Abstract

We read with interest the article recently published by Cherian et al.1 in Liver Transplantation. The authors presented a series of 24 liver transplants in human immunodeficiency virus (HIV)–positive recipients and focused on vascular complications. They reported that 8 of the 24 patients (33%) suffered a vascular complication; precisely 5 (20%) had hepatic artery thrombosis (HAT), 1 (4%) had a generalized arteriopathy (according to angiography), and 1 (4%) had endoarteritis (according to a histological analysis). Multiple arterial anastomoses were created in 8 of the 24 recipients, and 2 cases of HAT occurred in this group. The authors did not mention how many patients had undergone an aortohepatic bypass. In addition, 5 separate venous thrombotic events were detected in the 24 recipients. These data compared unfavorably with their experience with HIV-negative cases (ie, a 2.7% incidence of HAT among more than 2000 adult recipients over a 15-year period). The authors concluded that the prothrombotic state associated with the combination of HIV and liver disease was a cause of post-LT morbidity, in that 8 of the 24 recipients (33%) suffered a vascular thrombotic complication. Moreover, according to Cherian et al., there was a potential increase in the risk of HAT in the HIV-positive cohort versus the HIV-negative historical controls [3.2% versus 12%, P = 0.016 (Fisher's exact test)]. They suggested that multiple acquired and persistent thrombophilic abnormalities, such as protein C and S deficiencies and increased factor VIII concentrations, which are more frequently observed in HIV-infected patients versus healthy populations, might be a possible explanation for the high incidence of vascular complication in this HIV series.2, 3 The results reported for this series are not in accordance with the experience with liver transplantation in HIV-infected patients at our center. From 2004 to 2011, we performed liver transplantation for 32 HIV-positive patients. No cases of HAT were encountered. Vascular complications included 2 cases of early hepatic artery stenosis (within 30 days after transplantation) successfully treated with percutaneous transluminal angioplasty (PTA) and stenting, 1 case of early portal vein thrombosis (day 1) successfully treated with surgical thrombectomy, and 1 case of late hepatic vein stenosis (6 months after transplantation) successfully treated with PTA and stenting. The overall incidence was 12.5%. No separate venous thrombotic events were detected in our series. An aortohepatic bypass was used in 5 cases (15.6%); 4 patients received full right split liver grafts with an arterial anastomosis on the right hepatic artery. Complex arterial reconstructions at the back table were performed in 5 cases (15.6%). At a median follow-up of 33 months (range = 9-85 months), the resistive index of the hepatic artery according to color Doppler ultrasound was 0.64 ± 0.07; no cases of HAT were encountered, and this included 2 cases of arterial stenosis treated with PTA and stenting. Our posttransplant thrombotic prophylaxis policy consisted of low-molecular-weight heparin for 10 days followed by long-term anti-aggregation therapy with 100 mg of acetylsalicylic acid daily, and it did not differ from the policy for non-HIV cases. Historically, the incidence of HAT at our center has been 4.4%,4 which is perfectly within the range reported in the literature (1.6%-8%).5 In conclusion, according to our experience, liver transplantation for HIV-positive recipients is not associated with a higher incidence of any type of vascular complication and is especially not associated with HAT. Umberto Baccarani M.D. Ph.D. F.E.B.S.*, Stefania Bidinost M.D.*, Marcello Tavio M.D. , Pierluigi Viale M.D. , Gian Luigi Adani M.D., Ph.D.*, * Liver Transplant Unit Department of Medical and Biological Sciences University Hospital of Udine Udine, Italy, Infectious Disease Unit Hospital of Ancona Ancona, Italy, Institute of Infectious Diseases University Hospital of Bologna Bologna, Italy.

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