Nonalcoholic Fatty Liver Disease: How Is It Diagnosed and Treated? | Guidelines Consensus


In April 2022, the American Heart Association (AHA) issued a NAFLD) and a scientific statement on cardiovascular risk. NAFLD is an increasingly common disease affecting more than 25% of adults worldwide. This article mainly selects the guidelines for the diagnosis and screening of NAFLD, as well as potential interventions.

2022 AHA Scientific Statement: Diagnosis and Treatment of NAFLD

< span>1. NAFLD is very common, with a global prevalence of more than 25%, and its incidence increases with the incidence of obesity and metabolic syndrome.

2. Most NAFLD patients are undiagnosed. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are not useful for the diagnosis of NAFLD and nonalcoholic steatohepatitis (NASH) due to poor sensitivity and specificity. AST and ALT levels may be normal even in NASH patients. Liver biopsy is the gold standard for diagnosing NAFLD and NASH, but it is expensive and increases the risk of complications. Non-invasive diagnostic methods such as vibration-controlled transient elastography (FibroScan) are available but underused.

3. Most patients with hepatic steatosis do not progress to NASH, cirrhosis or hepatocellular carcinoma (HCC), But there is a subgroup meeting. It is difficult to determine which patients will develop disease progression, so imaging studies (possibly in conjunction with liver biopsy) are essential to monitor disease severity and progression. Routine liver ultrasonography is useful for showing hepatic steatosis, but it cannot quantify the extent of steatosis nor rule out hepatic steatosis because the technique is insensitive.

4. The occurrence of NAFLD is associated with insulin resistance, with or without diabetes, obesity (especially visceral obesity), metabolic syndrome and Dyslipidemia, including hypertriglyceridemia, increased free fatty acids, low high-density lipoprotein cholesterol, and small, dense low-density lipoprotein (LDL). Genetic factors (monogenic or polygenic) can modulate the risk of NAFLD development and progression to NASH.

5. NASH is an increasingly common cause of end-stage liver disease.

6. NASH is a contributing factor and marker of increased risk of atherosclerotic cardiovascular disease (ASCVD). Many risk factors for NAFLD are also risk factors for ASCVD. One component of increased ASCVD risk in NAFLD is attributed to individual risk factors, but the presence of NAFLD was associated with increased ASCVD risk compared with individuals with the same ASCVD risk factors without NAFLD.

7. NAFLD can be considered a risk-enhancing factor when assessing a patient’s ASCVD risk.

8. Lifestyle intervention is the key treatment intervention for NAFLD patients. Patients are strongly recommended to adjust their diet, increase physical activity, lose weight, and avoid alcohol. A 5%-10% weight loss can reverse liver steatosis and stabilize or reduce NASH in many patients, but this goal is often difficult to achieve. Improving insulin sensitivity, reducing hyperglycemia, and lowering triglycerides are additional goals of treatment.

9. Glucagon-like peptide-1 receptor agonists can moderately improve NAFLD, improve blood sugar, reduce body weight, and reduce major adverse cardiac events. Risk of vascular events.

10. Novel experimental drug therapies targeting various steps in the pathogenesis of NAFLD are under development, but most have limited efficacy and toxicity. It has been a limiting factor for some drugs.

11. Promotional materials about NAFLD can be used for patient education (see today’s next post).

References: Duell PB, Welty FK, Miller M, et al. Nonalcoholic Fatty Liver Disease and Cardiovascular Risk: A Scientific Statement From the American Heart Association[J]. Arterioscler Thromb Vasc Biol. 2022 Apr 14:101161ATV0000000000000153. doi: 10.1161/ATV.000000000000153.