Congenital Hypercoagulability and HITAssociated Thrombosis

Gardyn and associates (1995) reported a patient with fatal HIT and widespread microvascular thrombosis. The investigators identified heterozygous factor V Leiden (G1691A mutation) in this patient, and they speculated that this contributed to the severe clinical course. However, the complications may also have been related to the treatment with LMWH and warfarin.

The interaction between factor V Leiden and thrombotic sequelae of HIT was formally investigated in a study of 165 patients with HIT, 16 (9.7%) of whom had factor V Leiden (Lee et al., 1998). No increase in the number or severity of venous or arterial thrombosis was seen. This result is not surprising, as thrombosis occurs in about 50-75% of patients with HIT (Warkentin and Kelton, 1996). Thus, even if the most common congenital hypercoagulable disorders, factor V Leiden and the prothrombin G20210A mutation (each occurring in about 5% of the population), were strongly associated with increased risk for thrombosis in HIT, only a few HIT-associated thromboses could thereby be explained.

Carlsson and colleagues (2003) studied 142 patients with HIT (79 with thrombosis) to determine whether any of 10 established or putative platelet receptor or clotting factor polymorphisms (including factor V Leiden and pro-thrombin G20210A mutation) was associated with thrombosis. None was found.

Lindhoff-Last et al. (2002) also found no association between factor V Leiden or prothrombin G20210A mutation and thrombosis in a smaller study of 21 patients. However, they found that more HIT patients had elevated factor VIII levels (at mean 29 mo follow-up) than matched normal controls (16/21 vs. 4/21). The significance of this finding is unclear.

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