported. Age varied from 6 to 81 years (mean age 34.3 years). The management varied from only supportive to the administration of unfractionated heparin, low-molecular-weight heparin, and anti-vitamin K medications, accompanied by adequate replacement therapy. Evolution was fair or good in the majority of cases, but there were 10 fatalities. Risk factors were present in 61 patients. The most frequent of these were replacement therapy (35 cases), surgery (34), and old age (13). Some patients had more than one risk factor. Eleven patients had no risk factors. There are discrepancies in the prevalence of pulmonary embolism among different clotting disorders. The conditions most frequently affected are FVII deficiency and fibrinogen defects. The significance of the findings is discussed.
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PMID:Pulmonary embolism in congenital bleeding disorders: intriguing discrepancies among different clotting factors deficiencies. 2682 62