Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis

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Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis. / Saugel, Bernd; Lee, Marcel; Feichtinger, Stephanie; Hapfelmeier, Alexander; Schmid, Roland M; Siveke, Jens T.

In: J THROMB THROMBOLYS, Vol. 40, No. 1, 01.07.2015, p. 54-60.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

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Saugel, B, Lee, M, Feichtinger, S, Hapfelmeier, A, Schmid, RM & Siveke, JT 2015, 'Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis', J THROMB THROMBOLYS, vol. 40, no. 1, pp. 54-60. https://doi.org/10.1007/s11239-014-1124-z

APA

Saugel, B., Lee, M., Feichtinger, S., Hapfelmeier, A., Schmid, R. M., & Siveke, J. T. (2015). Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis. J THROMB THROMBOLYS, 40(1), 54-60. https://doi.org/10.1007/s11239-014-1124-z

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Bibtex

@article{ecc8e860b6df4db19b6a070df998767c,
title = "Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis",
abstract = "Liver cirrhosis, myeloproliferative disorders (MPDs) and prothrombotic mutations are aetiologic factors for portal vein thrombosis (PVT). The role and frequency of thrombophilic genetic risk factors in cirrhotic patients is not well established. In this case-control study, we investigated the frequency of Janus kinase 2 (JAK2) (JAK2 V617F), Factor V Leiden (FVL G1691A), and Prothrombin (G20210A) mutations in cirrhotic patients with PVT (LCi+/PVT+ group, n = 21) in comparison with two control collectives (cirrhotic patients without PVT, LCi+/PVT- group, n = 43; PVT patients without liver cirrhosis, LCi-/PVT+ group, n = 29). In the LCi+/PVT+ group, JAK2 V617F was present in 2/21 patients (10 %; p = 0.104 compared to LCi+/PVT-; p = 0.092 compared to LCi-/PVT+), whereas 0/43 LCi+/PVT- patients (0 %; p < 0.001 compared to LCi-/PVT+) and 9/29 LCi-/PVT+ patients (31 %) harboured this mutation. The FVL G1691A mutation was identified in 1/21 patients (5 %) in the LCi+/PVT+ group, in 5/43 patients (12 %) in the LCi+/PVT- group, and in 2/29 patients (7 %) in the LCi-/PVT+ group. The Prothrombin G20210A mutation was present in 0/21 LCi+/PVT+ patients (0 %), in 1/43 LCi+/PVT- patients (2 %), and in 4/29 patients (14 %) in the LCi-/PVT+ group. This study provides evidence that a relevant proportion of cirrhotic patients with PVT harbours a JAK2 V617F mutation.",
author = "Bernd Saugel and Marcel Lee and Stephanie Feichtinger and Alexander Hapfelmeier and Schmid, {Roland M} and Siveke, {Jens T}",
year = "2015",
month = jul,
day = "1",
doi = "10.1007/s11239-014-1124-z",
language = "English",
volume = "40",
pages = "54--60",
journal = "J THROMB THROMBOLYS",
issn = "0929-5305",
publisher = "Springer Netherlands",
number = "1",

}

RIS

TY - JOUR

T1 - Thrombophilic factor analysis in cirrhotic patients with portal vein thrombosis

AU - Saugel, Bernd

AU - Lee, Marcel

AU - Feichtinger, Stephanie

AU - Hapfelmeier, Alexander

AU - Schmid, Roland M

AU - Siveke, Jens T

PY - 2015/7/1

Y1 - 2015/7/1

N2 - Liver cirrhosis, myeloproliferative disorders (MPDs) and prothrombotic mutations are aetiologic factors for portal vein thrombosis (PVT). The role and frequency of thrombophilic genetic risk factors in cirrhotic patients is not well established. In this case-control study, we investigated the frequency of Janus kinase 2 (JAK2) (JAK2 V617F), Factor V Leiden (FVL G1691A), and Prothrombin (G20210A) mutations in cirrhotic patients with PVT (LCi+/PVT+ group, n = 21) in comparison with two control collectives (cirrhotic patients without PVT, LCi+/PVT- group, n = 43; PVT patients without liver cirrhosis, LCi-/PVT+ group, n = 29). In the LCi+/PVT+ group, JAK2 V617F was present in 2/21 patients (10 %; p = 0.104 compared to LCi+/PVT-; p = 0.092 compared to LCi-/PVT+), whereas 0/43 LCi+/PVT- patients (0 %; p < 0.001 compared to LCi-/PVT+) and 9/29 LCi-/PVT+ patients (31 %) harboured this mutation. The FVL G1691A mutation was identified in 1/21 patients (5 %) in the LCi+/PVT+ group, in 5/43 patients (12 %) in the LCi+/PVT- group, and in 2/29 patients (7 %) in the LCi-/PVT+ group. The Prothrombin G20210A mutation was present in 0/21 LCi+/PVT+ patients (0 %), in 1/43 LCi+/PVT- patients (2 %), and in 4/29 patients (14 %) in the LCi-/PVT+ group. This study provides evidence that a relevant proportion of cirrhotic patients with PVT harbours a JAK2 V617F mutation.

AB - Liver cirrhosis, myeloproliferative disorders (MPDs) and prothrombotic mutations are aetiologic factors for portal vein thrombosis (PVT). The role and frequency of thrombophilic genetic risk factors in cirrhotic patients is not well established. In this case-control study, we investigated the frequency of Janus kinase 2 (JAK2) (JAK2 V617F), Factor V Leiden (FVL G1691A), and Prothrombin (G20210A) mutations in cirrhotic patients with PVT (LCi+/PVT+ group, n = 21) in comparison with two control collectives (cirrhotic patients without PVT, LCi+/PVT- group, n = 43; PVT patients without liver cirrhosis, LCi-/PVT+ group, n = 29). In the LCi+/PVT+ group, JAK2 V617F was present in 2/21 patients (10 %; p = 0.104 compared to LCi+/PVT-; p = 0.092 compared to LCi-/PVT+), whereas 0/43 LCi+/PVT- patients (0 %; p < 0.001 compared to LCi-/PVT+) and 9/29 LCi-/PVT+ patients (31 %) harboured this mutation. The FVL G1691A mutation was identified in 1/21 patients (5 %) in the LCi+/PVT+ group, in 5/43 patients (12 %) in the LCi+/PVT- group, and in 2/29 patients (7 %) in the LCi-/PVT+ group. The Prothrombin G20210A mutation was present in 0/21 LCi+/PVT+ patients (0 %), in 1/43 LCi+/PVT- patients (2 %), and in 4/29 patients (14 %) in the LCi-/PVT+ group. This study provides evidence that a relevant proportion of cirrhotic patients with PVT harbours a JAK2 V617F mutation.

U2 - 10.1007/s11239-014-1124-z

DO - 10.1007/s11239-014-1124-z

M3 - SCORING: Journal article

C2 - 25115839

VL - 40

SP - 54

EP - 60

JO - J THROMB THROMBOLYS

JF - J THROMB THROMBOLYS

SN - 0929-5305

IS - 1

ER -