Key result
The PNPLA3 GG genotype significantly increased the risk of de novo NAFLD in long-term liver transplant recipients compared to CC and CG carriers (OR 14.2; 95% CI 1.78-113; P=0.012).
Why the study?
Do PNPLA3 I148M and TM6SF2 E167K polymorphisms affect the susceptibility to de novo NAFLD in long-term liver transplant recipients?
Cross-Sectional (n=65)
Do PNPLA3 I148M and TM6SF2 E167K polymorphisms affect the susceptibility to de novo NAFLD in long-term liver transplant recipients?
Odds Ratio: 14.2 (95% CI 1.78–113)
Absolute Event Rate: 33% vs 10%
p-value: p=0.012
The PNPLA3 I148M variant, particularly in combination with obesity, significantly increases the risk of de novo NAFLD in long-term liver transplant recipients.
May support weight control in obese PNPLA3 GG LT recipients to limit NAFLD risk; extends genetic associations to transplant survivors but remains hypothesis-generating.
De novo non-alcoholic fatty liver disease (NAFLD) is a common late complication for long-term survivors after liver transplantation. Genomic studies confirmed that PNPLA3 I148M and TM6SF2 E167K polymorphisms affected NAFLD susceptibility in the general population. However, this association was not validated in survivors after liver transplantation (LT). We performed a cross-sectional survey to investigate this relationship. A comprehensive survey, including anthropometric measurements, fasting venous blood sampling, ultrasound, and questionnaires was performed in the short-term. The clinical indications and patient's steatosis status before LT were collected from inpatient medical records. Sixty-five long-term recipients with a survival exceeding 10 years were enrolled in the final analysis. De novo NAFLD was more frequent in PNPLA3 GG carriers (0.33 vs 0.10 for GG vs CC + CG carriers, P = 0.018), while the genetic impact on NAFLD susceptibility was insignificant when categorized by the TM6SF2 polymorphism (0.19 in CC vs 0.14 in CT + TT carriers, P = 0.883). Multi-covariate analysis revealed that PNPLA3 exerted a significant genetic effect on de novo NAFLD following a recessive model (GG vs CC + CG, OR = 14.2, 95%CI: 1.78-113, P = 0.012). Compared to recipients with only the PNPLA3 GG allele or obesity (defined as body mass index > 25 kg/m(2)), steatosis was highly prevalent (71.4%) in PNPLA3 GG carriers with obesity. In conclusion, PNPLA3 I148M, but not TM6SF2 E167K, affects de novo NAFLD occurrence with a prominent interaction with obesity. Weight control might be a meaningful method to reduce the genetic susceptibility to NAFLD exerted by PNPLA3 variants.
No takes yet. Share an insight, caveat, or question.
Zhengtao Liu (2015) conducted a cross-sectional in De novo non-alcoholic fatty liver disease (NAFLD) (n=65). PNPLA3 I148M polymorphism (GG genotype) vs. CC + CG genotype was evaluated on De novo NAFLD (OR 14.2, 95% CI 1.78-113, p=0.012). The PNPLA3 GG genotype significantly increased the risk of de novo NAFLD in long-term liver transplant recipients compared to CC and CG carriers (OR 14.2; 95% CI 1.78-113; P=0.012).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: