Sefik-Bukilica, Mirjana

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  • Sefik-Bukilica, Mirjana (3)
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Author's Bibliography

Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis

Colić, Jelena; Pruner, Iva; Damjanov, Nemanja; Pekmezović, Tatjana; Sefik-Bukilica, Mirjana; Antović, Aleksandra

(Toronto : J Rheumatol Publ Co., 2022)

TY  - JOUR
AU  - Colić, Jelena
AU  - Pruner, Iva
AU  - Damjanov, Nemanja
AU  - Pekmezović, Tatjana
AU  - Sefik-Bukilica, Mirjana
AU  - Antović, Aleksandra
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1536
AB  - Objective. To assess thrombin generation, fibrin formation, and structure together with the fibrinolytic status in patients with systemic sclerosis (SSc) in relation to the occurrence of digital ulcers (DUs) during the course of disease. Methods. We studied variables of endothelial dysfunction, thrombin generation, overall hemostatic potential, and fibrin clot turbidity in plasma from 58 patients with SSc (39 with DU history and 19 DU-naive) and 46 matched healthy controls (HCs). Fibrin structure was visualized using scanning electron microscopy (SEM). Finally, 39 patients with a history of DUs were followed for 1.5 years and the predictive value of all investigated markers for new DU onset was explored. Results. Significantly enhanced endogenous thrombin potential (ETP) and prolonged clot lysis time (CLT) were found in patients with DUs compared to HCs. CLT was prolonged in patients with DUs compared to those without, showing good validity in identifying DUs with an area under the curve of 0.7 (95% CI 0.6-0.8). The levels of ETP and intercellular adhesion molecule 1 were independently associated with CLT. Over the follow-up period, 20 patients developed new DUs. CLT was prolonged (P  lt  0.001) in patients with new DU episodes, especially those with recurrent DUs. Regression analysis showed that the Raynaud phenomenon visual analog scale and CLT were predictors of new DUs (OR 1.1, 95% CI 1.0-1.1 and OR 1.2, 95% CI 1.1-1.3, respectively). SEM confirmed denser fibrin clots in patients with new DUs. Conclusion. Our results suggest that impaired fibrinolysis might have an emerging role in underlying digital vasculopathy and its progression in SSc.
PB  - Toronto : J Rheumatol Publ Co.
T2  - Journal of Rheumatology
T1  - Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis
EP  - 606
IS  - 6
SP  - 598
VL  - 49
DO  - 10.3899/jrheum.210931
ER  - 
@article{
author = "Colić, Jelena and Pruner, Iva and Damjanov, Nemanja and Pekmezović, Tatjana and Sefik-Bukilica, Mirjana and Antović, Aleksandra",
year = "2022",
abstract = "Objective. To assess thrombin generation, fibrin formation, and structure together with the fibrinolytic status in patients with systemic sclerosis (SSc) in relation to the occurrence of digital ulcers (DUs) during the course of disease. Methods. We studied variables of endothelial dysfunction, thrombin generation, overall hemostatic potential, and fibrin clot turbidity in plasma from 58 patients with SSc (39 with DU history and 19 DU-naive) and 46 matched healthy controls (HCs). Fibrin structure was visualized using scanning electron microscopy (SEM). Finally, 39 patients with a history of DUs were followed for 1.5 years and the predictive value of all investigated markers for new DU onset was explored. Results. Significantly enhanced endogenous thrombin potential (ETP) and prolonged clot lysis time (CLT) were found in patients with DUs compared to HCs. CLT was prolonged in patients with DUs compared to those without, showing good validity in identifying DUs with an area under the curve of 0.7 (95% CI 0.6-0.8). The levels of ETP and intercellular adhesion molecule 1 were independently associated with CLT. Over the follow-up period, 20 patients developed new DUs. CLT was prolonged (P  lt  0.001) in patients with new DU episodes, especially those with recurrent DUs. Regression analysis showed that the Raynaud phenomenon visual analog scale and CLT were predictors of new DUs (OR 1.1, 95% CI 1.0-1.1 and OR 1.2, 95% CI 1.1-1.3, respectively). SEM confirmed denser fibrin clots in patients with new DUs. Conclusion. Our results suggest that impaired fibrinolysis might have an emerging role in underlying digital vasculopathy and its progression in SSc.",
publisher = "Toronto : J Rheumatol Publ Co.",
journal = "Journal of Rheumatology",
title = "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis",
pages = "606-598",
number = "6",
volume = "49",
doi = "10.3899/jrheum.210931"
}
Colić, J., Pruner, I., Damjanov, N., Pekmezović, T., Sefik-Bukilica, M.,& Antović, A.. (2022). Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis. in Journal of Rheumatology
Toronto : J Rheumatol Publ Co.., 49(6), 598-606.
https://doi.org/10.3899/jrheum.210931
Colić J, Pruner I, Damjanov N, Pekmezović T, Sefik-Bukilica M, Antović A. Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis. in Journal of Rheumatology. 2022;49(6):598-606.
doi:10.3899/jrheum.210931 .
Colić, Jelena, Pruner, Iva, Damjanov, Nemanja, Pekmezović, Tatjana, Sefik-Bukilica, Mirjana, Antović, Aleksandra, "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis" in Journal of Rheumatology, 49, no. 6 (2022):598-606,
https://doi.org/10.3899/jrheum.210931 . .
5
2
1

Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)

Colić, Jelena; Pruner, Iva; Damjanov, Nemanja; Pekmezović, Tatjana; Sefik-Bukilica, Mirjana; Antović, Aleksandra

(J Rheumatol Publ Co, Toronto, 2022)

TY  - JOUR
AU  - Colić, Jelena
AU  - Pruner, Iva
AU  - Damjanov, Nemanja
AU  - Pekmezović, Tatjana
AU  - Sefik-Bukilica, Mirjana
AU  - Antović, Aleksandra
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1534
AB  - J Rheumatol 2022; doi: 10.3899/jrheum.210931

In the Methods section, under the subheading “Follow-up and study outcome,” the last sentence should be as follows: “All new DUs were recorded by contacting all 39 patients once every 1–3 months during follow-up.” The error does not affect the results or conclusions of the study.

This correction only applies to the April 1 First Release. The correct text appears in the print and online issues.
PB  - J Rheumatol Publ Co, Toronto
T2  - Journal of Rheumatology
T1  - Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)
EP  - 440
IS  - 5
SP  - 440
VL  - 49
DO  - 10.3899/jrheum.210931.C1
ER  - 
@article{
author = "Colić, Jelena and Pruner, Iva and Damjanov, Nemanja and Pekmezović, Tatjana and Sefik-Bukilica, Mirjana and Antović, Aleksandra",
year = "2022",
abstract = "J Rheumatol 2022; doi: 10.3899/jrheum.210931

In the Methods section, under the subheading “Follow-up and study outcome,” the last sentence should be as follows: “All new DUs were recorded by contacting all 39 patients once every 1–3 months during follow-up.” The error does not affect the results or conclusions of the study.

This correction only applies to the April 1 First Release. The correct text appears in the print and online issues.",
publisher = "J Rheumatol Publ Co, Toronto",
journal = "Journal of Rheumatology",
title = "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)",
pages = "440-440",
number = "5",
volume = "49",
doi = "10.3899/jrheum.210931.C1"
}
Colić, J., Pruner, I., Damjanov, N., Pekmezović, T., Sefik-Bukilica, M.,& Antović, A.. (2022). Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022). in Journal of Rheumatology
J Rheumatol Publ Co, Toronto., 49(5), 440-440.
https://doi.org/10.3899/jrheum.210931.C1
Colić J, Pruner I, Damjanov N, Pekmezović T, Sefik-Bukilica M, Antović A. Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022). in Journal of Rheumatology. 2022;49(5):440-440.
doi:10.3899/jrheum.210931.C1 .
Colić, Jelena, Pruner, Iva, Damjanov, Nemanja, Pekmezović, Tatjana, Sefik-Bukilica, Mirjana, Antović, Aleksandra, "Impaired Fibrinolysis Is Linked With Digital Vasculopathy and Onset of New Digital Ulcers in Systemic Sclerosis (vol 49, pg 598, 2022)" in Journal of Rheumatology, 49, no. 5 (2022):440-440,
https://doi.org/10.3899/jrheum.210931.C1 . .

-174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis

Jancić, Ivan; Arsenović-Ranin, Nevena; Sefik-Bukilica, Mirjana; Živojinović, Slađana; Damjanov, Nemanja; Spasovski, Vesna; Srzentić Dražilov, Sanja; Stanković, Biljana; Pavlović, Sonja

(Springer Heidelberg, Heidelberg, 2013)

TY  - JOUR
AU  - Jancić, Ivan
AU  - Arsenović-Ranin, Nevena
AU  - Sefik-Bukilica, Mirjana
AU  - Živojinović, Slađana
AU  - Damjanov, Nemanja
AU  - Spasovski, Vesna
AU  - Srzentić Dražilov, Sanja
AU  - Stanković, Biljana
AU  - Pavlović, Sonja
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/645
AB  - To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement  gt  1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-alpha) blockers in RA.
PB  - Springer Heidelberg, Heidelberg
T2  - Rheumatology International
T1  - -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis
EP  - 1486
IS  - 6
SP  - 1481
VL  - 33
DO  - 10.1007/s00296-012-2586-y
ER  - 
@article{
author = "Jancić, Ivan and Arsenović-Ranin, Nevena and Sefik-Bukilica, Mirjana and Živojinović, Slađana and Damjanov, Nemanja and Spasovski, Vesna and Srzentić Dražilov, Sanja and Stanković, Biljana and Pavlović, Sonja",
year = "2013",
abstract = "To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement  gt  1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-alpha) blockers in RA.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "Rheumatology International",
title = "-174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis",
pages = "1486-1481",
number = "6",
volume = "33",
doi = "10.1007/s00296-012-2586-y"
}
Jancić, I., Arsenović-Ranin, N., Sefik-Bukilica, M., Živojinović, S., Damjanov, N., Spasovski, V., Srzentić Dražilov, S., Stanković, B.,& Pavlović, S.. (2013). -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis. in Rheumatology International
Springer Heidelberg, Heidelberg., 33(6), 1481-1486.
https://doi.org/10.1007/s00296-012-2586-y
Jancić I, Arsenović-Ranin N, Sefik-Bukilica M, Živojinović S, Damjanov N, Spasovski V, Srzentić Dražilov S, Stanković B, Pavlović S. -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis. in Rheumatology International. 2013;33(6):1481-1486.
doi:10.1007/s00296-012-2586-y .
Jancić, Ivan, Arsenović-Ranin, Nevena, Sefik-Bukilica, Mirjana, Živojinović, Slađana, Damjanov, Nemanja, Spasovski, Vesna, Srzentić Dražilov, Sanja, Stanković, Biljana, Pavlović, Sonja, "-174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis" in Rheumatology International, 33, no. 6 (2013):1481-1486,
https://doi.org/10.1007/s00296-012-2586-y . .
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