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• W2752281075 abstract "See article in Hepatology Research 48: E335–E339 PNPLA3 as a liver steatosis risk factor following living-donor liver transplantation for hepatitis C H Miyaaki, S Miuma, N Taura, H Shibata, A Soyama, M Hidaka, M Takatsuki, S Eguchi and K Nakao See article in Hepatology Research 48: E162–E171 Effect of PNPLA3 I148M polymorphism on histologically proven non-alcoholic fatty liver disease in liver transplant recipients H Kim, KW Lee, K Lee, S Seo, MY Park, SW Ahn, SK Hong, KC Yoon, HS Kim, Y Choi, HW Lee, NJ Yi and KS Suh Assessment of the liver allograft after liver transplantation (LT) is an important issue in the effort to improve long-term survival. Because hepatitis B and C, which are the most important causes of recurrent disease, have been recently well controlled by antiviral therapy even after LT, hepatic steatosis is a relatively important major cause of chronic liver disease in the liver allograft.1 Metabolic syndrome (obesity, diabetes mellitus, hyperlipidemia, and hypertension) is common among patients undergoing LT.2 The nutritional status changes substantially after LT, which may contribute to aggravation of metabolic syndrome and fatty liver disease. Furthermore, these metabolic factors are considered to be exacerbated by immunosuppressive drugs and steroids and are important predictive factors for morbidity and mortality in the post-LT period. In particular, cyclosporine is reportedly associated with a high incidence of hypertension and hyperlipidemia,3 and tacrolimus is a known cause of diabetes mellitus.4 Hepatic steatosis is well known as an important late complication of LT. Hepatic steatosis, which is apparently unrelated to recurrent disease, is present in approximately 30% of post-LT biopsies.1, 5 Dumortier et al.5 reported that 31.1% of LT recipients developed hepatic steatosis after LT. Their multivariate analysis revealed seven independent risk factors for post-LT steatosis: post-LT obesity, a tacrolimus-based regimen, diabetes mellitus, hyperlipidemia, hypertension, alcoholic cirrhosis, and pre-existing donor graft steatosis. Interestingly, when LT recipients had zero, one, two, three, four, five, and six of these risk factors, post-LT steatosis occurred in 6.0%, 12.0%, 22.1%, 29.9%, 65.5%, 81.5%, and 100.0% of the recipients, respectively. Kim et al.6 also reported that pre-LT alcoholic cirrhosis, obesity at biopsy, and pre-existing donor graft steatosis were significant independent risk factors for post-LT non-alcoholic fatty liver disease (NAFLD). Like metabolic factors, genetic factors also influence the development of NAFLD. In particular, the single nucleotide polymorphism (SNP) rs738409 G allele in the patatin-like phospholipase domain-containing 3 gene (PNPLA3) has been identified as the most important genetic risk factor for the development of NAFLD.7, 8 Although the functional roles of the gene have not been well clarified, it is considered to play an important role in remodeling lipid droplets, promoting the extracellular release of retinol,9 and modulating endoplasmic reticulum stress.10 The SNP rs58542926 in the transmembrane 6 superfamily member 2 gene (TM6SF2) was also recently identified to be closely associated with the development of NAFLD11, 12 by modulating lipid metabolism, including the total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels, thus helping to protect against cardiovascular disease.12 Genetic factors also play important roles in post-LT NAFLD. One study showed that the presence of the SNP rs738409 G allele of PNPLA3 in the recipients, but not in the donors, is an independent risk factor for post-LT NAFLD.13 Furthermore, the multivariate analysis showed that recipients with the GG genotype had a 13.7-fold higher risk of graft steatosis than recipients with the CC genotype, independent of age, weight gain after LT, or underlying disease. Very recently, two similar articles in which the SNP rs738409 GG genotype in PNPLA3 was an independent and important predictor of the development of NAFLD after living-donor LT were published in Hepatology Research.14, 15 In these articles, Miyaaki et al.14 reported that histologically proven liver steatosis was present in 30.0% and steatohepatitis in 7.0% of recipients after living-donor LT for chronic hepatitis C in Japan. They showed that the SNP rs738409 GG genotype in PNPLA3 was a risk factor for the development of NAFLD in donors, but not in recipients. The average time to liver steatosis after LT was 2.74 ± 1.55 years. Additionally, the time to the development of liver steatosis differed significantly according to the donors’ rs738409 genotype (GG, 4.27 ± 1.09 years; GC, 8.33 ± 0.85 years; and CC, 11.23 ± 1.15 years; P = 0.002), but not the recipients’ genotype (P = not significant). Various laboratory markers, including age, body mass index at liver biopsy, bodyweight change, diabetes, dyslipidemia, and immunosuppressive drugs, were not significant. Kim et al.15 reported that histologically proven liver steatosis was present in 28.1% of patients at a mean time of 12.7 ± 2.0 months after living-donor LT. One year after LT, liver steatosis was present in 50.0% of homozygous recipients with the rs738409 GG genotype compared with 27.3% of heterozygous recipients with the G allele and 9.1% of homozygous recipients with the CC genotype; these differences were statistically significant. In contrast, the donor's genotype was not significantly associated with the development of NAFLD after LT. However, the development of NAFLD was remarkably increased after LT when both the recipient and donor showed a heterogeneous or homozygous genotype of the G allele compared with other genetic statuses (47.1% vs. 6.7%, respectively; P = 0.018). Moreover, the authors reported that the presence of the G allele in both the donor and recipient was the only significant predictive factor for post-LT NALFD in their multivariate analysis. Although both of the above-mentioned studies concluded that the SNP rs738409 G allele of PNPLA3 was an independent and important predictive factor for the development of NAFLD after LT, whether the G allele of recipients or donors is more important for the development of NAFLD remains controversial. Miyaaki et al.14 found that the G allele was a predictive factor in donors but not in recipients. These results differ from those in the previous study13 and those reported by Kim et al.15 Interestingly, however, Kim et al.15 also reported that the G allele in both the donor and recipient was the most important predictive factor; this is a very similar conclusion obtained by Dumortier et al.,5 who found that the development of NAFLD after LT was related to both the recipient (the “soil”) and the graft (the “seed”). As mentioned above, the SNP rs58542926 in TM6SF2 is an independent and important predictive factor for the development of NAFLD.11, 12 However, the influences of the SNP of this gene for the development of post-LT NALFD remain unclear. Further large-scale investigations are expected to clarify which combinations of these SNPs, including those in the PNPLA3 and TM6SF2 genes, are the most important predictive factors for post-LT NALFD. These studies14, 15 provide beneficial and interesting information that assists in our understanding of the mechanisms of development of NAFLD after living-donor LT." @default.
• W2752281075 created "2017-09-15" @default.
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• W2752281075 date "2018-02-01" @default.
• W2752281075 modified "2023-09-25" @default.
• W2752281075 title "Are donors or recipients a more important predictive factor for the development of non-alcoholic fatty liver disease after liver transplantation?" @default.
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• W2752281075 doi "https://doi.org/10.1111/hepr.12975" @default.
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