Recurrence Of Nonalcoholic Fatty Liver Disease Research Articles

Non-alcoholic fatty liver disease increases the risk of biochemical recurrence in high-grade metastatic prostate cancer patients.

Non-alcoholic fatty liver disease (NAFLD) has been reported to be helpful to identify high-risk individuals of developing prostate cancer. Our aim is to investigate the relationship between NAFLD and biochemical recurrence in metastatic prostate cancer patients. We retrospectively investigated 602 patients with metastatic prostate cancer receiving the androgen deprivation therapy. Liver fat was estimated with liver-to-spleen ratio by computed tomography (CT) scans. The relationship between NAFLD and biochemical recurrence was investigated with Cox models. The model for biochemical recurrence was adjusted for multiple variables. NAFLD was significantly associated with biochemical recurrence in patients with Gleason score ≥4+3 when adjusting for each of body mass index (hazards ratio [HR]=1.38; 95% confidence interval [CI]=1.08-1.77; p=0.01), visceral adipose tissue (HR=1.36; 95% CI=1.07-1.74; p=0.01), hypertension (HR=1.41; 95% CI=1.10-1.80; p=0.01), and diabetes mellitus (HR=1.42; 95% CI=1.11-1.82; p=0.01), using age and prostate-specific antigen level as potential confounder. The 2-year biochemical recurrence rate in the Gleason score ≥4+3 patients with and without NAFLD was 84.0% (100/119) and 72.2% (130/180), respectively (p=0.018). The median biochemical recurrence free survival of the Gleason score ≥4+3 patients with and without NAFLD were 17 and 21 months, respectively (p=0.005). NAFLD is an independent risk factor for biochemical recurrence in patients with high-grade metastatic prostate cancer. If validated in prospective studies, future research should test whether treatment of NAFLD can lead to better prognosis.

Extrahepatic organs in the development of non-alcoholic fatty liver disease in liver transplant patients.

Non-alcoholic fatty liver disease (NAFLD) is highly prevalent in patients who undergo liver transplantation (LT). Whereas there is huge data on NAFLD, little is known about NAFLD in LT. In this review, we aim to explore extrahepatic organs and their potential mechanisms in the development of NAFLD in LT patients and discuss current limitations in preclinical and clinical scenarios with suggestions for future study. The following keywords, such as NAFLD, NASH, liver transplant, therapy, pathogenesis and biomarkers, were set for literature retrieval. The articles which were published articles in English till 25th June 2020 in PubMed database were included, and there is no limit for the study design type. Following LT, there are significant shifts in the microbiota and farnesoid X receptor may be a potential therapeutic target for NAFLD in LT settings. The roles of probiotics and diet on NALFD remain inconclusive in LT background. Nevertheless, the adipokines and cytokines disorder and local insulin resistance of adipose tissue may contribute to NAFLD process. Bariatric surgeries are promising in controlling de novo and recurrent NAFLD with significant reduction in abdominal adipose tissue, despite the optimal timing is inconclusive in LT cases. Furthermore, circumstantial evidence indicates that miRNA-33a may function as a mediator bridging sarcopenia and NAFLD of post-LT. β-Hydroxy-β-Methyl-Butyrate treatment could improve muscle status in graft recipients and shows protective potential for NAFLD in LT settings. Gut, adipose tissue and muscle are intricately intertwined in promoting NAFLD in LT cases. Further animal studies are needed to deepen our understanding of mechanisms in multi-organ crosstalk. High quality clinical trials are warrant for making guidelines and developing management strategies on NAFLD after LT.

Relationship between the dynamics of non-alcoholic fatty liver disease and incident diabetes mellitus

The aim of the current study was to evaluate the association between changes in non-alcoholic fatty liver disease (NAFLD) over time and risk of incident diabetes mellitus (DM). In total, 3047 subjects without underlying DM were followed up for 14 years from the Anseong-Ansan cohort. NAFLD status was determined biennially using the hepatic steatosis index (HSI), and subjects were clustered into seven groups according to changes in HSI, body mass index (BMI), and homeostatic model assessment of insulin resistance (HOMA-IR): none, persistent, transient, transient resolved, resolved, incident, and recurrent NAFLD (Groups 1–7, respectively). Predictive abilities were compared between the dynamics of HSI and single time points. Regarding the changes in HSI, the risk of incident DM was highest in Group 2 (hazard ratio [HR] 2.710; P < 0.001), followed by Groups 7 (HR 2.062; P < 0.001) and 3 (HR 1.559; P = 0.027). The predictive ability for DM was powerful in order of HOMA-IR, HSI and BMI. The dynamics of NAFLD were less predictive of incident DM than single time-point NAFLD. In conclusion, NAFLD is more useful than BMI in predicting incident DM. However, NAFLD status at single time points can better predict incident DM than dynamic changes in HSI.

Genetic and Life Style Risk Factors for Recurrent Non-alcoholic Fatty Liver Disease Following Liver Transplantation.

Recurrent or de novo non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) following liver transplantation (LT) is a frequent event being increasingly recognized over the last decade, but the influence of recurrent NASH on graft and patient outcomes is not yet established. Taking into consideration the long term survival of liver transplanted patients and long term complications with associated morbidity and mortality, it is important to define and minimize risk factors for recurrent NAFLD/NASH. Metabolic syndrome, obesity, dyslipidemia, diabetes mellitus are life style risk factors that can be potentially modified by various interventions and thus, decrease the risk of recurrent NAFLD/NASH. On the other hand, genetic factors like recipient and/or donor PNPLA3, TM6SF2, GCKR, MBOAT7 or ADIPOQ gene polymorphisms proved to be risk factors for recurrent NASH. Personalized interventions to influence the different metabolic disorders occurring after LT in order to minimize the risks, as well as genetic screening of donors and recipients should be performed pre-LT in order to achieve diagnosis and treatment as early as possible.

A Single-Center Study of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis Recurrence in Recipients of Liver Transplant for Treatment of Nonalcoholic Steatohepatitis Cirrhosis.

Nonalcoholic steatohepatitis is a growing indication for liver transplant. We examined multiple granular elements to determine risk factors for recurrence of nonalcoholic steatohepatitis or recurrence of nonalcoholic fatty liver disease. This is a retrospective, single-center study of patients who underwent liver transplant for nonalcoholic steatohepatitis. Demographic differences were assessed with the Wilcoxon and Pearson tests for continuous and discrete variables, respectively. We used a linear mixed effects model to estimate mean changes in body mass index and laboratory measurements. Time to graft loss was analyzed with the Cox proportional hazards model. From 1998 to 2017, there were 275 patients at our center who underwent liver transplant as treatment for nonalcoholic steatohepatitis cirrhosis. Of these patients, 31 (11%) were diagnosed with recurrent nonalcoholic steatohepatitis and 60 (22%) had recurrent nonalcoholic fatty liver disease. Patients with or without recurrence of either nonalcoholic steatohepatitis or nonalcoholic fatty liver disease were similar with regard to Model for End-Stage Liver Disease score, body mass index, sex, ethnicity, comorbidity, and donor characteristics, including donor macrosteatosis. Exposures to several medication classes were examined, but there was no association with recurrence of either nonalcoholic steatohepatitis or nonalcoholic fatty liver disease. Changes in aspartate aminotransferase and alanine aminotransferase levels over time were correlated with recurrence of either nonalcoholic steatohepatitis or nonalcoholic fatty liver disease versus levels observed in the groups with no recurrent disease. There was no difference in graft survival for the groups with recurrence of either nonalcoholic steatohepatitis or nonalcoholic fatty liver disease. Recurrence of nonalcoholic fatty liver disease and recurrence of nonalcoholic steatohepatitis were not associated with increased mortality after liver transplant. There were notable steady increases in body mass index after transplant for all patients who received liver transplant as treatment for nonalcoholic steatohepatitis.

Utility of Metabolomic Biomarkers to Identify Nonalcoholic Fatty Liver Disease in Liver Transplant Recipients.

Background.Nonalcoholic fatty liver disease (NAFLD) is a rising indication for liver transplantation (LT). Identification of NAFLD recurrence and those at risk for more progressive disease after LT remains elusive as the diagnosis requires biopsy, which is invasive and impractical for serial monitoring. We therefore aimed to identify metabolites in the blood associated with recurrent NAFLD that could potentially be used for detection and monitoring.Methods.This cross-sectional pilot study included 37 LT recipients who underwent simultaneous liver biopsy and plasma collection for metabolomic analysis. Metabolic profiles were compared between patients with recurrent NAFLD, normal liver (negative control), and acute rejection (rejection control).Results.Univariate analysis revealed 14 metabolites that were significantly altered in patients with recurrence of NAFLD compared with negative controls and 19 compared with rejection controls (P < 0.05). In addition, metabolomic profiling identified 16 metabolites that distinguished nonalcoholic fatty liver versus nonalcoholic steatohepatitis. Metabolite class trends among patients with recurrent NAFLD following LT were consistent with prior metabolomics data in patients with NAFLD in the non-LT setting.Conclusions.In conclusion, we identified candidate metabolites that could be used in the clinical setting to noninvasively identify recurrent NAFLD and differentiate NAFL from the more progressive nonalcoholic steatohepatitis. Further investigation with a larger sample size is warranted to validate these results.

A weight regain of 1.5\xa0kg or more and lack of exercise are associated with nonalcoholic fatty liver disease recurrence in men

The importance of maintaining the remission of nonalcoholic fatty liver disease (NAFLD) has been overlooked. Here we aimed to clarify factors causing NAFLD recurrence. In this retrospective cohort study over 10.8 ± 5.4 years, we investigated 1260 male health check-up participants diagnosed with NAFLD who achieved remission. The data were compared between the maintained remission and recurrence group. Among all participants, 618 (49.0%) showed NAFLD recurrence at the last visit. Participants in the maintained remission group continued to lose weight (72.7 ± 9.1, 68.7 ± 8.5 and 68.2 ± 8.9 kg), whereas those in the recurrence group lost and regained weight (72.9 ± 9.9, 69.7 ± 9.3 and 73.0 ± 10.4 kg). Receiver operating characteristic curve analysis showed a weight regain of + 1.5 kg as the cutoff value for recurrence. The proportion of regular exercisers at the last visit was 34.6% in the maintained remission group and 24.5% in the recurrence group (p < 0.0001). Multivariable analysis revealed the amount of weight regain (in 1 kg increments; adjusted odds ratio, 1.29; 95% confidence interval, 1.24–1.34) and regular exercise at the last visit (adjusted odds ratio, 0.67; 95% confidence interval, 0.55–0.89) were independently associated with recurrence. These findings demonstrate a weight regain of 1.5 kg or more and lack of exercise were associated with NAFLD recurrence.

Liver-Related and Cardiovascular Outcome of Patients Transplanted for Nonalcoholic Fatty Liver Disease: A European Single-Center Study

The increasing rate of liver transplantation (LT) for nonalcoholic fatty liver disease (NAFLD) raises concerns on cardiovascular morbidity and mortality after LT in these patients. We collected variables regarding the presence of metabolic risk factors, NAFLD recurrence, cardiovascular morbidity, and overall survival at time of listing and after LT of 112 patients with NAFLD and a control group of 120 patients with hepatitis C (HCV). Metabolic syndrome and cardiovascular morbidity component rates (24.1% vs 12.5%) at the time of LT listing were higher in patients with NAFLD compared with patients with HCV (for all, P < .0390). Median follow-up after LT was 5.6 years in patients with NAFLD vs 13.5 years in patients with HCV (P=.0009). There was no difference in 6-weeks postoperative mortality (1.7% vs 2.5%) (P =1.0000). Metabolic syndrome components after LT were more frequent in patients with NAFLD than in patients with HCV (for all, P < .0008). The incidence of NAFLD 5 years after LT was higher in patients transplanted for NAFLD compared with HCV (43.5% vs 4.2%) (P < .0001). Patients with recurrent NAFLD more often had myocardial infarction compared with those without recurrence (8.3% vs 0%) (P=.0313). Five years after LT, cardiovascular morbidity was more frequent in the NAFLD group than in the HCV group (12.8% vs 9.3%) (P=.0256), whereas no difference in overall survival was observed. LT for NAFLD is associated with satisfactory 5-year outcomes; however, our data underscore the need for close monitoring and aggressive management of cardiovascular risk factors in these patients.

Nonalcoholic Fatty Liver Disease after Liver Transplant.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in the world. The rising prevalence of nonalcoholic steatohepatitis (NASH) has led to a 170% increase in NASH cirrhosis as the listing indication for liver transplantation from 2004 to 2013. As of 2018, NASH has overtaken hepatitis C as an indication for liver transplantation in the USA. After liver transplantation, the allograft often develops recurrent NAFLD among patients with known NASH cirrhosis. In addition to recurrent disease, de novo NAFLD has been reported in patients with other indications for liver transplantation. In this review, we will discuss the risk factors associated with recurrent and de novo NAFLD, natural course of the disease, and management strategies after liver transplantation.

Noninvasive markers of liver steatosis and fibrosis after liver transplantation - Where do we stand?

In the last two decades, advances in immunosuppressive regimens have led to fewer complications of acute rejection crisis and consequently improved short-term graft and patient survival. In parallel with this great success, long-term post-transplantation complications have become a focus of interest of doctors engaged in transplant medicine. Metabolic syndrome (MetS) and its individual components, namely, obesity, dyslipidemia, diabetes, and hypertension, often develop in the post-transplant setting and are associated with immuno-suppressive therapy. Nonalcoholic fatty liver disease (NAFLD) is closely related to MetS and its individual components and is the liver manifestation of MetS. Therefore, it is not surprising that MetS and its individual components are associated with recurrent or “de novo” NAFLD after liver transplantation (LT). Fibrosis of the graft is one of the main determinants of overall morbidity and mortality in the post-LT period. In the assessment of post-LT steatosis and fibrosis, we have biochemical markers, imaging methods and liver biopsy. Because of the significant economic burden of post-LT steatosis and fibrosis and its potential consequences, there is an unmet need for noninvasive methods that are efficient and cost-effective. Biochemical scores can overestimate fibrosis and are not a good method for fibrosis evaluation in liver transplant recipients due to frequent post-LT thrombocytopenia. Transient elastography with controlled attenuation parameter is a promising noninvasive method for steatosis and fibrosis. In this review, we will specifically focus on the evaluation of steatosis and fibrosis in the post-LT setting in the context of de novo or recurrent NAFLD.

Clinical and Genetic Risk Factors of Recurrent Nonalcoholic Fatty Liver Disease After Liver Transplantation.

INTRODUCTION:Nonalcoholic fatty liver disease (NAFLD) has been increasingly reported among recipients of liver transplantation (LT). We aimed to identify clinical and genetic risk factors responsible for the development of early recurrent NAFLD in nonalcoholic steatohepatitis transplant recipients.METHODS:Forty-six total single nucleotide polymorphisms with known association with NAFLD were tested among both recipient and donor liver samples in 66 LT recipients with nonalcoholic steatohepatitis to characterize influences on NAFLD recurrence at ∼1 year post-LT (median interval from LT to biopsy: 377 days).RESULTS:Recurrent NAFLD was identified in 43 (65.2%) patients, 20 (30.3%) with mild recurrence, and 23 (34.8%) with moderate to severe NAFLD. On adjusted analysis, change in the body mass index (BMI) (ΔBMI) was significantly associated with NAFLD recurrence, whereas post-LT diabetes mellitus was associated with increased severity of NAFLD recurrence. ADIPOR1 rs10920533 in the recipient was associated with increased risk of moderate to severe NAFLD recurrence, whereas the minor allele of SOD2 rs4880 in the recipient was associated with reduced risk. Similar reduced risk was noted in the presence of donor SOD2 rs4880 and HSD17B13 rs6834314 polymorphism.DISCUSSION:Increased BMI post-LT is strongly associated with NAFLD recurrence, whereas post-LT diabetes mellitus was associated with increased severity of NAFLD recurrence. Both donor and recipient SOD2 rs4880 and donor HSD17B13 rs6834314 single nucleotide polymorphisms may be associated with reduced risk of early NAFLD recurrence, whereas presence of the minor allele form of ADIPOR1 rs10920533 in the recipient is associated with increased severity NAFLD recurrence.

Characterization of Gut Microbiome in Liver Transplant Recipients With Nonalcoholic Steatohepatitis.

Twenty-one patients who received LT for NASH and had a protocol liver biopsy performed beyond 1-y post-LT were included prospectively (January 2018-December 2018). Genomic DNA extraction, next-generation sequencing, and quantitative PCR analysis were performed on stool samples collected within 1.1 ± 1.6 y from time of liver biopsy. Recurrent NAFLD was noted in 15 of the 21 included patients. Stool microbiome analysis at the genus level showed significant loss of Akkermansia and increasing Fusobacterium associated with NAFLD recurrence. Quantitative PCR analysis revealed significantly decreased relative abundance of Firmicutes in patients with NAFLD activity scores (NASs) ≥5 as compared with patients with lower NAS scores, whereas Bacteroidetes were significantly increased with higher NAS (P < 0.05). Firmicutes (P = 0.007) and Bifidobacterium group (P = 0.037) were inversely correlated, whereas Bacteroidetes (P = 0.001) showed a positive correlation with higher hepatic steatosis content. The Firmicutes/Bacteroidetes ratios were higher in patients without NAFLD or NASH as compared with patients diagnosed with NAFLD or NASH at the time of sample collection. Akkermansia, Firmicutes, and Bifidobacterium may play protective roles in the development of recurrent NAFLD in LT recipients, whereas Fusobacteria and Bacteroidetes may play pathogenic roles. These findings highlight the potential role of the "gut-liver" axis in the pathogenesis of NAFLD recurrence after LT.

Approach to prevention of non-alcoholic fatty liver disease after liver transplantation

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease and non-alcoholic steatohepatitis (NASH) related cirrhosis is third common indication for liver transplantation (LT). Patients who have NASH related cirrhosis and are candidates for LT often have multiple comorbidities. These comorbidities need to be addressed before and after transplantation as it affects overall survival. Like hepatitis B, hepatitis C, primary biliary cirrhosis, autoimmune hepatitis which recurs after transplantation, NASH also recurs after transplant however the impact of the recurrence on allograft and patient outcomes is unclear. Limited data suggests that it does not affect graft and patient survival. De novo NAFLD which is defined as occurrence of fatty liver in a patient who did not have fatty liver prior to LT can also occur in the allograft of patients transplanted for non-NAFLD liver disease. Obesity, hyperlipidemia, diabetes as well as steroid dose and duration after LT are common predictors of recurrence of NAFLD after transplantation. Studies on prevention and treatment of NASH in post-transplant patients are lacking. Prevention of weight gain, regular exercises, weight reducing surgery, limited steroid use or steroid free regimen have been tried with varying success. Future studies for the prevention of NAFLD/NASH are required especially in post liver transplant patient.

Recurrence of fatty liver disease following liver transplantation for NAFLD-related cirrhosis: Current status and challenges.

Non-alcoholic fatty liver disease (NAFLD) is emerging as a major health problem worldwide. NAFLD is a continuum of disease ranging from mild liver steatosis to severe steatohepatitis, which will ultimately lead to end-stage liver disease with high morbidity and mortality rates. This disorder is considered as a silent liver disease. The metabolic syndrome and its components are accounted as the major risk factors for the progression of NAFLD to NASH and cirrhosis. Liver transplantation is considered as an appropriate treatment for the end-stage disease. For the last two decades, NASH has been the most common reason for liver transplantation, especially in the developed countries; however, the outcome of post-transplantation in these patients is of a great concern. The recurrent NASH and NAFLD seem to be the usual issues in LT. Steatosis appears in more than 80% of LTs; however, re-transplantation caused by steatohepatitis is rare. Recently, several risk factors of the recurrent NAFLD, including age, donor steatosis, metabolic syndrome, and immunosuppressant agents, have been introduced. Among the metabolic syndrome components, obesity seriously has negative effects on the outcomes of post-liver transplantation in patients. Unfortunately, there is no standard medicine to prevent or treat the recurrent NAFLD; however, it seems that weight loss and lifestyle modification play critical roles in controlling or inhibiting the recurrent NAFLD or NASH.

Non-alcoholic Fatty Liver Disease: Growing Burden, Adverse Outcomes and Associations.

Nonalcoholic fatty liver disease (NAFLD) is a systemic disorder with a complex multifactorial pathogenesis and heterogenous clinical manifestations. NAFLD, once believed to be an innocuous condition, has now become the most common cause of chronic liver disease in many countries worldwide. NAFLD is already highly prevalent in the general population, and owing to a rising incidence of obesity and diabetes mellitus, the incidence of NAFLD and its impact on global healthcare are expected to increase in the future. A subset of patients with NAFLD develops progressive liver disease leading to cirrhosis, hepatocellular carcinoma, and liver failure. NAFLD has emerged as one of the leading causes of cirrhosis and hepatocellular carcinoma in recent years. Moreover, HCC can occur in NAFLD even in absence of cirrhosis. Compared with the general population, NAFLD increases the risk of liver-related, cardiovascular and all-cause mortality. NAFLD is bidirectionally associated with metabolic syndrome. NAFLD increases the risk and contributes to aggravation of the pathophysiology of atherosclerosis, cardiovascular diseases, diabetes mellitus, and chronic kidney disease. In addition, NAFLD is linked to colorectal polyps, polycystic ovarian syndrome, osteoporosis, obstructive sleep apnea, stroke, and various extrahepatic malignancies. Extended resection of steatotic liver is associated with increased risk of liver failure and mortality. There is an increasing trend of NAFLD-related cirrhosis requiring liver transplantation, and the recurrence of NAFLD in such patients is almost universal. This review discusses the growing burden of NAFLD, its outcomes, and adverse associations with various diseases.

Range of Normal Serum Aminotransferase Levels in Liver Transplant Recipients

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are used to monitor liver transplant recipients (LTR) but the reference range and context of its use is not well defined. We aimed to determine the healthy ranges in LTR without chronic liver disease. MethodsOne hundred and three LTR without chronic liver disease based on serology, transient elastography with controlled attenuated parameter, and ultrasound were included. A healthy range of aminotransferases was set to 95th percentile. An updated normal aminotransferase range was used to detect recurrence in post-liver transplantation (LT) with hepatitis C virus (HCV) and nonalcoholic fatty liver disease (NAFLD). ResultsThe normal ALT and AST range was 0 to 57 and 0 to 54 IU/L, respectively, in LTR and was not affected by age, sex, obesity, or choice of immunosuppressant. The diagnostic performance of serum ALT and AST to detect recurrence of NAFLD by a controlled attenuated parameter was poor with area under the receiver operating characteristic curve of 0.573 (95% confidence interval 0.493, 0.655; P = .08) and 0.537 (0.456, 0.618; P = .4), respectively. In contrast, the diagnostic performance of ALT and AST to detect recurrence of HCV after LT was 0.906 (0.868, 0.944; P < .001) and 0.925 (0.890, 0.959; P < .001), respectively. ConclusionThe updated aminotransferase range in LTR is higher than the general population and accurate for detecting recurrent HCV, but not NAFLD.

The ILTS Consensus Conference on NAFLD/NASH and Liver Transplantation: Setting the Stage.

The ILTS Consensus Conference on NAFLD/NASH and Liver Transplantation: Setting the Stage.

Nonalcoholic steatohepatitis: the new frontier for liver transplantation.

Nonalcoholic fatty liver disease (NAFLD) is a growing cause of chronic liver disease globally and nonalcoholic steatohepatitis is projected to become the most common indication for liver transplantation. The purpose of this review is to highlight key issues surrounding NAFLD as an indication for liver transplantation, including its increasing prevalence, outcomes related to liver transplantation, development of post liver transplant NAFLD and NAFLD in the liver donor pool. With the advent of direct-acting antiviral therapies, the proportion of patients on the liver transplant list or undergoing liver transplant for chronic hepatitis C infection is steadily decreasing. In contrast, the number transplants performed for NAFLD is increasing. By 2030, it is estimated that the incidence of decompensated cirrhosis and hepatocellular carcinoma will increase by 168 and 137%, respectively, and the number of deaths will increase by 178%. Liver transplantation cures cirrhosis but does not treat the underlying metabolic disease associated with NAFLD. Thus, strategies to control comorbidities in patients with NAFLD prior to transplant are needed to decrease waitlist mortality and the recurrence of NAFLD after liver transplant. NAFLD in the donor pool is also a growing concern. Strategies to minimize steatosis and expand the number of donors are critical to meet the growing demand for liver transplantation.

Long-term Outcomes in Patients Undergoing Liver Transplantation for Nonalcoholic Steatohepatitis-Related Cirrhosis.

Nonalcoholic steatohepatitis (NASH), a clinically aggressive variant of nonalcoholic fatty liver disease (NAFLD), is becoming an increasingly common indication for liver transplantation (LT); however, relatively little is known regarding its clinical course post-LT. The aim of the current study is to describe disease recurrence and clinical course after LT. All surviving patients transplanted for NASH at the authors' institution had transient elastography (TE) to evaluate hepatic steatosis and fibrosis. The charts of deceased patients were reviewed for liver biopsy to evaluate for disease recurrence. Finally, causes of mortality in these patients were evaluated. Of the 103 patients who met criteria, 56 had TE, whereas 34 had a liver biopsy. Steatosis was detected in 49 (87.5%) of the patients who had a TE and were defined to have recurrent NAFLD. Most patients had liver stiffness measurements consistent with no fibrosis (42.9%) or F1-F2 fibrosis (30.4%). Advanced fibrosis was noted in 26.8%, whereas 5.4% had cirrhosis but were clinically compensated. In patients with liver biopsy, 88.2% had recurrent NAFLD, whereas 41.2% had recurrent NASH. Bridging fibrosis was noted in 20.6% of patients but no patients had cirrhosis. Within the cohort, 32 patients died with the leading cause of mortality cancer (25%), infectious complications (25%), and cardiovascular disease (21.9%). Only 9% of deaths were attributable to graft cirrhosis. Recurrent NAFLD is common post-LT occurring in nearly 88% of all patients, whereas nearly a quarter of patients were noted to have advanced fibrosis.

Recurrence of graft steatosis after liver transplantation for cryptogenic cirrhosis in recently commenced liver transplant program

Non-alcoholic fatty liver disease (NAFLD) seems to recur in at least one third of patients transplanted for non-alcoholic steatohepatitis (NASH)-related cirrhosis. While, NASH recurrence does not seem to affect overall graft and patient survival up to 10 years, cardiovascular and infection-related morbidity and mortality seem to be increased in these patients. This report looks at the graft histology in patients who were transplanted for NASH-related cirrhosis after short-term follow up. We report a high prevalence of recurrent NAFLD in liver grafts post-transplant among five patients. The degree of steatosis noted among the recipients is alarming.