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Lp(a) is elevated across autoimmune diseases with limited evidence that anti-inflammatory therapy helps, systematic review of 13 studies (J Clin Lipidol 2026)

Original title: Lipoprotein(a) in selected autoimmune diseases: A systematic review of cardiovascular implications and anti-inflammatory interventions

J Clin Lipidol · · 6

Castillo-Córdoba EM, Mitta A, Romeo FJ

PROSPERO-registered (CRD420251121143) systematic review of 313 records, 13 studies meeting inclusion, examining Lp(a) elevation and the effect of anti-inflammatory or immunomodulatory therapy across autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, psoriasis, Behcet's disease, Takayasu arteritis). Elevated Lp(a) was frequently observed but with variable outcome associations: in lupus, higher Lp(a) correlated with renal involvement and inflammatory activity but inconsistently with cardiovascular outcomes; in rheumatoid arthritis, TNF inhibitor therapy did not significantly change Lp(a); Mendelian randomisation supported a causal link between psoriasis and elevated Lp(a); and in Takayasu arteritis and Behcet's disease, elevated Lp(a) was linked to vascular involvement. A population-based cohort showed additive cardiovascular risk when autoimmune disease and elevated Lp(a) co-occurred. The authors conclude Lp(a) elevation is common across autoimmune diseases and may add to ASCVD risk, but evidence that immunomodulatory therapy modifies Lp(a) remains limited.

Read the paper (DOI)PubMed

Original abstract

Background: Autoimmune diseases are associated with increased atherosclerotic cardiovascular disease (ASCVD) risk driven by chronic systemic inflammation and prothrombotic mechanisms. Lipoprotein(a) [Lp(a)] is a causal ASCVD risk factor with proinflammatory and antifibrinolytic properties; however, its role in autoimmune diseases and the impact of immunomodulatory therapies remain unclear.

Objective: To evaluate the consistency of Lp(a) elevation across autoimmune diseases and whether anti-inflammatory or immunomodulatory therapies modify circulating Lp(a) levels.

Methods: A Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020-guided systematic review registered in International Prospective Register of Systematic Reviews (PROSPERO)(CRD420251121143) was conducted. MEDLINE and Cochrane were searched for English-language studies (1990-2025) assessing Lp(a) in adults with autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, psoriasis, Behçet's disease, and Takayasu arteritis. Two reviewers independently screened studies and assessed quality using the Newcastle-Ottawa Scale. Findings were synthesized descriptively.

Results: Of 313 records, 13 studies met the inclusion criteria. Elevated Lp(a) was frequently observed, with variable outcome associations. In systemic lupus erythematosus, higher Lp(a) correlated with renal involvement and inflammatory activity, whereas cardiovascular associations were inconsistent. In rheumatoid arthritis, tumor necrosis factor inhibitor therapy did not significantly modify Lp(a). In psoriasis, Mendelian randomization supported a causal association between psoriasis and elevated Lp(a). In Takayasu arteritis and Behçet's disease, elevated Lp(a) was linked to vascular involvement. A population-based cohort demonstrated additive cardiovascular risk among individuals with autoimmune disease and elevated Lp(a).

Conclusion: Lp(a) elevation is common across autoimmune diseases and may contribute to excess ASCVD risk. Evidence for modification with immunomodulatory therapy is limited. Prospective studies are needed.

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Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.