Cardiovascular disease and chronic kidney disease represent two primary causes of death in NASH patients. Importantly, harmonisation of national NASH guidelines has yet to be achieved, and disparate detection and treatment methods are under development.
This primary care provider-oriented review aimed to present current information regarding NASH’s symptoms, its different means of detection, and possible treatment plans.
Despite NASH’s pathophysiological complexity, studies have shown a direct link to obesity, insulin resistance, lipotoxicity and an unhealthy diet, as well as to genetic predispositions to hepatic fat. The correlation between NAFLD and CVD is unclear, however, NAFLD leads to hypertension and coronary calcification which can be fatal. The diagnosis of NAFLD is exclusionary in nature, although the presence of T2D, metabolic syndrome, and dyslipidemia are indicators of its presence. Patients with such comorbidities are considered to be at high-risk of possessing NAFLD and progressing to NASH. Liver biopsy remains the gold standard for diagnosing NASH but retains significant risks related to invasiveness. Non-invasive diagnostic tools include the enhanced liver fibrosis (ELF) score and the low-cost FIB-4 index. Importantly, however, these only detect its advanced stages with high accuracy. Currency treatment for NAFLD includes weight loss via diets with monounsaturated fatty acids as a source of lipids. Bariatric surgery is also an option if the patient has a BMI of 35 kg/m2. The use of vitamin E or pioglitazone has also demonstrated promising clinical results although both compounds possess undeniable limitations which can lead to further lethal health problems. Currently, no pharmacologic agents have yet been approved for the treatment of NAFLD or NASH in the US or Europe. However, considerable clinical trial efforts are currently underway.