This guidance describes a wide spectrum of approaches toidentify the adults, young people and children with non-alcoholic fatty liverdisease (NAFLD) who have advanced liver fibrosis and are most at risk offurther complications.
It outlines the lifestyle changes and pharmacologicaltreatments that can manage NAFLD and advanced liver fibrosis. This guidance isdeveloped by a panel of expert hepatologist with data supported system.Guidance document is little different from guideline as guidelines are developedby a multidisciplinary panel of experts and rate the quality of the evidenceand the strength of each recommendation using the grading of recommendations,assessment development, and evaluation system. Guidancestatements are not recommendations, but help clinicians to understand andimplement the most recent evidence.This practice guidance is developed for use by physicians andother health professionals.
The data have been retrieved by an extensive PubMedsearch up to December 2017. Specific guidance statements are evidence basedwhenever possible, and, when such evidence is not available or is inconsistent,guidance statements are made based on the consensus opinion of the authors.Non-alcoholicfatty liver disease has been defined as the accumulation of fat in the liver inthe absence of recent or ongoing intake of significant amount of alcohol. Two criteria must be fulfilled for defining NAFLDNAFLD can be categorized histologically into nonalcoholic fattyliver (NAFL) or nonalcoholicSteatohepatitis. NAFL is defined as the presence of ?5% HSwithout evidence of hepatocellular injury in the form of hepatocyte ballooning.NASH is defined as the presence of ?5%HSand inflammation with hepatocyte injury (e.
g., ballooning), withor without any fibrosis.Till date, liver biopsy remains the gold standard for diagnosingNASH. Though, liver biopsy is not feasible in studies of the generalpopulation, there is no direct assessment of the incidence or prevalence ofNASH.
But, there have been some attempts to estimate the prevalence of NASH byindirect means. Worldwide, obesity remains the mostimportant and well-described risk factor for NAFLD. The results of severalcross-sectional studies and case-control studies have shown that people withNAFLD have higher waist circumference (WC) or BMI than those without NAFLD, andhave reported significant associations between abdominal obesity (OR =1.10-1.
13; 95% CI, 1.02-1.22 per 1-cm increase in WC) and NAFLD.(108) In theDionysos study, NAFLD was present in 94%, 67%, and 24.5% of the obese,overweight, and normal weight populations, respectively. Although themechanisms responsible for the increased risk of NAFLD with abdominal obesityhave not been fully elucidated, current findings suggest that obesity leads toinsulin resistance, which, in turns, leads to NAFLD.
At the other end of thedistribution, data on the prevalence of NAFLD among high-risk individuals withsevere obesity have become widely published. On average, these studies reportedthat 76% (range 33 to 99%) of the patients undergoing bariatric surgery havesteatosis, 37% (range 9.8 to 72.5%) have NASH, 23% (range 7.3 to 49%) fibrosis,and 5.8% (range 1.6 to 10%) cirrhosis.Several studies have described ahigher prevalence of NAFLD among people with type 2 diabetes compared withnondiabetics, with prevalence estimates ranging from 40% to 69.
5%. Moreover, arecent case-control study using proton-MRS demonstrated that people with type 2diabetes have on average 80% more liver fat than age-, weight-, and sex-matchedcontrols. This difference was not explained by the type of medications used.Furthermore, aspartate aminotransferase (AST) and alanine aminotransferase(ALT)underestimated liver fat content among people with diabetes; for any given ALTor AST level, adults with type 2 diabetes had 40 to 200% more liver fat thannondiabetic adults.Patients with type 2 diabetes not only have a higherprevalence of NAFLD, but also appear to have more severe forms of the disease,including NASH and fibrosis.
Dyslipidemia: Dyslipidemia that is characterized by hightriglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels predisposespatients to arthrosclerosis. Approximately 20–80% of NAFLD patients also havedyslipidemia. The prevalence of NAFLD inindividuals with dyslipidemia attending lipid clinics has been estimated to be50%.(29,30) A very common change in the metabolic profile among patients withT2DM, MS, and obesity is an alteration of serum lipid levels (dyslipidemia),suggesting a close relationship between T2DM, MS, and obesity and NAFLD.
It hasbeen shown that NASH significantly boosts the level of oxidized low-densitylipoprotein cholesterol (LDL-C). High LDL-C is a well-established risk factorfor arthrosclerosis. The most common form of dyslipidemia in NAFLD patients isatherogenic dyslipidemia, which is characterized by hypertriglyceridemia, lowHDL-C levels, and high LDL-C levels.
Age, sex, and ethnicity: NAFLD is seen in allage groups, prevalence peaks in the fourth decade in men and sixth decade inwomen. The prevalence of NAFLD in India above 20 years age was 18.9%.
Theprevalence of NAFLD increased with increasing age. More recent studies areshowing that the prevalence of NAFLD in men is equal to or greater than theprevalence in women. But these findings are not consistent with our population.
Recently in a large cohort, it revealed that NAFLD is more prevalent in femaleamong Bangladeshi population and prevalence of NASH was 42.4% in NAFLD which ismuch higher. In fact, both the prevalence of NAFLDand stage of liver disease appear to increase with age.Despiteusing different diagnostic tools, US population-based studies all found thatHispanics have the highest and non-Hispanic blacks have the lowest prevalenceof NAFLD. Echoing the racial/ethnic differences in the NAFLD prevalence,Younossi et al recently reported that NASH was independently associated withbeing Hispanic odds ratio (OR), 1.72; 95%CI: 1.
28-2.33 and inverselyassociated with being African-American (OR, 0.52; 95%CI: 0.34-0.78).
Furthermore, in a study using proton-MRS Peterson et al found that even afteradjusting for BMI and age, Asian Indian men have significantly higher HTcompared with their Caucasian counterparts (1.54 vs. 0.77%).
It is intriguing that most of the recent data suggestthat the ethnic differences reported for NAFLD may be explained by the geneticvariation related to the patatin-like phospholipase domain-containing protein 3(PNPLA-3) gene.(40) In summary, the incidence of NAFLD varies across the world,ranging from 28.01 per 1,000 person-years (95% CI, 19.34-40.57) to 52.34 per1,000 person years (95% CI, 28.31-96.77).
