Prevalence and clinical associations of posttransplant fatty liver disease

Lim, Lee Yong; Cheng, Chee Leong; Wee, Aileen; Lim, Seng Gee; Lee, Yin Mei; Sutedja, Dede Selamat; Costa, M. Da; Prabhakaran, K.; Wai, Chun-Tao

doi:10.1111/j.1478-3231.2006.01396.x

Cited by 72 publications

(71 citation statements)

References 17 publications

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“…(6,7) Genetic factors, such as patatin-like phospholipase domain containing 3 (PNPLA3) gene polymorphism, are associated with increased hepatic fat concentration. (10) Posttransplant NAFLD affects 18%-40% of liver transplantation (LT) recipients (11)(12)(13) and even 39%-70% (14,15) of those transplanted for NAFLD-related cirrhosis. Risk factors of posttransplant NAFLD include pretransplant and posttransplant obesity, (11)(12)(13) alcoholic cirrhosis as an indication for LT, posttransplant DM, hyperlipidemia, hypertension, tacrolimus (FK-506) administration, and pretransplant graft steatosis.…”

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“…(10) Posttransplant NAFLD affects 18%-40% of liver transplantation (LT) recipients (11)(12)(13) and even 39%-70% (14,15) of those transplanted for NAFLD-related cirrhosis. Risk factors of posttransplant NAFLD include pretransplant and posttransplant obesity, (11)(12)(13) alcoholic cirrhosis as an indication for LT, posttransplant DM, hyperlipidemia, hypertension, tacrolimus (FK-506) administration, and pretransplant graft steatosis. (11) In a study by Finkenstedt et al, (16) the PNPLA3 genotype of the recipient (but not the donor) was associated with the development of posttransplant steatosis.…”

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Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

et al. 2016

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Steatosis occurs frequently after liver transplantation (LT). We aimed to determine the prevalence of steatosis in adult LT recipients, to determine the effects of significant (>33%; grades 2-3) steatosis on patient survival, and to identify risk factors for the development of significant steatosis and its effect on fibrosis progression. We retrospectively examined 2360 posttransplant biopsies of 548 LT recipients. Survival was compared between patients with significant steatosis and those with grades 0-1 steatosis. Patients with significant steatosis were compared to controls without steatosis (grade 0) for clinical and laboratory factors and fibrosis progression. Steatosis was found in 309 (56.4%) patients, including 93 (17.0%) patients with significant steatosis. Steatohepatitis (nonalcoholic fatty liver disease activity score 5) was diagnosed in 57 (10.4%) patients. The prevalence of steatosis increased from 30.3% at 1 year to 47.6% at 10 years after LT (P < 0.001). Survival times did not differ between groups (P 5 0.29). On multivariate analysis of pretransplant factors and initial immunosuppression (IS), alcohol-induced cirrhosis (P < 0.001) and high body mass index (BMI; P 5 0.002) were associated with the development of significant steatosis, whereas increased levels of alkaline phosphatase (P 5 0.01) and mycophenolate mofetil given initially (P 5 0.009) appeared to protect against significant steatosis. On multivariate analysis of posttransplant factors, high BMI (P < 0.001), serum triglycerides (P < 0.001), alcohol consumption (P 5 0.005), and type 2 diabetes mellitus (P 5 0.048) were associated with significant steatosis, whereas high creatinine (P 5 0.02) appeared to protect against significant steatosis. Significant steatosis was not associated with a higher fibrosis stage (P 5 0.62). Posttransplant steatosis affects 56.4% of LT recipients, and the prevalence increases with time after LT. Recipient factors and types of IS affect the risk for significant steatosis, which is not associated with a higher fibrosis stage or worse patient survival.Liver Transplantation 22 644-655 2016 AASLD.

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Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

et al. 2016

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“…Th e diff erence was, however, not statistically signifi cant. It is important to note that only half of the patients in this cohort had donor biopsy fi ndings available for comparison ( 6 ). In the present study, the prevalence of allograft steatosis at implantation was 30.2 % among those who developed de novo NAFLD compared with 12.6 % among those who did not ( 8 ).…”

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“…Poordad et al ( 5 ) reported four cases of de novo NAFLD that developed early in the post-transplant setting. In another report, NAFLD developed in 40 % of LT recipients aft er a mean follow-up of 44 months ( 6 ). NASH was seen in 13 % .…”

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Non-Alcoholic Fatty Liver Disease After Liver Transplantation: A Case of Nurture and Nature

Ong

Younossi

2010

American Journal of Gastroenterology

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Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Most patients with cryptogenic cirrhosis are considered to have had " burned out NAFLD. " Although the recurrence and progression of NAFLD after liver transplantation (LT) have been shown previously, the incidence of de novo NAFLD after LT has not been extensively reported. In this issue of the American Journal of Gastroenterology , Dumortier et al. report the incidence of de novo post-LT NAFLD. Although most of the risk factors for post-LT NAFLD are similar to those for primary NAFLD, hepatic steatosis in the donor livers and a pre-transplant diagnosis of alcoholic liver disease remain independent risk factors. Although there are some limitations, this study provides the largest cohort of patients for whom post-LT NAFLD is reported. Am J Gastroenterol 2010; 105:621 -623; doi: 10.1038/ajg.2009 Non-alcoholic fatty liver disease (NAFLD) is currently recognized as one of the most common forms of chronic liver disease. Natural history studies have shown that a proportion of patients, especially those with non-alcoholic steatohepatitis (NASH), will develop progressive liver disease, leading to end-stage liver disease and hepatocellular carcinoma ( 1 ). Moreover, recurrence of NAFLD aft er liver transplantation (LT) is common ( 2 ). Th e risk factors for recurrent NAFLD include post-transplant diabetes, obesity, and hypertriglyceridemia ( 1 ). Progression from simple steatosis to NASH and cirrhosis and even allograft failure has been demonstrated ( 1,3 ).De novo NAFLD aft er LT, however, is not as well studied. Its incidence, risk factors, and natural history are not currently well defi ned. In an early report, 25 % of patients with cholestatic liver disease were noted to develop a fatty liver aft er LT. As pretransplant characteristics as well as explants ' histology were not described for this group of patients, it is diffi cult to determine whether this group had concomitant NAFLD at the time of transplantation and thus whether developing a fatty liver aft er transplant simply represented recurrent disease ( 4 ). Poordad et al. ( 5 ) reported four cases of de novo NAFLD that developed early in the post-transplant setting. In another report, NAFLD developed in 40 % of LT recipients aft er a mean follow-up of 44 months ( 6 ). NASH was seen in 13 % . Seo et al. ( 7 ) reported an incidence of 18 % for NAFLD and 9 % for NASH aft er an average follow-up of 28 months. Th ese early reports are, however, limited by small sample sizes and the relative predominance of chronic hepatitis C as an indication for LT, which has been associated with hepatic steatosis, especially HCV genotype 3 infection. Moreover, the liver biopsies in these studies were performed for clinical indications in the majority of cases as opposed to protocol biopsies, a fact that may aff ect the estimation of the incidence of NAFLD in the post-transplant setting.In this issue of the American Journal of Gastroenterology , Dumortier et al. ( 8 ) report their ...

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Posttransplant metabolic syndrome: An epidemic waiting to happen

et al. 2009

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With increasing survival after orthotopic liver transplantation (OLT), metabolic syndrome and its individual components, including diabetes mellitus, hypertension, dyslipidemia, and obesity, are increasingly being identified and contributing to cardiovascular complications and late morbidity and mortality. The prevalence of posttransplant metabolic syndrome (PTMS) and its individual components has been found to be higher post-OLT versus a comparable population without OLT. The development of nonalcoholic fatty liver disease (NAFLD) after liver transplantation for non-NAFLD cirrhosis is also being increasingly recognized. A number of predictors have been identified as potential risk factors related to these complications. The pretransplant risk factors include immunosuppression, a higher age at transplant, male gender, a history of smoking, the pretransplant body mass index, pre-OLT diabetes, the etiology of the underlying liver disease that resulted in OLT (hepatitis C, cryptogenic cirrhosis, or alcohol), an increased donor body mass index, and marital status. Although there is an increased risk of cardiovascular events, rejection, and infection among patients with PTMS, the overall impact on long-term survival and mortality remains inconclusive. Strategies to reduce the development of metabolic syndrome after transplantation should include lifestyle modifications involving alterations in diet and increased physical activity. Additional measures that may be potentially beneficial include the use of lipid-lowering agents, the optimal control of blood glucose, and the use of tacrolimus instead of cyclosporine. With the availability of liver transplantation as an effective therapy for chronic end-stage liver disease and with over 90% survival at 1 year and over 70% survival at 5 years, the occurrence of MS after liver transplantation is being increasingly recognized. 4 Patients after transplantation can develop a number of well-recognized complications, which include infection, graft rejection, vascular and biliary disorders, renal insufficiency, neurological and psychiatric disorders, chronic

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Prevalence and clinical associations of posttransplant fatty liver disease

Abstract: Posttransplant steatosis is common after liver transplant even in patients transplanted for non-NAFLD-related liver diseases. However, it is mostly benign during our follow-up, with only 13% developing steatohepatitis and none with fibrosis or cirrhosis.

Cited by 72 publications

References 17 publications

Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

Non-Alcoholic Fatty Liver Disease After Liver Transplantation: A Case of Nurture and Nature

Posttransplant metabolic syndrome: An epidemic waiting to happen

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