phenprocoumon and Activated-Protein-C-Resistance

Several genetic liver diseases can be treated by liver transplantation (LT). However, some genetic defects also may be acquired by this procedure. We describe a patient who developed recurrent deep-vein thromboses after LT for hepatitis C virus-associated hepatocellular carcinoma on the basis of a homozygous Leiden mutation of the factor V gene in the donor liver. Liver donors with a history of venous thrombosis should be screened for the presence of activated protein C (APC) resistance. In addition, we recommend looking for APC resistance in liver recipients who develop venous thromboembolic disease in the post-LT course. Molecular analysis of donor tissue may be necessary to make a definite diagnosis of factor V Leiden mutation in these patients. As a consequence, intensified postoperative thromboprophylaxis or lifelong anticoagulant therapy may be necessary if this thrombophilic gene defect is detected.

Topics: Activated Protein C Resistance; Anticoagulants; Factor V; Female; Humans; Liver Transplantation; Living Donors; Middle Aged; Phenprocoumon; Recurrence; Venous Thrombosis

Topics: 3' Untranslated Regions; Activated Protein C Resistance; Anticoagulants; Chemical and Drug Induced Liver Injury; Female; Genetic Predisposition to Disease; Heparin, Low-Molecular-Weight; Heterozygote; Humans; Hypoprothrombinemias; Liver Function Tests; Middle Aged; Phenprocoumon; Prothrombin; Recurrence; Thrombophilia; Venous Thrombosis

Resistance to activated protein C, caused by a single point mutation in the factor V gene (Arg506Gln or FV Leiden), is the most prevalent single risk factor associated with venous thromboembolic disease. The aim of this study was to investigate the effectiveness of standard oral anticoagulant therapy (OAT) in patients with the Arg506Gln mutation compared with a matched control group. The study compared selected variables in 27 patients carrying the Arg506Gln mutation with 27 sex- and age-matched controls in steady state oral anticoagulant treatment (OAT). The study showed that similar doses of vitamin K antagonists in carriers and noncarriers suppress and generate a uniform distribution of coagulation markers in steady state OAT. Thus, it seems that OAT with standard treatment doses is just as effective in patients with the Arg506Gln mutation as in comparable controls without the mutation.

Topics: Activated Protein C Resistance; Adolescent; Adult; Aged; Aged, 80 and over; Anticoagulants; Arginine; Case-Control Studies; Factor V; Female; Glycine; Humans; Immunoenzyme Techniques; Linear Models; Male; Middle Aged; Phenprocoumon; Point Mutation; Polymerase Chain Reaction; Statistics, Nonparametric; Warfarin