BACKGROUND OF THE STUDY

Non-alcoholic fatty liver disease (NAFLD) was believed to be a disease of the industrialized world, primarily related to sedentary life-style. However, a growing body of literature has highlighted NAFLD as a global epidemic. Studies have suggested a wide amount of diversity in prevalence based on country of interest. The average prevalence in Europe is 20–30% and in China appears to be 5–24%. In India, the prevalence is estimated to be between 16–38.6%. This is believed to be due to the increasing industrialization of these nations, along with changes in lifestyle and diet. Furthermore, recent studies have also suggested that Non-alcoholic steatohepattis (NASH)/NAFLD can also affect seemingly non-obese Asians. This has come to be known as the ‘Asian Paradox’— as a disease that is associated with high BMI in the Western world may not predict accurately the risk of developing NAFLD in the Asian world (Sital Singh, Gabriela N. Kuftinec and Souvik Sarkar et al., 2017).

 NAFLD is pathologically defined as accumulation of fat, mainly triglycerides, in hepatocytes, with no evidence of significant alcohol consumption or other secondary causes. This includes the entire spectrum of fatty liver conditions, ranging from simple hepatic steatosis through steatohepatitis to cirrhosis. NAFLD is one of the most common metabolic liver disorders, and its incidence is increasing rapidly. The prevalence of NAFLD is between 6.3% and 33% depending on the population, and is expected to rise in the future as the rate of obesity increases, populations become older, and physical activity levels decrease (Yong-ho Lee et al., 2014).

The exponential rise of the disease over the last two decades has been accentuated by the swift rise in levels of sedentary lifestyle, low levels of physical activity across age groups, and consumption of nutritionally imbalanced diets, which, more often than not, results in metabolically excess calorie intake.NAFLD is currently estimated to affect around 25% of the population worldwide. In India, the numbers are slightly higher at 28.1% in the average risk population and only likely to increase in the coming times (Tushar Prabhakar et al., 2023).

            Non-alcoholic fatty liver disease is the most common chronic liver disease with a worldwide prevalence of 20– 30%. Obesity entails a 3.5-fold increased risk of developing NAFLD, and the prevalence of NAFLD therefore mirrors the steady increase of obesity globally .NAFLD is strongly associated with the metabolic syndrome and type 2 diabetes mellitus. The potentially progressive nature of the disease is well established, and NAFLD will become the leading cause for liver transplantation in the next few years .NAFLD encompasses a histological spectrum ranging from isolated steatosis, i.e., non-alcoholic fatty liver (NAFL), to non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). NASH is characterized by hepatocellular accumulation of fat accompanied by lobular inflammation and ballooning of hepatocytes. Until recently, NAFL has been considered a benign disease and NASH the progressive disease state with risk of development of liver related complications and increased mortality from hepatic and non-hepatic causes.(Mattias Ekstedt et al., 2017).

            NAFLD is a spectrum that comprises two main histological phenotypes with varying prognoses: NAFL or simple steatosis and non-alcoholic steatohepatitis (NASH). The latter is an advanced inflammatory form of NAFLD that confers higher risk of fibrosis, end-stage liver disease and cardiovascular disease mortality. NAFLD progression is closely related to insulin resistance, obesity and type 2 diabetes, and is influenced by environmental factors (eg, dietary fructose and alcohol; dysbiosis. (Shaheen Tomah et el., 2021).

                                                NEED FOR STUDY

NAFLD is a condition having hepatic steatosis with or without inflammation, fibrosis and hepatic manifestations. NAFLD mainly comprises of Non Alcoholic Fatty Liver and Non Alcoholic Steatohepatitis (Milic & Stim et al., 2012).

In NAFL, fat accumulation is present in the liver, without any significant inflammation. Whereas in NASH fat accumulation at liver is present along with the inflammation which is remarkably distinguished by the histopathological findings (Chalasani et al., 2018).

            Nonalcoholic fatty liver disease is characterized by evidence of hepatic steatosis as determined by either imaging or histology, associated with any metabolic factor. Other liver diseases, such as alcoholic liver disease, viral liver disease, and drug-induced liver disorder, are excluded Nonalcoholic fatty liver disease has become the most prevalent cause of chronic liver disease worldwide and is now the fastest-growing indication for liver transplantation among waitlist registrants.In recent years, hepatocellular carcinoma based on non-viral liver disease has increased, and the need for a screening method has become urgent.. (Katsutoshi Tokushig et.al.,2020)

NAFLD is one of the most prevalent diseases among both developed as well as in developing countries. It affects around 20-30 percent adults worldwide (Fan & Farrell, 2009). The main etiology behind NAFLD is "Triple Hit behaviour phenotype" including Sedentary Behaviour, Low physical activity and Poor diet are mainly responsible. (Marchesini, Petta & Dalle 2016)

Evidence from patients that have undergone serial liver biopsies over an interval of several years demonstrates that the progression of NAFLD from steatosis to NASH and fibrosis is not linear and is probably more dynamic than previously thought; the fibrosis progression rate in simple steatosis is estimated to be 14 years per stage of fibrosis, and the fibrosis progression rate in NASH is estimated at 7 years per stage of fibrosis. Data published in the past few years suggest that risk of liver-related mortality in NAFLD grows exponentially as the stage of fibrosis increases. Furthermore, evidence from familial aggregation and twin studies have shown a heritable component to NAFLD. Interestingly, the genetic susceptibility for the development of steatosis and fibrosis might be shared (Zobair Younossi et al., 2017).