TY  - JOUR
AU  - Pruner, Iva
AU  - Farm, Maria
AU  - Tomić, Branko
AU  - Gvozdenov, Maja
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Soutari, Nida Mahmoud Hourani
AU  - Antović, Aleksandra
AU  - Radojković, Dragica
AU  - Antović, Jovan P.
AU  - Đorđević, Valentina
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1375
AB  - BACKGROUND: Thrombosis is a major global disease burden with almost 60% of cases related to underlying heredity and most cases still idiopathic. Synonymous single nucleotide polymorphisms (sSNPs) are considered silent and phenotypically neutral. Our previous study revealed a novel synonymous FII c.1824C gt  T variant as a potential risk factor for pregnancy loss, but it has not yet been associated with thrombotic diseases. METHODS: To determine the frequency of the FII c.1824C gt  T variant we have sequenced patients' DNA. Prothrombin RNA expression was measured by quantitative PCR. Functional analyses included routine hemostasis tests, western blotting and ELISA to determine prothrombin levels in plasma, and global hemostasis assays for thrombin and fibrin generation in carriers of the FII c.1824C gt  T variant. Scanning electron mi- croscopy was used to examine the structure of fibrin clots. RESULTS: Frequency of the FII c.1824C gt  T variant was significantly increased in patients with venous thromboembolism and cerebrovascular insult. Examination in vitro demonstrated increased expression of prothrombin mRNA in FII c.1824C gt  T transfected cells. Our ex vivo study of FII c.1824C gt  T carriers showed that the presence of this variant was associated with hyperprothrom-binemia, hypofibrinolysis, and formation of densely packed fibrin clots resistant to fibrinolysis. CONCLUSION: Our data indicate that FII c.1824C gt  T, although a synonymous variant, leads to the development of a prothrombotic phenotype and could represent a new prothrombotic risk factor. As a silent variant, FII c.1824C gt  T would probably be overlooked during genetic screening, and our results show that it could not be detected in routine laboratory tests.
PB  - Oxford Univ Press Inc, Cary
T2  - Clinical Chemistry
T1  - The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor
EP  - 389
IS  - 2
SP  - 379
VL  - 66
DO  - 10.1093/clinchem/hvz015
ER  - 

@article{
author = "Pruner, Iva and Farm, Maria and Tomić, Branko and Gvozdenov, Maja and Kovač, Mirjana and Miljić, Predrag and Soutari, Nida Mahmoud Hourani and Antović, Aleksandra and Radojković, Dragica and Antović, Jovan P. and Đorđević, Valentina",
year = "2020",
abstract = "BACKGROUND: Thrombosis is a major global disease burden with almost 60% of cases related to underlying heredity and most cases still idiopathic. Synonymous single nucleotide polymorphisms (sSNPs) are considered silent and phenotypically neutral. Our previous study revealed a novel synonymous FII c.1824C gt  T variant as a potential risk factor for pregnancy loss, but it has not yet been associated with thrombotic diseases. METHODS: To determine the frequency of the FII c.1824C gt  T variant we have sequenced patients' DNA. Prothrombin RNA expression was measured by quantitative PCR. Functional analyses included routine hemostasis tests, western blotting and ELISA to determine prothrombin levels in plasma, and global hemostasis assays for thrombin and fibrin generation in carriers of the FII c.1824C gt  T variant. Scanning electron mi- croscopy was used to examine the structure of fibrin clots. RESULTS: Frequency of the FII c.1824C gt  T variant was significantly increased in patients with venous thromboembolism and cerebrovascular insult. Examination in vitro demonstrated increased expression of prothrombin mRNA in FII c.1824C gt  T transfected cells. Our ex vivo study of FII c.1824C gt  T carriers showed that the presence of this variant was associated with hyperprothrom-binemia, hypofibrinolysis, and formation of densely packed fibrin clots resistant to fibrinolysis. CONCLUSION: Our data indicate that FII c.1824C gt  T, although a synonymous variant, leads to the development of a prothrombotic phenotype and could represent a new prothrombotic risk factor. As a silent variant, FII c.1824C gt  T would probably be overlooked during genetic screening, and our results show that it could not be detected in routine laboratory tests.",
publisher = "Oxford Univ Press Inc, Cary",
journal = "Clinical Chemistry",
title = "The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor",
pages = "389-379",
number = "2",
volume = "66",
doi = "10.1093/clinchem/hvz015"
}

Pruner, I., Farm, M., Tomić, B., Gvozdenov, M., Kovač, M., Miljić, P., Soutari, N. M. H., Antović, A., Radojković, D., Antović, J. P.,& Đorđević, V.. (2020). The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor. in Clinical Chemistry
Oxford Univ Press Inc, Cary., 66(2), 379-389.
https://doi.org/10.1093/clinchem/hvz015

Pruner I, Farm M, Tomić B, Gvozdenov M, Kovač M, Miljić P, Soutari NMH, Antović A, Radojković D, Antović JP, Đorđević V. The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor. in Clinical Chemistry. 2020;66(2):379-389.
doi:10.1093/clinchem/hvz015 .

Pruner, Iva, Farm, Maria, Tomić, Branko, Gvozdenov, Maja, Kovač, Mirjana, Miljić, Predrag, Soutari, Nida Mahmoud Hourani, Antović, Aleksandra, Radojković, Dragica, Antović, Jovan P., Đorđević, Valentina, "The Silence Speaks, but We Do Not Listen: Synonymous c.1824C  gt  T Gene Variant in the Last Exon of the Prothrombin Gene as a New Prothrombotic Risk Factor" in Clinical Chemistry, 66, no. 2 (2020):379-389,
https://doi.org/10.1093/clinchem/hvz015 . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Mitić, Gorana
AU  - Miković, Zeljko
AU  - Mandić, Vesna
AU  - Miljić, Predrag
AU  - Mitrović, Mirjana
AU  - Tomić, Branko
AU  - Bereczky, Zsuzsanna
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1287
AB  - Background: Inherited antithrombin (AT) deficiency is a rare autosomal dominant disorder, caused by mutations in the SERPINC1 gene. The most common clinical presentation in AT deficient patients includes venous thrombosis and pulmonary embolism, while the association of AT deficiency and its effect on the development of pregnancy complications has been less studied. The aim of our research was to evaluate the effect of AT deficiency types, determined by genotyping, on pregnancy outcomes. Methods: A retrospective cohort study included 28 women with AT deficiency, and their 64 pregnancies were analyzed. Results: With regard to live birth rate, a significant difference was observed among women who were carriers of different SERPINC1 mutations, as the rate varied from 100% in cases of type I to the extremely low rate of 8% for women with type II HBS (AT Budapest 3) in the homozygous variant, P=0.0005. All pregnancies from the type I group, even untreated ones, resulted in live births. In women with AT Budapest 3 in homozygous variant the overall live birth rate increased to 28.5% in the treated pregnancies. In this group the highest incidence of fetal death was observed of 62%; repeated fetal losses in 30%; fetal growth restriction in 22% and placental abruption in 7% of all pregnancies. Conclusion: Our study results indicate a difference between type I and type II AT deficiency. The risk of pregnancy related VTE was equally present in both groups, except for AT Budapest 3 in the heterozygous variant, while adverse pregnancy outcomes were strictly related to type II, especially AT Budapest 3 in the homozygous variant.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - The influence of specific mutations in the AT gene (SERPINC1) on the type of pregnancy related complications
EP  - 19
SP  - 12
VL  - 173
DO  - 10.1016/j.thromres.2018.11.006
ER  - 

@article{
author = "Kovač, Mirjana and Mitić, Gorana and Miković, Zeljko and Mandić, Vesna and Miljić, Predrag and Mitrović, Mirjana and Tomić, Branko and Bereczky, Zsuzsanna",
year = "2019",
abstract = "Background: Inherited antithrombin (AT) deficiency is a rare autosomal dominant disorder, caused by mutations in the SERPINC1 gene. The most common clinical presentation in AT deficient patients includes venous thrombosis and pulmonary embolism, while the association of AT deficiency and its effect on the development of pregnancy complications has been less studied. The aim of our research was to evaluate the effect of AT deficiency types, determined by genotyping, on pregnancy outcomes. Methods: A retrospective cohort study included 28 women with AT deficiency, and their 64 pregnancies were analyzed. Results: With regard to live birth rate, a significant difference was observed among women who were carriers of different SERPINC1 mutations, as the rate varied from 100% in cases of type I to the extremely low rate of 8% for women with type II HBS (AT Budapest 3) in the homozygous variant, P=0.0005. All pregnancies from the type I group, even untreated ones, resulted in live births. In women with AT Budapest 3 in homozygous variant the overall live birth rate increased to 28.5% in the treated pregnancies. In this group the highest incidence of fetal death was observed of 62%; repeated fetal losses in 30%; fetal growth restriction in 22% and placental abruption in 7% of all pregnancies. Conclusion: Our study results indicate a difference between type I and type II AT deficiency. The risk of pregnancy related VTE was equally present in both groups, except for AT Budapest 3 in the heterozygous variant, while adverse pregnancy outcomes were strictly related to type II, especially AT Budapest 3 in the homozygous variant.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "The influence of specific mutations in the AT gene (SERPINC1) on the type of pregnancy related complications",
pages = "19-12",
volume = "173",
doi = "10.1016/j.thromres.2018.11.006"
}

Kovač, M., Mitić, G., Miković, Z., Mandić, V., Miljić, P., Mitrović, M., Tomić, B.,& Bereczky, Z.. (2019). The influence of specific mutations in the AT gene (SERPINC1) on the type of pregnancy related complications. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 173, 12-19.
https://doi.org/10.1016/j.thromres.2018.11.006

Kovač M, Mitić G, Miković Z, Mandić V, Miljić P, Mitrović M, Tomić B, Bereczky Z. The influence of specific mutations in the AT gene (SERPINC1) on the type of pregnancy related complications. in Thrombosis Research. 2019;173:12-19.
doi:10.1016/j.thromres.2018.11.006 .

Kovač, Mirjana, Mitić, Gorana, Miković, Zeljko, Mandić, Vesna, Miljić, Predrag, Mitrović, Mirjana, Tomić, Branko, Bereczky, Zsuzsanna, "The influence of specific mutations in the AT gene (SERPINC1) on the type of pregnancy related complications" in Thrombosis Research, 173 (2019):12-19,
https://doi.org/10.1016/j.thromres.2018.11.006 . .

TY  - CONF
AU  - Gvozdenov, Maja
AU  - Pruner, Iva
AU  - Tomić, Branko
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Antić, Darko
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1136
PB  - Nature Publishing Group, London
C3  - European Journal of Human Genetics
T1  - Functional analyses of the FIIc.*64_*66del gene variant and its potential role in fetal loss etiology
EP  - 828
SP  - 827
VL  - 26
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1136
ER  - 

@conference{
author = "Gvozdenov, Maja and Pruner, Iva and Tomić, Branko and Kovač, Mirjana and Miljić, Predrag and Antić, Darko and Đorđević, Valentina and Radojković, Dragica",
year = "2018",
publisher = "Nature Publishing Group, London",
journal = "European Journal of Human Genetics",
title = "Functional analyses of the FIIc.*64_*66del gene variant and its potential role in fetal loss etiology",
pages = "828-827",
volume = "26",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1136"
}

Gvozdenov, M., Pruner, I., Tomić, B., Kovač, M., Miljić, P., Antić, D., Đorđević, V.,& Radojković, D.. (2018). Functional analyses of the FIIc.*64_*66del gene variant and its potential role in fetal loss etiology. in European Journal of Human Genetics
Nature Publishing Group, London., 26, 827-828.
https://hdl.handle.net/21.15107/rcub_imagine_1136

Gvozdenov M, Pruner I, Tomić B, Kovač M, Miljić P, Antić D, Đorđević V, Radojković D. Functional analyses of the FIIc.*64_*66del gene variant and its potential role in fetal loss etiology. in European Journal of Human Genetics. 2018;26:827-828.
https://hdl.handle.net/21.15107/rcub_imagine_1136 .

Gvozdenov, Maja, Pruner, Iva, Tomić, Branko, Kovač, Mirjana, Miljić, Predrag, Antić, Darko, Đorđević, Valentina, Radojković, Dragica, "Functional analyses of the FIIc.*64_*66del gene variant and its potential role in fetal loss etiology" in European Journal of Human Genetics, 26 (2018):827-828,
https://hdl.handle.net/21.15107/rcub_imagine_1136 .

TY  - JOUR
AU  - Miljić, Predrag
AU  - Gvozdenov, Maja
AU  - Takagi, Y.
AU  - Takagi, A.
AU  - Pruner, Iva
AU  - Dragojević, M.
AU  - Tomić, Branko
AU  - Bodrozić, J.
AU  - Kojima, T.
AU  - Radojković, Dragica
AU  - Đorđević, Valentina
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1045
AB  - Background: The recently reported c.1787G gt 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 gt 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.
PB  - Wiley, Hoboken
T2  - Journal of Thrombosis and Haemostasis
T1  - Clinical and biochemical characterization of the prothrombin Belgrade mutation in a large Serbian pedigree: new insights into the antithrombin resistance mechanism
EP  - 677
IS  - 4
SP  - 670
VL  - 15
DO  - 10.1111/jth.13618
ER  - 

@article{
author = "Miljić, Predrag and Gvozdenov, Maja and Takagi, Y. and Takagi, A. and Pruner, Iva and Dragojević, M. and Tomić, Branko and Bodrozić, J. and Kojima, T. and Radojković, Dragica and Đorđević, Valentina",
year = "2017",
abstract = "Background: The recently reported c.1787G gt 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 gt 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.",
publisher = "Wiley, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Clinical and biochemical characterization of the prothrombin Belgrade mutation in a large Serbian pedigree: new insights into the antithrombin resistance mechanism",
pages = "677-670",
number = "4",
volume = "15",
doi = "10.1111/jth.13618"
}

Miljić, P., Gvozdenov, M., Takagi, Y., Takagi, A., Pruner, I., Dragojević, M., Tomić, B., Bodrozić, J., Kojima, T., Radojković, D.,& Đorđević, V.. (2017). Clinical and biochemical characterization of the prothrombin Belgrade mutation in a large Serbian pedigree: new insights into the antithrombin resistance mechanism. in Journal of Thrombosis and Haemostasis
Wiley, Hoboken., 15(4), 670-677.
https://doi.org/10.1111/jth.13618

Miljić P, Gvozdenov M, Takagi Y, Takagi A, Pruner I, Dragojević M, Tomić B, Bodrozić J, Kojima T, Radojković D, Đorđević V. Clinical and biochemical characterization of the prothrombin Belgrade mutation in a large Serbian pedigree: new insights into the antithrombin resistance mechanism. in Journal of Thrombosis and Haemostasis. 2017;15(4):670-677.
doi:10.1111/jth.13618 .

Miljić, Predrag, Gvozdenov, Maja, Takagi, Y., Takagi, A., Pruner, Iva, Dragojević, M., Tomić, Branko, Bodrozić, J., Kojima, T., Radojković, Dragica, Đorđević, Valentina, "Clinical and biochemical characterization of the prothrombin Belgrade mutation in a large Serbian pedigree: new insights into the antithrombin resistance mechanism" in Journal of Thrombosis and Haemostasis, 15, no. 4 (2017):670-677,
https://doi.org/10.1111/jth.13618 . .

TY  - CONF
AU  - Bodrozić, J.
AU  - Miljić, P.
AU  - Gojnić, M.
AU  - Vasić, D.
AU  - Đorđević, Valentina
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/942
AB  - Background:Venous thromboembolism is one of the leading causes ofmaternal morbidity and mortality. The role of inherited thrombophiliain occurrence and localization of pregnancy related thrombosis is notclear.Aims:To investigate the influence of hereditary thrombophilia onlocalization and extent of thrombosis in women with thromboemboliccomplications during pregnancy and puerperium.Methods:We conducted a retrospective analysis of 212 consecutivewomen with pregnancy related deep vein thrombosis of lower extremi-ties (LE) or pulmonary embolism (PE) who were referred to our insti-tution for thrombophilia testing from January 2004 to December2015. When DVT of LE was present with PE, the event was accountedas PE. Thrombosis of superficial veins was excluded. All thromboticepisodes were confirmed with duplex ultrasonography and CT pneu-moangiography. In all women following causes of hereditary throm-bophilia were tested: factor V Leiden and prothrombin G20210Amutations, antithrombin, protein C and protein S deficiency. Bloodfor thrombophilia testing was obtained at least 3 months after cessa-tion of anticoagulant therapy.Results:Out of 212 women with pregnancy related thrombosis, 33(15,6%) developed PE, 73 (34,4%) developed unilateral thrombosis ofboth proximal and distal veins, 63 (29,7%) of proximal, and 36 (17%)of distal veins. Seven women (3,3%) developed concomitant bilateralthrombosis of deep veins of lower extremities. Hereditary throm-bophilia testing was positive in 82/212 (38,7%) women. Prevalence ofinherited thrombophilia was significantly higher in women with mas-sive DVT (proximal+distal veins) and in women with isolated DVT ofproximal veins than in women with PE and isolated DVT of distalveins.Conclusions:According to our results, inherited thrombophilia influ-ences localization and extent of pregnancy related thrombosis. Surpris-ingly, prevalence of thrombophilia was low in women who developedpregnancy related pulmonary embolism.
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Inherited thrombophilia influences localization and extent of pregnancy related deep venous thrombosis
EP  - 160
SP  - 160
VL  - 14
UR  - https://hdl.handle.net/21.15107/rcub_imagine_942
ER  - 

@conference{
author = "Bodrozić, J. and Miljić, P. and Gojnić, M. and Vasić, D. and Đorđević, Valentina",
year = "2016",
abstract = "Background:Venous thromboembolism is one of the leading causes ofmaternal morbidity and mortality. The role of inherited thrombophiliain occurrence and localization of pregnancy related thrombosis is notclear.Aims:To investigate the influence of hereditary thrombophilia onlocalization and extent of thrombosis in women with thromboemboliccomplications during pregnancy and puerperium.Methods:We conducted a retrospective analysis of 212 consecutivewomen with pregnancy related deep vein thrombosis of lower extremi-ties (LE) or pulmonary embolism (PE) who were referred to our insti-tution for thrombophilia testing from January 2004 to December2015. When DVT of LE was present with PE, the event was accountedas PE. Thrombosis of superficial veins was excluded. All thromboticepisodes were confirmed with duplex ultrasonography and CT pneu-moangiography. In all women following causes of hereditary throm-bophilia were tested: factor V Leiden and prothrombin G20210Amutations, antithrombin, protein C and protein S deficiency. Bloodfor thrombophilia testing was obtained at least 3 months after cessa-tion of anticoagulant therapy.Results:Out of 212 women with pregnancy related thrombosis, 33(15,6%) developed PE, 73 (34,4%) developed unilateral thrombosis ofboth proximal and distal veins, 63 (29,7%) of proximal, and 36 (17%)of distal veins. Seven women (3,3%) developed concomitant bilateralthrombosis of deep veins of lower extremities. Hereditary throm-bophilia testing was positive in 82/212 (38,7%) women. Prevalence ofinherited thrombophilia was significantly higher in women with mas-sive DVT (proximal+distal veins) and in women with isolated DVT ofproximal veins than in women with PE and isolated DVT of distalveins.Conclusions:According to our results, inherited thrombophilia influ-ences localization and extent of pregnancy related thrombosis. Surpris-ingly, prevalence of thrombophilia was low in women who developedpregnancy related pulmonary embolism.",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Inherited thrombophilia influences localization and extent of pregnancy related deep venous thrombosis",
pages = "160-160",
volume = "14",
url = "https://hdl.handle.net/21.15107/rcub_imagine_942"
}

Bodrozić, J., Miljić, P., Gojnić, M., Vasić, D.,& Đorđević, V.. (2016). Inherited thrombophilia influences localization and extent of pregnancy related deep venous thrombosis. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 14, 160-160.
https://hdl.handle.net/21.15107/rcub_imagine_942

Bodrozić J, Miljić P, Gojnić M, Vasić D, Đorđević V. Inherited thrombophilia influences localization and extent of pregnancy related deep venous thrombosis. in Journal of Thrombosis and Haemostasis. 2016;14:160-160.
https://hdl.handle.net/21.15107/rcub_imagine_942 .

Bodrozić, J., Miljić, P., Gojnić, M., Vasić, D., Đorđević, Valentina, "Inherited thrombophilia influences localization and extent of pregnancy related deep venous thrombosis" in Journal of Thrombosis and Haemostasis, 14 (2016):160-160,
https://hdl.handle.net/21.15107/rcub_imagine_942 .

TY  - CONF
AU  - Miljić, P.
AU  - Bodrozić, J.
AU  - Pruner, Iva
AU  - Đorđević, Valentina
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/956
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Antithrombin resistance caused by c.1787G  gt  a mutation in prothrombin gene: rare but strong inherited thrombophilia
EP  - 97
SP  - 97
VL  - 14
UR  - https://hdl.handle.net/21.15107/rcub_imagine_956
ER  - 

@conference{
author = "Miljić, P. and Bodrozić, J. and Pruner, Iva and Đorđević, Valentina",
year = "2016",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Antithrombin resistance caused by c.1787G  gt  a mutation in prothrombin gene: rare but strong inherited thrombophilia",
pages = "97-97",
volume = "14",
url = "https://hdl.handle.net/21.15107/rcub_imagine_956"
}

Miljić, P., Bodrozić, J., Pruner, I.,& Đorđević, V.. (2016). Antithrombin resistance caused by c.1787G  gt  a mutation in prothrombin gene: rare but strong inherited thrombophilia. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 14, 97-97.
https://hdl.handle.net/21.15107/rcub_imagine_956

Miljić P, Bodrozić J, Pruner I, Đorđević V. Antithrombin resistance caused by c.1787G  gt  a mutation in prothrombin gene: rare but strong inherited thrombophilia. in Journal of Thrombosis and Haemostasis. 2016;14:97-97.
https://hdl.handle.net/21.15107/rcub_imagine_956 .

Miljić, P., Bodrozić, J., Pruner, Iva, Đorđević, Valentina, "Antithrombin resistance caused by c.1787G  gt  a mutation in prothrombin gene: rare but strong inherited thrombophilia" in Journal of Thrombosis and Haemostasis, 14 (2016):97-97,
https://hdl.handle.net/21.15107/rcub_imagine_956 .

TY  - JOUR
AU  - Mitrović, Mirjana
AU  - Suvajdžić, Nada
AU  - Elezović, Ivo
AU  - Bogdanović, Andrija
AU  - Đorđević, Valentina
AU  - Miljić, Predrag
AU  - Djunić, Irena
AU  - Gvozdenov, Maja
AU  - Čolović, Nataša
AU  - Virijević, Marijana
AU  - Leković, Danijela
AU  - Vidović, Ana
AU  - Tomin, Dragica
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/891
AB  - Introduction: Thrombotic events (TE) appear to be more common in acute promyelocytic leukemia (APL) than in other acute leukemias, with reported prevalence ranging from 2 to 10-15%. Materials and Methods: We retrospectively analyzed the data on TE appearance in 63 APL patients. Results: TE occured in 13 (20.6%) cases, four arterial (6.3%) and nine venous (14.3%). TE were more frequently diagnosed after initiation of weekly D-dimer monitoring (7 TE during 20 months vs 6 during 76 months, P = 0.032). Patients with and without venous thrombosis were significantly different regarding female/male ratio (P = 0.046), PT (P = 0.022), a PTT (P = 0.044), ISTH DIC score (P = 0.001), bcr3 (P = 0.02) and FLT3-ITD (P = 0.028) mutation. The most significant risk factor for venous TE occurrence in multivariate analysis was FLT3-ITD mutation (P = 0.034). PAI-1 4G/4G polymorphism was five times more frequent in patients with venous TE than without it (P = 0.05). Regarding risk factors for arterial TE we failed to identify any. Conclusions: We have demonstrated that APL-related TE rate is higher than previously reported and that weekly D-dimer monitoring might help to identify patients with silent thrombosis. Moreover, our study suggests a possible relationship between venous TE occurrence and several laboratory findings (PT, aPTT, ISTH DIC score, bcr3 isoform, FLT3-ITD mutation and PAI 4G/4G). Prophylactic use of heparin might be considered in patients with ISTH DIC score  lt  5, bcr3 isoform, FLT3-ITD mutation and PAI 4G/4G.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - Thrombotic events in acute promyelocytic leukemia
EP  - 593
IS  - 4
SP  - 588
VL  - 135
DO  - 10.1016/j.thromres.2014.11.026
ER  - 

@article{
author = "Mitrović, Mirjana and Suvajdžić, Nada and Elezović, Ivo and Bogdanović, Andrija and Đorđević, Valentina and Miljić, Predrag and Djunić, Irena and Gvozdenov, Maja and Čolović, Nataša and Virijević, Marijana and Leković, Danijela and Vidović, Ana and Tomin, Dragica",
year = "2015",
abstract = "Introduction: Thrombotic events (TE) appear to be more common in acute promyelocytic leukemia (APL) than in other acute leukemias, with reported prevalence ranging from 2 to 10-15%. Materials and Methods: We retrospectively analyzed the data on TE appearance in 63 APL patients. Results: TE occured in 13 (20.6%) cases, four arterial (6.3%) and nine venous (14.3%). TE were more frequently diagnosed after initiation of weekly D-dimer monitoring (7 TE during 20 months vs 6 during 76 months, P = 0.032). Patients with and without venous thrombosis were significantly different regarding female/male ratio (P = 0.046), PT (P = 0.022), a PTT (P = 0.044), ISTH DIC score (P = 0.001), bcr3 (P = 0.02) and FLT3-ITD (P = 0.028) mutation. The most significant risk factor for venous TE occurrence in multivariate analysis was FLT3-ITD mutation (P = 0.034). PAI-1 4G/4G polymorphism was five times more frequent in patients with venous TE than without it (P = 0.05). Regarding risk factors for arterial TE we failed to identify any. Conclusions: We have demonstrated that APL-related TE rate is higher than previously reported and that weekly D-dimer monitoring might help to identify patients with silent thrombosis. Moreover, our study suggests a possible relationship between venous TE occurrence and several laboratory findings (PT, aPTT, ISTH DIC score, bcr3 isoform, FLT3-ITD mutation and PAI 4G/4G). Prophylactic use of heparin might be considered in patients with ISTH DIC score  lt  5, bcr3 isoform, FLT3-ITD mutation and PAI 4G/4G.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Thrombotic events in acute promyelocytic leukemia",
pages = "593-588",
number = "4",
volume = "135",
doi = "10.1016/j.thromres.2014.11.026"
}

Mitrović, M., Suvajdžić, N., Elezović, I., Bogdanović, A., Đorđević, V., Miljić, P., Djunić, I., Gvozdenov, M., Čolović, N., Virijević, M., Leković, D., Vidović, A.,& Tomin, D.. (2015). Thrombotic events in acute promyelocytic leukemia. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 135(4), 588-593.
https://doi.org/10.1016/j.thromres.2014.11.026

Mitrović M, Suvajdžić N, Elezović I, Bogdanović A, Đorđević V, Miljić P, Djunić I, Gvozdenov M, Čolović N, Virijević M, Leković D, Vidović A, Tomin D. Thrombotic events in acute promyelocytic leukemia. in Thrombosis Research. 2015;135(4):588-593.
doi:10.1016/j.thromres.2014.11.026 .

Mitrović, Mirjana, Suvajdžić, Nada, Elezović, Ivo, Bogdanović, Andrija, Đorđević, Valentina, Miljić, Predrag, Djunić, Irena, Gvozdenov, Maja, Čolović, Nataša, Virijević, Marijana, Leković, Danijela, Vidović, Ana, Tomin, Dragica, "Thrombotic events in acute promyelocytic leukemia" in Thrombosis Research, 135, no. 4 (2015):588-593,
https://doi.org/10.1016/j.thromres.2014.11.026 . .

TY  - JOUR
AU  - Pruner, Iva
AU  - Đorđević, Valentina
AU  - Gvozdenov, Maja
AU  - Tomić, Branko
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Radojković, Dragica
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/830
AB  - Recurrent pregnancy loss (RPL) is a health problem affecting up to 5% of women of reproductive age. Several thrombophilic risk factors might contribute to RPL. To investigate relationship between a novel C20068T gene variant in the 3' end of prothrombin gene and RPL, we tested 153 women with RPL and 111 controls for the presence of this gene variant. In patients, we have detected four heterozygous (2.61%) and no homozygous carriers. In controls, no carriers were detected. Our results indicate higher prevalence of C20068T gene variant in women with RPL but this difference was not statistically significant. However, in patients who suffered 5 or more RPL, frequency of C20068T gene variant was significantly increased compared to controls (12.5% vs. 0%, P = 0.02). This is the first study which points out a possible role of C20068T gene variant in etiology of RPL, but larger studies should be carried out to confirm our findings.
PB  - Društvo genetičara Srbije, Beograd
T2  - Genetika-Belgrade
T1  - The c20068t gene variant in the 3 ' end of the prothrombin gene and recurrent pregnancy loss: a pilot study
EP  - 476
IS  - 2
SP  - 469
VL  - 47
DO  - 10.2298/GENSR1502469P
ER  - 

@article{
author = "Pruner, Iva and Đorđević, Valentina and Gvozdenov, Maja and Tomić, Branko and Kovač, Mirjana and Miljić, Predrag and Radojković, Dragica",
year = "2015",
abstract = "Recurrent pregnancy loss (RPL) is a health problem affecting up to 5% of women of reproductive age. Several thrombophilic risk factors might contribute to RPL. To investigate relationship between a novel C20068T gene variant in the 3' end of prothrombin gene and RPL, we tested 153 women with RPL and 111 controls for the presence of this gene variant. In patients, we have detected four heterozygous (2.61%) and no homozygous carriers. In controls, no carriers were detected. Our results indicate higher prevalence of C20068T gene variant in women with RPL but this difference was not statistically significant. However, in patients who suffered 5 or more RPL, frequency of C20068T gene variant was significantly increased compared to controls (12.5% vs. 0%, P = 0.02). This is the first study which points out a possible role of C20068T gene variant in etiology of RPL, but larger studies should be carried out to confirm our findings.",
publisher = "Društvo genetičara Srbije, Beograd",
journal = "Genetika-Belgrade",
title = "The c20068t gene variant in the 3 ' end of the prothrombin gene and recurrent pregnancy loss: a pilot study",
pages = "476-469",
number = "2",
volume = "47",
doi = "10.2298/GENSR1502469P"
}

Pruner, I., Đorđević, V., Gvozdenov, M., Tomić, B., Kovač, M., Miljić, P.,& Radojković, D.. (2015). The c20068t gene variant in the 3 ' end of the prothrombin gene and recurrent pregnancy loss: a pilot study. in Genetika-Belgrade
Društvo genetičara Srbije, Beograd., 47(2), 469-476.
https://doi.org/10.2298/GENSR1502469P

Pruner I, Đorđević V, Gvozdenov M, Tomić B, Kovač M, Miljić P, Radojković D. The c20068t gene variant in the 3 ' end of the prothrombin gene and recurrent pregnancy loss: a pilot study. in Genetika-Belgrade. 2015;47(2):469-476.
doi:10.2298/GENSR1502469P .

Pruner, Iva, Đorđević, Valentina, Gvozdenov, Maja, Tomić, Branko, Kovač, Mirjana, Miljić, Predrag, Radojković, Dragica, "The c20068t gene variant in the 3 ' end of the prothrombin gene and recurrent pregnancy loss: a pilot study" in Genetika-Belgrade, 47, no. 2 (2015):469-476,
https://doi.org/10.2298/GENSR1502469P . .

TY  - CONF
AU  - Đorđević, Valentina
AU  - Pruner, Iva
AU  - Gvozdenov, Maja
AU  - Tomić, Branko
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Radojković, Dragica
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/806
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - The possible role of c.1824c  gt  t prothrombin gene variant in pathogenesis of thrombophilia
EP  - 460
SP  - 460
VL  - 13
UR  - https://hdl.handle.net/21.15107/rcub_imagine_806
ER  - 

@conference{
author = "Đorđević, Valentina and Pruner, Iva and Gvozdenov, Maja and Tomić, Branko and Kovač, Mirjana and Miljić, Predrag and Radojković, Dragica",
year = "2015",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "The possible role of c.1824c  gt  t prothrombin gene variant in pathogenesis of thrombophilia",
pages = "460-460",
volume = "13",
url = "https://hdl.handle.net/21.15107/rcub_imagine_806"
}

Đorđević, V., Pruner, I., Gvozdenov, M., Tomić, B., Kovač, M., Miljić, P.,& Radojković, D.. (2015). The possible role of c.1824c  gt  t prothrombin gene variant in pathogenesis of thrombophilia. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 13, 460-460.
https://hdl.handle.net/21.15107/rcub_imagine_806

Đorđević V, Pruner I, Gvozdenov M, Tomić B, Kovač M, Miljić P, Radojković D. The possible role of c.1824c  gt  t prothrombin gene variant in pathogenesis of thrombophilia. in Journal of Thrombosis and Haemostasis. 2015;13:460-460.
https://hdl.handle.net/21.15107/rcub_imagine_806 .

Đorđević, Valentina, Pruner, Iva, Gvozdenov, Maja, Tomić, Branko, Kovač, Mirjana, Miljić, Predrag, Radojković, Dragica, "The possible role of c.1824c  gt  t prothrombin gene variant in pathogenesis of thrombophilia" in Journal of Thrombosis and Haemostasis, 13 (2015):460-460,
https://hdl.handle.net/21.15107/rcub_imagine_806 .

TY  - CONF
AU  - Pruner, Iva
AU  - Đorđević, Valentina
AU  - Gvozdenov, Maja
AU  - Tomić, Branko
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Radojković, Dragica
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/706
PB  - Pergamon-Elsevier Science Ltd, Oxford
C3  - Thrombosis Research
T1  - The c20068t gene variant in the 3 ' end of the prothrombin gene is the risk factor for recurrent pregnancy loss
EP  - S108
SP  - S108
VL  - 133
DO  - 10.1016/S0049-3848(14)50343-X
ER  - 

@conference{
author = "Pruner, Iva and Đorđević, Valentina and Gvozdenov, Maja and Tomić, Branko and Kovač, Mirjana and Miljić, Predrag and Radojković, Dragica",
year = "2014",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "The c20068t gene variant in the 3 ' end of the prothrombin gene is the risk factor for recurrent pregnancy loss",
pages = "S108-S108",
volume = "133",
doi = "10.1016/S0049-3848(14)50343-X"
}

Pruner, I., Đorđević, V., Gvozdenov, M., Tomić, B., Kovač, M., Miljić, P.,& Radojković, D.. (2014). The c20068t gene variant in the 3 ' end of the prothrombin gene is the risk factor for recurrent pregnancy loss. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 133, S108-S108.
https://doi.org/10.1016/S0049-3848(14)50343-X

Pruner I, Đorđević V, Gvozdenov M, Tomić B, Kovač M, Miljić P, Radojković D. The c20068t gene variant in the 3 ' end of the prothrombin gene is the risk factor for recurrent pregnancy loss. in Thrombosis Research. 2014;133:S108-S108.
doi:10.1016/S0049-3848(14)50343-X .

Pruner, Iva, Đorđević, Valentina, Gvozdenov, Maja, Tomić, Branko, Kovač, Mirjana, Miljić, Predrag, Radojković, Dragica, "The c20068t gene variant in the 3 ' end of the prothrombin gene is the risk factor for recurrent pregnancy loss" in Thrombosis Research, 133 (2014):S108-S108,
https://doi.org/10.1016/S0049-3848(14)50343-X . .

TY  - JOUR
AU  - Kovač, Mirjana
AU  - Mitić, Gorana
AU  - Miljić, Predrag
AU  - Miković, Zeljko
AU  - Mandić, Vesna
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Bereczky, Zsuzsanna
AU  - Muszbek, Laszlo
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/722
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - Poor pregnancy outcome in women with homozygous type-II HBS antithrombin deficiency
EP  - 1160
IS  - 6
SP  - 1158
VL  - 133
DO  - 10.1016/j.thromres.2014.03.025
ER  - 

@article{
author = "Kovač, Mirjana and Mitić, Gorana and Miljić, Predrag and Miković, Zeljko and Mandić, Vesna and Đorđević, Valentina and Radojković, Dragica and Bereczky, Zsuzsanna and Muszbek, Laszlo",
year = "2014",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Poor pregnancy outcome in women with homozygous type-II HBS antithrombin deficiency",
pages = "1160-1158",
number = "6",
volume = "133",
doi = "10.1016/j.thromres.2014.03.025"
}

Kovač, M., Mitić, G., Miljić, P., Miković, Z., Mandić, V., Đorđević, V., Radojković, D., Bereczky, Z.,& Muszbek, L.. (2014). Poor pregnancy outcome in women with homozygous type-II HBS antithrombin deficiency. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 133(6), 1158-1160.
https://doi.org/10.1016/j.thromres.2014.03.025

Kovač M, Mitić G, Miljić P, Miković Z, Mandić V, Đorđević V, Radojković D, Bereczky Z, Muszbek L. Poor pregnancy outcome in women with homozygous type-II HBS antithrombin deficiency. in Thrombosis Research. 2014;133(6):1158-1160.
doi:10.1016/j.thromres.2014.03.025 .

Kovač, Mirjana, Mitić, Gorana, Miljić, Predrag, Miković, Zeljko, Mandić, Vesna, Đorđević, Valentina, Radojković, Dragica, Bereczky, Zsuzsanna, Muszbek, Laszlo, "Poor pregnancy outcome in women with homozygous type-II HBS antithrombin deficiency" in Thrombosis Research, 133, no. 6 (2014):1158-1160,
https://doi.org/10.1016/j.thromres.2014.03.025 . .

TY  - JOUR
AU  - Đorđević, Valentina
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Murata, M.
AU  - Takagi, A.
AU  - Pruner, Iva
AU  - Francuski, D.
AU  - Kojima, T.
AU  - Radojković, Dragica
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/629
PB  - Wiley-Blackwell, Hoboken
T2  - Journal of Thrombosis and Haemostasis
T1  - A novel prothrombin mutation in two families with prominent thrombophilia - the first cases of antithrombin resistance in a Caucasian population
EP  - 1939
IS  - 10
SP  - 1936
VL  - 11
DO  - 10.1111/jth.12367
ER  - 

@article{
author = "Đorđević, Valentina and Kovač, Mirjana and Miljić, Predrag and Murata, M. and Takagi, A. and Pruner, Iva and Francuski, D. and Kojima, T. and Radojković, Dragica",
year = "2013",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "A novel prothrombin mutation in two families with prominent thrombophilia - the first cases of antithrombin resistance in a Caucasian population",
pages = "1939-1936",
number = "10",
volume = "11",
doi = "10.1111/jth.12367"
}

Đorđević, V., Kovač, M., Miljić, P., Murata, M., Takagi, A., Pruner, I., Francuski, D., Kojima, T.,& Radojković, D.. (2013). A novel prothrombin mutation in two families with prominent thrombophilia - the first cases of antithrombin resistance in a Caucasian population. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 11(10), 1936-1939.
https://doi.org/10.1111/jth.12367

Đorđević V, Kovač M, Miljić P, Murata M, Takagi A, Pruner I, Francuski D, Kojima T, Radojković D. A novel prothrombin mutation in two families with prominent thrombophilia - the first cases of antithrombin resistance in a Caucasian population. in Journal of Thrombosis and Haemostasis. 2013;11(10):1936-1939.
doi:10.1111/jth.12367 .

Đorđević, Valentina, Kovač, Mirjana, Miljić, Predrag, Murata, M., Takagi, A., Pruner, Iva, Francuski, D., Kojima, T., Radojković, Dragica, "A novel prothrombin mutation in two families with prominent thrombophilia - the first cases of antithrombin resistance in a Caucasian population" in Journal of Thrombosis and Haemostasis, 11, no. 10 (2013):1936-1939,
https://doi.org/10.1111/jth.12367 . .

TY  - CONF
AU  - Bodrozić, J.
AU  - Miljić, Predrag
AU  - Gojnić, M.
AU  - Đorđević, Valentina
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/634
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Prevalence of hereditary thrombophilia is the highest in women who developed pregnancy related thrombosis during first trimester
EP  - 868
SP  - 867
VL  - 11
UR  - https://hdl.handle.net/21.15107/rcub_imagine_634
ER  - 

@conference{
author = "Bodrozić, J. and Miljić, Predrag and Gojnić, M. and Đorđević, Valentina",
year = "2013",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Prevalence of hereditary thrombophilia is the highest in women who developed pregnancy related thrombosis during first trimester",
pages = "868-867",
volume = "11",
url = "https://hdl.handle.net/21.15107/rcub_imagine_634"
}

Bodrozić, J., Miljić, P., Gojnić, M.,& Đorđević, V.. (2013). Prevalence of hereditary thrombophilia is the highest in women who developed pregnancy related thrombosis during first trimester. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 11, 867-868.
https://hdl.handle.net/21.15107/rcub_imagine_634

Bodrozić J, Miljić P, Gojnić M, Đorđević V. Prevalence of hereditary thrombophilia is the highest in women who developed pregnancy related thrombosis during first trimester. in Journal of Thrombosis and Haemostasis. 2013;11:867-868.
https://hdl.handle.net/21.15107/rcub_imagine_634 .

Bodrozić, J., Miljić, Predrag, Gojnić, M., Đorđević, Valentina, "Prevalence of hereditary thrombophilia is the highest in women who developed pregnancy related thrombosis during first trimester" in Journal of Thrombosis and Haemostasis, 11 (2013):867-868,
https://hdl.handle.net/21.15107/rcub_imagine_634 .

TY  - CONF
AU  - Miljić, Predrag
AU  - Bodrozić, J.
AU  - Đorđević, Valentina
AU  - Antović, Aleksandra
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/635
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Molecular markers of blood hipercoagulability and values of overall coagulation potential in double heterozygotes for the FV Leiden and FII G20210A mutation
EP  - 1014
SP  - 1013
VL  - 11
UR  - https://hdl.handle.net/21.15107/rcub_imagine_635
ER  - 

@conference{
author = "Miljić, Predrag and Bodrozić, J. and Đorđević, Valentina and Antović, Aleksandra",
year = "2013",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Molecular markers of blood hipercoagulability and values of overall coagulation potential in double heterozygotes for the FV Leiden and FII G20210A mutation",
pages = "1014-1013",
volume = "11",
url = "https://hdl.handle.net/21.15107/rcub_imagine_635"
}

Miljić, P., Bodrozić, J., Đorđević, V.,& Antović, A.. (2013). Molecular markers of blood hipercoagulability and values of overall coagulation potential in double heterozygotes for the FV Leiden and FII G20210A mutation. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 11, 1013-1014.
https://hdl.handle.net/21.15107/rcub_imagine_635

Miljić P, Bodrozić J, Đorđević V, Antović A. Molecular markers of blood hipercoagulability and values of overall coagulation potential in double heterozygotes for the FV Leiden and FII G20210A mutation. in Journal of Thrombosis and Haemostasis. 2013;11:1013-1014.
https://hdl.handle.net/21.15107/rcub_imagine_635 .

Miljić, Predrag, Bodrozić, J., Đorđević, Valentina, Antović, Aleksandra, "Molecular markers of blood hipercoagulability and values of overall coagulation potential in double heterozygotes for the FV Leiden and FII G20210A mutation" in Journal of Thrombosis and Haemostasis, 11 (2013):1013-1014,
https://hdl.handle.net/21.15107/rcub_imagine_635 .

TY  - CONF
AU  - Elezović, Ivo
AU  - Antić, Darko
AU  - Miljić, Predrag
AU  - Mitrović, Mirjana
AU  - Đorđević, Valentina
AU  - Stojanović, Ljudmila
AU  - Marković, Olivera
AU  - Kovač, Mirjana
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/592
PB  - Pergamon-Elsevier Science Ltd, Oxford
C3  - Thrombosis Research
T1  - Clinical manifestation in hereditary thrombophilias and managenemt of thrombosis, pregnancy and delivery
EP  - S133
SP  - S133
VL  - 130
DO  - 10.1016/j.thromres.2012.08.084
ER  - 

@conference{
author = "Elezović, Ivo and Antić, Darko and Miljić, Predrag and Mitrović, Mirjana and Đorđević, Valentina and Stojanović, Ljudmila and Marković, Olivera and Kovač, Mirjana",
year = "2012",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Clinical manifestation in hereditary thrombophilias and managenemt of thrombosis, pregnancy and delivery",
pages = "S133-S133",
volume = "130",
doi = "10.1016/j.thromres.2012.08.084"
}

Elezović, I., Antić, D., Miljić, P., Mitrović, M., Đorđević, V., Stojanović, L., Marković, O.,& Kovač, M.. (2012). Clinical manifestation in hereditary thrombophilias and managenemt of thrombosis, pregnancy and delivery. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 130, S133-S133.
https://doi.org/10.1016/j.thromres.2012.08.084

Elezović I, Antić D, Miljić P, Mitrović M, Đorđević V, Stojanović L, Marković O, Kovač M. Clinical manifestation in hereditary thrombophilias and managenemt of thrombosis, pregnancy and delivery. in Thrombosis Research. 2012;130:S133-S133.
doi:10.1016/j.thromres.2012.08.084 .

Elezović, Ivo, Antić, Darko, Miljić, Predrag, Mitrović, Mirjana, Đorđević, Valentina, Stojanović, Ljudmila, Marković, Olivera, Kovač, Mirjana, "Clinical manifestation in hereditary thrombophilias and managenemt of thrombosis, pregnancy and delivery" in Thrombosis Research, 130 (2012):S133-S133,
https://doi.org/10.1016/j.thromres.2012.08.084 . .

TY  - JOUR
AU  - Đorđević, Valentina
AU  - Pruner, Iva
AU  - Rakićević, Ljiljana
AU  - Kovač, Mirjana
AU  - Miković, Danijela
AU  - Miljić, Predrag
AU  - Antonijević, Nebojša
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/505
AB  - Tromboze dubokih vena (TDV) su multifaktorijalno oboljenje koje se javlja sa učestalošću 1/1000 stanovnika godišnje. Mutacije FV Leiden, FII G20210A i MTHFR C677T predstavljaju genetske faktore za nastanak venskih tromboza. Cilj ove studije je da se utvrdi učestalost FV Leiden, FII G20210A i MTHFR C677T mutacija kod bolesnika sa TDV gornjih ili donjih ekstremiteta. Studija je obuhvatila 119 bolesnika podeljenih u dve grupe. Grupa bolesnika sa TDV donjih ekstremiteta brojila je 77, a grupa sa TDV gornjih ekstremiteta 42 bolesnika. Prisustvo FV Leiden, FII G20210A i MTHFR C677T mutacija dokazivano je umnožavanjem odgovarajućeg fragmenta gena pomoću lančane reakcije umnožavanja polimerazom i digestijom dobijenih fragmenata restrikcionim enzimima (PCR-RFLP).Učestalost FV Leiden mutacije, u grupi bolesnika sa TDV donjih ekstremiteta, iznosila je 26,0% u heterozigotnom obliku i 1,3% u homozigotnom obliku. U grupi bolesnika sa TDV gornjih ekstremiteta, učestalost heterozigotnih nosilaca iznosila je 7,2%. Mutacija FII G20210A bila je prisutna kod 15,6% ispitanika u grupi bolesnika sa TDV donjih ekstremiteta u heterozigotnom obliku, dok je u grupi sa TDV gornjih ekstremiteta ova mutacija bila zastupljena sa 7,2% u heterozigotnom i 2,3% u homozigotnom obliku. Učestalost MTHFR C677T mutacije kod bolesnika sa TDV donjih ekstremiteta iznosila je 42,8% u heterozigotnom obliku i 13% u homozigotnom obliku, a kod TDV gornjih ekstremiteta 52,4% u heterozigotnom obliku i 9,5% u homozigotnom obliku.Mutacije FV Leiden i FII G20210A predstavljaju značajne faktore rizika za nastanak TDV donjih ekstremiteta. Kod TDV gornjih ekstremiteta ove mutacije su manje zastupljene i potrebno je sprovesti dalja istraživanja koja obuhvataju veći broj bolesnika. MTHFR C677T mutacija je manje značajan faktor rizika i treba ga razmatrati samo u slučajevima kada se pojavljuje u kombinaciji sa drugim faktorima rizika.
AB  - Deep vein thrombosis (DVT) is a multifactorial disease that occurs with frequency of 1/1000 per year. The FV Leiden, FII G20210A and MTHFR C677T mutations represent genetic factors for the occurrence of vein thrombosis. The goal of this study was to determine the frequency of these mutations in patients with DVT of upper and lower limbs. The study encompassed 119 patients divided in two groups. The group of patients with the lower limbs thrombosis included 77 patients, while the upper limbs thrombosis group included 42 patients. The presence of FV Leiden, FII G20210A and MTHFR C677T mutations was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. In patients with DVT of lower limbs, the frequency of FV Leiden mutation was 26,0% in heterozygous form and 1,3% in homozygous form. In the group of patients with DVT of upper limbs, the frequency of heterozygous carriers was 7.2%. In patients with DVT of lower limbs, FII G20210A mutation occurred in heterozygous form in 15.6% subjects, and in the group with DVT of upper limbs the frequency was 7.2% in heterozygous and 2.3% in homozygous form. The frequency of MTHFR C677T mutation in patients with lower limbs DVT was 42.8% in heterozygous form and 13% in homozygous form, while in the group of patients with upper limbs DVT, the frequency was 52.4% in heterozygous form and 9.5% in homozygous form. The FV Leiden and FII G20210A mutations represent significant risk factors for the occurrence of DVT of lower limbs. These mutations are less frequent in DVT of upper limbs and more extensive further studies are needed to determine their potential role. The MTHFR C677T mutation represents less significant risk factor for lower limb DVT and should be taken into account only in cases when it occurs in combination with other risk factors.
PB  - Društvo genetičara Srbije, Beograd
T2  - Genetika-Belgrade
T1  - Mutacije FV Leiden, FII G20210A i MTHFR C677T kao faktori rizika za nastanak tromboze dubokih vena gornjih i donjih ekstremiteta
T1  - FV Leiden, FII G20210A and MTHFR C677T mutations in patients with lower or upper limb deep vein thrombosis
EP  - 380
IS  - 2
SP  - 371
VL  - 43
DO  - 10.2298/GENSR1102371D
ER  - 

@article{
author = "Đorđević, Valentina and Pruner, Iva and Rakićević, Ljiljana and Kovač, Mirjana and Miković, Danijela and Miljić, Predrag and Antonijević, Nebojša and Radojković, Dragica",
year = "2011",
abstract = "Tromboze dubokih vena (TDV) su multifaktorijalno oboljenje koje se javlja sa učestalošću 1/1000 stanovnika godišnje. Mutacije FV Leiden, FII G20210A i MTHFR C677T predstavljaju genetske faktore za nastanak venskih tromboza. Cilj ove studije je da se utvrdi učestalost FV Leiden, FII G20210A i MTHFR C677T mutacija kod bolesnika sa TDV gornjih ili donjih ekstremiteta. Studija je obuhvatila 119 bolesnika podeljenih u dve grupe. Grupa bolesnika sa TDV donjih ekstremiteta brojila je 77, a grupa sa TDV gornjih ekstremiteta 42 bolesnika. Prisustvo FV Leiden, FII G20210A i MTHFR C677T mutacija dokazivano je umnožavanjem odgovarajućeg fragmenta gena pomoću lančane reakcije umnožavanja polimerazom i digestijom dobijenih fragmenata restrikcionim enzimima (PCR-RFLP).Učestalost FV Leiden mutacije, u grupi bolesnika sa TDV donjih ekstremiteta, iznosila je 26,0% u heterozigotnom obliku i 1,3% u homozigotnom obliku. U grupi bolesnika sa TDV gornjih ekstremiteta, učestalost heterozigotnih nosilaca iznosila je 7,2%. Mutacija FII G20210A bila je prisutna kod 15,6% ispitanika u grupi bolesnika sa TDV donjih ekstremiteta u heterozigotnom obliku, dok je u grupi sa TDV gornjih ekstremiteta ova mutacija bila zastupljena sa 7,2% u heterozigotnom i 2,3% u homozigotnom obliku. Učestalost MTHFR C677T mutacije kod bolesnika sa TDV donjih ekstremiteta iznosila je 42,8% u heterozigotnom obliku i 13% u homozigotnom obliku, a kod TDV gornjih ekstremiteta 52,4% u heterozigotnom obliku i 9,5% u homozigotnom obliku.Mutacije FV Leiden i FII G20210A predstavljaju značajne faktore rizika za nastanak TDV donjih ekstremiteta. Kod TDV gornjih ekstremiteta ove mutacije su manje zastupljene i potrebno je sprovesti dalja istraživanja koja obuhvataju veći broj bolesnika. MTHFR C677T mutacija je manje značajan faktor rizika i treba ga razmatrati samo u slučajevima kada se pojavljuje u kombinaciji sa drugim faktorima rizika., Deep vein thrombosis (DVT) is a multifactorial disease that occurs with frequency of 1/1000 per year. The FV Leiden, FII G20210A and MTHFR C677T mutations represent genetic factors for the occurrence of vein thrombosis. The goal of this study was to determine the frequency of these mutations in patients with DVT of upper and lower limbs. The study encompassed 119 patients divided in two groups. The group of patients with the lower limbs thrombosis included 77 patients, while the upper limbs thrombosis group included 42 patients. The presence of FV Leiden, FII G20210A and MTHFR C677T mutations was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. In patients with DVT of lower limbs, the frequency of FV Leiden mutation was 26,0% in heterozygous form and 1,3% in homozygous form. In the group of patients with DVT of upper limbs, the frequency of heterozygous carriers was 7.2%. In patients with DVT of lower limbs, FII G20210A mutation occurred in heterozygous form in 15.6% subjects, and in the group with DVT of upper limbs the frequency was 7.2% in heterozygous and 2.3% in homozygous form. The frequency of MTHFR C677T mutation in patients with lower limbs DVT was 42.8% in heterozygous form and 13% in homozygous form, while in the group of patients with upper limbs DVT, the frequency was 52.4% in heterozygous form and 9.5% in homozygous form. The FV Leiden and FII G20210A mutations represent significant risk factors for the occurrence of DVT of lower limbs. These mutations are less frequent in DVT of upper limbs and more extensive further studies are needed to determine their potential role. The MTHFR C677T mutation represents less significant risk factor for lower limb DVT and should be taken into account only in cases when it occurs in combination with other risk factors.",
publisher = "Društvo genetičara Srbije, Beograd",
journal = "Genetika-Belgrade",
title = "Mutacije FV Leiden, FII G20210A i MTHFR C677T kao faktori rizika za nastanak tromboze dubokih vena gornjih i donjih ekstremiteta, FV Leiden, FII G20210A and MTHFR C677T mutations in patients with lower or upper limb deep vein thrombosis",
pages = "380-371",
number = "2",
volume = "43",
doi = "10.2298/GENSR1102371D"
}

Đorđević, V., Pruner, I., Rakićević, L., Kovač, M., Miković, D., Miljić, P., Antonijević, N.,& Radojković, D.. (2011). Mutacije FV Leiden, FII G20210A i MTHFR C677T kao faktori rizika za nastanak tromboze dubokih vena gornjih i donjih ekstremiteta. in Genetika-Belgrade
Društvo genetičara Srbije, Beograd., 43(2), 371-380.
https://doi.org/10.2298/GENSR1102371D

Đorđević V, Pruner I, Rakićević L, Kovač M, Miković D, Miljić P, Antonijević N, Radojković D. Mutacije FV Leiden, FII G20210A i MTHFR C677T kao faktori rizika za nastanak tromboze dubokih vena gornjih i donjih ekstremiteta. in Genetika-Belgrade. 2011;43(2):371-380.
doi:10.2298/GENSR1102371D .

Đorđević, Valentina, Pruner, Iva, Rakićević, Ljiljana, Kovač, Mirjana, Miković, Danijela, Miljić, Predrag, Antonijević, Nebojša, Radojković, Dragica, "Mutacije FV Leiden, FII G20210A i MTHFR C677T kao faktori rizika za nastanak tromboze dubokih vena gornjih i donjih ekstremiteta" in Genetika-Belgrade, 43, no. 2 (2011):371-380,
https://doi.org/10.2298/GENSR1102371D . .

TY  - CONF
AU  - Đorđević, Valentina
AU  - Pruner, Iva
AU  - Kovač, Mirjana
AU  - Miljić, Predrag
AU  - Antonijević, Nebojša
AU  - Kojić, Snežana
AU  - Radojković, Dragica
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/473
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Three novel 3 ' end prothrombin gene polymorphisms and their association with thrombophilia
EP  - 873
SP  - 873
VL  - 9
UR  - https://hdl.handle.net/21.15107/rcub_imagine_473
ER  - 

@conference{
author = "Đorđević, Valentina and Pruner, Iva and Kovač, Mirjana and Miljić, Predrag and Antonijević, Nebojša and Kojić, Snežana and Radojković, Dragica",
year = "2011",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Three novel 3 ' end prothrombin gene polymorphisms and their association with thrombophilia",
pages = "873-873",
volume = "9",
url = "https://hdl.handle.net/21.15107/rcub_imagine_473"
}

Đorđević, V., Pruner, I., Kovač, M., Miljić, P., Antonijević, N., Kojić, S.,& Radojković, D.. (2011). Three novel 3 ' end prothrombin gene polymorphisms and their association with thrombophilia. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 9, 873-873.
https://hdl.handle.net/21.15107/rcub_imagine_473

Đorđević V, Pruner I, Kovač M, Miljić P, Antonijević N, Kojić S, Radojković D. Three novel 3 ' end prothrombin gene polymorphisms and their association with thrombophilia. in Journal of Thrombosis and Haemostasis. 2011;9:873-873.
https://hdl.handle.net/21.15107/rcub_imagine_473 .

Đorđević, Valentina, Pruner, Iva, Kovač, Mirjana, Miljić, Predrag, Antonijević, Nebojša, Kojić, Snežana, Radojković, Dragica, "Three novel 3 ' end prothrombin gene polymorphisms and their association with thrombophilia" in Journal of Thrombosis and Haemostasis, 9 (2011):873-873,
https://hdl.handle.net/21.15107/rcub_imagine_473 .

TY  - CONF
AU  - Elezović, I
AU  - Antić, Darko
AU  - Miljić, Predrag
AU  - Đorđević, Valentina
AU  - Stojanović, L.
AU  - Marković, O.
AU  - Kovač, Mirjana
PY  - 2011
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/475
PB  - Wiley-Blackwell, Hoboken
C3  - Journal of Thrombosis and Haemostasis
T1  - Thrombosis and pregnancy in hereditary thrombophilias
EP  - 429
SP  - 429
VL  - 9
UR  - https://hdl.handle.net/21.15107/rcub_imagine_475
ER  - 

@conference{
author = "Elezović, I and Antić, Darko and Miljić, Predrag and Đorđević, Valentina and Stojanović, L. and Marković, O. and Kovač, Mirjana",
year = "2011",
publisher = "Wiley-Blackwell, Hoboken",
journal = "Journal of Thrombosis and Haemostasis",
title = "Thrombosis and pregnancy in hereditary thrombophilias",
pages = "429-429",
volume = "9",
url = "https://hdl.handle.net/21.15107/rcub_imagine_475"
}

Elezović, I., Antić, D., Miljić, P., Đorđević, V., Stojanović, L., Marković, O.,& Kovač, M.. (2011). Thrombosis and pregnancy in hereditary thrombophilias. in Journal of Thrombosis and Haemostasis
Wiley-Blackwell, Hoboken., 9, 429-429.
https://hdl.handle.net/21.15107/rcub_imagine_475

Elezović I, Antić D, Miljić P, Đorđević V, Stojanović L, Marković O, Kovač M. Thrombosis and pregnancy in hereditary thrombophilias. in Journal of Thrombosis and Haemostasis. 2011;9:429-429.
https://hdl.handle.net/21.15107/rcub_imagine_475 .

Elezović, I, Antić, Darko, Miljić, Predrag, Đorđević, Valentina, Stojanović, L., Marković, O., Kovač, Mirjana, "Thrombosis and pregnancy in hereditary thrombophilias" in Journal of Thrombosis and Haemostasis, 9 (2011):429-429,
https://hdl.handle.net/21.15107/rcub_imagine_475 .

TY  - CONF
AU  - Miljić, Predrag
AU  - Heylen, Evelien
AU  - Willemse, Johan
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Colović, Milica
AU  - Elezović, Ivo
AU  - Hendriks, Dirk
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/426
AB  - Although the maintenance of precise balance between coagulation and fibrinolysis is of utmost importance for normal haemostasis, until recently these two systems were considered as completely separate mechanisms involved in the process of formation and dissolution of blood clot. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently described attenuator of the fibrinolytic rate and is considered to be the molecular link between coagulation and fibrinolysis. TAFI circulates in plasma as an inactive precursor and its conversion in active enzyme (TAFIa) occurs by the action of thrombin or plasmin, but most efficiently by thrombin in the presence of its cofactor thrombomodulin. Once generated, TAFI down-regulates fibrinolysis by removing C-terminal lysine residues from partially degraded fibrin; thereby preventing the upregulation of plasminogen binding and activation. Because TAFI is activated by thrombin on one side, and acts as the attenuator of fibrinolysis on another side, it enables fine synchronization between these two systems. The antifibrinolytic function of TAFI mostly depends on TAFI concentration, the rate of its activation and the half-life of TAFIa in plasma. Changes in thrombin generation can have a profound effect on the rate of TAFI activation, and consequently on the rate of fibrinolysis. Therefore, it has been hypothesized that increased thrombin generation seen in thrombophilia patients may enhance TAFI activation, leading to a hypofibrinolytic state, which may further contribute to the thrombotic tendency. However, the results of several studies, in which relation between TAFI level and the occurrence of thromboembolic complications in carriers of hereditary thrombophilia have been investigated, were not consistent.
PB  - Srpsko lekarsko društvo, Beograd
C3  - Srpski arhiv za celokupno lekarstvo
T1  - Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis
EP  - 78
SP  - 74
VL  - 138
DO  - 10.2298/SARH10S1074M
ER  - 

@conference{
author = "Miljić, Predrag and Heylen, Evelien and Willemse, Johan and Đorđević, Valentina and Radojković, Dragica and Colović, Milica and Elezović, Ivo and Hendriks, Dirk",
year = "2010",
abstract = "Although the maintenance of precise balance between coagulation and fibrinolysis is of utmost importance for normal haemostasis, until recently these two systems were considered as completely separate mechanisms involved in the process of formation and dissolution of blood clot. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently described attenuator of the fibrinolytic rate and is considered to be the molecular link between coagulation and fibrinolysis. TAFI circulates in plasma as an inactive precursor and its conversion in active enzyme (TAFIa) occurs by the action of thrombin or plasmin, but most efficiently by thrombin in the presence of its cofactor thrombomodulin. Once generated, TAFI down-regulates fibrinolysis by removing C-terminal lysine residues from partially degraded fibrin; thereby preventing the upregulation of plasminogen binding and activation. Because TAFI is activated by thrombin on one side, and acts as the attenuator of fibrinolysis on another side, it enables fine synchronization between these two systems. The antifibrinolytic function of TAFI mostly depends on TAFI concentration, the rate of its activation and the half-life of TAFIa in plasma. Changes in thrombin generation can have a profound effect on the rate of TAFI activation, and consequently on the rate of fibrinolysis. Therefore, it has been hypothesized that increased thrombin generation seen in thrombophilia patients may enhance TAFI activation, leading to a hypofibrinolytic state, which may further contribute to the thrombotic tendency. However, the results of several studies, in which relation between TAFI level and the occurrence of thromboembolic complications in carriers of hereditary thrombophilia have been investigated, were not consistent.",
publisher = "Srpsko lekarsko društvo, Beograd",
journal = "Srpski arhiv za celokupno lekarstvo",
title = "Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis",
pages = "78-74",
volume = "138",
doi = "10.2298/SARH10S1074M"
}

Miljić, P., Heylen, E., Willemse, J., Đorđević, V., Radojković, D., Colović, M., Elezović, I.,& Hendriks, D.. (2010). Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis. in Srpski arhiv za celokupno lekarstvo
Srpsko lekarsko društvo, Beograd., 138, 74-78.
https://doi.org/10.2298/SARH10S1074M

Miljić P, Heylen E, Willemse J, Đorđević V, Radojković D, Colović M, Elezović I, Hendriks D. Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis. in Srpski arhiv za celokupno lekarstvo. 2010;138:74-78.
doi:10.2298/SARH10S1074M .

Miljić, Predrag, Heylen, Evelien, Willemse, Johan, Đorđević, Valentina, Radojković, Dragica, Colović, Milica, Elezović, Ivo, Hendriks, Dirk, "Thrombin Activatable Fibrinolysis Inhibitor (TAFI): A Molecular Link Between Coagulation and Fibrinolysis" in Srpski arhiv za celokupno lekarstvo, 138 (2010):74-78,
https://doi.org/10.2298/SARH10S1074M . .

TY  - JOUR
AU  - Pruner, Iva
AU  - Đorđević, Valentina
AU  - Miljić, Predrag
AU  - Kovač, Mirjana
AU  - Antonijević, Nebojša
AU  - Rakićević, Ljiljana
AU  - Radojković, Dragica
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/441
AB  - Recurrent fetal loss (RFL) is common health problem affecting up to 5% of women of reproductive age. It has been shown that plasma thrombin-activatable fibrinolysis inhibitor (TAFI) concentrations increase during pregnancy and return to baseline levels soon after delivery. The +1040C/T single nucleotide polymorphism in coding region of TAFI gene is associated with TAFI blood levels. The aim of our study was to investigate the relationship between +1040C/T polymorphism in TAFI gene and idiopathic RFL. Study was carried out in a group of 120 women (61 controls and 59 women with idiopathic RFL). The R1040C/T polymorphism was detected by restriction fragment length polymorphism PCR. Increased frequency of +1040T/T genotype was observed in a study group, but without statistically significant difference. Carriers of T/T genotype have increased risk of fetal loss by 1.23-fold, compared with carriers of C/C (95% CI 0.462-3.277; P=0.7) and 1.34-fold compared with carriers of C/T genotype (95% CI 0.501-3.601; P=0.6). C allele is associated with reduced risk of recurrent fetal loss compared with T allele (OR 0.91; 95% CI 0.545-1.533; P=0.7). In conclusion, we observed increased frequency of +1040T/T genotype in a patient group, suggesting that this genotype could be potential risk factor for idiopathic RFL. Further investigation should be carried out in order to establish the role of this polymorphism in the etiology of idiopathic recurrent miscarriages. Blood Coagul Fibrinolysis 21: 679-682
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Blood Coagulation & Fibrinolysis
T1  - +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss
EP  - 682
IS  - 7
SP  - 679
VL  - 21
DO  - 10.1097/MBC.0b013e32833e426d
ER  - 

@article{
author = "Pruner, Iva and Đorđević, Valentina and Miljić, Predrag and Kovač, Mirjana and Antonijević, Nebojša and Rakićević, Ljiljana and Radojković, Dragica",
year = "2010",
abstract = "Recurrent fetal loss (RFL) is common health problem affecting up to 5% of women of reproductive age. It has been shown that plasma thrombin-activatable fibrinolysis inhibitor (TAFI) concentrations increase during pregnancy and return to baseline levels soon after delivery. The +1040C/T single nucleotide polymorphism in coding region of TAFI gene is associated with TAFI blood levels. The aim of our study was to investigate the relationship between +1040C/T polymorphism in TAFI gene and idiopathic RFL. Study was carried out in a group of 120 women (61 controls and 59 women with idiopathic RFL). The R1040C/T polymorphism was detected by restriction fragment length polymorphism PCR. Increased frequency of +1040T/T genotype was observed in a study group, but without statistically significant difference. Carriers of T/T genotype have increased risk of fetal loss by 1.23-fold, compared with carriers of C/C (95% CI 0.462-3.277; P=0.7) and 1.34-fold compared with carriers of C/T genotype (95% CI 0.501-3.601; P=0.6). C allele is associated with reduced risk of recurrent fetal loss compared with T allele (OR 0.91; 95% CI 0.545-1.533; P=0.7). In conclusion, we observed increased frequency of +1040T/T genotype in a patient group, suggesting that this genotype could be potential risk factor for idiopathic RFL. Further investigation should be carried out in order to establish the role of this polymorphism in the etiology of idiopathic recurrent miscarriages. Blood Coagul Fibrinolysis 21: 679-682",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Blood Coagulation & Fibrinolysis",
title = "+1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss",
pages = "682-679",
number = "7",
volume = "21",
doi = "10.1097/MBC.0b013e32833e426d"
}

Pruner, I., Đorđević, V., Miljić, P., Kovač, M., Antonijević, N., Rakićević, L.,& Radojković, D.. (2010). +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss. in Blood Coagulation & Fibrinolysis
Lippincott Williams & Wilkins, Philadelphia., 21(7), 679-682.
https://doi.org/10.1097/MBC.0b013e32833e426d

Pruner I, Đorđević V, Miljić P, Kovač M, Antonijević N, Rakićević L, Radojković D. +1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss. in Blood Coagulation & Fibrinolysis. 2010;21(7):679-682.
doi:10.1097/MBC.0b013e32833e426d .

Pruner, Iva, Đorđević, Valentina, Miljić, Predrag, Kovač, Mirjana, Antonijević, Nebojša, Rakićević, Ljiljana, Radojković, Dragica, "+1040 C/T polymorphism in coding region of thrombin-activatable fibrinolysis inhibitor gene and the risk of idiopathic recurrent fetal loss" in Blood Coagulation & Fibrinolysis, 21, no. 7 (2010):679-682,
https://doi.org/10.1097/MBC.0b013e32833e426d . .

TY  - CONF
AU  - Elezović, V.
AU  - Miljić, Predrag
AU  - Antić, Darko
AU  - Stojanović, L.
AU  - Marković, O.
AU  - Đorđević, Valentina
AU  - Kovač, Mirjana
PY  - 2010
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/411
PB  - Ferrata Storti Foundation, Pavia
C3  - Haematologica-The Hematology Journal
T1  - Clinical manifestation of antiphospholipid antibodies
EP  - 759
SP  - 759
VL  - 95
UR  - https://hdl.handle.net/21.15107/rcub_imagine_411
ER  - 

@conference{
author = "Elezović, V. and Miljić, Predrag and Antić, Darko and Stojanović, L. and Marković, O. and Đorđević, Valentina and Kovač, Mirjana",
year = "2010",
publisher = "Ferrata Storti Foundation, Pavia",
journal = "Haematologica-The Hematology Journal",
title = "Clinical manifestation of antiphospholipid antibodies",
pages = "759-759",
volume = "95",
url = "https://hdl.handle.net/21.15107/rcub_imagine_411"
}

Elezović, V., Miljić, P., Antić, D., Stojanović, L., Marković, O., Đorđević, V.,& Kovač, M.. (2010). Clinical manifestation of antiphospholipid antibodies. in Haematologica-The Hematology Journal
Ferrata Storti Foundation, Pavia., 95, 759-759.
https://hdl.handle.net/21.15107/rcub_imagine_411

Elezović V, Miljić P, Antić D, Stojanović L, Marković O, Đorđević V, Kovač M. Clinical manifestation of antiphospholipid antibodies. in Haematologica-The Hematology Journal. 2010;95:759-759.
https://hdl.handle.net/21.15107/rcub_imagine_411 .

Elezović, V., Miljić, Predrag, Antić, Darko, Stojanović, L., Marković, O., Đorđević, Valentina, Kovač, Mirjana, "Clinical manifestation of antiphospholipid antibodies" in Haematologica-The Hematology Journal, 95 (2010):759-759,
https://hdl.handle.net/21.15107/rcub_imagine_411 .

TY  - JOUR
AU  - Nagorni-Obradović, L. J.
AU  - Miljić, Predrag
AU  - Đorđević, Valentina
AU  - Pesut, D. P.
AU  - Jovanović, D.
AU  - Stojsić, J.
AU  - Stević, R.
AU  - Radojković, Dragica
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/372
AB  - 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.
PB  - Macedonian Acad Sciences Arts, Skopje
T2  - Balkan Journal of Medical Genetics
T1  - The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products
EP  - 75
IS  - 2
SP  - 69
VL  - 12
DO  - 10.2478/v10034-010-0007-7
ER  - 

@article{
author = "Nagorni-Obradović, L. J. and Miljić, Predrag and Đorđević, Valentina and Pesut, D. P. and Jovanović, D. and Stojsić, J. and Stević, R. and Radojković, Dragica",
year = "2009",
abstract = "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.",
publisher = "Macedonian Acad Sciences Arts, Skopje",
journal = "Balkan Journal of Medical Genetics",
title = "The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products",
pages = "75-69",
number = "2",
volume = "12",
doi = "10.2478/v10034-010-0007-7"
}

Nagorni-Obradović, L. J., Miljić, P., Đorđević, V., Pesut, D. P., Jovanović, D., Stojsić, J., Stević, R.,& Radojković, D.. (2009). The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products. in Balkan Journal of Medical Genetics
Macedonian Acad Sciences Arts, Skopje., 12(2), 69-75.
https://doi.org/10.2478/v10034-010-0007-7

Nagorni-Obradović LJ, Miljić P, Đorđević V, Pesut DP, Jovanović D, Stojsić J, Stević R, Radojković D. The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products. in Balkan Journal of Medical Genetics. 2009;12(2):69-75.
doi:10.2478/v10034-010-0007-7 .

Nagorni-Obradović, L. J., Miljić, Predrag, Đorđević, Valentina, Pesut, D. P., Jovanović, D., Stojsić, J., Stević, R., Radojković, Dragica, "The prothrombin factor ii g20210a mutation with pulmonary thromboembolism and a normal level of fibrin degradation products" in Balkan Journal of Medical Genetics, 12, no. 2 (2009):69-75,
https://doi.org/10.2478/v10034-010-0007-7 . .

TY  - JOUR
AU  - Heylen, Evelien
AU  - Miljić, Predrag
AU  - Willemse, Johan
AU  - Đorđević, Valentina
AU  - Radojković, Dragica
AU  - Colović, Milica
AU  - Elezović, Ivo
AU  - Hendriks, Dirk
PY  - 2009
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/399
AB  - Introduction: It is considered that high plasma levels of procarboxypeptidase U (proCPU or TAFI) can promote the development of thrombosis, but data comparing proCPU levels in thrombophilia carriers and healthy subjects are rather scarce. Moreover, the results of previous studies on the risk of thrombosis related to high proCPU concentration in this population were not consistent. Although the 325 polymorphism, of proCPU has a significant effect on the CPU half-life, it's influence on the risk of thrombosis or spontaneous pregnancy loss in carriers of hereditary thrombophilia is not clear. Materials and Methods: The study population consisted of 144 thrombophilic patients (94 heterozygous and 10 homozygous carriers of FV Leiden, 26 heterozygous carriers of the prothrombin G20210A variation and 14 double carriers of FV Leiden and FII variation) and 69 healthy controls. Results: The results show that patients with inherited thrombophilia have a tendency toward lower mean proCPU plasma levels compared to healthy controls, however, this difference was only significant in carriers of FII G20210A (p = 0.014). A higher frequency of the most stable Ile325Ile proCPU was seen among carriers of I'll G20210A mutation compared to the control group (19% vs 7%; p = 0.186). In the second part of the study proCPU as a risk factor for thrombosis was evaluated. In heterozygous carriers of FV Leiden or FII G20210A high levels of proCPU conferred to an almost 4-fold increased risk for spontaneous onset thrombosis. The more stable Ile325Ile proCPU seems to impose a higher risk for clinical manifestation of the thrombophilic condition. Finally, a significant positive correlation between F1 + 2 and proCPU concentration was seen. Conclusion: The increased risk of thrombosis in thrombophilia patients is not only ascribable to an increased thrombin generation, but also high levels of proCPU and the presence of the 325Ile genotype tip the balance towards thrombotic tendency even further.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Thrombosis Research
T1  - Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia
EP  - 432
IS  - 4
SP  - 427
VL  - 124
DO  - 10.1016/j.thromres.2009.01.005
ER  - 

@article{
author = "Heylen, Evelien and Miljić, Predrag and Willemse, Johan and Đorđević, Valentina and Radojković, Dragica and Colović, Milica and Elezović, Ivo and Hendriks, Dirk",
year = "2009",
abstract = "Introduction: It is considered that high plasma levels of procarboxypeptidase U (proCPU or TAFI) can promote the development of thrombosis, but data comparing proCPU levels in thrombophilia carriers and healthy subjects are rather scarce. Moreover, the results of previous studies on the risk of thrombosis related to high proCPU concentration in this population were not consistent. Although the 325 polymorphism, of proCPU has a significant effect on the CPU half-life, it's influence on the risk of thrombosis or spontaneous pregnancy loss in carriers of hereditary thrombophilia is not clear. Materials and Methods: The study population consisted of 144 thrombophilic patients (94 heterozygous and 10 homozygous carriers of FV Leiden, 26 heterozygous carriers of the prothrombin G20210A variation and 14 double carriers of FV Leiden and FII variation) and 69 healthy controls. Results: The results show that patients with inherited thrombophilia have a tendency toward lower mean proCPU plasma levels compared to healthy controls, however, this difference was only significant in carriers of FII G20210A (p = 0.014). A higher frequency of the most stable Ile325Ile proCPU was seen among carriers of I'll G20210A mutation compared to the control group (19% vs 7%; p = 0.186). In the second part of the study proCPU as a risk factor for thrombosis was evaluated. In heterozygous carriers of FV Leiden or FII G20210A high levels of proCPU conferred to an almost 4-fold increased risk for spontaneous onset thrombosis. The more stable Ile325Ile proCPU seems to impose a higher risk for clinical manifestation of the thrombophilic condition. Finally, a significant positive correlation between F1 + 2 and proCPU concentration was seen. Conclusion: The increased risk of thrombosis in thrombophilia patients is not only ascribable to an increased thrombin generation, but also high levels of proCPU and the presence of the 325Ile genotype tip the balance towards thrombotic tendency even further.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Thrombosis Research",
title = "Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia",
pages = "432-427",
number = "4",
volume = "124",
doi = "10.1016/j.thromres.2009.01.005"
}

Heylen, E., Miljić, P., Willemse, J., Đorđević, V., Radojković, D., Colović, M., Elezović, I.,& Hendriks, D.. (2009). Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia. in Thrombosis Research
Pergamon-Elsevier Science Ltd, Oxford., 124(4), 427-432.
https://doi.org/10.1016/j.thromres.2009.01.005

Heylen E, Miljić P, Willemse J, Đorđević V, Radojković D, Colović M, Elezović I, Hendriks D. Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia. in Thrombosis Research. 2009;124(4):427-432.
doi:10.1016/j.thromres.2009.01.005 .

Heylen, Evelien, Miljić, Predrag, Willemse, Johan, Đorđević, Valentina, Radojković, Dragica, Colović, Milica, Elezović, Ivo, Hendriks, Dirk, "Procarboxypeptidase U (TAFI) contributes to the risk of thrombosis in patients with hereditary thrombophilia" in Thrombosis Research, 124, no. 4 (2009):427-432,
https://doi.org/10.1016/j.thromres.2009.01.005 . .

TY  - JOUR
AU  - Perunicić, Jovan
AU  - Antonijević, Nebojša
AU  - Miljić, Predrag
AU  - Đorđević, Valentina
AU  - Miković, Danijela
AU  - Kovač, Mirjana
AU  - Đokić, Milan
AU  - Mrdović, Igor
AU  - Nikolić, Aleksandra
AU  - Vasiljević, Zorana
PY  - 2008
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/320
AB  - Treatment of patients with heparin-induced thrombocytopenia type II (HIT II) and thrombosis in some cases that represents a clinical challenge, which, if unrecognized, may lead to treatment delay or disease progression with potentially lethal outcome. We present a case of a 19-year-old patient with antiphospholipid syndrome, factor V (FV) Leiden mutation in heterozygous state, and venous thromboembolism. The patient was subjected to intravenous infusions of unfractionated heparin (UFH), and 16 days after the beginning of the treatment, his condition worsened, with thrombocytopenia and extension of thrombosis. Whereas the patient had a high clinical score for HIT II, functional and antigenic assays for the presence of HIT antibodies were negative. After repeated negative functional and antigenic assays, pseudo-HIT was suspected and nadroparin was introduced, which resulted in further worsening of the clinical presentation. Disease remission, along with complete normalization of platelet count, was finally accomplished with the introduction of lepirudin. The presence of multiple comorbid states, such as antiphospholipid syndrome, can potentially make laboratory confirmation of disease more difficult in patients with HIT II. In our opinion, it is of great importance that HIT II diagnosis be primarily clinical and that laboratory test results are carefully interpreted, especially when HIT is indicated by high clinical score values.
PB  - Springer, Dordrecht
T2  - Journal of Thrombosis and Thrombolysis
T1  - Clinical challenge: heparin-induced thrombocytopenia type II (HIT II) or pseudo-HIT in a patient with antiphospholipid syndrome
EP  - 146
IS  - 2
SP  - 142
VL  - 26
DO  - 10.1007/s11239-007-0076-y
ER  - 

@article{
author = "Perunicić, Jovan and Antonijević, Nebojša and Miljić, Predrag and Đorđević, Valentina and Miković, Danijela and Kovač, Mirjana and Đokić, Milan and Mrdović, Igor and Nikolić, Aleksandra and Vasiljević, Zorana",
year = "2008",
abstract = "Treatment of patients with heparin-induced thrombocytopenia type II (HIT II) and thrombosis in some cases that represents a clinical challenge, which, if unrecognized, may lead to treatment delay or disease progression with potentially lethal outcome. We present a case of a 19-year-old patient with antiphospholipid syndrome, factor V (FV) Leiden mutation in heterozygous state, and venous thromboembolism. The patient was subjected to intravenous infusions of unfractionated heparin (UFH), and 16 days after the beginning of the treatment, his condition worsened, with thrombocytopenia and extension of thrombosis. Whereas the patient had a high clinical score for HIT II, functional and antigenic assays for the presence of HIT antibodies were negative. After repeated negative functional and antigenic assays, pseudo-HIT was suspected and nadroparin was introduced, which resulted in further worsening of the clinical presentation. Disease remission, along with complete normalization of platelet count, was finally accomplished with the introduction of lepirudin. The presence of multiple comorbid states, such as antiphospholipid syndrome, can potentially make laboratory confirmation of disease more difficult in patients with HIT II. In our opinion, it is of great importance that HIT II diagnosis be primarily clinical and that laboratory test results are carefully interpreted, especially when HIT is indicated by high clinical score values.",
publisher = "Springer, Dordrecht",
journal = "Journal of Thrombosis and Thrombolysis",
title = "Clinical challenge: heparin-induced thrombocytopenia type II (HIT II) or pseudo-HIT in a patient with antiphospholipid syndrome",
pages = "146-142",
number = "2",
volume = "26",
doi = "10.1007/s11239-007-0076-y"
}

Perunicić, J., Antonijević, N., Miljić, P., Đorđević, V., Miković, D., Kovač, M., Đokić, M., Mrdović, I., Nikolić, A.,& Vasiljević, Z.. (2008). Clinical challenge: heparin-induced thrombocytopenia type II (HIT II) or pseudo-HIT in a patient with antiphospholipid syndrome. in Journal of Thrombosis and Thrombolysis
Springer, Dordrecht., 26(2), 142-146.
https://doi.org/10.1007/s11239-007-0076-y

Perunicić J, Antonijević N, Miljić P, Đorđević V, Miković D, Kovač M, Đokić M, Mrdović I, Nikolić A, Vasiljević Z. Clinical challenge: heparin-induced thrombocytopenia type II (HIT II) or pseudo-HIT in a patient with antiphospholipid syndrome. in Journal of Thrombosis and Thrombolysis. 2008;26(2):142-146.
doi:10.1007/s11239-007-0076-y .

Perunicić, Jovan, Antonijević, Nebojša, Miljić, Predrag, Đorđević, Valentina, Miković, Danijela, Kovač, Mirjana, Đokić, Milan, Mrdović, Igor, Nikolić, Aleksandra, Vasiljević, Zorana, "Clinical challenge: heparin-induced thrombocytopenia type II (HIT II) or pseudo-HIT in a patient with antiphospholipid syndrome" in Journal of Thrombosis and Thrombolysis, 26, no. 2 (2008):142-146,
https://doi.org/10.1007/s11239-007-0076-y . .

TY  - JOUR
AU  - Đorđević, Valentina
AU  - Rakićević, Ljiljana
AU  - Miljić, Predrag
AU  - Miković, Danijela
AU  - Kovač, Mirjana
AU  - Radojković, Dragica
AU  - Savić, Ana
PY  - 2005
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/212
AB  - FV Leiden mutacija je veoma značajan genetički faktor rizika za pojavu venskog tromboembolizma (VTE). U okviru ove studije analizirana je klinička slika i uticaj stečenih i genetičkih faktora rizika u grupi od 100 bolesnika, nosilaca FV Leiden mutacije (95 heterozigota i 5 homozigota). Devedeset jedan bolesnik je imao VTE, sa trombozom dubokih vena donjih ekstremiteta kao najčešćom manifestacijom. Kod 68,6% žena bio je prisutan neki od stečenih faktora rizika, dok je to bio slučaj kod 28,6% muškaraca. Mutacija FII G20210A je detektovana kod 9,5%, MTHFR 677TT kod 8,4%, a obe mutacije su bile prisutne u 2,1% heterozigotnih nosilaca FV Leiden mutacije. Rezultati ove studije ukazuju na značaj poznavanja udruženih faktora rizika kod pacijenata koji su nosioci FV Leiden mutacije.
AB  - FV Leiden mutation is an important genetic risk factor for venous thromboembolsm (VTE). In this study we have analyzed clinical manifestation and the impact of other genetic and acquired risk factors in 100 patients (95 heterozygous and 5 homozygous) carriers of FV Leiden mutation. Among these patients, 91 experienced VTE, with down limb deep vein thrombosis as the most frequent manifestation. An acquired risk factor was present in 68.6% of women, whereas this was the case in 28.6% of men. FIIG20210A was present in 9.5%, MTHFR 677TT in 8.4% and both mutations in 2.1% of the heterozygous FV Leiden carriers. Our results suggest that knowledge of coexisting factors predisposing to VTE is very important for FV Leiden mutation carriers and may contribute to the prevention of VTE episodes.
PB  - Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd
T2  - Jugoslovenska medicinska biohemija
T1  - Uticaj stečenih i genetičkih faktora na ispoljavanje trombofilije kod nosilaca FV Leiden mutacije
T1  - Impact of acquired and genetic factors on thrombophilic phenotype in FV Leiden mutation carriers
EP  - 146
IS  - 2
SP  - 141
VL  - 24
DO  - 10.2298/JMH0502141D
ER  - 

@article{
author = "Đorđević, Valentina and Rakićević, Ljiljana and Miljić, Predrag and Miković, Danijela and Kovač, Mirjana and Radojković, Dragica and Savić, Ana",
year = "2005",
abstract = "FV Leiden mutacija je veoma značajan genetički faktor rizika za pojavu venskog tromboembolizma (VTE). U okviru ove studije analizirana je klinička slika i uticaj stečenih i genetičkih faktora rizika u grupi od 100 bolesnika, nosilaca FV Leiden mutacije (95 heterozigota i 5 homozigota). Devedeset jedan bolesnik je imao VTE, sa trombozom dubokih vena donjih ekstremiteta kao najčešćom manifestacijom. Kod 68,6% žena bio je prisutan neki od stečenih faktora rizika, dok je to bio slučaj kod 28,6% muškaraca. Mutacija FII G20210A je detektovana kod 9,5%, MTHFR 677TT kod 8,4%, a obe mutacije su bile prisutne u 2,1% heterozigotnih nosilaca FV Leiden mutacije. Rezultati ove studije ukazuju na značaj poznavanja udruženih faktora rizika kod pacijenata koji su nosioci FV Leiden mutacije., FV Leiden mutation is an important genetic risk factor for venous thromboembolsm (VTE). In this study we have analyzed clinical manifestation and the impact of other genetic and acquired risk factors in 100 patients (95 heterozygous and 5 homozygous) carriers of FV Leiden mutation. Among these patients, 91 experienced VTE, with down limb deep vein thrombosis as the most frequent manifestation. An acquired risk factor was present in 68.6% of women, whereas this was the case in 28.6% of men. FIIG20210A was present in 9.5%, MTHFR 677TT in 8.4% and both mutations in 2.1% of the heterozygous FV Leiden carriers. Our results suggest that knowledge of coexisting factors predisposing to VTE is very important for FV Leiden mutation carriers and may contribute to the prevention of VTE episodes.",
publisher = "Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd",
journal = "Jugoslovenska medicinska biohemija",
title = "Uticaj stečenih i genetičkih faktora na ispoljavanje trombofilije kod nosilaca FV Leiden mutacije, Impact of acquired and genetic factors on thrombophilic phenotype in FV Leiden mutation carriers",
pages = "146-141",
number = "2",
volume = "24",
doi = "10.2298/JMH0502141D"
}

Đorđević, V., Rakićević, L., Miljić, P., Miković, D., Kovač, M., Radojković, D.,& Savić, A.. (2005). Uticaj stečenih i genetičkih faktora na ispoljavanje trombofilije kod nosilaca FV Leiden mutacije. in Jugoslovenska medicinska biohemija
Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd., 24(2), 141-146.
https://doi.org/10.2298/JMH0502141D

Đorđević V, Rakićević L, Miljić P, Miković D, Kovač M, Radojković D, Savić A. Uticaj stečenih i genetičkih faktora na ispoljavanje trombofilije kod nosilaca FV Leiden mutacije. in Jugoslovenska medicinska biohemija. 2005;24(2):141-146.
doi:10.2298/JMH0502141D .

Đorđević, Valentina, Rakićević, Ljiljana, Miljić, Predrag, Miković, Danijela, Kovač, Mirjana, Radojković, Dragica, Savić, Ana, "Uticaj stečenih i genetičkih faktora na ispoljavanje trombofilije kod nosilaca FV Leiden mutacije" in Jugoslovenska medicinska biohemija, 24, no. 2 (2005):141-146,
https://doi.org/10.2298/JMH0502141D . .