No abstract available.
Non-alcoholic Fatty Liver Disease

Humans ; MicroRNAs ; Non-alcoholic Fatty Liver Disease

Humans ; Non-alcoholic Fatty Liver Disease

No abstract available.
Aging* ; Non-alcoholic Fatty Liver Disease*

No abstract available.
Diabetes Mellitus ; Non-alcoholic Fatty Liver Disease

Background: Weight loss, though difficult to attain and sustain over time, remains the cornerstone of non-alcoholic fatty liver disease (NAFLD) treatment. We aimed to describe weight changes among NAFLD patients. Methods: This was a retrospective, cohort study of consecutively-identified NAFLD patients with >2 clinic visits from March2007–April2018. Weight changes from baseline were categorized into weight gain, weight loss, and no change. Baseline liver and metabolic biochemistries and non-invasive liver fibrosis tests were correlated with the final weight changes. Succeeding weight changes after the initial follow-up visits were used to determine sustainability of weight loss. Results: Of the 240 patients included, 123 (51.2%), 93 (38.8%), and 24 (10%) had weight gain, weight loss, and no change, respectively. Only 12.5% had >5% weight loss. Duration of follow-up was significantly longer for patients with weight loss (p<0.001). None of the baseline demographic and laboratory data were associated with weight loss. Patients with weight loss also did not have significant changes to their biochemistries and non-invasive liver fibrosis tests compared to patients with weight gain/no change. Compared to patients with weight gain after the initial follow-up, where only 11.8% were able to lose weight on the final visit, 73.1% of patients who lost weight after the initial follow-up were able to sustain their weight loss on the final visit. Conclusions Weight loss is achieved in only a third of NAFLD patients. Although 73% of patients who lost weight initially were able to sustain it, patients who gained weight after the 1st follow-up were unlikely to lose weight on further follow-up.
Non-alcoholic Fatty Liver Disease ; Weight Loss

Cirrhosis is the result of chronic liver disease due to a variety of causes. It is deemed to be cryptogenic when the leading cause cannot be identified despite extensive laboratory, radiological and pathological investigations. The prevalence of cryptogenic cirrhosis diagnosis has been dramatically reduced in recent years due to the advanced achievement in diagnostic medicine, whereby it is attributed to only about less than 5% of cirrhosis cases. Here, we present a case of a 16-year-old boy with nonsignificant family history, was not taking any regular medication, and presented with progressive intermittent jaundice for a few years due to liver cirrhosis. Although an extensive investigation has been done, the etiology of the cirrhotic liver was still unknown. He had no features to support nonalcoholic steatohepatitis. He was in Child’s Grade B and prophylactically treated with a regular dose of propranolol to prevent portal hypertension complication while waiting for a liver transplant. This case report served the objective of showing that despite the advances in medical diagnostic techniques, cryptogenic cirrhosis is still used as a diagnosis in cases of chronic liver disease of unknown etiology.
Non-alcoholic Fatty Liver Disease ; Cirrhosis, Cryptogenic

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent causes of chronic liver disease worldwide which is often seen in patients with metabolic abnormalities such as those with obesity and insulin resistance. On the other hand, sarcopenia is a generalized and progressive skeletal muscle disorder characterized by low muscle strength, low muscle quality, low physical performance, or a combination of the three. Both disease entities share several underlying risk factors and pathophysiologic mechanisms. These include: (1) cardiometabolic overlaps such as insulin resistance, chronic systemic inflammation, decreased vitamin D levels, sex hormone modifications; (2) muscle-related factors such as those mitigated by myostatin signaling, and myokines (i.e., irisin); and (3) liver-dysfunction related factors such as those associated with growth hormone/insulin-like growth factor 1 Axis, hepatokines (i.e., selenoprotein P and leukocyte cell-derived chemotaxin-2), fibroblast growth factors 21 and 19 (FGF21 and FGF19), and hyperammonemia. This narrative review will examine the pathophysiologic overlaps that can explain the links between NAFLD and sarcopenia. Furthermore, this review will explore the emerging roles of nonpharmacologic (e.g., weight reduction, diet, alcohol, and smoking cessation, and physical activity) and pharmacologic management (e.g., roles of β-hydroxy-β-methylbutyrate, branched-chain amino acid supplements, and testosterone therapy) to improve care, intervention sustainability, and acceptability for patients with sarcopenia-associated NAFLD.
Non-alcoholic Fatty Liver Disease ; Sarcopenia

No abstract available.
Fibrosis* ; Liver Diseases* ; Liver* ; Non-alcoholic Fatty Liver Disease*

No abstract available.
Fibrosis* ; Liver Diseases* ; Liver* ; Non-alcoholic Fatty Liver Disease*