Posttransplant liver steatosis occurs frequently and can affect patient outcome. Our aim was to clarify the risk factors for steatosis or steatohepatitis after living donor liver transplantation (LT) through a retrospective examination of recent 100 living donor LT recipients and their liver donors.
Liver biopsy was performed at 1 year after LT and each year, thereafter, or as needed due to abnormal liver enzyme levels, with a median follow-up of 4 years (2-10 years).
Liver steatosis (≥5%) was identified in 33 cases, with steatohepatitis identified in 9 of 33 patients with liver steatosis. Recipients with liver steatosis were younger than those without steatosis (53.4 ± 9.5 years vs 57.6 ± 9.9 years, respectively; P = 0.045). Of note, the prevalence of steatosis was significantly higher among LT recipients who received a graft from a donor with steatosis than without (60% vs 23%, respectively; P = 0.001). Donor steatosis was also associated with steatohepatitis in recipients after LT (steatohepatitis/simple steatosis, 88%:50%). On multivariate analysis, younger recipient age (P = 0.023) and donor steatosis (P = 0.005) were independent risk factors of liver steatosis after LT. Among the 33 recipients in our study group, 26 were assessed by serial liver biopsies, with 6 showing progression of the nonalcoholic fatty liver disease activity score. An increase in body weight was predictive of steatosis progression after LT (P = 0.005).
Age and donor steatosis influence the risk of liver steatosis and steatohepatitis in recipients after LT. The clinical course of steatosis is relatively benign, with only 19% developing nonalcoholic fatty liver disease activity score and 7.6% significant fibrosis.
1 Department of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki, Japan.
2 Department of Surgery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Received 24 January 2018. Revision received 16 May 2018.
Accepted 4 June 2018.
The authors declare no funding or no conflicts of interest.
H.M. participated in the study design, statistical analysis, data interpretation, article preparation, literature search. S.M. participated in the data collection. N.T. participated in the data collection. H.S. participated in the data collection. R.S. participated in the data collection. A.S. participated in the data collection. M.H. participated in the data collection. M.T. participated in the data collection. S.E. participated in the data collection. K.N. participated in the data interpretation.
Correspondence: Hisamitsu Miyaaki, MD, Department of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan. (firstname.lastname@example.org).