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Copyright ©The Author(s) 2020.
World J Gastroenterol. Mar 28, 2020; 26(12): 1273-1285
Published online Mar 28, 2020. doi: 10.3748/wjg.v26.i12.1273
Table 3 Genes and their single nucleotide polymorphisms investigated in association with non-alcoholic fatty liver disease after liver transplantation
Ref.Etiology/Population
Genes and best 95%CI ORKey points
N (no steatosis/steatosis)
Míková et al[37]VariousDonor TM6SF2: rs58542926 (1.28-4.42); Donor PNPLA3: rs738409 (1.28-3.27); Additive: TM6SF2 + PNPLA3 (2.01-13.0); Recipient NS for allDonor TM6SF2 A allele and PNPLA3 G allele are associated with steatosis in both univariate and multivariate adjusted analyses
European
139/129The additive effect of donor TM6SF2 A allele and donor PNPLA3 G allele is strongly associated with steatosis
No association when recipients SNPs were analyzed
John et al[40]HCVRecipient adiponectin: rs1501299 (1.09-5.5), rs266729 (0.14-0.75); rs2241766, rs17300539 – NS; Donor – NS for allRecipient but not donor adiponectin rs1501299 GG genotype is significantly, but weakly associated with de novo steatosis after adjustment for race and HCV genotype
North American
72/39
Kim et al[39]VariousRecipient PNPLA3: rs738409 (1.00-9.34)1; Donor – NS; Additive donor + recipent: (1.32-117.0)2If both, donor and recipient have G allele, the recipient has higher risk for steatosis weak association, small number of patients
Eastern Asian
23/9
Trunečka et al[38]VariousDonor PNPLA3: rs738409 (1.05-1.75); Recipient PNPLA3: rs738409 (1.02-1.57)PNPLA3 G allele in donors [OR (95%CI) = 1.62 (1.12-2.33)], but not in recipients is independently associated with steatosis after adjustment for age, disease etiology, BMI, diabetes, hypertension, therapy and lipids
European
89/87