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Abstract
Purpose
Effective treatment of dyslipidemia with lipid-lowering agents is pivotal in the management of metabolic-associated fatty liver disease (MAFLD) for preventing cardiovascular complications. We explored the associations between improvements in liver injuries indicated by changes in transaminases and a reduction in lipid levels in MAFLD patients with dyslipidemia and elevated transaminases during lipid-lowering therapies.
Methods
This prospective, cohort study enrolled consecutive MAFLD patients with hyperlipidemia and elevated transaminases. Patients were divided into a group receiving lipid-lowering agents and an age-, sex- and baseline lipid level-matched control group without receiving lipid-lowering agents. Clinical visits were performed at the 1st month and then every 3 months for 1 year.
Results
This study included 541 MAFLD patients (lipid-lowering group: 325 patients; control group: 216 patients). Compared with controls, there was a substantially greater reduction in alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transpeptidase (GGT), triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) in the lipid-lowering group after 12 months (all P < 0.05). The decrease in ALT was positively correlated with the decrease in TC (r = 0.332), TG (r = 0.180), LDL-c (r = 0.253) and apolipoprotein E (ApoE) (r = 0.119), while the decrease in AST was positively correlated with the decrease in TC (r = 0.228) and LDL-c (r = 0.192) (all P<0.05). The greater range of reduction in blood lipids (TC/TG/LDL-c), the higher the transaminase and GGT normalization rate (all P<0.05). Multivariate analysis confirmed that a TG decrease of over 50% remained an independent predictor of transaminase and GGT normalization (OR 2.07, 95% CI 1.12–3.84, P=0.020).
Conclusion
Lipid-lowering to target levels might be beneficial to liver injury improvements in MAFLD patients with dyslipidemia when receiving lipid-lowering agents.
Abbreviations
MAFLD, metabolic-associated fatty liver disease; CVD, cardiovascular disease; NAFLD, nonalcoholic fatty liver disease; BMI, body mass index; T2DM, type 2 diabetes; DBP, diastolic blood pressure; WC, waist circumference; SBP, systolic blood pressure; ALT, alanine aminotransferease; AST, aspartate aminotransferase; GGT, gamma glutamyltranspeptidase; TC, total cholesterol; LDL-c, low-density lipoprotein cholesterol; TG, triglyceride; ApoA-1, apolipoprotein A-1; HDL-c, high-density lipoprotein cholesterol; ApoB, apolipoprotein B; LP-A, lipoprotein-A; ApoE, apolipoprotein E; UA, uric acid; FFA, free fatty acid; FBG, fasting blood glucose; FINS, fasting insulin; HOMA-IR, homeostatic model assessment of insulin resistance; hs-CRP, high-sensitivity C-reactive protein; HbA1c, glycated hemoglobin; FIB-4, Fibrosis-4; LSM, liver stiffness measurement; NFS, NAFLD fibrosis score; LFC, liver fat content.
Data Sharing Statement
All data generated or analyzed during this study are included in this published article.
Ethics Approval
The study protocol was approved by the local ethics committee (IEC for clinical research and animal trials of the First Affiliated Hospital of Sun Yat-sen University) [2014 No. 112], and was in accordance with the ethical standards of the 1964 Declaration of Helsinki.
Acknowledgments
We are grateful to Professor Aihua Lin in School of Public Health, Sun Yat-sen University for her assistance in statistical analysis of this study.
Disclosure
The authors declare that they have no competing interests in this work.