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Published on: May 6, 2014
Proprotein convertase subtilisin/kexin type 9 is associated with atherosclerosis in patients with Behcet's disease
Rabia Aydogan Baykara1, Pinar Diydem Yilmaz2, Mevlüt Hakan Göktepe3
1Department of Physical Medicine and Rehabilitation, Malatya Turgut Ozal University, Malatya, Turkey.
Insights
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is independently associated with subclinical atherosclerosis in Behcet
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Biochemistry
Background:
- Behcet's disease (BD) is linked to increased cardiovascular disease risk.
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) accelerates atherosclerosis.
- Subclinical atherosclerosis markers like carotid artery intima-media thickness (cIMT) are crucial in BD patients.
Purpose of the Study:
- To investigate the relationship between PCSK9 levels and cIMT in BD patients.
- To determine if PCSK9 is associated with BD disease activity.
- To explore PCSK9 as a potential biomarker for atherosclerosis in BD.
Main Methods:
- A case-control study involving 58 BD patients and 58 healthy controls.
- Measurement of carotid artery intima-media thickness (cIMT).
- Quantification of serum PCSK9 levels and assessment of BD disease activity.
Main Results:
- BD patients exhibited significantly higher cIMT and PCSK9 levels compared to controls.
- A significant independent association was found between PCSK9 and cIMT (p < 0.050).
- No independent association was observed between PCSK9 and BD disease activity.
Conclusions:
- PCSK9 is strongly and independently associated with subclinical atherosclerosis in Behcet's disease.
- PCSK9 may serve as a marker for atherosclerosis in BD patients.
- The association between PCSK9 and BD disease activity appears limited.
Objectives:
The incidence of cardiovascular disease is increased in patients with Behcet's disease (BD). Proprotein convertase subtilisin/kexin type 9 (PCSK9) causes the acceleration of atherosclerosis. We aimed to investigate whether there is a relationship between PCSK9 with carotid artery intima-media thickness (cIMT), a marker of subclinical atherosclerosis, and BD disease activity.
Methods:
Fifty-eight patients with BD and 58 age-, gender-, and body mass index (BMI)-matched healthy control subjects were included in the study. The disease activity of the patients was estimated. Individuals' cIMT values were measured, and PCSK9 levels were studied.
Results:
Patients with BD' cIMT (0.51 ± 0.1 vs 0.41 ± 0.1 mm, p < .001) and PCSK9 (623.2 ± 101.7 ± 10.1 vs 528.3 ± 242.7 ng/ml, p = .007), values were significantly higher than the control group. In stepwise regression analysis, there was an independent relationship between cIMT with PCSK9 (β = 0.179, p < .050). There was no independent relationship between disease activities with PCSK9. Based on the ROC curve analysis, the PCSK9 optimal cutoff value for cIMT was 595.1 ng/ml, sensitivity 66.7%, specificity 64.7% (AUC = 0.672; 95% CI: 0.530-0.815, p = .040).
Conclusion:
There is a strong independent association between subclinical atherosclerosis and PCSK9 in patients with BD. There may be no independent association between PCSK9 and disease activity.
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