Recurrence of Primary Sclerosing Cholangitis After Living Donor Liver Transplantation

Sumihito Tamura; Yasuhiko Sugawara; Junichi Kaneko; Yuichi Matsui; Junichi Togashi; Masatoshi Makuuchi


Liver International. 2007;27(1):86-94. 

In This Article

Patients and Methods

A total of 348 patients underwent liver transplantation at our institution between April 1996 and October 2005. During this period, nine patients (3%) underwent LDLT for end-stage liver disease secondary to PSC. The clinical records of these recipients and of the respective live donors were subjected to analysis.

The pretransplantation diagnosis of PSC was based on the criteria described previously.[9] In brief, (1) the presence of a cholestatic biochemical profile for 6 months or more, (2) typical findings on cholangiogram, and (3) histopathologic findings of the explant liver consistent with PSC. Other potential causes of progressive cholestatic liver disease, such as primary biliary cirrhosis, sarcoidosis, choledochal cysts, and chronic obstruction secondary to biliary stone disease, were excluded in all patients. The occurrence of events suggestive of hepatic decompensation were considered to indicate advanced PSC, which supported the decision to perform LDLT. Model for end-stage liver disease and modified Mayo risk scores for PSC were determined for all patients. The model for end-stage liver disease score was calculated for all patients using an Internet-based calculator ( The modified Mayo risk score for PSC was calculated using the following formula: R = 0.03 × age (years)+0.54 loge (bilirubin [mg/dl])+0.54 loge (asparate aminotransferase [U/l])+1.24 (variceal bleeding [no = 0; yes = 1]−0.84 × albumin (g/dl)) as described previously.[18]

Complete donor-recipient HLA typing was performed prospectively as part of the pre-LDLT workup, as described.[19] In brief, HLA class I typing was performed using a standard complement-dependent microcytotoxicity assay with a Terasaki HLA tray (One Lambda Inc., Los Angeles, CA). Serologic HLA-DR typing was performed using a two-color fluorescence assay. In six cases (Cases 2-4, 6-9), high-resolution polymerase chain reaction (PCR)-based DNA typing was available for the HLA-DRB1 locus using the sequence-based typing (PCR-SBT) method with the AlleleSEQR DRB1 typing kit (Atria Genetics Inc., San Francisco, CA).

Our selection of live liver donors, surgical techniques, and immunosuppression regimen for LDLT is described elsewhere.[20,21] In brief, living donors were selected after considering their age, blood type, graft size, liver function, and desire to volunteer. Total liver volume of the donor was determined by computed tomography volumetry, and standard liver volume of the recipient was calculated as described previously in order to determine the necessary liver volume.[22]

In our series, grafts procured from live liver donors are flushed with University of Wisconsin solution and stored on ice. The median cold and warm ischemic times of the PSC cases were 122 (range 64-195) and 70 min (range 46-100), respectively. Those of our entire LDLT registry are 113 (range 11-394) and 70 min (22-237). In all the PSC cases, biliary drainage was accomplished by a bilioenteric anastomosis between the graft hepatic duct and a roux-en-Y jejunal loop. The immunosuppression regimen consisted of steroid induction with tacrolimus and steroids for maintenance, as previously described.[23]

Protocol biopsy or protocol cholangiograms were not performed. Vascular patency of the graft was evaluated by Doppler ultrasonography twice daily during the first 2 weeks following transplantation,[24] and thereafter whenever the results of liver function tests were greater than two times the upper normal limit.

The diagnosis of recurrent PSC was made according to the definition,[15] with modifications with the use of drip infusion cholangiography with multidetector-row helical computer-assisted tomography or magnetic resonance cholangiopancreatography instead of percutaneous transhepatic cholangiogram. In brief, the diagnosis of recurrent PSC was based on the following two major criteria: (1) a confirmed diagnosis of PSC transplantation in the explanted liver, and (2) a cholangiogram showing nonanastomotic biliary strictures of the intrahepatic biliary tree with beading and irregularity occurring 90 days posttransplantation. Nonanastomotic biliary strictures developing within the first 90 days posttransplantation are excluded as the majority of nonanastomotic biliary strictures related to ischemic damage as a result of ischemia reperfusion-induced injury occur within this period.[15] Exclusion criteria included the presence of other causes of biliary strictures, such as hepatic artery thrombosis, chronic ductopenic rejection, ABO blood-type incompatibility, and anastomotic bile duct strictures related to surgical reconstruction.


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