Oral anticoagulants and cyclosporin A

Haematologica vol. 85(8):August 2000 min-K dependent proteins, revealed that the affected amino acid was highly conserved, indicating an important structural or functional role. The search for other established thrombophilic genetic risk factors such as protein S and antithrombin deficiency, factor V Leiden, methylene tetrahydrofolate reductase C677T variant, and prothrombin G20210A variant revealed that only one patient was heterozygous for the prothrombin variant (Figure 1). Family analysis revealed that individuals with the same mutation responsible for PC deficiency and prothrombin variant, had no clinical thrombosis. These data show that thrombosis can be the result of multiple acquired and genetic factors interacting with a consequent synergistic effect, possibly, including factors which still remain unknown. In each family the deficiency cosegregates with the mutation (Table 1), indicating that the defect is the likely cause of PC deficiency in these patients. Our results corroborate that recurrent mutations are very frequent in PC deficiency, since three of our identified mutations were previously described in other countries and two of them involved the hypermutable region of CPG dinucleotides.