Nonalcoholic Steatohepatitis: Case-Based Focused on Pediatric and Adult Guidelines

Abstract

Nonalcoholic fatty liver disease (NAFLD) comprises a continuum of conditions associated with insulin resistance and obesity in the absence of secondary causes of hepatic steatosis (alcohol, medication, genetic disorders, hepatitis, etc.) The milder, benign form of NAFLD is simple fatty liver or steatosis. Fatty infiltration affects more than 5% of the liver.1 This is determined by histologic exam, direct quantification or imaging. The range progresses to nonalcoholic steatohepatitis (NASH) and culminates in fibrosis and cirrhosis. Histologic changes include ballooning degeneration of hepatocytes, the presence of Mallory bodies, macrovesicular steatosis, lobular or portal inflammation.2\xa0 \nNAFLD is now the foremost cause of childhood, adolescent and adult chronic hepatic disease. The pediatric and adult obesity epidemic makes NAFLD a potentially ubiquitous hepatic pathology amongst all patients.3,4,5 The increase of obese children and adults with obesity correlates to the rise of NAFLD cases. In adults, the rate of NAFLD increase is paired with the epidemics of obesity and Type 2 Diabetes (T2DM).4,5 Data proposes hepatic-related mortality may be due to NASH ultimately progressing to cirrhosis.3,4 NAFLD is linked to pediatric and adult cardiovascular risk and morbidity.4,6 Non-invasive biomarkers and the gold standard of liver biopsy not only diagnose but assist in targeted therapies.6 Most pharmacologic therapy for NAFLD is in trial stages for patients of all ages. Pioglitazone is favored in adults who have NAFLD/NASH and T2DM.7 The gut biome is also impactful. Lifestyle modifications of diet and exercise can reduce the public health burden of this disease.7,8,9,10