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To the Editor:

Multiple acquired and persistent thrombophilic abnormalities have been observed in HIV-infected patients leading authors to recognize HIV infection as a prothombotic state with potential implications after transplantation (1). Recently, five cases of arterial complications in 24 HIV-infected liver transplant recipients have been reported by Cherian et al. (2) including three cases of hepatic artery thrombosis (HAT). The rate of HAT in the HIV-positive and the HIV-negative recipients was 12% and 3.2%, respectively (p = 0.016). The authors concluded that there is a trend toward an increased risk of HAT in this population and recommended a full coagulopathy screen at the transplant assessment and a risk-adapted case-by-case consideration of antithrombotic prophylaxis for HIV-infected recipients.

Our experience is different. In September 2003, a prospective study of liver transplantation (LT) in HIV-infected patients was approved by our IRB. Until December 2011, 34 LTs have been performed in 32 HIV-infected recipients using whole grafts from deceased donors. All patients, except one, met the criteria of the Spanish Consensus Document for this type of transplant (3). The median (range of) recipient age, MELD score and donor age were 44 years (33–61), 13 points (7–24) and 55 years (26–76), respectively. The liver disease etiology was HCV in 25 patients, coinfection HCV/HBV in six patients and unknown in one patient. The pretransplant HIV RNA load was <50 copies/mL in 29 recipients, and the median pretransplant CD4 count was 286 cells/μL (49–836). Three patients with a right hepatic artery from the superior mesenteric artery required back-bench reconstruction. At the time of writing, after a median follow-up of 26.5 months (0–99), none of our HIV-infected patients have developed post-transplant HAT or venous complications. One recipient (3%) presented hepatic artery stenosis and was successfully treated with angioplasty. This patient had a single arterial anastomosis and a hepaticojejunostomy for the biliary reconstruction. Unfortunately, the patient died 9 months after LT due to an aggressive HCV recurrence. Two differences between our series and the London series could account for the different rate of arterial complications (3% vs. 12%): the incidence of complex arterial reconstruction (9% and 33%, respectively) and the proportion of patients with detectable pretransplant HIV RNA load (10% and 33%, respectively). On the other hand, in a review of recent literature we found reports of approximately 200 LTs in HIV-infected recipients worldwide; among these, we identified six cases of vascular complications including four cases of HAT, one case of hepatic artery rupture and one case of venous occlusion (4). Both our experience and that indicated in the literature compare well with the 3% to 5% reported incidence of HAT after LT in HIV-negative recipients (5).

In summary, our results and those in the literature do not confirm the suggested trend toward an increased risk of HAT after LT in HIV-infected patients, and therefore the use of antithrombotic prophylaxis does not seem to be justified. We need larger prospective studies to determine whether the described thrombophilic abnormalities observed in the HIV-infected patients may affect the development of vascular complications after LT.

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