ABSTRACT
Dahlback was the first to notice the phenomenon of activated protein C resistance (APC-R), which is the most common cause of inherited thrombophilia.3,4 Later, Bertina et al5 found the molecular basis of APCR, namely, the factor V Leiden (FVL) mutation, R506Q, in which arginine (R) is replaced by glutamine (Q) at position 506 in the factor V gene. The mutant FVL is more slowly inactivated by protein C than wild-type factor V.6 APC-R, which is not related to this mutation (acquired APC-R), has also been found to be an independent risk factor for VTE.7,8 Acquired APC-R is associated with a number of clinical conditions, including pregnancy,9 oral contraceptive use,10 and antiphospholipid syndrome.11
