Delve into the latest in medical education resources for NASH. Explore new studies, teaching methodologies, and advancements shaping NASH education for healthcare professionals.
Up to 30% of patients with non-alcoholic fatty liver disease (NAFLD) progress to non-alcoholic steatohepatitis (NASH), significantly increasing their risk of fibrosis and associated adverse outcomes. As such, ensuring the early identification of NAFLD and NASH in at-risk patients is a clinical priority.
Changing the terminology from NAFLD, non-alcoholic fatty liver disease, to MAFLD, metabolic dysfunction-associated fatty liver disease, has been an ongoing debate. MAFLD is based upon an individual having hepatic steatosis, as well as either type 2 diabetes mellitus, obesity (or being overweight) or if at a normal weight, two or more metabolic risk abnormalities.
Patients with non-alcoholic fatty liver disease (NAFLD) are at risk of progressing to inflammatory non-alcoholic steatohepatitis (NASH), a NAFLD subtype associated with fibrosis, cirrhosis, and hepatocellular carcinoma.
Seeking the perfect NASH biomarker may be unrealistic; versatility is key. A diverse biomarker pool adapts to varied clinical contexts and settings. FIB-4, a cost-effective marker, can be supplemented by complex multimarkers for NASH therapeutic trials. Embracing diagnostic imperfections is crucial for flexible biomarker algorithms.
The rising healthcare costs of NASH highlight the need for early intervention. Higher FIB-4 scores correlate with increased healthcare expenses. Early-stage intervention can reduce the burden on patients and the healthcare system.
Heterogeneity in cut-off points for non-invasive fibrosis tests impacts NAFLD risk stratification. Standardized guidelines could improve consistency and accuracy in identifying patients requiring specialist care.
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.
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.
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.