Dyslipidemia is one of the most common diseases worldwide. It is known as one of the most dangerous “silent killer” due to its late, and usually fatal manifestations. It has a strong association with atherosclerosis [1]. Our study investigates the association between the development of atherosclerosis and the thrombotic risk observed in patients with dyslipidemia. This association is demonstrated by analysis of various lipoprotein particles, including atherogenic and non-atherogenic, and their relation with homocysteine as a marker of thrombosis.
Patients undergoing personalized weight reduction and lifestyle changes program were recruited at the cardiology ambulance of the 1st Department of Internal Medicine, Pavol Jozef Šafárik University in Košice, Slovakia. The selected individuals were divided into the study group (n = 6, average age 36 ± 8 years) and control group (n = 6, average age 31 ± 6 years). The analysis of the cholesterol in low-density lipoprotein and high-density lipoprotein sub-particles was performed by Lipoprint® Lipoprotein Subfractions Testing System. Statistical analysis was performed using SPSS Statistics 22 (IBM).
Dyslipidemic patients included in the study group had total cholesterol (TC) values above 5 mmol/L (average 6.25 ± 0.77 mmol/L) and low-density lipoprotein-cholesterol (LDL-C) above 3 mmol/L (average 4.00 ± 0.68 mmol/L). Control group consisted of individuals without dyslipidemia. Homocysteine values varied widely in both groups.
Pearson's statistical analysis showed that the correlation between homocysteine concentration and the levels of TC, triacylglycerol, LDL-C and high-density lipoprotein-cholesterol (HDL-C) was not significant, but we did not even find the expected positive correlation between homocysteine and TC and LDL-C value[2]. Cholesterol in subfractions appears to be a more sensitive marker. Cholesterol in the atherogenic fractions like in VLDL, IDL A, B, C, and LDL 3 showed a positive correlation with homocysteine, while less atherogenic or anti-atherogenic fractions like LDL 1, 2, HDL 2, and 3 were reciprocally correlated with homocysteine. Spearman's non-parametric analysis in dyslipidemic patients showed a statistically significant positive correlation between homocysteine and the cholesterol in the large subfraction HDL 1 (Spearman's rho 0.89, p = 0.019). Spearman's non-parametric analysis in the control group individuals showed a statistically significant positive correlation between homocysteine and the cholesterol in the intermediate subfractions HDL 6 and 7 (Spearman's rho 0.89, p = 0.019 for both). The divergent regression trends between homocysteine and the large HDL sub-particles 1, 4, 6, and 7 observed in dyslipidemic and non-dyslipidemic patients suggest a modification of these particles during abnormal lipid metabolism in dyslipidemia.
The first results of this project indicate the importance of monitoring the relation of homocysteine concentration and the cholesterol level in lipoprotein subfractions in a large scale. Our results are aimed to assist in the management, whether in the diagnosis or in the treatment of dyslipidemic patients, making it more personal.
Key words: dyslipidemia, cholesterol, lipoprotein, homocysteine
This work was supported by grant no. VEGA 1/0910/16.
Comments to the work
Hello, very useful work you did. However, I want to point your attention on terminology, I do not agree on indicating DISLIPIDEMIA as a disease itself, it is the symptom of the diseases (e.g. diabetes mellitus). Second question is about drawing your conlusions: even the correleations between HCy and other measured parameters (TC, TGA, LDL-C, HDL-C) were not significant you have emphasized "the importance of monitoring the relation of homocysteine concentration and the cholesterol level in lipoprotein subfractions in a large scale." So on what fact is based that outcome? I would recommend to refine that judgment at the end of the abstract or weaken that formulation respectively. Best regards, ZB
Re: Comments to the work
Good morning, thank you for your contribution.
On the first hand, I do not agree on saying that dyslipidemia is a symptom of a disease, mostly it is considered itself a disease. As you mentioned, according to terminology, a disease is defined as a disorder of structure or function in a human, animal, or plant, especially that produces specific symptoms or that affects a specific location and is not simply a direct result of a physical injury. If we compare it with the definition of symptom, which it is understood as a physical or mental feature, which is regarded as indicating a condition of disease, particularly such as feature that is apparent to the patient. On ICD-10, all different forms of dyslipidemia are described as Disorders of lipoprotein metabolism and other lipidemias (E-78), so does many other literature, which they include the different clinical manifestations (signs and symptoms) of each specific type of disorder.
On the other hand, when we speak about monitoring the results in a large scale is based on the fact that the sample is too small, thus the results cannot be extrapolated or generalized to the population. The results of our study should be confirmed by performing more studies and with larger samples. In addition, the statement is supported by the fact that we promote the management and treatment of the patient from a more personalized point of view, because many healthy patients may have already risk of dyslipidemia complications, while dyslipidemic patients may have lower risk.