Liver transplantation in human immunodeficiency virus-infected patients: procoagulant, but is antithrombotic prophylaxis required?

Cherian, P Thomas; Alrabih, Wesal; Douiri, Abdel; Quaglia, Alberto; Heneghan, Michael A; O'Grady, John; Rela, Mohamed; Heaton, Nigel D

Liver transplantation (LT) for human immunodeficiency virus (HIV)-positive recipients with end-stage liver disease has become an accepted practice. However, because these patients are increasingly being recognized as prothrombotic, we reviewed their posttransplant thrombotic complications. Because morphological changes might be responsible in part for this prothrombotic state, we also conducted a histopathological review of explants from HIV-positive patients. Between 1990 and 2010, 24 of 3502 recipients (including 23 adults) were HIV-positive at LT. These patients and their postoperative courses were reviewed with a particular focus on vascular complications, risk factors, and outcomes. Another patient in whom HIV was detected 12 years after LT was also examined. Among the 24 HIV-positive LT recipients (17 males and 22 whole liver grafts; median age = 40 years), 5 developed arterial complications [including 3 cases of hepatic artery thrombosis (HAT), 1 case of generalized arteriopathy (on angiography), and 1 case of endoarteritis (on histological analysis)]. Multiple arterial anastomoses were performed in 8 of the 24 recipients, and HAT occurred twice within this anastomosis group. The outcomes of the 3 patients with HAT included retransplantation, biliary stenting for ischemic cholangiopathy followed by retransplantation, and observation only. In addition, 5 separate venous thrombotic events were detected in the 24 recipients during this period. Moreover, the delayed-HIV recipient developed delayed HAT and subsequently ischemic cholangiopathy and was being assessed for retransplantation at the time of this writing. In conclusion, the prothrombotic state associated with combined HIV and liver disease is a cause of morbidity after LT: 8 of the 24 recipients (33%) in this series suffered vascular thrombotic complications. There is a potential increase in the risk of HAT: the rate for the HIV-positive cohort was higher than the rate for historical HIV-negative controls [12% versus 3.2%, P = 0.016 (Fisher's exact test)]. The minimization of complex arterial reconstruction, coagulopathy screening, and risk-adapted antithrombotic chemoprophylaxis appear to be reasonable precautions.