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Donor factor V leiden mutation and vascular thrombosis following liver transplantation
Author(s) -
Hirshfield Gideon,
Collier Jane D.,
Brown Karen,
Taylor Craig,
Frick Thomas,
Baglin Trevor P.,
Alexander Graeme J.M.
Publication year - 1998
Publication title -
liver transplantation and surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1074-3022
DOI - 10.1002/lt.500040108
Subject(s) - factor v leiden , thrombosis , liver transplantation , medicine , cardiology , transplantation , gastroenterology , venous thrombosis
The most commonly detected hypercoagulable state involves an abnormal factor V protein synthesized by the liver in which arginine at position 506 is replaced by glutamine as a result of a single‐point mutation in the factor V gene (factor V Leiden). Liver transplantation is complicated by hepatic vascular thrombosis in up to 15% of cases, resulting in graft loss in most instances. This retrospective study examined the effect of the factor V Leiden mutation on the risk of hepatic vessel thrombosis after liver transplantation. The mutation was sought by polymerase chain reaction and Mnl I digestion of DNA where available from 214 recipients and 276 donors receiving 319 liver transplants. No donors or patients were homozygous for the factor V Leiden mutation. The prevalence of the heterozygous mutation was 19 of 276 (6.9%) in donors and 19 of 214 (8.9%) in recipients. Forty‐one thrombotic episodes occurred after transplantation in the 276 transplants in which donor DNA was available for analysis; 22 involved the hepatic artery, 9 involved the portal vein, and 10 were deep venous thromboses. A donor factor V Leiden mutation was detected in the donor in 6 of 41 (14.6%) with any thrombotic event compared with 13 of 235 (5.5%) without ( P = 0.03). The relative risk of any thrombosis with this mutation was therefore 2.32 (95% confidence interval [CI], 1.12–4.81). The factor V Leiden mutation was present in the donor in 4 of 31 (12.9%) cases complicated by hepatic vessel thrombosis (which always led to graft loss or death) and 15 of 245 (6.1%) cases without ( P = 0.16). The relative risk of hepatic vessel thrombosis in the presence of this allele was therefore 2.00 (95% CI, 0.78–5.14). As anticipated, the presence of this allele in the recipient was not associated with deep venous or hepatic vessel thrombosis. The factor V Leiden mutation in the donor liver is not a major risk factor for hepatic vessel thrombosis and subsequent graft loss after liver transplantation.