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Donor liver steatosis: A risk factor for early new‐onset diabetes after liver transplantation

AIMS/INTRODUCTION: To investigate whether donor liver steatosis increases the incidence of new‐onset diabetes after transplantation (NODAT) in liver transplant recipients. MATERIALS AND METHODS: We retrospectively analyzed liver transplant recipients at Zhongshan Hospital, Shanghai, China, from Apri...

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Detalles Bibliográficos
Autores principales: Xue, Mengjuan, Lv, Chaoyang, Chen, Xianying, Liang, Jing, Zhao, Chenhe, Zhang, Yao, Huang, Xiaowu, Sun, Qiman, Wang, Ting, Gao, Jian, Zhou, Jian, Yu, Mingxiang, Fan, Jia, Gao, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334314/
https://www.ncbi.nlm.nih.gov/pubmed/27511316
http://dx.doi.org/10.1111/jdi.12560
Descripción
Sumario:AIMS/INTRODUCTION: To investigate whether donor liver steatosis increases the incidence of new‐onset diabetes after transplantation (NODAT) in liver transplant recipients. MATERIALS AND METHODS: We retrospectively analyzed liver transplant recipients at Zhongshan Hospital, Shanghai, China, from April 2001 to December 2014. The final analysis involved 763 patients. The cumulative incidence of NODAT at 1, 3, 5 and 10 years after liver transplantation was investigated. Furthermore, according to the findings of donor liver biopsy before transplantation, patients were divided into steatotic and non‐steatotic donor liver groups, and NODAT incidence was compared between these groups. Multivariate Cox regression was used to explore the risk factors for NODAT in the patients. RESULTS: Of the 763 donors, 309 (40.5%) had liver steatosis. At the end of follow up, 130 (42.1%) patients in the steatotic donor liver group developed NODAT, an incidence that exceeded that in the non‐steatotic donor liver group (P = 0.001). The cumulative incidence of NODAT among all patients at 1, 3, 5, and 10 years after transplantation was 33, 43, 50 and 56%, respectively. The cumulative incidences of NODAT at 1, 3, 5 and 10 years in the steatotic donor liver group were significantly higher than those in the non‐steatotic donor liver group (P = 0.003). Multivariate Cox regression analyses showed that donor liver steatosis was an independent risk factor for NODAT among liver transplant recipients, after other potential risk factors were adjusted for (hazard ratio 1.774, 95% confidence interval: 1.025–3.073; P = 0.041). CONCLUSIONS: Donor liver steatosis increases NODAT incidence among liver transplant recipients.