Resolution of Preoperative Portal Vein Thrombosis After Administration of Antithrombin III in Living Donor Liver Transplantation: Case Report H. Imai, H. Egawa, M. Kajiwara, A. Nakajima, Y. Ogura, E. Hatano, M. Ueda, Y. Kawaguchi, T. Kaido, Y. Takada, and S. Uemoto ABSTRACT A 59-year-old man with hepatitis C virus–associated liver cirrhosis was transferred to our hospital to undergo living donor liver transplantation. Coagulation was impaired (pro- thrombin time [International Normalized Ratio], 3.27), and antithrombin III (AT-III) activity was 23% (normal, 87%–115%). Contrast-enhanced computed tomography scans revealed portal vein thrombosis (PVT) from the junction between the splenic and superior mesenteric vein to the porta hepatica; the portal vein was completely obstructed (PVT). To prevent further development of PVT, 1500 U of AT-III was administered for 3 days, elevating the AT-III activity to 50%. A contrast-enhanced computed tomography scan obtained 9 days after AT-III administration showed resolution of PVT. Living donor liver transplantation was safely performed without portal vein grafting. Thus, a low AT-III concentration may have an important role in the pathogenesis of PVT in patients with cirrhosis. P ORTAL VEIN THROMBOSIS (PVT) is a serious problem in patients with cirrhosis who are candidates for liver transplantation (OLT). The role of surgical tech- niques to overcome PVT during OLT is controversial. We believe that thorough planning is essential for a successful outcome in patients with PVT. 1,2 Although it has been suggested that anticoagulation may result in recanalization in more than 80% of patients with newly diagnosed PVT, the (42.1%) recanalization rate in candidates for OLT is not completely satisfactory. 3,4 The pathogenesis of PVT is not well understood in cirrhosis. Clarifying the mechanism of PVT formation in liver cirrhosis may contribute to the treatment of preexisting PVT in OLT. Herein, we report the case of a patient with cirrhosis with PVT that resolved after administration of antithrombin III (AT-III) therapy before living donor liver transplantation (LDLT), which suggests a role for AT-III in the pathogenesis of PVT in liver cirrhosis. CASE REPORT A 59-year-old man who had been diagnosed with hepatitis C virus infection in the 1990s was taken to a hospital because of massive hematemesis in February 2007. Emergent endoscopy showed rup- tured esophageal varices, which was treated using endoscopic varicose ligation. Because of hemorrhagic shock, liver failure and hepatic coma developed. Although the hepatic coma improved with conservative treatment, jaundice and ascites were refractory. Subsequently, the patient was transferred to our hospital to undergo living donor liver transplantation (OLT) in April 2007. Laboratory findings at admission were as follows: aspartate amino- transferase, 64 IU/L (normal range, 13–33 IU/L); alanine amino- transferase, 38 IU/L (normal, 8 – 42 IU/L); alkaline phosphatase, 344 IU/L (normal, 115–359 IU/L); total bilirubin, 11.4 mg/dL (normal, 0.3–1.3 mg/dL); and direct bilirubin, 5.6 mg/dL (normal, 0.1– 0.2 mg/dL). Hepatitis B surface antigen was negative, and hepatitis C virus antibody was positive. Coagulation ability was impaired, with prothrombin time, 24 seconds (normal range, 10.2–13.4 seconds); prothrombin time (International Normalized ratio), 3.27 (normal, 0.91–1.24); activated partial thromboplastin time, 45 seconds (normal, 26.2–39.3 seconds); and AT-III activity, 23% (normal, 87%–115%). Class C liver disease was diagnosed (Child-Pugh score, 13); the Model for End-Stage Liver Disease score was 30. Contrast-enhanced computed tomography (CT) scans re- vealed severe atrophy of the liver, splenomegaly, and a splenorenal shunt. In addition, PVT from the junction of the splenic and superior mesenteric veins to the porta hepatica was noted, and the portal vein (PV) was completely obstructed (Fig 1A–C). This PVT was not seen on the CT scan performed in March 2007. To prevent further From the Department of Hepatobiliary Pancreas and Trans- plant Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. Address reprint requests to Hiroto Egawa, PhD, Graduate School of Medicine, Kyoto University, 54 Kawara-cho, Shogoin Sakyo-ku, Kyoto 606-8507, Japan. E-mail: egawa@kuhp.kyoto-u.ac.jp © 2009 Published by Elsevier Inc. 0041-1345/09/$–see front matter 360 Park Avenue South, New York, NY 10010-1710 doi:10.1016/j.transproceed.2008.10.104 Transplantation Proceedings, 41, 3931–3933 (2009) 3931