The Current View of Nonalcoholic Fatty Liver Disease-Related Hepatocellular Carcinoma

Kogiso, Tomomi; Tokushige, Katsutoshi

doi:10.3390/cancers13030516

Cited by 20 publications

(20 citation statements)

References 86 publications

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“…46 The current Japanese NAFLD/NASH guidelines recommend a 2-step risk stratification process including screening for serum markers of fibrosis or platelet counts, the fibrosis-4 index or the NAFLD fibrosis score. 47 Depending on the risk of fibrosis, subsequent liver elastography or biopsy is recommended. Ultrasound-based HCC screening may be performed in male patients with F2/F3 fibrosis, female patients with F3 fibrosis and in all patients with cirrhosis.…”

Section: Surveillancementioning

confidence: 99%

NAFLD-driven HCC: Safety and efficacy of current and emerging treatment options

Foerster

Gairing

Müller

et al. 2022

Journal of Hepatology

177

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In light of a global rise in obesity and type 2 diabetes, non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) represent an increasingly important underlying aetiology of hepatocellular carcinoma (HCC). HCCs arising from lipotoxicity-mediated chronic inflammation are characterised by several unique features: in contrast to virally driven HCC, up to 50% of NAFLD-HCC occurs in patients without cirrhosis and annual HCC incidence is comparatively low, complicating current surveillance strategies. On average, patients are older and are more frequently diagnosed at an advanced stage. While locoregional treatments are probably equally effective regardless of HCC aetiology, the picture is less clear for systemic therapy. Tyrosine kinase inhibitors are probably equally effective, while there have been initial signals that immune checkpoint inhibitors may be less effective in NAFLD-HCC than in viral HCC. Current international clinical practice guidelines for HCC do not consider aetiology, as there are insufficient data to draw specific conclusions or to recommend aetiology-specific modifications to the current management of patients with HCC. However, in light of the growing relevance of NAFLD-HCC, future clinical trials should assess whether HCC aetiologyand NAFLD/NASH in particularinfluence the safety and efficacy of a given treatment.

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Section: Surveillancementioning

confidence: 99%

NAFLD-driven HCC: Safety and efficacy of current and emerging treatment options

Foerster

Gairing

Müller

et al. 2022

Journal of Hepatology

177

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“…Some NAFLD patients eventually develop nonalcoholic steatohepatitis (NASH), cirrhosis, hepatocellular carcinoma, liver failure, and cardiovascular disease (CVD), which is also a major cause of mortality in NAFLD patients. [7][8][9] The prevention of CVD is important for the improvement of mortality, and early detection of high CVD risk patients is a clinically important issue. Diabetes mellitus (DM), hypertension, and dyslipidemia are well known to be risk factors of CVD, which are parts of the metabolic syndrome; NAFLD has also been associated with CVD risk.…”

Section: Introductionmentioning

confidence: 99%

Liver fibrosis and fatty liver as independent risk factors for cardiovascular disease

Tamaki

Kurosaki

Takahashi

et al. 2021

J of Gastro and Hepatol

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Background and Aim:The association between liver fibrosis, fatty liver, and cardiovascular disease (CVD) risk is unknown. Hence, this study aimed to investigate the association of liver fibrosis and fatty liver with CVD risk independent of already known CVD risk comorbidities. Methods: This is a prospective study registered with the University Hospital Medical Information Network clinical trial registry (UMIN000036175). Liver fibrosis was assessed by serum fibrosis markers including FIB-4, nonalcoholic fatty liver disease fibrosis score (NFS), and Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA + -M2BP), whereas fatty liver was diagnosed by ultrasonography. CVD risk was evaluated using the Framingham risk score (FRS), and a high CVD risk was defined as an FRS ≥ 20%. Results: A total of 3512 subjects were enrolled, and high CVD risk (FRS ≥ 20%) was observed in 17.5%. Advanced fibrosis (FIB-4 ≥ 2.67, NFS ≥ 0.675, and WFA + -M2BP ≥ 1.0) and the presence of fatty liver were significantly associated with high CVD risk independent of diabetes mellitus, dyslipidemia, and hypertension. When subjects were stratified by liver fibrosis and fatty liver, subjects with advanced fibrosis and fatty liver have the highest odds for high CVD risk (odds ratio [OR]: 5.90-35.6), followed by subjects with advanced fibrosis and without fatty liver (OR: 2.53-9.62) using subjects without advanced fibrosis and fatty liver as a reference. Conclusions: Liver fibrosis and fatty liver were associated with CVD risk independent of already known CVD risk comorbidities. The assessment of liver fibrosis and fatty liver may be useful to identify high CVD risk subjects. collection. NT analyzed data. MK and NI clinically revised the manuscript and supervised the study. NI, MK, and NI obtained funding. All authors read and approved the final version of the manuscript.

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“…A review detailing the epidemiology of NAFLD-related HCC by Kogiso et al is included in this special edition of MDPI Cancers [ 20 ]. Here, we will briefly summarize key epidemiologic concepts and predictions relevant to this review.…”

Section: Epidemiology and Predictionsmentioning

confidence: 99%

“…This stems from the notion that HCC develops more commonly in advanced liver disease, i.e., late-stage fibrosis or cirrhosis, and HCC screening is currently only recommended for NAFLD patients with cirrhosis [ 7 , 70 ]. However, the approach is problematic as NAFLD-related HCC often develops in the absence of cirrhosis [ 4 , 23 , 71 , 72 ], though this is unclear and may vary by population [ 20 , 70 , 73 ]. Nonetheless, patients with NAFLD-related HCC are often diagnosed at a later stage compared to their viral and alcoholic counterparts and advances in screening and prevention are needed [ 3 , 72 , 74 ].…”

Section: Clinical Approach To Nafld and Nafld-related Hccmentioning

confidence: 99%

Abnormal Metabolism in the Progression of Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma: Mechanistic Insights to Chemoprevention

Orabi

Berger

Brown

2021

Cancers

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Nonalcoholic fatty liver disease (NAFLD) is on the rise and becoming a major contributor to the development of hepatocellular carcinoma (HCC). Reasons for this include the rise in obesity and metabolic syndrome in contrast to the marked advances in prevention and treatment strategies of viral HCC. These shifts are expected to rapidly propel this trend even further in the coming decades, with NAFLD on course to become the leading etiology of end-stage liver disease and HCC. No Food and Drug Administration (FDA)-approved medications are currently available for the treatment of NAFLD, and advances are desperately needed. Numerous medications with varying mechanisms of action targeting liver steatosis and fibrosis are being investigated including peroxisome proliferator-activated receptor (PPAR) agonists and farnesoid X receptor (FXR) agonists. Additionally, drugs targeting components of metabolic syndrome, such as antihyperglycemics, have been found to affect NAFLD progression and are now being considered in the treatment of these patients. As NAFLD drug discovery continues, special attention should be given to their relationship to HCC. Several mechanisms in the pathogenesis of NAFLD have been implicated in hepatocarcinogenesis, and therapies aimed at NAFLD may additionally harbor independent antitumorigenic potential. This approach may provide novel prevention and treatment strategies.

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The Current View of Nonalcoholic Fatty Liver Disease-Related Hepatocellular Carcinoma

Cited by 20 publications

References 86 publications

NAFLD-driven HCC: Safety and efficacy of current and emerging treatment options

NAFLD-driven HCC: Safety and efficacy of current and emerging treatment options

Liver fibrosis and fatty liver as independent risk factors for cardiovascular disease

Abnormal Metabolism in the Progression of Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma: Mechanistic Insights to Chemoprevention

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