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.

Significant correlation was found between the results of histology and 1H MRS measurement of liver fat content. The method is suitable for non-invasive repetitive examination of liver fat in liver-transplants patients between protocol biopsies and for the screening of steatosis in other liver diseases.

Purpose: To examine changes in the brain before liver transplantation caused by the accumulation of paramagnetic ion deposits and to investigate recovery after liver transplantation over a long-term horizon. Materials and Methods:Fifteen patients indicated for liver transplantation, 26 patients up to 2 years after, and 40 patients 8-15 years after liver transplantation were subjected to MR relaxometry. T 1 and T 2 relaxation times in the basal ganglia, thalamus, and white matter were evaluated.Results: Relaxometry revealed a shortening of the relaxation times due to the deposition of paramagnetic ions in the basal ganglia before liver transplantation (P < 0.05), complete normalization of the relaxation times shortly after transplantation in the globus pallidus and caudate nucleus, and partial recovery of T 2 in the putamen. Relaxation times remained stable even 15 years posttransplantation. Increased relaxation times posttransplantation were found in the white matter and thalamus. Conclusion:The shortening of the relaxation times observed in the basal ganglia before liver transplantation was caused by paramagnetic ion deposition. The recovery observable within 2 years after transplantation was permanent, and no recurrence of paramagnetic ion deposition was observed even 15 years posttransplantation. Changes in the white matter and thalamus after transplantation were attributed to damage caused by permanent exposure to immunosuppressants. HEPATIC ENCEPHALOPATHY (HE) is a neuropsychiatric complication accompanying chronic or acute liver failure (1) characterized by cognitive deficits and disturbances of fine motor control. The pathogenic mechanisms related to HE are still not completely understood. HE is probably a consequence of a low-grade chronic cerebral edema and represents a primary gliopathy. HE symptoms may be caused by altered synaptic transmission due to impaired glialneuronal communication. Ammonium plays a key role in HE development (2). A higher permeability of the blood-brain barrier and increased brain ammonia uptake in patients with liver cirrhosis have been observed (3). A low grade cerebral edema that alters the functioning of astrocytes (which are also responsible for cerebral ammonia detoxification) is therefore hypothesized to be the cause of HE.A higher permeability of the blood-brain barrier is also responsible for the deposition of some paramagnetic ions. Their presence in the basal ganglia of patients with hepatic encephalopathy is indicated by signal alterations in computed tomography (CT) scans and in MRI (4-7), particularly in the globus pallidus. A strong hyperintense signal on T 1 -weighted and a hypointense signal on T 2 -weighted images have been observed due to substantial T 1 and T 2 shortening. Similar changes have also been reported in patients suffering from other chronic liver diseases (with or without encephalopathy), patients receiving long-term parenteral nutrition, or patients intoxicated by manganese (8-10).Manganese (Mn) is hypothesized to be responsible for these relaxa...

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