Activated Protein C Resistance (APCR) and Placental Fibrin Deposition

Abstract 

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 2.1s with the Coatest^® classic test and subjects (n=11) with an APC ratio in the normal range, greater than 2.1s (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.

Keywords: Activated protein C resistance (APCR), Placental fibrin deposition, Placental histological abnormalities, Thrombophilia