Hepatic steatosis after pediatric liver transplant

被引:10
|
作者
Perito, Emily R. [1 ,2 ]
Vase, Tabitha [6 ]
Ramachandran, Rageshree [3 ]
Phelps, Andrew [4 ]
Jen, Kuang-Yu [7 ]
Lustig, Robert H. [1 ]
Feldstein, Vickie A. [4 ]
Rosenthal, Philip [1 ,5 ]
机构
[1] Univ Calif San Francisco, Dept Pediat, 550 16th St,5th Floor,Box 0136, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA
[4] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA
[5] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA
[6] Univ Calif San Francisco, Sch Med, San Francisco, CA USA
[7] Univ Calif Davis, Dept Pathol & Lab Med, Davis, CA 95616 USA
基金
美国国家卫生研究院;
关键词
FAMILIAL INTRAHEPATIC CHOLESTASIS; FATTY LIVER; METABOLIC SYNDROME; DIAGNOSTIC-ACCURACY; ALLOGRAFT FIBROSIS; SCORING SYSTEM; CHILDREN; BIOPSY; ADOLESCENTS; PREVALENCE;
D O I
10.1002/lt.24773
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatic steatosis develops after liver transplantation (LT) in 30% of adults, and nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in nontransplanted children. However, posttransplant steatosis has been minimally studied in pediatric LT recipients. We explored the prevalence, persistence, and association with chronic liver damage of hepatic steatosis in these children. In this single-center study of pediatric patients transplanted 1988-2015 (n = 318), 31% of those with any posttransplant biopsy (n = 271) had >= 1 biopsy with steatosis. Median time from transplant to first biopsy with steatosis was 0.8 months (interquartile range [IQR], 0.3-6.5 months) and to last biopsy with steatosis was 5.5 months (IQR, 1.0-24.5 months); 85% of patients with steatosis also had for-cause biopsies without steatosis. All available for-cause biopsies were re-evaluated (n = 104). Of 9 biopsies that could be interpreted as nonalcoholic steatohepatitis (NASH)/borderline NASH, with steatosis plus inflammation or ballooning, 8 also had features of cholestasis or rejection. Among 70 patients with surveillance biopsies 3.6-20.0 years after transplant, only 1 overweight adolescent had a biopsy with NAFLD (grade 1 steatosis, mild inflammation, no ballooning or fibrosis)-despite a 30% prevalence of overweight/obesity in the cohort and 27% with steatosis on previous for-cause biopsy. Steatosis on preceding for-cause biopsy was not associated with portal (P = 0.49) or perivenular fibrosis (P = 0.85) on surveillance biopsy. Hepatic steatosis commonly develops early after transplant in children and adolescents, but it rarely persists. Biopsies that did have steatosis with NASH characteristics were all for-cause, mostly in patients with NAFLD risk factors and/or confounding causes of liver damage. Prospective studies that follow children into adulthood will be needed to evaluate if and when hepatic steatosis presents a longterm risk for pediatric LT recipients.
引用
收藏
页码:957 / 967
页数:11
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