Hepatic steatosis is associated with intrahepatic cholestasis and transient hyperbilirubinemia during regeneration after living donor liver transplantation.

Research paper by Jai Young JY Cho, Kyung-Suk KS Suh, Hae Won HW Lee, Eung-Ho EH Cho, Sung Hoon SH Yang, Yong Beom YB Cho, Nam-Joon NJ Yi, Min A MA Kim, Ja-June JJ Jang, Kuhn Uk KU Lee

Indexed on: 12 Sep '06Published on: 12 Sep '06Published in: Transplant International


A clear understanding of the mechanisms in steatotic livers that trigger cholestasis or hyperbilirubinemia after living donor liver transplantation (LDLT) remains elusive. We hypothesized that microarchitectural disturbance might occur within regenerating steatotic livers without impairment of hepatic proliferative activity. Liver biopsy specimens from 67 LDLT recipients taken at the 10th postoperative day were scored for the numbers of portal tracts per area (nPT/A) of liver tissue and for intrahepatic cholestasis, and immunostained by proliferating cell nuclear antigen (PCNA) and Ki-67. The preoperative degree of macrovesicular steatosis (MaS) was independently associated with cholestasis after LDLT (P < 0.001). Serum total bilirubin results on the 1st, 3rd, and 7th days post-LDLT in MaS+ (5-30% of MaS; n = 37) patients were significantly higher than those in MaS- (<5% of MaS; n = 30) patients (P = 0.030, 0.042, and 0.019, respectively). Mean numbers of positively stained hepatocytes were 53.1 +/- 12.0 in patients with MaS and 48.0 +/- 17.1 in those without MaS by PCNA (P = 0.390), and 24.4 +/- 10.5 and 24.0 +/- 14.0 by Ki-67 (P = 0.940). However, a significant negative correlation was found between the degree of MaS and nPT/A (P = 0.013), and nPT/A was correlated with the grade of histological cholestasis (r = 0.350, P = 0.039). Intrahepatic cholestasis and hyperbilirubinemia after LDLT could be caused by scanty morphologic change of portal tract during steatotic liver regeneration.