Activated protein C resistance (APCR) and placental fibrin deposition.
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.
Sedano
S
S
National Diagnostics Centre, National University of Ireland, Galway, Ireland. sara.sedano@nuigalway.ie
Gaffney
G
G
Mortimer
G
G
Lyons
M
M
Cleary
B
B
Murray
M
M
Maher
M
M
D020016:Activated Protein C Resistance / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D006801:Humans; D010920:Placenta / Q000503:physiopathology*; D011247:Pregnancy; D019851:Thrombophilia / Q000235:genetics
D005337:Fibrin