Nonalcoholic fatty liver disease

Brunt, Elizabeth M.; Wong, Vincent W. S.; Nobili, Valério; Day, Christopher P.; Sookoian, Silvia; Maher, Jacquelyn J.; Bugianesi, Elisabetta; Sirlin, Claude B.; Neuschwander‐Tetri, Brent A.; Rinella, Mary E.

doi:10.1038/nrdp.2015.80

Cited by 696 publications

(643 citation statements)

References 251 publications

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“…Only liver fragments that were at least 1.5 cm in length and included eight portal tracts were considered to be appropriate for histological assessment. The presence of steatotic hepatocytes at a concentration of >5% in a liver tissue section was accepted as the histological criterion for the diagnosis of NAFLD (14). NAFLD activity score (NAS) was used to diagnose NAFLD (15).…”

Section: Histological Evaluationmentioning

confidence: 99%

The development of a clinical score for the prediction of nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease using routine parameters

Li¹,

Jian-hui²,

Zhang³

et al. 2015

Turk J Gastroenterol

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Background/Aims: To develop a clinical score for the prediction of nonalcoholic steatohepatitis (NASH) using routine parameters in patients with nonalcoholic fatty liver disease who had abnormal liver function tests and/or fatty liver detected by ultrasonography. Materials and Methods: To identify parameters associated with the presence of NASH by evaluating anthropometric characteristics and routine biomarkers of 82 patients with histologically proven NAFLD and to develop a clinical score for predicting NASH according to the area under the curve of receiver operating characteristics (AUC) of parameters. Results: Four parameters [alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), C-reactive protein (CRP), and apolipoprotein B (ApoB)/apolipoprotein A1 (ApoA1) ratio] were significantly linked to NASH. The AUROCs of ALT, GGT, CRP, and ApoB/ApoA1 ratio for the prediction of NASH were 0.829, 0.892, 0.708, and 0.712, respectively. The AUROC of the combined clinical score for the prediction of NASH was 0.904 (95% CI, 0.885-1.002) at a cut-off of 3.8 points with a sensitivity of 90.2%, specificity of 87.0%, positive predictive value of 88.3%, and negative predictive value of 91.5%. Conclusion: In the present study, a clinical score was developed for the noninvasive prediction of NASH; the score was based on a combination of routine biochemical parameters and was useful in distinguishing NASH from NAFLD.

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Section: Histological Evaluationmentioning

confidence: 99%

The development of a clinical score for the prediction of nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease using routine parameters

Li¹,

Jian-hui²,

Zhang³

et al. 2015

Turk J Gastroenterol

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“…Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disorder that exhibits complex phenotypic diversity 1. The scope of the histologic disease severity varies, ranging from a relatively benign and mild condition known as simple (bland) steatosis or nonalcoholic fatty liver (NAFL) to a more severe histologic picture characterized by liver cell injury, a mixed inflammatory lobular infiltrate, and variable fibrosis, referred to as nonalcoholic steatohepatitis (NASH) 2.…”

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confidence: 99%

“…Irrespective of whether NAFL and NASH should be considered as having different long‐term clinical impact, it is clear that the progression of NASH into more aggressive phenotypes, including NASH fibrosis and NASH cirrhosis and eventually hepatocellular carcinoma (HCC), imposes a tremendous public health problem of epidemic proportions 1, 3…”

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confidence: 99%

Metastasis‐associated lung adenocarcinoma transcript 1 as a common molecular driver in the pathogenesis of nonalcoholic steatohepatitis and chronic immune‐mediated liver damage

Sookoian

Flichman

Garaycoechea

et al. 2018

Hepatology Communications

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Long noncoding RNAs (lncRNAs) are functional molecules that orchestrate gene expression. To identify lncRNAs involved in nonalcoholic fatty liver disease (NAFLD) severity, we performed a multiscale study that included: (a) systems biology modeling that indicated metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) as a candidate lncRNA for exploring disease‐related associations, (b) translational exploration in the clinical setting, and (c) mechanistic modeling. MALAT1 liver profiling was performed in three consecutive phases, including an exploratory stage (liver samples from patients with NAFLD who were morbidly obese [n = 47] and from 13 individuals with normal liver histology); a replication stage (patients with NAFLD and metabolic syndrome [n =49]); and a hypothesis‐driven stage (patients with chronic hepatitis C and autoimmune liver diseases, [n = 65]). Liver abundance of MALAT1 was associated with NAFLD severity (P = 1 × 10–6); MALAT1 expression levels were up‐regulated 1.75‐fold (P = 0.029) and 3.6‐fold (P = 0.012) in patients with nonalcoholic steatohepatitis compared to those diagnosed with simple steatosis (discovery and replication set, respectively; analysis of covariance adjusted by age, homeostasis model assessment, and body mass index). Quantification of liver vascular endothelial growth factor A messenger RNA, a target of MALAT1, revealed a significant correlation between the two RNAs (R, 0.58; P = 5 × 10–8). Increased levels of MALAT1 were also associated with autoimmune liver diseases. Interactome assessment uncovered significant biological pathways, including Janus kinase‐signal transducers and activators of transcription and response to interferon‐γ. Conclusion: Deregulated expression of MALAT1 stratifies patients into the histologic phenotypes associated with NAFLD severity. MALAT1 up‐regulation seems to be a common molecular mechanism in immune‐mediated chronic inflammatory liver damage. This suggests that convergent pathophenotypes (inflammation and fibrosis) share similar molecular mediators. (Hepatology Communications 2018;2:654‐665)

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“…Hepatic steatosis develops by interactions among genetic, metabolic, and environmental factors (8). Sedentary lifestyle and excess caloric or inappropriate intake (high glucose, high fructose, high fat, or high cholesterol diet) are well-known environmental factors associated with hepatic steatosis and NAFLD/NASH.…”

Section: “Multiple-parallel Hit” Pathogenesis Of Nashmentioning

confidence: 99%

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

Kim

Lee

2018

Front. Endocrinol.

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Non-alcoholic fatty liver disease (NAFLD) is an emerging global health problem and a potential risk factor for type 2 diabetes, cardiovascular disease, and chronic kidney disease. Nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, is a predisposing factor for development of cirrhosis and hepatocellular carcinoma. The increasing prevalence of NASH emphasizes the need for novel therapeutic approaches. Although therapeutic drugs against NASH are not yet available, fundamental insights into the pathogenesis of NASH have been made during the past few decades. Multiple therapeutic strategies have been developed and are currently being explored in clinical trials or preclinical testing. The pathogenesis of NASH involves multiple intracellular/extracellular events in various cell types in the liver or crosstalk events between the liver and other organs. Here, we review current findings and knowledge regarding the pathogenesis of NASH, focusing on the most recent advances. We also highlight hormone-based therapeutic approaches for treatment of NASH.

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Nonalcoholic fatty liver disease

Cited by 696 publications

References 251 publications

The development of a clinical score for the prediction of nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease using routine parameters

The development of a clinical score for the prediction of nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease using routine parameters

Metastasis‐associated lung adenocarcinoma transcript 1 as a common molecular driver in the pathogenesis of nonalcoholic steatohepatitis and chronic immune‐mediated liver damage

Pathogenesis of Nonalcoholic Steatohepatitis and Hormone-Based Therapeutic Approaches

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