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Thrombophilic Factors (thrombophilic + factor)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Thrombophilic Factors Do Not Predict Outcomes in Renal Transplant Recipients Under Prophylactic Acetylsalicylic Acid

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2010
L. Ghisdal
A cohort of recipients of renal transplant after 2000 (N = 310) was prospectively screened on the day of transplantation and 1 month later for a panel of 11 thrombophilic factors to assess their effect on posttransplant outcomes. All patients received prophylactic acetylsalicylic acid, started before transplantation. The rate of thromboembolic events or acute rejection episodes during the first posttransplant year (primary composite endpoint) was 16.7% among patients free of thrombophilic factor (N = 60) and 17.2% in those with ,1 thrombophilic factor (N = 250) (p > 0.99). The incidence of the primary endpoint was similar among patients free of thrombophilic factors and those with ,2 (N = 135), or ,3 (N = 53) factors (16.3% and 15.1% respectively; p = 1) and in patients who remained thrombophilic at 1 month (15.7%; p = 0.84). None of the individual thrombophilic factor present at the day of transplantation was associated with the primary endpoint. The incidence of cardiovascular events at 1-year, serum creatinine at 1-year, 4-year actuarial graft and patient survival were not influenced by the presence of ,1 thrombophilic factor at baseline (p = NS). In conclusion, the presence of thrombophilic factors does not influence thromboembolic events, acute rejection, graft or patient survival in patients transplanted after 2000 and receiving prophylactic acetylsalicylic acid. [source]

Multiple thrombophilic factors in a patient with Budd,Chiari syndrome

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2002
V. BRANCACCIO
Myeloproliferative disorders are the main cause of Budd,Chiari syndrome in western countries. Inherited or acquired thrombophilic factors have also been implicated. A novel mutation of the prothrombin gene (G,A20210) has only been described in a few cases of Budd,Chiari syndrome so far. Venous thrombosis is often the result of multiple concomitant thrombophilic factors. We report the case of a patient with essential thrombocythemia and Budd,Chiari syndrome in which heterozygosity for both factor V Leiden and the mutation G20210A of the prothrombin gene were identified. [source]

Double inherited thrombophilias and adverse pregnancy outcomes: Fashion or science?

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 5 2010
Giovanni Larciprete
Abstract Aim:, To determine to what extent double inherited thrombophilias are associated with adverse obstetric complications correlated with fetoplacental insufficiency, such as preeclampsia, hemolytic anemia elevated liver enzymes and low platelet count (HELLP) syndrome, gestational hypertension, fetal growth restriction (FGR), intrauterine death (ID), abruptio placentae and disseminated intravascular coagulopathy. Methods:, Pregnant women coming to delivery were retrospectively divided into two groups: group A (controls) and group B (cases). Patients belonging to group B had one of the following: severe preeclampsia, HELLP syndrome, gestational hypertension, FGR, intrauterine death, abruptio placentae of disseminated intravascular coagulopathy. We detected methylenetetrahydrofolate reductase (MTHFR) A1298C, MTHFR C677T, factor V Leiden, PAI-1, mutant prothrombin G20210A, plasma homocysteine, antithrombin III, protein S and activated protein C resistance. Normal pregnant women or pregnant women with double defects were enrolled in this study. Results:, The combination of MTHFR C677T mutation with PAI-1 (5G/5G) mutation was significantly linked with the occurrence of ID. HELLP syndrome was significantly related to the simultaneous presence of factor VIII and X mutations. The combination of MTHFR C677T with factor VIII mutation and the combination of factor II and V mutations were significantly related to the occurrence of abruptio placentae. We found an association between double isoforms MTHFR mutation and FGR. Conclusion:, It seems that some thrombophilias and a combination of thrombophilic factors carry a greater risk than others for a given adverse outcome. Further studies are needed to check the link between thrombophilic gene mutations and adverse pregnancy outcomes, such as recurrent miscarriages and deep venous thrombosis. [source]

Budd-Chiari syndrome in Sweden: epidemiology, clinical characteristics and survival , an 18-year experience

LIVER INTERNATIONAL, Issue 2 2009
Rupesh Rajani
Abstract Background: The exact incidence and prevalence of Budd-Chiari syndrome (BCS) is unknown in the general population. Published reports differ in terms of the clinical characteristics, effects of therapy and survival. Aims: To investigate the epidemiology, clinical presentation and survival in patients with BCS. Methods: Retrospective multicentre study in Sweden reviewing the medical records of all patients with BCS 1986,2003, identified from the computerised diagnosis database of 11 hospitals, including all university hospitals and liver transplantation centres. Results: Forty-three patients with BCS were identified, of whom nine (21%) had concomitant portal vein thrombosis. The mean age-standardised incidence and prevalence rates in 1990,2001 were calculated to be 0.8 per million per year and 1.4 per million inhabitants respectively. Myeloproliferative disorders (38%), thrombophilic factors (31%) and oral contraceptives (30%) were common aetiological factors. Two or more risk factors were present in 44%. In 23%, no risk factor was evident. The median follow-up time was 2.7 years. Seventy-two percent were on anticoagulant therapy during follow-up. Transjugular intrahepatic portosystemic shunting, surgical shunting procedures and liver transplantation were performed in 4, 6 and 18 patients respectively. Nineteen patients died. The overall transplantation-free survival at 1, 5 and 10 years was 47, 28 and 17% respectively. Conclusions: Budd-Chiari syndrome is a rare disorder; the mean age-standardised incidence and prevalence rates in Sweden in 1990,2001 were calculated to be 0.8 per million per year and 1.4 per million inhabitants respectively. The presence of a myeloproliferative disorder was a common aetiological factor in our cohort and about half of the patients had a multifactorial aetiology. The transplantation-free survival was poor. [source]