scholarly journals From lipoprotein apheresis to proprotein convertase subtilisin/kexin type 9 inhibitors: Impact on low-density lipoprotein cholesterol and C-reactive protein levels in cardiovascular disease patients

2018 ◽  
Vol 25 (17) ◽  
pp. 1843-1851 ◽  
Author(s):  
Maria G Zenti ◽  
Anna Altomari ◽  
Maria G Lupo ◽  
Margherita Botta ◽  
Enzo Bonora ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Proprotein Convertase ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein Apheresis ◽  
Reactive Protein ◽  
Cholesterol Levels

In this observational study, we compared the effect of lipoprotein apheresis and evolocumab or alirocumab on levels of lipoprotein cholesterol, triglycerides and inflammatory markers (C reactive protein and interleukin 6) in cardiovascular patients ( n = 9). Patients were monitored during the last year of lipoprotein apheresis followed by six months of treatment with proprotein convertase subtilisin/kexin type 9 inhibitors. The biochemical parameters were determined pre- and post- every apheresis procedure for 12 months and then after one, three and six months of treatment with evolocumab (140 mg every two weeks [Q2W]) or alirocumab (75 mg or 150 mg every two weeks [Q2W]). Lipoprotein apheresis significantly reduced low-density lipoprotein cholesterol levels from 138 ± 32 mg/dl to 46 ± 16 mg/dl ( p < 0.001), with an inter-apheresis level of 114 ± 26 mg/dl. Lipoprotein(a) was also reduced from a median of 42 mg/dl to 17 mg/dl ( p < 0.01). Upon anti-proprotein convertase subtilisin/kexin type 9 therapy, low-density lipoprotein cholesterol levels were similar to post-apheresis (59 ± 25, 41 ± 22 and 42 ± 21mg/dl at one, three and six months, respectively) as well as those of lipoprotein(a) (18 mg/dl). However, an opposite effect was observed on high-density lipoprotein cholesterol levels: –16.0% from pre- to post-apheresis and +34.0% between pre-apheresis and proprotein convertase subtilisin/kexin type 9 inhibitors. Apheresis significantly reduced high-sensitivity C-reactive protein levels (1.5 ± 1.2 mg/l pre-apheresis to 0.6 ± 0.6 mg/l post-apheresis), while no changes were found upon proprotein convertase subtilisin/kexin type 9 mAbs administration. In conclusion, our study demonstrated that, by switching from lipoprotein apheresis to anti-proprotein convertase subtilisin/kexin type 9 therapies, patients reached similar low-density lipoprotein cholesterol and lipoprotein(a) levels, increased those of high-density lipoprotein cholesterol, and showed no changes on high-sensitivity C-reactive protein.

scholarly journals Relationship between C-reactive protein and features of the metabolic syndrome in military pilots in the Serbia and Montenegro

2005 ◽  
Vol 62 (11) ◽  
pp. 811-819
Author(s):  
Aleksandra Jovelic ◽  
Goran Radjen ◽  
Stojan Jovelic ◽  
Marica Markovic
Keyword(s):  
Metabolic Syndrome ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Reactive Protein

Background/Aim. C-reactive protein is an independent predictor of the risk of cardiovascular events and diabetes mellitus in apparently healthy men. The relationship between C-reactive protein and the features of metabolic syndrome has not been fully elucidated. To assess the cross-sectional relationship between C-reactive protein and the features of metabolic syndrome in healthy people. Methods. We studied 161 military pilots (agee, 40?6 years) free of cardiovascular disease, diabetes mellitus and active inflammation on their regular annual medical control. Age, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, fasting glucose, glycosylated hemoglobin, blood pressure, smoking habit, waist circumference and body mass index were evaluated. Plasma C-reactive protein was measured by the immunonephelometry (Dade Behring) method. Metabolic syndrome was defined according to the National Cholesterol Education Program Expert Panel. Results. The mean C-reactive protein concentrations in the subjects grouped according to the presence of 0, 1, 2 and 3 or more features of the metabolic syndrome were 1.11, 1.89, 1.72 and 2.22 mg/L, respectively (p = 0.023) with a statistically, significant difference between those with 3, and without metabolic syndrome (p = 0.01). In the simple regression analyses C-reactive protein did not correlate with the total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, body mass index and blood pressure (p > 0.05). In the multiple regression analysis, waist circumference (? = 0.411, p = 0.000), triglycerides to high density lipoprotein cholesterol ratio (? = 0.774, p = 0.000), smoking habit (? = 0.236, p = 0.003) and triglycerides (? = 0.471, p = 0.027) were independent predictors of C-reactive protein. Conclusions. Our results suggested a cross-sectional independent correlation between the examined cardiovascular risk factors as the predominant features of metabolic syndrome and C-reactive protein in the group of apparently healthy subjects. The lack of correlation of C-reactive protein with the total cholesterol and low density lipoprotein cholesterol in our study may suggest their different role in the process of atherosclerosis and the possibility to determine C-reactive protein in order to identify high-risk subjects not identified with cholesterol screening.

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