Objective To detect the level of serum proprotein convertase subtilisin/kexin type 9 (PCSK9) in patients with systemic lupus erythematosus (SLE) and investigate the correlation between PCSK9 level and disease parameters. Methods Forty-seven SLE patients and 30 age, sex-matched healthy controls (HCs) were included in our research. Traditional cardiovascular disease (CVD) risk factors were compared between the two groups. The level of serum PCSK9 was examined by ELISA. Carotid intima-media thickness (cIMT) was measured by carotid ultrasound. According to the measured value of cIMT, SLE patients were divided into SLE-AS (cIMT≥1.0 mm) and SLE-NonAS (cIMT<1.0 mm) subgroups. Atherogenic factors and PCSK9 levels were compared between the two subgroups. Univariate correlational analysis of PCSK9 levels and disease parameters was conducted in the SLE patients. Results No difference was found in the total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), ApoA1, ApoB, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), fasting blood-glucose (FBG), body mass index (BMI) or uric acid (UA) between the SLE patients and HCs. However, the higher ratio of cIMT thickening and the elevation of serum PCSK9 levels were observed in the SLE patients as compared with the HCs. No significant difference in the traditional risk factors for CVD was found, but significant difference in the level of C-reactive protein (CRP) existed between the SLE-AS subgroup and SLE-NonAS subgroup. The level of serum PCSK9 in the SLE-AS subgroup was significantly higher than that in the SLE-NonAS subgroup. PCSK9 concentrations were positively correlated with CRP levels, but not correlated obviously with the age, SLEDAI, lipids parameters (TC, LDL-C, ApoA1, ApoB, TG, HDL-C), BMI or UA levels. This tendency seemed to be more significant in the female patients. Conclusion Elevated level of serum PCSK9 can be observed in SLE patients, especially in those with thickening of cIMT. PCSK9 may be associated with atherogenic inflammation in SLE.