Editor—Pre-eclampsia is a heritable endothelial disorder, which is unique to pregnancy1 and characteristically associated with haemostatic and thrombophilic abnormalities. This association has led to the identification of a number of gene variants that might confer thrombophilic risk in pre-eclampsia. An increased carrier rate for two of these polymorphisms, factor V Leiden2 and the thermolabile variant of methylenetetrahydrofolate reductase (MTHFR),3has been reported in some women with pre-eclampsia. However, we have been unable to replicate these findings in our own East Anglian population.4

We have now looked at two further candidate thrombophilic polymorphisms in our pre-eclampsia cohort that are involved in the regulation of vascular thrombosis. The first is the 20210G>A polymorphism in the 3′ UTR region of the prothrombin (PT) gene that causes a modest rise in plasma prothrombin levels,5 and is reportedly associated with severe pre-eclampsia in an Israeli cohort.6 The second is a coding variant (98C>T) in exon 2 of theGPIIIa gene that provides the common beta subunit for several β3-integrins including the platelet fibrinogen receptor. This polymorphism causes a 33Leu>Pro substitution and the existence of two antigenically distinct forms of the mature GPIIb/IIIa antigen on platelets (the Pl(A) antigens 1 and 2). Loss of functional GPIIIa is associated with a rare bleeding disorder (Glanzmann's thrombasthenia) and the 33Pro variant itself has been associated with risk of premature acute coronary syndromes and stroke in young white women.7