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The significance of antiphospholipid antibodies in liver recipients
A Furmańczyk-Zawiska1, O Tronina, T Baczkowska
1Department of Transplantation Medicine and Nephrology, Transplantation Institute, Medical University of Warsaw, Warsaw, Poland.
Background:
The presence of antiphospholipid antibodies (APLAs) may be associated with increased thrombotic risk. Liver graft thrombosis may necessitate retransplantation.
Aim:
To determine the prevalence of APLAs among liver recipients and to investigate the relationship between APLAs and liver graft thrombosis.
Materials And Methods:
We included 33 Caucasian patients aged 22 to 75 years who displayed stable liver graft function (21 women and 12 men). The patients were divided into 2 subgroups: high thrombotic risk subgroup T(-) and at low risk T(+) subgroups. The T(-) included 25 patients, T(+) included 8 recipients with a history of severe thrombosis. We investigated: lupus anticoagulant, anticardiolipin antibodies (aCL), anti-β2-glycoprotein I antibodies (anti-β2GPI), antiprothrombin antibodies (immunoglobulin (Ig)G and IgM isotype), protein C and S activities, factor VIII, antithrombin, ADAMTS-13 and anti-ADAMTS-13. The 2 determinations were performed at an interval of 6 months. The mean follow-up was 19.5 ± 4.6 months.
Results:
The most commonly detected antibodies were anti-β2GPI IgM (25%) and aCL IgG (15.63%). Comparing the prevalence of APLAs between T(-) and T(+), we observed a significant difference only for aCL IgM (P = .0183), which was not confirmed on a second determination after 6 months. We noted correlations between aCL IgM and number of thrombotic episodes (P = .0040) and between aCL IgM and anti-β2GPI IgM (P = .0074; rho 0.45). Despite receiving low-molecular-weight heparin or aspirin recurrence of thrombosis occurred in 4 T(+) patients: 3 hepatic artery thrombosis and 1 splenic artery thrombosis. Only 1 patient had APLAs; the other 2, protein C or S deficiency and the fourth, a normal test.
Conclusions:
The prevalence of APLAs in liver recipients is greater than that in the general population. The usefulness of APLAs as a marker of thrombosis was not demonstrated suggesting multifactorial etiologies of liver graft thrombosis.
