Activated Protein C Resistance (APCR) and Placental Fibrin Deposition
Autor: | Mark Lyons, Majella Maher, S. Sedano, Margaret Murray, G. Mortimer, Brendan Cleary, G Gaffney |
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Rok vydání: | 2008 |
Předmět: |
medicine.medical_specialty
Placenta Intrauterine growth restriction Thrombophilia Gastroenterology Fibrin Pregnancy Internal medicine Recurrent miscarriage Coagulopathy medicine Humans Activated Protein C Resistance biology Placental abruption Obstetrics and Gynecology medicine.disease Thrombosis Reproductive Medicine Immunology biology.protein Female Activated protein C resistance Developmental Biology |
Zdroj: | Placenta. 29:833-837 |
ISSN: | 0143-4004 |
DOI: | 10.1016/j.placenta.2008.06.012 |
Popis: | Activated protein C resistance (APCR) results in an 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 or equal to 2.1 s with the Coatest ® classic test and subjects ( n = 11) with an APC ratio in the normal 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. |
Databáze: | OpenAIRE |
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