Patatin-Like Phospholipase Domain-Containing 3 I148M Variant Is Associated with Liver Steatosis and Fat Distribution in Chronic Hepatitis B

Zampino, Rosa; Coppola, Nicola; Cirillo, Grazia; Boemio, Adriana; Grandone, Anna; Stanzione, Maria; Capoluongo, Nicolina; Marrone, Aldo; Macera, Margherita; Sagnelli, E.; Adinolfi, Luigi Elio; Giudice, Emanuele Miraglia del

doi:10.1007/s10620-015-3716-7

Cited by 12 publications

(9 citation statements)

References 35 publications

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“…Some studies have demonstrated that the GG genotype effect the risk of HCC development (Falleti et al, 2011;Sato et al, 2014), while most other studies have reported no such association (Nischalke et al, 2011;Guyot et al, 2013;Friedrich et al, 2014). For patients with HBV infection, recent data reported that PNPLA3 polymorphism was independently associated with hepatic steatosis, but not with advanced fibrosis and HCC development (Vigano et al, 2013;Brouwer et al, 2015;Zampino et al, 2015). As a result, these data, as well as our report, suggest an apparent weaker or even no effect of PNPLA3 polymorphism on the risk of HCC in patients with chronic viral hepatitis as compared to those with fatty liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases

Khlaiphuengsin¹,

Kiatbumrung²,

Payungporn³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Background: The aim of this study was to evaluate any association between a single nucleotide polymorphism (SNP) in the patatin-like phospholipase domain containing 3 (PNPLA3) (rs738409, C>G) and the development and prognosis in patients with hepatocellular carcinoma (HCC). Materials and Methods: Two hundred heathy controls and 388 HCC cases were included: 211 with HBV, 98 patients with HCV, 29 with alcoholic steatohepatitis (ASH) and 52 with non-alcoholic steatohepatitis (NASH). The SNP was determined by real-time PCR based on TaqMan assays. Results: The prevalence of rs738409 genotypes CC, CG and GG in controls was 91 (45.5%), 88 (44.0%), and 21 (10.5%), respectively, while the corresponding genotypes in all patients with HCC was 158 (40.7%), 178 (45.9%), and 52 (13.4%). The GG genotype had significantly higher distribution in patients with ASH/NASH-related HCC compared with controls (OR=2.34, 95% CI=1.16-4.71, P=0.018), and viral-related HCC cases (OR=2.15, 95% CI=1.13-4.08, P=0.020). However, the frequency of the GG genotype was similar between controls and patients with viral-related HCC. At initial diagnosis, HBV-related HCC were larger and at more advanced BCLC stage than the other HCC groups. There were no significant differences between the GG and non-GG groups regarding clinical characteristics, tumor stage and overall survival. Conclusions: These data suggest an influence of the PNPLA3 polymorphism on the occurrence of HCC in patients with ASH/NASH but not among those with chronic viral hepatitis. However, the polymorphism was not associated with the prognosis of HCC.

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Section: Discussionmentioning

confidence: 99%

Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases

Khlaiphuengsin¹,

Kiatbumrung²,

Payungporn³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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“…In chronic hepatitis B, the association between PNPLA3 and liver damage seems to be limited to liver fat and inflammation but not fibrosis accumulation per se [40][41][42][43][44]. This link does not seem to be modulated by hepatitis B virus genotypes [40,41].…”

Section: Key Pointmentioning

confidence: 94%

PNPLA3 gene in liver diseases

Trépo

Romeo

Zucman‐Rossi

et al. 2016

Journal of Hepatology

232

196

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“…58 A similar result has been reported in a separate study of 99 individuals with hepatitis B in which the I148M homozygotes had an OR ¼ 13.9 (95% CI 2.2-86.9; p ¼ 0.005) for the presence of severe steatosis compared with individuals lacking this allele. 55 This allele has not been associated with fibrosis or cirrhosis in multiple studies. 55,59,60…”

Section: Effects In Other Liver Diseasesmentioning

confidence: 99%

“…35 The serum ALT level increasing allele at TRIB1 (rs2954021) significantly associates with increased serum levels of total cholesterol, serum LDL-C, serum triglycerides, and serum alkaline phosphatase, but decreased levels of serum HDL-C. 35,53 Variants near TRIB1 have also been associated with adiponectin. 55 The finding that some, but not all genetic variants that predispose to development of NAFLD predispose to related metabolic disease, suggests that genetics may help explain in part the imperfect correlation of these traits with each other. That is, some of the correlation seen between developing metabolic disease may be due to having shared genetic elements that predispose to more than one metabolic abnormality.…”

Section: Pleiotropies Effects On Related Metabolic Traits and Diseasesmentioning

confidence: 99%

Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease

2015

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Nonalcoholic fatty liver disease (NAFLD) is caused by hepatic steatosis, which can progress to nonalcoholic steatohepatitis, fibrosis/cirrhosis, and hepatocellular carcinoma in the absence of excessive alcohol consumption. Nonalcoholic fatty liver disease will become the number one cause of liver disease worldwide by 2020. Nonalcoholic fatty liver disease is correlated albeit imperfectly with obesity and other metabolic diseases such as diabetes, hyperlipidemia, and cardiovascular disease, but exactly how having one of these diseases contributes to the development of other metabolic diseases is only now being elucidated. Development of NAFLD and related metabolic diseases is genetically influenced in the population, and recent genome-wide association studies (GWASs) have discovered genetic variants that associate with these diseases. These GWAS-associated variants cannot only help us to identify individuals at high risk of developing NAFLD, but also to better understand its pathophysiology so that we can develop more effective treatments for this disease and related metabolic diseases in the future.

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Patatin-Like Phospholipase Domain-Containing 3 I148M Variant Is Associated with Liver Steatosis and Fat Distribution in Chronic Hepatitis B

Abstract: In our CHB patients, the PNPLA3 polymorphisms influenced the development of liver steatosis, but not fibrosis status. The association of PNPLA3 p.I148M with liver steatosis increased with the greater amount of abdominal fat, irrespective of BMI.

Cited by 12 publications

References 35 publications

Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases

Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases

PNPLA3 gene in liver diseases

Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease

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