A SYSTEMATIC REVIEW OF FOLLOW-UP DISEASE PROGRESSION IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER

Аннотация

Hepatosteatosis is defined as an excessive accumulation of triglycerides in hepatocytes. There are 2 main conditions associated with hepatic steatosis: non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFFLD). In addition, various causes are listed in the pathogenesis of hepatic steatosis, such as metabolic, nutritional, drug (chemotherapy and steroids), and hepatitis C virus (HCV) infection. 1 The natural course of hepatic steatosis varies depending on the etiology and concomitant conditions such as inflammation and fibrosis, which can progress to cirrhosis and liver failure. Therefore, it is important to diagnose and quantify liver steatosis. Liver biopsy is currently the gold standard for evaluating a patient with suspected liver steatosis.[1] However, there are potential drawbacks to liver biopsy, such as sampling error, variability in interpretation, cost, and associated morbidity. Therefore, imaging techniques are commonly used for this purpose. In this article, we will review the etiology, imaging patterns, and quantification of hepaticsteatosis usingtraditional andadvanced imaging techniques. Key words: Hepatosteatosis, metabolic syndrome, NAFLD, metabolically healthy obesity, ultrasonography NAFLD is the most common form of hepatic steatosis and affects 30%-40% of men and 15%-20% of women in the general population. This disease is considered a hepatic manifestation of metabolic syndrome and has a strong association with insulin resistance, atherosclerosis, obesity, dyslipidemia, and hypertension[3]. Risk factors for NAFLD include insulin resistance and metabolic syndrome i.e., three or more of the following: obesity, diabetes mellitus, hypertension, low high-density lipoprotein levels, and high triglyceride levels. Among these, obesity is the most common risk factor. However, people with normal body weight (body mass index [BMI; kg/m2 ] Compared to healthy people, patients with lean NAFLD had higher metabolic syndrome occurrence, diastolic blood pressure, hemoglobin A1c, and insulin resistance. Additionally, biochemical and hematologic markers, such as serum ALT, AST, Gamma glutamyl peptidase (γ-GT), and total bilirubin levels, were higher in patients with lean NAFLD than in healthy participants [1].Although the prevalence of metabolic syndrome in lean NAFLD was lower than in obese NAFLD, the impact of lean NAFLD was a stronger risk factor for higher rates of all-cause mortality, cirrhosis, and HCC than obese NAFLD.reported that patients with lean NAFLD showed advanced fibrosis stage, higher incidence of metabolic comorbidities, and higher all-cause mortality thanobese NAFLD. Additionally ,that patients with lean NAFLD had a higher risk forcirrhosis, HCC thanobese NAFLD. Theseresults suggest theimportant role ofmetabolic disorders in this population. The etiology of lean NAFLD is assumed to be based on central obesity and visceral fat Therefore, the BMI-driven approach for NAFLD may need to be reappraised. BMI does not entirely explain the association between visceral fat and NAFLD. 98,7:ROTCAFTCAPMI .SECNEICSLACIDEM,5202,yaM,5emuloV gro.srehsilbupcimedaca.www Moreover, the relationship between lean NAFLD and metabolic syndrome is still not fully understood, and more long-term studies are required[2]. Obese patients present with significant variations in metabolic abnormalities, such as hyperglycemia, hypertension, and dyslipidemia. Recently, these patients have been classified into different subphenotypes depending on their metabolic health status. Metabolically healthy obesity (MHO) is a concept derived from clinical observations that some obese people do not present with common metabolic abnormalites; the implications of this for the development of NAFLD across its subphenotypes remain vague. In a study that included 4,432 MHO people, 2,145 patients (48.4%) were presented NAFLD simultaneously. On the contrary, in 225 patients with NAFLD, 14 (6.2%) were metabolically healthy. MHO was considered as a risk factor of NAFLD development. [3]As mentioned earlier, the definition of NAFLD must exclude other causes that can result in inflammation and fatty changes. The significant amount of alcohol intake that differentiates NAFLD from alcoholic fatty liver disease ranges from 10 to 40 g (pure alcohol) a day, and this range varies between studies. The EASL guideline defined the amount of significant alcohol consumption as ≥210 g in men and ≥140 g in women weekly.3 These criteria were also applied in the Korean Association for the Study of Liver NAFLD guidelines.4 In the AASLD guidelines, the standard alcohol drink was defined as 14 g of pure alcohol, and significant alcohol consumption was defined as more than 21 standard drinks in men and 14 in women per week.[2] Recently, it has been suggested that the term NAFLD does not reflect theheterogeneous pathogenesis or various courses of fatty liver disease. Furthermore, the overestimation of the exclusion of alcohol has induced deba