PanNASH covers commented articles ans publications to acquire sufficient information, understanding, and skills to cope with NASH/NAFLD healthcare demands.
Physicians often underestimate or overestimate fibrosis severity in NASH, leading to concerns about appropriate treatment. Standardized interpretations of risk stratification tools are needed.
Patients with T2D complications have a 4.5x greater risk of developing fibrosis, independent of HbA1c levels. FIB-4 index can help identify diabetic patients at highest risk, improving primary care screening.
Fatty liver disease (FLD) is found to be the strongest independent predictor of increased heart rate and reduced left ventricular volumes, and positively predicts cardiac remodelling
FIB4 and VCTE show promise in predicting prognosis for NAFLD patients. These non-invasive tests offer an alternative to liver biopsies for risk stratification. Quick and easily prescribed, they can streamline referrals and specialized management. A sequential algorithm with FIB4 and VCTE may improve NAFLD care.
Recurrence of NASH/NAFLD after liver transplantation requires attention. Factors include weight gain, post-transplant diabetes, and immunosuppressant drugs. Donor-related genetic risk factors also contribute. A multidisciplinary approach is essential for prevention and management.
Exercise training is 3.5 times more likely to achieve clinically meaningful treatment response in liver fat compared to standard clinical care for NAFLD patients, independent of significant weight loss.
Fatty liver disease can be caused by many different autosomal recessive diseases. One includes Wilson’s disease, a condition which leads to abnormal copper accumulation in multiple organs. Cirrhosis is common in up to 30% of cases, as well as steatosis and steatohepatitis. Cystic fibrosis is another example, where steatosis is common and liver disease occurs in 0.1-3.6% of patients. Furthermore, alpha-1-antitrypsin deficiency and lysosomal acid lipase deficiency have been linked to steatosis accumulation, although have little research into their pathogenesis.
Non-alcoholic fatty liver disease (NAFLD) has a more progressive form, non-alcoholic steatohepatitis (NASH). In both conditions, inflammation is a key driver of the pathogenesis. There are various causes of metabolic injury in the conditions, leading to the activation of different immune cells such as hepatic Kupffer cells.
Non-alcoholic fatty liver disease (NAFLD) has a more progressive form, non-alcoholic steatohepatitis (NASH). In both conditions, inflammation is a key driver of the pathogenesis. Current treatments mostly focus on promoting weight loss (through encouraging lifestyle changes, or, if necessary, bariatric surgery) and improving comorbidities through pharmacotherapy, such as type 2 diabetes.
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disease encompassing simple hepatic steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC).
Although it is known that non-alcoholic steatohepatitis (NASH) increases the risk of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma, no pharmacologic therapy has yet been approved to treat it.
Non-alcoholic fatty liver disease (NAFLD) is estimated to affect 25% of the world’s adult population. In 20% of these patients, NAFLD further develops into non-alcoholic steatohepatitis (NASH), which itself represents a leading cause of progression to liver cirrhosis and hepatocellular carcinoma.