Transplantation · 2005
Resistance to activated protein C caused by factor V Leiden mutation and orthotopic liver transplantation.
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Loew Andreas, Jacob Dietmar, Neuhaus Peter, Riess Hanno
Аннотация
BACKGROUND: Factor V (FV)-dependent resistance to activated protein C (APCR) is most likely caused by a point mutation in the FV gene, the so-called FV Leiden mutation (FV:Q506), which is a common risk factor predisposing to venous thromboembolism. Little is known about the role of FV:Q506 in recipients of human liver grafts and the significance of acquired APCR caused by orthotopic liver transplantation (OLT).
METHODS: We screened blood samples of 720 patients who underwent OLT by genotyping for FV:Q506 and by testing for APCR with two highly FV-specific tests. Apart from the existing medical records, we obtained clinical data from 551 patients on thromboembolic events (TEs) by means of a questionnaire.
RESULTS: We found 49 (6.8%) heterozygous carriers of FV:Q who did not show APCR after OLT. One patient, heterozygous for FV:Q506, displayed APCR after OLT. In 35 (4.9%) noncarriers of FV:Q we detected APCR after OLT. In comparison with noncarriers, carriers of FV:Q506 demonstrated more TE before transplantation (7% vs. 28%, P<0.0005; relative risk 4.0 [95% confidence interval, 2.3-6.9]); this was also true for Budd-Chiari syndrome (1.8% vs. 10%, P<0.005). At a median follow-up of 5 years (0, 13-12 years), we found a higher incidence of TE after transplantation in patients with "acquired" APCR (16.7% vs. 4,3%; P=0.01; relative risk 3.9 [95% confidence interval, 1.7-9.0]), which included one patient with life-threatening TE during the early postoperative phase.
CONCLUSIONS: APCR caused by FV:Q506 before OLT is a risk factor for TE. OLT-related "acquired" APCR should be considered a risk factor for venous thromboembolism.
METHODS: We screened blood samples of 720 patients who underwent OLT by genotyping for FV:Q506 and by testing for APCR with two highly FV-specific tests. Apart from the existing medical records, we obtained clinical data from 551 patients on thromboembolic events (TEs) by means of a questionnaire.
RESULTS: We found 49 (6.8%) heterozygous carriers of FV:Q who did not show APCR after OLT. One patient, heterozygous for FV:Q506, displayed APCR after OLT. In 35 (4.9%) noncarriers of FV:Q we detected APCR after OLT. In comparison with noncarriers, carriers of FV:Q506 demonstrated more TE before transplantation (7% vs. 28%, P<0.0005; relative risk 4.0 [95% confidence interval, 2.3-6.9]); this was also true for Budd-Chiari syndrome (1.8% vs. 10%, P<0.005). At a median follow-up of 5 years (0, 13-12 years), we found a higher incidence of TE after transplantation in patients with "acquired" APCR (16.7% vs. 4,3%; P=0.01; relative risk 3.9 [95% confidence interval, 1.7-9.0]), which included one patient with life-threatening TE during the early postoperative phase.
CONCLUSIONS: APCR caused by FV:Q506 before OLT is a risk factor for TE. OLT-related "acquired" APCR should be considered a risk factor for venous thromboembolism.