Lipids & metabolic liver disease
Interplay among lipoprotein(a), hepatic and vascular damage in individuals with metabolic dysfunction
Authors' conclusion
The results of this study suggest that liver damage is more likely the cause of reduced plasma Lp(a) levels rather than a consequence. Assessing plasma Lp(a) levels and the extent of liver damage could improve the prediction of vascular damage.
Study context
- Population
- Individuals with metabolic dysfunction (Liver-Bible cohort) and Milan Biobank808 with genomic information
- Participants
- 859 individuals
- Outcome
- Combined effects of Lp(a) levels on liver and vascular damage
Methodological detailsGenome-wide association studies (GWAS), polygenic risk scores
- GWAS
- Polygenic risk scores
Main finding
As reported in the abstract
Determinants of Lp(a) and relation to LSM (Liver-Bible)
- Genetic variation in the LPA gene was the strongest determinant of Lp(a), followed by liver stiffness measurement (LSM)
- Circulating Lp(a) levels, but not genetic predisposition, inversely related to LSM
Observational data: associations, not effects.
Further findings
Carotid atherosclerotic plaques in participants with more severe insulin resistance (n = 250)
- Lp(a) levels, OR
- 6.7 (95% CI 1.0-53.0, p = 0.046)
- LSM, OR
- 13.7 (95% CI 1.4-172.2, p = 0.023)
- Regardless of traditional cardiovascular risk factors
Milan Biobank (n = 6963): genetically predicted Lp(a) and MASLD
- Genetically predicted higher Lp(a) levels tended to increase risk of liver-related outcomes
- Genetically predicted MASLD associated with lower circulating Lp(a) levels
Original publication
Interplay among lipoprotein(a), hepatic and vascular damage in individuals with metabolic dysfunction. Cardiovasc Diabetol. Published 26 November 2025. doi:10.
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