Associations of Elevated Lipoprotein(a) with C-Reactive Protein and Type 2 Diabetes in a Multiethnic Population
TL;DR
Findings support the emerging concept that Lp(a) may function as a molecular-inflammatory mediator potentially contributing to residual cardiovascular risk and highlight the importance of incorporating Lp(a) assessment into cardiometabolic risk stratification, particularly in high-risk populations.
Abstract
Background: Lipoprotein(a) [Lp(a)] is a genetically determined, pro-atherogenic lipoprotein enriched in oxidized phospholipids and increasingly recognized as a key potential contributor to residual cardiovascular and inflammatory risk. However, data on its distribution and cardiometabolic associations in Middle Eastern populations remain limited. This study aimed to evaluate the prevalence of elevated Lp(a) and its association with type 2 diabetes (T2D), systemic inflammation, and ethnic variation in a multiethnic cohort. Methods: In this cross-sectional study, data from 2083 adults aged ≥ 18 years residing in Kuwait were collected through the Kuwait Diabetes Epidemiology Program (KDEP) at Dasman Diabetes Institute between 2011 and 2014 using random sampling. Plasma Lp(a) concentrations, cardiometabolic parameters, and high-sensitivity C-reactive protein (CRP) were measured. Elevated Lp(a) was defined as ≥ 50 mg/dL according to established clinical guidelines. Associations of elevated Lp(a) with T2D and CRP were assessed using multivariable Poisson regression models to estimate adjusted prevalence ratios. Results: The overall prevalence of elevated Lp(a) was 41.2%, exceeding global estimates. Significant ethnic variation was observed, with Arabs exhibiting the highest prevalence. After adjustment for potential confounders, individuals with T2D had a higher prevalence of elevated Lp(a) (APR = 1.166) and diabetes status significantly modified the association between CRP and elevated Lp(a) interaction (APR = 1.015), thus supporting a link between Lp(a) and systemic inflammation. Conclusions: Elevated Lp(a) was highly prevalent in this multiethnic Middle Eastern population and was independently associated with T2D and systemic inflammation. These findings support the emerging concept that Lp(a) may function as a molecular-inflammatory mediator potentially contributing to residual cardiovascular risk and highlight the importance of incorporating Lp(a) assessment into cardiometabolic risk stratification, particularly in high-risk populations.