Open AccessHepatic steatosis is associated with intrahepatic cholestasis and transient hyperbilirubinemia during regeneration after living donor liver transplantation
Author(s) -
Cho Jai Young,
Suh KyungSuk,
Lee Hae Won,
Cho EungHo,
Yang Sung Hoon,
Cho Yong Beom,
Yi NamJoon,
Kim Min A,
Jang JaJune,
Lee Kuhn UK
Publication year - 2006
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2006.00355.x
Subject(s) - cholestasis , medicine , steatosis , gastroenterology , liver transplantation , liver regeneration , proliferating cell nuclear antigen , transplantation , hepatology , pathology , regeneration (biology) , immunohistochemistry , biology , microbiology and biotechnology
Summary 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.