Limited value of plasma cytokeratin-18 as a biomarker for NASH and fibrosis in patients with non-alcoholic fatty liver disease

Cusi, Kenneth; Chang, Zhihui; Harrison, S.A.; Lomonaco, Romina; Bril, Fernando; Orsak, Beverly; Ortiz-López, Carolina; Hecht, Joan; Feldstein, Ariel E.; Webb, Amy; Louden, Christopher; Goros, Martin; Tio, Fermin O.

doi:10.1016/j.jhep.2013.07.042

Cited by 226 publications

(186 citation statements)

References 32 publications

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“…Our data underscore the need to directly assess hepatic histology from the high risk participants we identified in order to validate more precise non-invasive diagnostic panels and to determine the need and targets for therapeutic interventions and prevention. Our observation that 52% of a population-based Mexican American cohort has NAFLD by ultrasound extends our prior work and substantiates studies where Hispanic individuals were recruited from primary care and gastroenterology clinics from military facilities [16] . This burden of disease parallels the high prevalence of obesity, diabetes and lipid abnormalities in these populations.…”

Section: Discussionsupporting

confidence: 86%

Burden of nonalcoholic fatty liver disease and advanced fibrosis in a Texas Hispanic community cohort

Pan

Fisher‐Hoch

Chen

et al. 2015

WJH

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Section: Discussionsupporting

confidence: 86%

Burden of nonalcoholic fatty liver disease and advanced fibrosis in a Texas Hispanic community cohort

Pan

Fisher‐Hoch

Chen

et al. 2015

WJH

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“…Cytokeratin-18 fragments (CK-18), which are generated during cell death (M65 fragments) or apoptosis (M30 fragments), have modest accuracy for the diagnosis of NASH (66% sensitivity, 82% specificity) [33,34] . CK-18 changes parallel histological improvement but do not perform better than alanine transaminase (ALT) in identifying histological responders [35] .…”

Section: Steatohepatitis Nashmentioning

confidence: 99%

EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease

2016

Journal of Hepatology

3,460

1,817

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DefinitionNAFLD is characterised by excessive hepatic fat accumulation, associated with insulin resistance (IR), and defined by the presence of steatosis in >5% of hepatocytes according to histological analysis or by the proton density fat fraction (PDFF, providing a rough estimation of the volume fraction of fatty material in the liver) >5.6% assessed by proton magnetic resonance spectroscopy ( 1 H-MRS) or quantitative fat/water selective magnetic resonance imaging (MRI). NAFLD includes two pathologically distinct conditions with different prognoses: nonalcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH); the latter covers a wide spectrum of disease severity, including fibrosis, cirrhosis and hepatocellular carcinoma (HCC) ( table 2 ).The diagnosis of NAFLD requires exclusion of both secondary causes and a daily alcohol consumption ≥ 30 g for men and 20 g for women [1] . The relationship between alcohol and liver injury depends on several cofactors (type of alcoholic beverage, drinking patterns, duration of exposure, individual/genetic susceptibility), rendering simple quantitative thresholds at least partly arbitrary. Specifically, patients consuming moderate amounts of alcohol may be still predisposed to NAFLD if they have metabolic risk factors. Of note, the overall impact of metabolic risk factors on the occurrence of steatosis appears to be higher than that of alcohol in these patients [3] . The definitive diagnosis of NASH requires a liver biopsy. Recommendations• Patients with IR and/or metabolic risk factors (i.e., obesity or metabolic syndrome (MetS)) should undergo diagnostic procedures for the diagnosis of NAFLD, which relies on the demonstration of excessive liver fat (A1) • Individuals with steatosis should be screened for secondary causes of NAFLD, including a careful assessment of alcohol intake. The interaction between moderate amounts of alcohol and metabolic factors in fatty liver should always be considered (A1) • Other chronic liver diseases, that may coexist with NAFLD, should be identified as this might result in more severe liver injury (B1) Prevalence and IncidenceNAFLD is the most common liver disorder in Western countries, affecting 17-46% of adults, with differences according to the diagnostic method, age, sex and ethnicity [4] . It parallels the prevalence of MetS and its components, which also increases the risk of more advanced disease, both in adults and in children. NAFLD is also present in 7% of normalweight (lean) persons [5] , more frequently in females, at a younger age and with normal liver enzymes. Their liver disease may nonetheless be progressive [6] .NAFLD incidence has rarely been measured. It was 20-86/1,000 person-years based on elevated liver enzymes and/or on ultrasound (US), and 34/1,000 per year by 1 H-MRS [7] . The need for NAFLD screening in the community has been questioned given the high direct and indirect costs of testing, the low predictive value of non-invasive tests, the risks of liver biopsy and the lack of effective treatments [8] . Ho...

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“…Increased liver enzymes have been found to highly related with NASH, however, may not be reliable [31] . Lately, it has come to the literature a new model namely the fragment of keratin 18 (CK18), which is for now, the best marker for detecting NASH, however showed lower accuracy with sensitivity (60%) [32] .…”

Section: Diagnosismentioning

confidence: 99%

Role of diet on non-alcoholic fatty liver disease: An updated narrative review

Papandreou

Andreou

2015

WJH

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The purpose of this article review is to update what is known about the role of diet on non-alcoholic fatty liver disease (NAFLD). NAFLD is the most common cause of chronic liver disease in the developed world and is considered to be a spectrum, ranging from fatty infiltration of the liver alone (steatosis), which may lead to fatty infiltration with inflammation known as non alcoholic steatohepatitis While the majority of individuals with risk factors like obesity and insulin resistance have steatosis, only few people may develop steatohepatitis. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Weight loss alone by dietary changes has been shown to lead to histological improvement in fatty liver making nutrition therapy to become a cornerstone of treatment for NAFLD. Supplementation of vitamin E, C and omega 3 fatty acids are under consideration with some conflicting data. Moreover, research has been showed that saturated fat, trans-fatty acid, carbohydrate, and simple sugars (fructose and sucrose) may play significant role in the intrahepatic fat accumulation. However, true associations with specific nutrients yet to be clarified.

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Limited value of plasma cytokeratin-18 as a biomarker for NASH and fibrosis in patients with non-alcoholic fatty liver disease

Cited by 226 publications

References 32 publications

Burden of nonalcoholic fatty liver disease and advanced fibrosis in a Texas Hispanic community cohort

Burden of nonalcoholic fatty liver disease and advanced fibrosis in a Texas Hispanic community cohort

EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease

Role of diet on non-alcoholic fatty liver disease: An updated narrative review

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