Browsing by Author "Miljic, P. (6604038486)"

[No abstract available]

Essentials Prothrombin Belgrade mutation leads to antithrombin resistance. Clinical and biochemical phenotypes in a large family with this mutation were investigated. In carriers, we detected decreased factor II activity and increased endogenous thrombin potential. Prothrombin Belgrade mutation represents a strong prothrombotic risk factor. Summary: Background The recently reported c.1787G>A mutation in the prothrombin gene leads to Arg596Gln replacement in the protein molecule (prothrombin Belgrade). This substitution impairs binding of antithrombin to thrombin and results in inherited thrombophilia, known as antithrombin resistance. Objectives We aimed to elucidate the clinical and biochemical characteristics of thrombophilia associated with antithrombin resistance in a large Serbian family with the prothrombin Belgrade mutation. Patients and methods Nineteen family members were investigated, among whom 10 were carriers of the c.1787G>A mutation. In all subjects the clinical phenotype was determined and laboratory investigations of hemostatic parameters were performed. Results Six out of the 10 mutation carriers developed thromboembolic events, mainly deep venous and mesenteric vein thrombosis. The median age of the first thrombotic event was 26.5 (12–41) years, whereas the incidence rate of first thrombosis was 2.2% per year. In all mutation carriers prothrombin activity was significantly decreased in comparison with non-carriers, clearly distinguishing each group. However, the presence of the mutation did not affect the prothrombin antigen level in plasma. The endogenous thrombin potential was significantly increased in all carriers in comparison with non-carriers, indicating the presence of blood hypercoagulability. Interestingly, levels of D-dimer and the F1+2 fragment were similar in both groups. Conclusions Although rare, the prothrombin Belgrade mutation represents strong thrombophilia with early onset of thrombosis in the investigated family. According to our results, decreased prothrombin activity may be a simple screening test for detection of this mutation in thrombotic patients. © 2017 International Society on Thrombosis and Haemostasis

Background: Cardiovascular morbidity in adult patients with growth hormone deficiency (GHD) and hypopituitarism is increased. Clustering of cardiovascular risk factors leading to endothelial dysfunction and impaired fibrinolysis has also been reported and may account for progression to overt vascular changes in these patients. However, effect of long lasting GH replacement therapy on fibrinolytic capacity in GH deficient patients has not been investigated so far. Objective: To investigate fibrinolysis before and after challenge with venous occlusion in GHD patients with hypopituitarism before and during one year of growth hormone replacement. Design: Hospital based, interventional, prospective study. Investigated subjects: Twenty one patient with GHD and fourteen healthy control subjects matched for age, sex and body mass index (BMI). Methods: Anthropometric, metabolic and fibrinolytic parameters were measured at the start and after three, six and twelve months of treatment with human recombinant GH. Results: At baseline GHD patients had significantly impaired fibrinolysis compared to healthy persons. During treatment with GH, significant changes were observed in insulin like growth factor 1(IGF-1) [from baseline 6.9(2.4-13.5) to 22.0(9.0-33.0) nmol/l after one month of treatment; p < 0.01] and fibrinolysis. Improvement in fibrinolysis was mostly attributed to improvement of stimulated endothelial tissue plasminogen activator (t-PA) release in response to venous occlusion [from baseline 1.1(0.4-2.6) to 1.9(0.5-8.8) after one year of treatment; p < 0.01]. Conclusion: Growth hormone replacement therapy has favorable effects on t-PA release from endothelium and net fibrinolytic capacity in GHD adults, which may contribute to decrease their risk of vascular complications. © 2013 Elsevier Ltd.

Background: Cardiovascular morbidity in adult patients with growth hormone deficiency (GHD) and hypopituitarism is increased. Clustering of cardiovascular risk factors leading to endothelial dysfunction and impaired fibrinolysis has also been reported and may account for progression to overt vascular changes in these patients. However, effect of long lasting GH replacement therapy on fibrinolytic capacity in GH deficient patients has not been investigated so far. Objective: To investigate fibrinolysis before and after challenge with venous occlusion in GHD patients with hypopituitarism before and during one year of growth hormone replacement. Design: Hospital based, interventional, prospective study. Investigated subjects: Twenty one patient with GHD and fourteen healthy control subjects matched for age, sex and body mass index (BMI). Methods: Anthropometric, metabolic and fibrinolytic parameters were measured at the start and after three, six and twelve months of treatment with human recombinant GH. Results: At baseline GHD patients had significantly impaired fibrinolysis compared to healthy persons. During treatment with GH, significant changes were observed in insulin like growth factor 1(IGF-1) [from baseline 6.9(2.4-13.5) to 22.0(9.0-33.0) nmol/l after one month of treatment; p < 0.01] and fibrinolysis. Improvement in fibrinolysis was mostly attributed to improvement of stimulated endothelial tissue plasminogen activator (t-PA) release in response to venous occlusion [from baseline 1.1(0.4-2.6) to 1.9(0.5-8.8) after one year of treatment; p < 0.01]. Conclusion: Growth hormone replacement therapy has favorable effects on t-PA release from endothelium and net fibrinolytic capacity in GHD adults, which may contribute to decrease their risk of vascular complications. © 2013 Elsevier Ltd.

AIM: The aim of the study was to analyze the effectiveness of the application of DDAVP (desmopressin) and Hemate P with cryoprecipitate pre- and postpartum in patients with von Willebrand disease. METHODS: We monitored 32 patients with von Willebrand disease during the study period 1993-2003. DDAVP was applied in the 36th/37th week of gestation and cryoprecipitate and fresh frozen plasma were applied 1 day before and 3 days after delivery. DDAVP treatment continued for 4 weeks. Factor VIII (Hemate P) at the day of delivery RESULTS: No complications occurred in the studied population. CONCLUSION: Precipitation of DDAVP, Hemate P, and cryoprecipitate may help in the treatment of pregnant women with von Willebrand disease.

Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.

Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.