Peer-Reviewed Journal Details
Mandatory Fields
Sedano, S,Gaffney, G,Mortimer, G,Lyons, M,Cleary, B,Murray, M,Maher, M
2008
September
Placenta
Activated protein C resistance (APCR) and placental fibrin deposition
Published
()
Optional Fields
activated protein C resistance (APCR) placental fibrin deposition placental histological abnormalities thrombophilia FACTOR-V-LEIDEN RISK-FACTORS VENOUS THROMBOEMBOLISM PATHOLOGICAL FEATURES GROWTH RESTRICTION REDUCTASE GENE PREGNANCY LOSS FETAL THROMBOPHILIA THROMBOSIS
29
833
837
Activated protein C resistance (APCR) results in all ineffective anticoagulant response leading to an increased risk of thrombosis, particularly during pregnancy. Adverse pregnancy Outcomes including pre-eclampsia (PET), intrauterine growth restriction (IUGR), recurrent miscarriage and placental abruption have been linked with thrombotic lesions compromising the utero-placental Circulation. Using histological Staining including Martius Scarlet Blue (MSB) and Haematoxylin and Eosin (H&E) and microscopy, we Studied placental fibrin deposition and histological abnormalities in Subjects (n = 23) with APCR (APCR group), based on a ratio of less than OF equal to 2.1 s with the Coatest (R) classic test and Subjects (n = 11) with an APC ratio in the nomal range, greater than 2.1 s (APCN group). Fibrin deposition was significantly higher (3.3-fold) in the APCR group compared to the APCN group. An inverse correlation between APC ratio and placental fibrin deposition was determined for the Study group. Histological abnormalities were more than 2-fold higher in the APCR group compared to the APCN group. Molecular screening identified common thrombophilic mutations, FVL and FII-G20210A in the APCR group but not in the APCN group. (C) 2008 Elsevier Ltd. All rights reserved.
DOI 10.1016/j.placenta.2008.06.012
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