Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) is a natural circulating inhibitor of the LDL receptor. There is evidence that PCSK9 is a risk factor for coronary artery disease. In this study we aimed to determine factors associated with PCSK9 in patients with DMt2, according to statin treatment. Material included 116 consecutive patients with DMt2. Fasting serum lipids were determined enzymatically, apolipoproteins B100, A1 by immunoturbidimetry, apo C3, B48, pentraxin 3 (PTX3) and PCSK9 by ELISA, glycated hemoglobin A1c by HPLC. In the examined group 67 persons were statins users. Mean (SD) age of patients was 59.1 (11.1) years, HbA1c 8.6 (2.4%). Mean (SD) values of serum LDL-cholesterol were 2.6 (1.16) mmol/l and of serum PCSK9 255,4 (106,97) ng/ml. Patients treated with statins were older and had lower LDL-C: 2.38 (1.1) vs. 2.96 (1.2) mmol/l, p<0.05, apoB 100: 81.8 (20.6) vs. 99.7 (29.8) mg/dl, p<0.001 and higher waist circumference p<0,05. We did not observe differences in PCSK9 between patients receiving and not receiving statins: 248.6 (99.9) vs. 272.1 (112.5) ng/ml, p=0.2488 respectively. Median (IR) of apo B48 was lower in statin treated patients: 3529 (2370) vs. 5136.5 (3424.5) ng/dl, p<0.01. Correlation analysis revealed in both groups of patients significant correlation between PSCK9 and total cholesterol, LDL-C, triglycerides, PTX3 and apo B100. In statin users PCSK9 concentration was associated with apo A1 (p<0.001) and apo B48 (p<0.05). In patients not taking statins negative correlation between HbA1c and PCSK9 was found (p <0.05). The results indicate, that circulating PCSK9 is significantly associated with atherogenic markers - LDL-C, apo B 100, triglycerides and inflammation marker PTX3; in statin users also with apo A1, a negative risk marker, and apo B 48. In patients not taking statins significant negative association between PCSK9 and HbA1c was noted. These associations might be of value in understanding the pathways involved in atherosclerosis and dyslipidemia, mediated by PCSK9.
M. Walus-Miarka: None. M. Kapusta: None. E. Kawalec: None. B. Idzior-Walus: None.