Asia–Pacific Working Party on Non-alcoholic Fatty Liver Disease guidelines 2017—Part 1: Definition, risk factors and assessment
Journal
Journal of Gastroenterology and Hepatology (Australia)
Journal Volume
33
Journal Issue
1
Pages
70-85
Date Issued
2018
Author(s)
Wong V.W.-S.
Chan W.-K.
Chitturi S.
Chawla Y.
Dan Y.Y.
Duseja A.
Fan J.
Goh K.-L.
Hamaguchi M.
Hashimoto E.
Kim S.U.
Lesmana L.A.
Lin Y.-C.
Sollano J.
Wong S.K.-H.
Wong G.L.-H.
Chan H.L.-Y.
Farrell G.
Abstract
Since the publication of the guidelines for the assessment and management of non‑alcoholic fatty liver disease (NAFLD) by the Asia–Pacific Working Party on NAFLD in 2007,1 our understanding of the clinical characteristics and natural history of NAFLD has improved, and there have been developments in the assessment and treatment of NAFLD. It is therefore timely to update the guidelines in light of new evidence. This document presents the recommendations of the Asia–Pacific Working Party on NAFLD. The exercise was supported by the Journal of Gastroenterology and Hepatology Foundation. Members performed a systematic review of the literature on specified domains of interest, thereby allowing them to provide recommendations on different aspects of the clinical assessment and management of patients with NAFLD. The contents and statements were then discussed through face-to-face meetings and e-mail communications. The statements in this document follow the Grading of Recommendation Assessment, Development, and Evaluation approach (Table 1).2 The final grading of evidence and recommendations was determined by majority vote. These guidelines cover various aspects in the management of NAFLD, including diagnosis, screening, assessment, and treatment. While most evidence came from studies on adults identified to be at risk of metabolic disorder and after exclusion of other liver diseases, two special populations are included in this document. NAFLD in children and adolescents is becoming increasingly prevalent and may have devastating consequences owing to the long duration of fatty liver disease. In addition, chronic viral hepatitis is highly prevalent in Asia–Pacific countries, and the impact of concomitant fatty liver, a much discussed topic both for hepatitis B and C, is re-evaluated here for its long-term clinical significance and implications for patient care. A clear, reproducible definition of NAFLD is required for clinical practice and epidemiological studies because there are several causes of fatty liver and steatohepatitis, each with differing management implications and clinical outcomes. An unresolved definitional and semantic challenge is that two or more etiological factors commonly interact to influence the incidence, severity, and outcome of fatty liver. The current established “negative” definition of NAFLD requires (i) evidence of hepatic steatosis by either imaging or histology and (ii) absence of other causes of hepatic fat accumulation from conditions such as significant alcohol consumption, hepatitis C, medication use, or hereditary disorders. While it has been acknowledged that “in the majority of patients” NAFLD is associated with metabolic risk factors such as obesity, diabetes mellitus, and dyslipidemia, this fails to identify overnutrition (as opposed to established obesity) as pivotal, or to account for the approximately 25% of patients in Asian cohorts who have fatty liver but are not obese. However, the vast majority of such “non-obese NAFLD” patients exhibit insulin resistance. In this respect, it is also critical to note that family history of diabetes (genetic predisposition) and prediabetes as well as established diabetes are commonly associated with NAFLD. Finally, it has now been clearly demonstrated that loss of 10% of bodyweight (in overweight persons) completely reverses all elements of non-alcoholic steatohepatitis (“NASH”) pathology, including liver fibrosis. This cements the role of overnutrition in the causation of NAFLD. Review articles from Europe have tended towards a more positive definition of NAFLD, as did the original Asia–Pacific Guidelines of 2007. The recommended definition for the 11th Revision of the International Classification of Diseases is “NAFLD is characterized by fatty liver (defined as earlier) related to over-nutrition in the absence of excessive alcohol consumption.” The majority of cases of NAFLD show steatosis with no or minimal liver inflammation. The term favored by the American Association for the Study of Liver Diseases (AASLD) for this, non-alcoholic fatty liver, has not been adopted by the 11th Revision of the International Classification of Diseases as it seems ambiguous. Specifically, all NAFLD cases have fatty liver, whether steatohepatitis (NASH) is present or not. Instead, if the pathology is known, the terminology should be “NAFLD without NASH” or “simple steatosis,” “NASH,” and “with or without fibrosis or cirrhosis” for either category. Between 10% and 25% of NAFLD cases show steatohepatitis, that is, NASH. The hallmarks are conspicuous hepatocyte injury (especially ballooning and apoptosis) and substantial liver inflammation. NASH is more likely to be associated with liver fibrosis than cases showing only steatosis. Notwithstanding the likely importance of NASH in leading to fibrosis, it is the presence of fibrosis (with or without NASH) that predicts progression to cirrhosis in clinical outcome studies. Hepatocellular carcinoma (HCC) is a complication of NAFLD, but not exclusively among cases that progressed to cirrhosis (including cases of “cryptogenic cirrhosis”). Besides, it is unclear if a patient must have NASH before progressing to NAFLD-related HCC. No more than one standard drink per day (i.e. 70 g ethanol per week) for women and no more than two standard drinks per day (i.e. 140 g ethanol per week) for men have been used by the National Institutes of Health NASH clinical research network and widely adopted for clinical studies. The relevance of this standard to the populations in the Asia–Pacific region was discussed in the 2007 Guidelines. The proposed levels of alcohol intake are based on evidence about daily alcohol intake and risk of cirrhosis. The “cut-off” values have been set lower than the apparent “threshold levels” so as to avoid the issue of overlap between alcoholic liver disease and obesity, type 2 diabetes (T2DM), and metabolic syndrome in progression to cirrhosis. Patients who may be drinking at safe levels at the time of presentation with liver disease may have a past history of chronic excessive alcohol intake for a prolonged period of time and may have cirrhosis. Lifetime alcohol intake is therefore important and needs to be incorporated into history taking. Over the past three decades, changing Western lifestyles and dietary habits, in addition to relatively high rates of genetic predisposition in several community groups, have increased the prevalence of NAFLD in the Asia–Pacific region. On the basis of hepatic imaging, recent studies suggest that a quarter (95% confidence interval [CI]: 23.3–31.9%) of the general population in Asia has NAFLD, but the proportion of patients with advanced liver fibrosis diagnosed by transient elastography (TE) appears to be low (3.7% among NAFLD patients).3 Obesity, dyslipidemia, T2DM, and metabolic syndrome are established risk factors for developing NAFLD. In addition, several other risk factors for NAFLD have been identified in the Asia–Pacific region. These include hypothyroidism, polycystic ovary syndrome, obstructive sleep apnea, hypopituitarism, and hypogonadism. There may be subtle differences in the phenotype distribution of NAFLD between Asia–Pacific and Western countries. Of particular interest are more frequent “lean NAFLD” and the urban–rural differences of prevalence rates of NAFLD in Asia.4 In addition, Asian people are particularly susceptible, partly owing to body composition differences in fat and muscle and genetic susceptibility via predisposition to T2DM, PNPLA3 SNPs, and polymorphisms in apolipoprotein 3.5 On the other hand, the natural history of NAFLD and its progression to cirrhosis and HCC (when this occurs) is over several decades; the fact that NAFLD in Asian countries may be more recent than in North and South America, for example, may also influence the present distribution of disease phenotypes towards the milder end of the pathological spectrum. There are limited studies evaluating the incidence of NAFLD and the prevalence of NASH in the general population. In Japan, pooled regional NAFLD incidence rate estimates are 52.3 (95%CI: 28.1–96.8) per 1000 person-years.6 Incident NAFLD is not uncommon among Chinese people who are not obese; for instance, 8.9% of lean subjects developed NAFLD during a 5-year follow-up.6 Because the diagnosis of NASH requires a liver biopsy, the population prevalence of NASH in Asia is currently unknown. Among Asian liver biopsy series, NASH can be found in 63.5% (95%CI: 47.7–76.8). In natural history studies involving paired liver biopsies, around 25% of patients may progress from simple steatosis to NASH in 3 years.7 Non-alcoholic steatohepatitis is the most common cause of cirrhosis and HCC in patients without other known etiological causes of liver disease worldwide. Thus, 63.3% of formerly designated cryptogenic cirrhosis cases could finally be attributed to NAFLD because cryptogenic cirrhosis is more associated with metabolic syndrome than other causes of cirrhosis. A study from Japan found that 17 of 320 HCC cases (5.3%) were either associated with NASH or had unknown (“cryptogenic”) etiology.8 “Cryptogenic” HCC also accounted for 5.4% of all HCCs in Korea. null syndrome and its null (i.e. null and null are null common in cryptogenic cirrhosis and HCC null null literature from Asia also null a null null between NAFLD and HCC in null null null null null null The majority of null HCC patients either did not have null cirrhosis or cirrhosis was well null null null null with null B and null cirrhosis with other null However, null from null null long-term studies from this null with null null of liver null are required to null the prevalence and incidence of HCC in NAFLD null null in null NASH patients in null null general null is to null null the null importance of null null and null factors in null the prevalence of NAFLD and its liver null in different null null null null null of the vast Asia–Pacific region. null of the prevalence of NAFLD in children and adolescents null widely between null studies. null liver null null null null null that the prevalence of NAFLD was null in null null children null null to null null null study from null null the prevalence was null in null to null null in null null null the prevalence of NAFLD in null children (defined as the body null null null null null null by null and null null null null null null null that null of null null null children and adolescents had null null However, the null prevalence of NAFLD may be null by this null because liver null is relatively null for null cases with hepatic fat null null null null null null null is null used to null NAFLD null The prevalence of null null levels null null was null in null adolescents null null to null null in the null National Health and null null null null A null study of null null children null null null null a prevalence of null null null of null null null null for null in the general population is likely to be null null in null and null null in null null There are null null null null null as a null null for NAFLD as the null null of null null is not well established and null levels null not null the null null of NAFLD in children or null The standard diagnosis of NASH null on liver null null There were no studies to null NASH prevalence by this null in the Asia–Pacific region. In the null null null null used null null to null liver steatosis. null found that the prevalence of NAFLD and NASH was null and null null among null null of the cause of null null study in null null children null null was null by null null of NAFLD and NASH were null and null null null cirrhosis has been null in children as null as null null of null A recent null null that the pooled prevalence estimates did not null by null region in the general population among children and null In null in clinical studies of null null the prevalence estimates null by null null null null in the studies from Asia null than studies from Europe null and North null null It should be null that null null used in different studies could null null NAFLD prevalence null null and insulin null are null risk factors for the null of NAFLD (Table null The null of null null genetic null and null null null by null null null null null null and null may null the susceptibility to NAFLD. null the prevalence of NAFLD null with null and with the null null the null null among null null and susceptibility to NAFLD null null null liver can also be null by null factors including null null and null null the liver pathology in such cases may be null from NAFLD null to overnutrition and null null or null null such as excessive null intake null excessive fat null null insulin null and bodyweight null null null intake null excessive fat intake also null to increased null null of both null and null fatty null null insulin null null null null by null null and muscle and null the null of null in null null null null null hepatic null of null fatty null and null null null null of the majority of liver null null null null is also increased by null null null to null increased null of null to fatty null in the null Thus, insulin null with null null null with the increased null null of both null and null fatty null null to null excessive accumulation of null null in the null It is widely null that null is the most significant risk null for null null However, null null that has not null null to null is also null important null of NAFLD null null Thus, bodyweight null after null null of null as well as bodyweight null from null to null are both risk factors for null NAFLD, in both null and null null null studies in null null that the null null null both null of the null null null by null to null null and null metabolic null null null hepatic null null null null null null null null and could null null null a null null null null be null in null NAFLD, no null has null been null about null The null null of PNPLA3 null is associated with the null of hepatic null null the null null of PNPLA3 null is associated with lower hepatic null null The null of null is associated with the hepatic null null A null between the null polymorphisms of null and hepatic null null has been null but so have null null a null found no significant null between null polymorphisms and risk of null NAFLD is associated with null null in the null null null null with the general population because of null increased null null null The most common causes of null in patients with NAFLD are null disease and null null by null disease. null NAFLD appears to be null null with null null and null null in a null null of null The null risk factors for the null of advanced fibrosis or cirrhosis are advanced null null null obesity, and null null null null studies for the incidence and null of NAFLD in the general population null that the incidence rate of NAFLD was around null during a null to null null null and null of patients with NAFLD had null during that null It is well known that null null is null related to NAFLD null and null loss is associated with NAFLD null It is null null that simple steatosis is null a null null clinical null null NASH can progress to null null in null cases null null to HCC. However, recent null studies have demonstrated that simple steatosis has the null to progress to NASH with the null of null null and that the presence and null of fibrosis, null of the diagnosis of null null the long-term null null null null to a null review and null of null null the null fibrosis progression rate in patients with simple steatosis was null null null with null null in patients with null null null null in null of null A null risk null for such progression is more null null null on null liver null The null null of NASH null in advanced null a null null to as null null null null studies have null that patients with null null null a null null rate to patients with cirrhosis null by the hepatitis null null null the rate of null of HCC was lower null HCC null null about null 5-year null null null null fatty liver disease can null to cirrhosis and null in null null null to null of HCC can be null to cryptogenic null the majority of such cases are null to be null to null null studies in Asian countries such as null Japan, and null suggest that the null of NASH to HCC is lower than in the null and is in the region of null The incidence of HCC in NAFLD is null in patients who have cirrhosis. In null null the null null incidence of developing HCC among null NAFLD patients was null but it was null null more likely among null with advanced fibrosis. Among null the incidence of HCC was null in null null In addition, null and diabetes null are null risk factors for HCC and null the risk of HCC with other null null hepatitis B and null null The null and diabetes null has null a null null in incidence of null null null has now null the most null null cause for liver null in the null null from South null null the null null null NAFLD HCC has null from null to null over the null null There is null evidence that HCC can null in patients with NASH without null of liver null null null have null that null of NASH HCC cases null not show evidence of liver null null null and the risk of null HCC appears to be null with NAFLD null with other null Recommendation null null fatty liver disease should be null as the cause of liver disease in null patient who is overweight and in null hepatitis B or C, alcoholic liver null null liver diseases, and null metabolic null have been null Liver disease may present with null liver null null null null in null and null null a null null between null null and null in bodyweight is a null to null null imaging null null should be used to null steatosis. null null other null such as null null null null by null may provide null null null null null history null for null and current alcohol null A null null including null of bodyweight null null null and null null null null habits, null null and null of null null is a null to null NAFLD null A null or family history of T2DM, null null null null null and high null null null null fatty liver, and cirrhosis is null null In null null diagnosis could be null with positive null of risk factors for NAFLD, exclusion of other null and null of fatty liver by hepatic null null null null null with null null and null null a diagnosis of NAFLD is null null On the other hand, null for liver biopsy null null on the null of confidence that other conditions have been null null as null hepatitis and null liver null and whether null to null NAFLD other than null null by null null or null null are null null such as null into a clinical null of null null null null null for risk factors are discussed in the null on null null of null null (TE) or other null may be used to null liver null null the null for NASH null not NASH and for various null of fibrosis have not null been null null null can be a basis for null the null null of null null by null null including null of liver null In addition, null null is null null approach to steatosis null as discussed in null in the null null In patients with null liver null null liver null null the null are null liver biopsy or null after null null This is null in null in the null on null null of liver fibrosis. null fatty liver disease is the most common cause of chronic liver disease and is null to null null to null of the general null However, only a null proportion of the general population has null liver disease because of NAFLD. In a null study on null subjects in null null NAFLD null on null null null null was null in null null advanced fibrosis null on liver null null was found in only null null subjects found to have NAFLD on population null may null from null null as well as assessment null and treatment null other null of the metabolic syndrome to null the risk of null disease. However, the null of such null approach is unknown. On the other hand, the prevalence of NAFLD and null liver disease is null high among patients with diabetes null and null In a study on null patients with diabetes null null null the null of patients with increased null null with null and liver null null null with advanced null was null and null null In a null null the prevalence of NAFLD null on null null null null and advanced fibrosis null on liver null null was null and null null among null null In null study on null patients with null null null null null NAFLD, null and advanced fibrosis were null in null null and null null These null of patients null null most of the null null for null While the current null of null null null treatment is a null null to null null community null null all or null with risk null the null of null null with null of 10% of bodyweight are now such that it can be null that null null by NAFLD, with null increased null null null null to null disease and common null null to be null of the null and importance of null the null consequences of NAFLD. null null levels are not null for null for NAFLD as null may be null in patients with null liver disease null to null and null may be increased in null patients with only simple steatosis. null is a null null null null a null null null was found to have null null null and null null for the diagnosis of null However, it is null null and may be null null for null fatty null The null null null has been null to be null for the null of significant hepatic steatosis and may be null as a null null for NAFLD, null null as well as for null progress null to null null and null null null liver null null is performed null allowing assessment of the null of liver disease at the null null null the null null there null null null in the natural history of null null null null long-term null of null and null of null (Table null These null a null null on null for null Recommendation null Liver biopsy is null for the diagnosis of null as opposed to the other liver phenotypes of NAFLD. However, it is null null and null null with a null low risk of null and null null null null and null in null by null may null null in null with a null null of null patients or in a community null a liver biopsy is not null null as a general null null null liver null may null be null for patients with NAFLD who are null to have null chronic liver null null null there is a null to null NASH from other chronic liver diseases, null null null The null and null of new imaging null and null null can null the clinical null for liver null Non-alcoholic steatohepatitis is null as the presence of hepatic null null and hepatocyte injury null null null steatosis null steatosis null or steatosis with inflammation. The null null is as null null null and null null ballooning null null null null null null null null null null null null null null fibrosis, and null of fibrosis. null of fibrosis and null null have been null to be null important null for null but not null for the diagnosis for null null null In null steatosis and null chronic null are more null than in null and null ballooning and null null are not null The null null null null null null or null null for the null of fibrosis, and null null for null In null the NASH null null null null null developed and null the NAFLD null null null as a null null to null treatment null and disease progression in clinical null null was not developed to null null it was developed as a null null for clinical null but null in this null has now been null by the null null and null null null and null recommended null of NASH null without fibrosis null The null null is the null null of the null for steatosis null null null null and ballooning null null A null of null than or null to null null with a diagnosis of null null null than 3 null with null and null of 3 or null are null as null null null to fibrosis, null null null to null fibrosis in the null null null null or null null null of null fibrosis without null fibrosis is null as null null 2 is characterized by null and null fibrosis. null 3 is null as null fibrosis, and null null as cirrhosis. The null null fatty liver null of progression null null and null null and fibrosis null null null null null null The null null is based on null null of null null null and null null for null null liver, NAFLD, and NASH. The null null null of the null null of steatosis null null null and fibrosis null The null null null of ballooning null and null inflammation. It is important to note that steatosis null not include null but this is null null in the null null this is because the null of steatosis is not a null null of null liver null null null null null on the null null On the basis of the null null null a null null null null NAFLD null null been null for null null of children null null null null clinical and null null null null null null null null null null null null null clinical and null null null null null null null null null null null null null uncommon null null null null null null null null null null null null null null null null be used as a null null null null null with null null null null null null null null subtle null null null null null with null steatosis null null null null null null null null null steatosis null No null in null null null but not as null null null null null with null steatosis null than null null null null null null null null null null null null null null null null null on patients null null null imaging time null null null null null null null null of common clinical and null null have been used in clinical studies. While null of null null null null of liver fat null null null null to simple null null for null to null the presence of NAFLD. In null the null of steatosis null its null null of null liver fat null may not be null to the outcome of NAFLD or its null of NASH null null on null null and Liver null null liver null is null from null null and null null null null and null null NAFLD liver fat null estimates liver fat null (in null with a null null of metabolic syndrome, T2DM, null null null null null null and the null null null is a null null null null of null null null null apolipoprotein null null null null null null null null null null null and null The issue of null is that null of the null null null and null may not be null null in null null null null is the most common null imaging null for patients with null liver null or null null An null in the null of the liver null null null than the null of the null null null null and null null are the null imaging null of fatty null A null null based on null null null was found to null well with null null However, null null not null well in null null null and may null the diagnosis null of null if steatosis is null null null null null null null null and null null null null null by the null null or null null null of a null null null has demonstrated null null null in null null with null null null null characteristics null null null from null to null for steatosis null null to null for steatosis null and null to null for steatosis null null null null has the null of null null null null null than null null and null null can be null null with liver null null null null and null may be used to null NAFLD by null the presence of steatosis and to null its null null the null null null the null for NASH null null and for advanced fibrosis or cirrhosis null no or other null of null null null null null null null null null null null from the null null of hepatocyte null null null null null null null null null the null null well with null null of hepatic null An null null null null of null is null used to null fatty liver with high null null null null null null fat null null is null null null that null fat null of the null null null null null a null null of liver fat in null null of null null is null more null to null null in liver fat in clinical null as it is more null than the null steatosis null in null null in the liver fat null null has null null of null for steatosis null null the null null were null by the presence of null null null high null of null the null and null of null null null are the null null in null null null null to the general population. null null null null null the null of null null null a null null of null null null null null have been developed to null NAFLD. The null null null hepatocyte null through the null of a null null of null In null both null and null null null null null null through the null of both null and null null null null is null increased in null It has demonstrated null null null for NAFLD null null null but null null null for NASH null simple null null The null is null the null null null in clinical null The null was also null for limited null at a null null of null null null it null as a null null for null null A null of null studies null that null null had null null of null to null NASH null null null other null null null with null null or null null null null null null for NASH null null in patients with NAFLD. null the null null is null null is null to be used null but null either as the null null null with a low null or null of a null null null is null null that is exclusively null by null null with null in null and null null null is associated with NAFLD and null null the null null in null levels null in different studies null it null to be the null null null in null null is null null null that is null null with null a null null null null null and null null was used to null NASH or null null null null null null null its null with NASH or null with null null null of liver null null null including null null and null null null may be null null of null but are null to null as null null on null null null is null by the null null as null null null null null null null null null null null and null levels of null null null null null null null null and null null It has null null null for NASH null null and null NASH null null It has null null with null null and so null be null null are highly null null null null of null null null that null null null at the null null null null can null null of null null null have been increasingly null in the null and diagnosis of NAFLD and null The null and null levels were null in NASH null null with patients with simple null Because fibrosis is the most null null null the only null null null for null null in NAFLD, including HCC null and null null fibrosis assessment is of null clinical null null for null and HCC should be null in null of cirrhosis. Because of the null of liver biopsy discussed in the null Liver histology null null null and null null have been developed to null liver fibrosis. Over the past several decades, null of null null with clinical null including NAFLD fibrosis null null null null null null null and null null liver fibrosis null null null and null have null null null null null null null used to null the null of liver null null In addition, null of null null null long-term null such as the risk of null diabetes and null null and null null However, each of the null studies appears to have used its null null null as a null of null no widely null null values to null patients at low and high risk have been null null null to null liver null include null null null null null null and null null elastography null A recent null null that null had high null and null null used to identify fibrosis in patients with null However, null to null of null null null null null null among patients with high null null The null of null null can null the null rate of null in null null but null null is null null null null null elastography has also null null null in patients with NAFLD null null null was the most null of the null null assessment null However, null is not widely null and is null used in clinical practice because of the high null null studies in this region have null the null null of null null of liver biopsy among Asian patients with null null null have null that the null null of null null and null null can null more null null than that null by either null null However, null null null null and as a null the null implications of various values have not null been null null Thus, at the present null the clinical null of such null to avoid liver biopsy null null null A null null of null null is that most null have been performed in studies null a null null Thus, the null of the null to null the natural history of disease and to null null or null to null null null null The null incidence of developing HCC in NASH cirrhosis is null and the null of such cases is null null null over null null null null from the null suggest that null null null for HCC null is null null the risk of developing HCC is null per null null all NASH patients with cirrhosis should null HCC null null to patients with cirrhosis from other null null null null null is the most null null null null the null and null of null in the null fatty liver is not null This may null in null null for null imaging and null the null of null The null of null null null null null The issue of HCC null in null null of patients with NAFLD was null in the null on null HCC. However, the null risk for each fibrosis null is null so it is not null to null null of HCC null for null patients in the Asian null or null The risk of developing HCC in patients with null without advanced fibrosis is null low with null population studies showing that the incidence of HCC null null HCC after null null null that null null increased risk of HCC in null NASH include PNPLA3 null null null null null obesity, null null null and family null These factors may null null null risk null for screening, thereby null null However, as null there is null null or null null to null null null and this is null important null for null null null null is null to the null of both NAFLD and metabolic null null studies have demonstrated that patients with NAFLD have a null prevalence of null of metabolic syndrome including obesity, T2DM, and null null null In Asian null NAFLD null null the risk of null diabetes null by null to null The null of diabetes null with NAFLD null null metabolic null and null null null studies of NAFLD patients show that advanced fibrosis (NASH) have null increased null from null null null Asian studies have null that NAFLD is null null risk null for null null null null as well as null null null However, the null of null for NAFLD in patients with null null disease or null null disease in NAFLD patients is null to be null null fatty liver null null null is null associated with a null prevalence of chronic null null null the null of this null null between different cohorts of NAFLD null among Asian NAFLD patients null by null or null liver null a null null null with null to null null in null risk has been found null null null null null Asian studies have null increased risk of null null in NAFLD null In both null and null null the risk of null null and carcinoma in NAFLD patients is null to null and null null null null with patients without NAFLD. These null null null in NASH patients than among null with simple steatosis. However, no null null null null in NAFLD patients have been performed to null null null the current null null null null fatty liver disease is null associated with obstructive sleep null and null A null of null studies null null to null obstructive sleep null found a null to null increased risk of NAFLD including NASH and advanced fibrosis with obstructive sleep null null the risk of obstructive sleep null among NAFLD patients is not null null women with null NAFLD have been null to have lower null null null than null without null null the prevalence of null null in Chinese men was increased among null with null Recommendation null The null null null to null null null null for null null null The null of this null was supported by the Journal of Gastroenterology and Hepatology Foundation.
SDGs
Other Subjects
adiponectin; cytokeratin 18; ghrelin; leptin; resistin; retinol binding protein 4; alcohol consumption; anamnesis; blood analysis; clinical assessment; consensus development; decompensated liver cirrhosis; e-mail; echography; fatty liver; human; incidence; insulin resistance; liver biopsy; liver cell carcinoma; liver cirrhosis; liver fibrosis; liver histology; medical history; nonalcoholic fatty liver; nuclear magnetic resonance imaging; overnutrition; physical examination; practice guideline; prevalence; priority journal; Review; screening; thrombocyte count; transient elastography; adolescent; Asia; child; gastroenterology; nonalcoholic fatty liver; organization and management; Pacific islands; risk assessment; risk factor; virus hepatitis; Adolescent; Asia; Child; Gastroenterology; Hepatitis, Viral, Human; Humans; Non-alcoholic Fatty Liver Disease; Pacific Islands; Practice Guidelines as Topic; Prevalence; Risk Assessment; Risk Factors; Systematic Reviews as Topic
Publisher
Blackwell Publishing
Type
review