- Consistent inverse association between Lp(a) levels and MASLD severity.
- Lower Lp(a) reflects hepatic synthetic impairment and altered lipoprotein handling, not protection from cardiovascular disease.
- Recognise this paradox to improve Lp(a) interpretation and cardiovascular risk stratification in patients with MASLD.
Curr Cardiol Rep. 2026 Aug 8;28(1):76. doi: 10.1007/s11886-026-02399-9.
ABSTRACT
PURPOSE OF REVIEW: Lipoprotein(a) [Lp(a)] remains a well-established, genetically determined predictor of cardiovascular risk due to its pro-atherogenic and pro-thrombotic effects. This review examines the paradoxical relationship between Lp(a) and metabolic dysfunction-associated steatotic liver disease (MASLD), where Lp(a) levels decline with advanced fibrosis despite persistently elevated cardiovascular disease (CVD) risk.
RECENT FINDINGS: Studies consistently show an inverse association between Lp(a) and MASLD severity. Evidence suggests that lower Lp(a) levels are a consequence of hepatic dysfunction rather than protective against cardiovascular disease. Additionally, selective hepatic insulin resistance increases VLDL production, diverting apoB100 from Lp(a) assembly, while insulin directly suppresses apolipoprotein(a) synthesis. Genetic variants linked to MASLD may further impair hepatic lipid secretion and reduce Lp(a). Lower Lp(a) levels in MASLD likely reflect impaired hepatic synthetic function rather than reduced cardiovascular risk. Recognizing this paradox may improve risk stratification and interpretation of Lp(a) in patients with MASLD.
PMID:42570162 | DOI:10.1007/s11886-026-02399-9
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