ISOLATED FAMILIAL PLASMINOGEN DEFICIENCY MAY NOT BE A RISK FACTOR FORTHROMBOSIS

Despite many reports of individuals with congenital plasminogen defici ency and thrombosis, there is still uncertainty whether heterozygous d eficiency represents a real thrombophilic risk factor or simply a coin cidental finding. We have addressed this issue by testing for plasmino gen deficiency in a cohort of 9611 blood donors. Out of 66 donors with reduced plasminogen activity on two occasions 28 were shown to have a familial deficiency stale (including 3 with dysplasminogenaemia). Our observed prevalence rate for familial plasminogen deficiency, calcula ted at 2.9/1000 (95% CI=1.9-4.2 per 1000), was not significantly diffe rent from that calculated from published reports of congenital plasmin ogen deficiency in thrombotic cohorts (5.4/1000). Furthermore, with on ly two exceptions, all 80 donors and relatives with familial deficienc y were asymptomatic with regard to thrombosis-including a 29 year old donor with suspected compound heterozygous hypoplasminogenaemia. These findings add further weight to the argument that familial heterozygou s plasminogen deficiency, at least in isolation, does not constitute a significant thrombotic risk factor. However, it remains uncertain whe ther plasminogen deficiency, when combined with other thrombophilic co nditions, may become more clinically important.