Hepatic macrosteatosis in the US pediatric deceased liver donor population

被引:3
作者
Purvis, Joshua W. [1 ]
Orandi, Babak J. [1 ]
Dhall, Deepti [2 ]
McLeod, Chandler [1 ]
Gutierrez Sanchez, Luz Helena [3 ]
Gray, Meagan [4 ]
Frey, Kayla [1 ]
Sheikh, Saulat S. [1 ]
Cannon, Robert M. [1 ]
Terrault, Norah A. [5 ]
Lewis, Cora E. [6 ]
Locke, Jayme E. [1 ]
机构
[1] Univ Alabama Birmingham, Dept Surg, Div Transplantat, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA
[3] Univ Alabama Birmingham, Dept Pediat, Div Pediat Gastroenterol Hepatol & Nutr, Birmingham, AL USA
[4] Univ Alabama Birmingham, Dept Med, Div Gastroenterol & Hepatol, Birmingham, AL 35294 USA
[5] Univ Southern Calif, Keck Sch Med, Dept Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90007 USA
[6] Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA
关键词
LI biopsy; macrosteatosis; obesity; pediatric liver transplant; FATTY LIVER; CHILDHOOD OBESITY; DISEASE; STEATOSIS; CHILDREN; ADOLESCENT;
D O I
10.1111/petr.14155
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Introduction The pediatric obesity epidemic is associated with early development of hepatic macrosteatosis, a hallmark of non-alcoholic fatty LI disease, which is thought to be more rapidly progressive in children than adults. Macrosteatosis in adult allografts is associated with allograft loss, but this has not been examined in pediatric donors. Methods We studied all pediatric potential whole LI donors (2005-2018) who had a LI biopsy in the SRTR (n = 862) and whose LI was transplanted (n = 862). Macrosteatosis was abstracted from biopsy reports and compared to values in the SRTR standard analytic file. Recipients of macrosteatotic pediatric allografts were matched 1:1 to recipients of non-macrosteatotic pediatric allografts by propensity score matching on donor/recipient variables. All-cause allograft loss was estimated via Kaplan-Meier analysis and Cox proportional hazards model. Results From 2005 to 2018, the proportion of pediatric donors (age >= 2 years) with obesity increased (14.8% to 21.7%; p < .001), as did the proportion of pediatric deceased whole LI-only donor allografts with macrosteatosis (n = 10 648; 1.8% to 3.9%; p < .001). The median degree of macrosteatosis among macrosteatotic donors was 10% (IQR 5-30). There were no significant differences in all-cause allograft loss between recipients of pediatric LI allografts with and without macrosteatosis at 90 days (p = .11) or 1 year (p = .14) post-transplant in Kaplan-Meier analysis or a Cox proportional hazards model (p > .05). Conclusion Obese pediatric LI donors have increased over time and were more likely to have hepatic macrosteatosis; however, pediatric macrosteatosis did not appear to adversely affect recipient outcomes.
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