Key result
Among Chinese adults, the highest versus lowest quartile of Lp(a) was associated with lower odds of NAFLD (OR 0.28; 95% CI 0.20-0.41) and elevated liver stiffness (OR 0.31; 95% CI 0.21-0.45).
Why the study?
Are higher levels of Lipoprotein(a) and systemic inflammatory indices associated with hepatic steatosis and liver stiffness in Chinese adults?
Cross-Sectional (n=1,345)
Are higher levels of Lipoprotein(a) and systemic inflammatory indices associated with hepatic steatosis and liver stiffness in Chinese adults?
Higher circulating Lp(a) is inversely associated with FibroTouch-derived hepatic steatosis and liver stiffness in Chinese adults, suggesting a complex relationship between Lp(a) and liver fat/fibrosis.
Background Lipoprotein(a) [Lp(a)] is synthesized mainly in the liver, whereas blood cell-derived inflammatory indices reflect systemic immune–inflammatory status. We examined their associations with FibroTouch-assessed hepatic steatosis and liver stiffness in Chinese adults. Methods This hospital-based cross-sectional study included 1,345 Chinese adults. Nonalcoholic fatty liver disease (NAFLD) was defined as controlled attenuation parameter (CAP) ≥248 dB/m, and elevated liver stiffness as liver stiffness measurement (LSM) ≥8 kPa. Multivariable logistic and linear regression, restricted cubic spline (RCS), receiver operating characteristic (ROC), joint-exposure, subgroup, and sensitivity analyses were performed. Results Higher Lp(a) quartiles were associated with lower prevalences of NAFLD and elevated liver stiffness and with lower CAP and LSM values. After full adjustment, the highest versus lowest quartile was associated with lower odds of NAFLD (odds ratio [OR], 0.28; 95% confidence interval [CI], 0.20–0.41) and elevated liver stiffness (OR, 0.31; 95% CI, 0.21–0.45). RCS analyses showed significant inverse associations without evidence of nonlinearity. Higher Lp(a) was also associated with lower CAP (β, −14.40; 95% CI, −17.79 to −11.01) and LSM (β, −0.58; 95% CI, −0.83 to −0.33). The Lp(a)–systemic immune-inflammation index (SII) combination showed the highest discrimination for NAFLD, whereas Lp(a)–systemic inflammation response index (SIRI) performed best for elevated liver stiffness. When added to the fully adjusted model, the corresponding areas under the ROC curve (AUCs) were 0.762 and 0.811, respectively, and exceeded those of established noninvasive fibrosis scores. Low Lp(a) combined with high inflammatory burden was associated with the highest odds of both outcomes. Conclusions Among Chinese adults, higher circulating Lp(a) was inversely associated with FibroTouch-derived hepatic steatosis and liver stiffness. Combining Lp(a) with systemic inflammatory indices may provide complementary information for noninvasive cross-sectional assessment.
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Huang et al. (2026) conducted a cross-sectional in Hepatic steatosis and liver stiffness (n=1,345). Lipoprotein(a) vs. Lowest quartile of Lipoprotein(a) was evaluated on Nonalcoholic fatty liver disease (NAFLD) (OR 0.28, 95% CI 0.20-0.41). Among Chinese adults, the highest versus lowest quartile of Lp(a) was associated with lower odds of NAFLD (OR 0.28; 95% CI 0.20-0.41) and elevated liver stiffness (OR 0.31; 95% CI 0.21-0.45).
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