The role of hereditary antithrombotic protein defects in juvenile deep vein
thrombosis (DVT) was evaluated. Fifty six young patients (age <45 yr) with
doppler-proven DVT were investigated for the presence of resistance to act
ivated protein C (APC-R), lupus anticoagulant (LA), anticardiolipin antibod
ies and deficiencies of protein C, protein S, ATIII activities. Fifty nine
normal healthy individuals served as controls. APC-R was observed to be the
commonest defect underlying the Indian DVT as seen in 39.2% of patients fo
llowed by elevated ACA (5.3%), PAI (2.8%), presence of LA (2.8%) and reduce
d ATIII levels (2.8%). None of the subjects had protein C or S deficiency.
APC-R was associated with ATIII deficiency in one case, and elevated ACA in
two cases. In two subjects, APC-R was associated with elevated PAI levels.
Patients with more than one prothrombotic factor had a higher prevalence o
f pulmonary thromboembolism, suggesting that the thrombogenic potential of
APC-R is enhanced by the presence of coexisting hereditary or acquired prot
hrombotic defect.