Risk factors for non-alcoholic fatty liver disease are common in patients with non-B non-C hepatocellular carcinoma in India

David, Deepu; Raghavendran, Anantharam; Goel, Ashish; Kumar, C Bharath; Kodiatte, Thomas Alex; Burad, Deepak; Abraham, Priya; Ramakrishna, B. S.; Joseph, Philip; Ramachandran, Jeyamani; Eapen, CE

doi:10.1007/s12664-017-0785-x

Cited by 21 publications

(15 citation statements)

References 38 publications

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“…In a meta-analysis, White et al 20 showed that 60 per cent of HCC related to NASH had underlying cirrhosis and also documented a lower risk of HCC in NASH compared to those having HCV infection. In India, 72 per cent of non-B non-C HCC has shown the presence of underlying cirrhosis21. Cirrhosis of any aetiology (viral hepatitis, alcohol or MS) is considered to be a precursor to HCC22.…”

Section: Epidemiology Of Nafld/ Nash-associated Hccmentioning

confidence: 99%

“…Genetic mutation or oxidative stress causing necro-inflammation and hepatocarcinogenesis has been thought to be the underlying mechanism and these patients have a 200-fold increased risk of HCC development than non-HH patients5657. In a retrospective analysis, David et al 21 showed that 85 per cent of the patients with non-B non-C HCC had at least one risk factor for NAFLD.…”

Section: Risk Factors Of Hcc In Nafldmentioning

confidence: 99%

“…Its progression into necroinflammation, fibrosis and steatohepatitis has been explained by ’two-hit’ and ’multi-parallel hit’ theories. After development of hepatic steatosis, other factors such as obesity, IR and genetic mutations act as a 'second hit’ or ’multiple parallel hits’ at molecular level, leading to hepatocarcinogenesis521. In a case series of 11 patients of NASH-HCC, 91 per cent were found to have obesity, diabetes, hypertension and dyslipidaemia, which contributed to carcinogenic potential in NASH58.…”

Section: Pathophysiology Of Nafld/ Nash-hccmentioning

confidence: 99%

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Non-alcoholic fatty liver disease associated with hepatocellular carcinoma: An increasing concern

2019

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Hepatocellular carcinoma (HCC) is the sixth most common cancer in world and third largest cause of cancer-related deaths. The last few decades have witnessed the emergence of non-viral causes of HCC, the most important being non-alcoholic fatty liver disease (NAFLD). NAFLD ranges from simple steatosis in the absence of excessive alcohol intake to non-alcoholic steatohepatitis (NASH) with or without cirrhosis. About 3-15 per cent of the obese patients with NASH progress to cirrhosis and about 4-27 per cent of NASH with cirrhosis patients transform to HCC. It is also known that HCC can develop de novo in patients with NASH without the presence of cirrhosis. Yearly cumulative incidence of NASH-related HCC is low (2.6%) compared to four per cent of viral-HCC. NAFLD has been associated with risk factors such as metabolic syndrome, insulin resistance, altered gut flora and persistent inflammation. Due to alarming rise in metabolic diseases, both in the developing as well as the developed world, it is expected that the incidence of NAFLD/NASH-HCC would rise manifold in future. No definite guidelines have been drawn for surveillance and management of NAFLD/NASH-associated HCC. It is thus important to discuss the entity of HCC in NAFLD at length with special focus on its epidemiology, risk factors, pathophysiology, diagnosis, clinical presentation and prevention.

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Section: Epidemiology Of Nafld/ Nash-associated Hccmentioning

confidence: 99%

Section: Risk Factors Of Hcc In Nafldmentioning

confidence: 99%

Section: Pathophysiology Of Nafld/ Nash-hccmentioning

confidence: 99%

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Non-alcoholic fatty liver disease associated with hepatocellular carcinoma: An increasing concern

2019

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“…The analysis of patients with chronic HCV infection, in addition to alcohol abuse and dependence, indicated that elevated proton pump activity increased the risk of hepatic decompensation and hepatocellular carcinoma (3). According to the study of non-alcoholic fatty liver disease (NAFLD) in Indian patients, 11 patients with a history of considerable alcohol consumption had at least one risk factor for NAFLD, including alcohol-associated HCC (4). Asian countries have been reported to have a high incidence of HBV infection.…”

Section: Introductionmentioning

confidence: 99%

“…Asian countries have been reported to have a high incidence of HBV infection. A previous study of the Indian population demonstrated a lower prevalence of HBV infection of unknown origin (4); however, the direct role of alcohol in the carcinogenesis of HCC, or the mechanism underlying alcohol-induced hepatotoxicity associated with alcohol metabolites, oxidative stress and iron metabolism, are yet to be elucidated (2,5). The administration of alcohol/diethyl nitrosamine/carbon tetrachloride in mice successfully induced an α-fetoprotein-secreting HCC model in adult male BALB/c mice.…”

Section: Introductionmentioning

confidence: 99%

ACTG1 and TLR3 are biomarkers for alcohol‑associated hepatocellular carcinoma

Gao

Tan

et al. 2018

Oncol Lett

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Alcohol consumption is a risk factor for the development of hepatocellular carcinoma (HCC); however, the association between alcohol and HCC remains unknown. The present study aimed to identify key genes related to alcohol-associated HCC to improve the current understanding of the pathology of this disease. Alcohol-associated and non-alcohol-associated HCC samples in the GSE50579 dataset of the Gene Omnibus Database were analyzed to investigate altered gene expression. Integrated bioinformatics methods were employed to clarify the biological functions of the differentially expressed genes (DEGs), including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and protein-protein interactions (PPIs). The present study reported that candidate biomarker micro (mi)RNAs via TargetScan Human 7.1. DEGs and their associated miRNAs (according to bioinformatics analysis) were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Additionally, 284 EGs from the GSE50579 dataset were revealed. In GO term analysis, DEGs were closely associated with the ‘regulation of nucleic acid metabolism’. KEGG pathway analysis indicated that the DEGs were tightly engaged in the ‘VEGF and VEGF receptor signaling network’, ‘proteoglycan syndecan-mediated signaling events’, ‘erbB receptor signaling’ and ‘β1 integrin cell surface interactions’. According to the results of PPI and heat map analysis, the main hub genes were centrin 3 (CETN3), Toll-like receptor 3 (TLR3), receptor tyrosine-protein kinase (ERBB4), heat shock protein family member 8, actin γ1 (ACTG1) and α-smooth muscle actin. it was demonstrated that the ACTG1, TLR3, miR-6819-3p and miRΝΑ (miR)-6877-3P had undefined associations. Furthermore, RT-qPCR analysis revealed that miR-6819-3p and miR-6877-3P may enhance the expression levels of ACTG1 and inhibit the expression levels of TLR3 in alcohol-associated HCC tissues. TLR3 and ACTG1 were proposed as potential biomarkers of alcohol-associated HCC. Investigation into the regulatory functions of miR-6819-3p and miR-6877-3P may provide novel insights into the treatment of alcohol-associated HCC.

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First‐line sorafenib sequential therapy and liver disease etiology for unresectable hepatocellular carcinoma using inverse probability weighting: A multicenter retrospective study

et al. 2021

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Background and Aims Sequential therapy with molecular‐targeted agents (MTAs) is considered effective for unresectable hepatocellular carcinoma (HCC) patients. This study purposed to evaluate the efficacy of sequential therapy with sorafenib (SORA) as a first‐line therapy and to investigate the therapeutic impact of SORA in nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steato hepatitis (NASH)‐related HCC. Methods We evaluated 504 HCC patients treated with SORA (Study‐1). The times of administration for sorafenib from 2009 to 2015, 2016 to 2017, and 2018 and later were defined as the early‐, mid‐, and late‐term periods, respectively. Among them, 180 HCC patients treated with SORA in addition to MTAs in the mid‐ and late‐term periods were divided into groups based on disease etiology (NAFLD or NASH [n = 37] and viral or alcohol [n = 143]), and outcomes were compared after inverse probability weighting (IPW) (Study‐2). Results Overall survival (OS) of HCC patients who received sequential MTA therapy after first‐line SORA was significantly longer. The median survival times (MST) were 12.6 versus 17.6 versus 17.4 months in the early‐term group, mid‐term group, and the later‐time group (early vs. mid, p = 0.014, early vs. later. p = 0.045), respectively. (Study‐1). In Study‐2, there was no significant differences in OS between the Virus/alcohol group and the NAFLD/NASH group in patients who received sequential therapy (MST was 23.4 and 27.0 months p = 0.173, respectively). The NAFLD or NASH, female sex, albumin‐bilirubin (ALBI) grade 2b, and major Vp (Vp3/Vp4) were significant factors for OS treated with SORA. Conclusions Sequential therapy with SORA as the first‐line treatment improved the prognosis of unresectable HCC patients and was effective regardless of HCC etiology.

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Risk factors for non-alcoholic fatty liver disease are common in patients with non-B non-C hepatocellular carcinoma in India

Abstract: Eighty-five percent of the patients with non-B non-C HCC had at least one risk factor for NAFLD. None of the study patients had occult hepatitis B infection. NAFLD is emerging as the major etiological contributing factor for non-B non-C HCC in India.

Cited by 21 publications

References 38 publications

Non-alcoholic fatty liver disease associated with hepatocellular carcinoma: An increasing concern

Non-alcoholic fatty liver disease associated with hepatocellular carcinoma: An increasing concern

ACTG1 and TLR3 are biomarkers for alcohol‑associated hepatocellular carcinoma

First‐line sorafenib sequential therapy and liver disease etiology for unresectable hepatocellular carcinoma using inverse probability weighting: A multicenter retrospective study

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