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Blood, 15 February 2001, Vol. 97, No. 4, pp. 844-849
PLENARY PAPER
Acquired activated protein C resistance is associated with lupus
anticoagulants and thrombotic events in pediatric patients with
systemic lupus erythematosus
Christoph Male,
Lesley Mitchell,
James Julian,
Patricia Vegh,
Penny Joshua,
Margaret Adams,
Michelle David, and
Maureen E. Andrew
From the Hamilton Civic Hospitals Research Centre,
Hamilton, Canada; Hospital for Sick Children, Toronto, Canada;
Hôpital Ste. Justine, Montreal, Canada.
Acquired activated protein C resistance (APCR) has been
hypothesized as a possible mechanism by which antiphospholipid
antibodies (APLAs) cause thrombotic events (TEs). However, available
evidence for an association of acquired APCR with APLAs is limited.
More importantly, an association of acquired APCR with TEs has not been
demonstrated. The objective of the study was to determine, in pediatric
patients with systemic lupus erythematosus (SLE), whether (1) acquired
APCR is associated with the presence of APLAs, (2) APCR is associated
with TEs, and (3) there is an interaction between APCR and APLAs in
association with TEs. A cross-sectional cohort study of 59 consecutive,
nonselected children with SLE was conducted. Primary clinical outcomes
were symptomatic TEs, confirmed by objective radiographic tests.
Laboratory testing included lupus anticoagulants (LAs), anticardiolipin
antibodies (ACLAs), APC ratio, protein S, protein C, and factor V
Leiden. The results revealed that TEs occurred in 10 (17%) of 59 patients. Acquired APCR was present in 18 (31%) of 58 patients.
Acquired APCR was significantly associated with the presence of LAs but not ACLAs. Acquired APCR was also significantly associated with TEs.
There was significant interaction between APCR and LAs in the
association with TEs. Presence of both APCR and LAs was associated with
the highest risk of a TE. Protein S and protein C concentrations were
not associated with the presence of APLAs, APCR, or TEs. Presence of
acquired APCR is a marker identifying LA-positive patients at high risk
of TEs. Acquired APCR may reflect interference of LAs with the protein
C pathway that may represent a mechanism of LA-associated TEs.
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