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. 2025 Jul;54(4):302-310.
doi: 10.1080/03009742.2025.2488096. Epub 2025 May 6.

Dysregulated serum lipid profile and atherosclerosis in untreated female Takayasu arteritis patients: a propensity score-matched analysis

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Dysregulated serum lipid profile and atherosclerosis in untreated female Takayasu arteritis patients: a propensity score-matched analysis

Q Zang et al. Scand J Rheumatol. 2025 Jul.

Abstract

Objective: Recent studies suggest that dyslipidaemia may play a critical role in the progression of cardiovascular disease in Takayasu arteritis (TA), although the exact relationship between dyslipidaemia and TA disease activity remains unclear, which is the focus of this study.

Method: We evaluated dyslipidaemia and atherosclerosis in a cohort of untreated female patients. Fifty untreated female patients with TA (median age 30 years) and 98 healthy controls matched for age and body mass index (median age 30 years) were assessed for lipid profiles [total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (ApoA1), ApoB, ApoE, lipoprotein(a)], inflammatory markers [C-reactive protein (CRP), erythrocyte sedimentation rate (ESR)], and atherosclerotic plaque frequency.

Results: TA patients exhibited significantly higher levels of TG and the non-HDL-C/HDL-C ratio than the control group, whereas TC, HDL-C, LDL-C, and ApoA1 levels were significantly lower. Pearson's correlation analysis indicated a positive correlation between CRP and ApoB, as well as the non-HDL-C/HDL-C ratio, and negative correlations with TG, HDL-C, and ApoA1. Atherosclerotic plaques were detected in 14.3% of the TA patients. Multivariate regression analysis revealed that the presence of atherosclerotic plaques was associated only with age, independent of inflammatory markers and lipoprotein levels.

Conclusion: The results of this study indicate that untreated female TA patients exhibit a markedly dysregulated serum lipid profile. Atherosclerosis in early TA was not related to lipids or markers of inflammation.

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