S M Schuetze1, M Linenberger. 1. Department of Medicine, University of Washington Medical Center, Seattle 98195-7710, USA.
Abstract
BACKGROUND: Orthotopic liver transplantation (OLT) is frequently complicated by thrombotic events that may threaten the viability of the allograft and severely compromise the overall outcome in these patients. Although multiple prothrombotic pathogenic mechanisms may be involved, a role for inadequate natural anticoagulant levels in the early postoperative period has been postulated. METHODS: We describe a case of a woman who suffered multiple thrombotic complications after a second OLT. Prospective assays of procoagulant and natural anticoagulant factor levels, in addition to screening tests for a variety of inherited and acquired hypercoagulable states, were carried out. RESULTS: Serial studies confirmed an acquired, isolated deficiency of Protein S associated with the second transplanted liver. Protein S levels were normal after the patient's first and third OLTs. There was no laboratory evidence of other underlying prothrombotic conditions. CONCLUSIONS: This unusual case of acquired Protein S deficiency demonstrates that the hypercoagulable phenotype may develop in the recipient of a liver from a heterozygous deficient donor. Furthermore, isolated low Protein S may be causally associated with hepatic artery thrombosis after OLT.
BACKGROUND: Orthotopic liver transplantation (OLT) is frequently complicated by thrombotic events that may threaten the viability of the allograft and severely compromise the overall outcome in these patients. Although multiple prothrombotic pathogenic mechanisms may be involved, a role for inadequate natural anticoagulant levels in the early postoperative period has been postulated. METHODS: We describe a case of a woman who suffered multiple thrombotic complications after a second OLT. Prospective assays of procoagulant and natural anticoagulant factor levels, in addition to screening tests for a variety of inherited and acquired hypercoagulable states, were carried out. RESULTS: Serial studies confirmed an acquired, isolated deficiency of Protein S associated with the second transplanted liver. Protein S levels were normal after the patient's first and third OLTs. There was no laboratory evidence of other underlying prothrombotic conditions. CONCLUSIONS: This unusual case of acquired Protein S deficiency demonstrates that the hypercoagulable phenotype may develop in the recipient of a liver from a heterozygous deficient donor. Furthermore, isolated low Protein S may be causally associated with hepatic artery thrombosis after OLT.