RESUMO
INTRODUCTION: Atherosclerosis might diminish the nutrient supply to intervertebral discs (IVD), leading to disc herniation. Therefore, there is interest in determining the possible association between the blood lipid profile and lumbar disc herniation (LDH). We aimed to evaluate the association between blood lipids and LDH in a homogeneous group of patients, controlling for age- and sex-specific effects. MATERIAL AND METHODS: This is a case-control study which consisted of 100 individuals (mean age: 41.25 ±9.09; 50 men and 50 women), classified into two groups, as follows. Group I (G-I) consisted of 50 patients who underwent surgery for symptomatic LDH, while group II (G-II) consisted of 50 patients with nonspecific complaints of a headache, but with no previous history of back and/or leg pain, recruited among patients admitted to the outpatient clinic at the time of the study, and whose age and sex were matched to the study group. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose, and hemoglobin A1c levels were measured. The TC/HDL-C ratio was calculated. Blood pressure, waist circumference, body mass index, and the history of smoking were included in the analysis. RESULTS: The mean values of the TC, TG, LDL-C, HDL-C levels and TC/HDL-C ratio were 198.38, 132.76, 131.9, 40.38 mg/dl and 5.09, respectively. No statistically significant relationship between the blood lipid profile and LDH was identified in this population. CONCLUSIONS: Blood lipid levels in this young adult Turkish population did not predict LDH, and may not be a leading cause of IVD ischemia and IVD degeneration.
RESUMO
The role of sialic acid (SA) in the pathogenesis of atherosclerosis and as a predictor of cardiovascular events has attracted much attention in recent years. However, most studies investigating the role of total and lipid-bound sialic acids (TSA and LSA) in the pathogenesis of atherosclerosis lack information on the reason for the elevated SA concentrations in coronary heart disease and myocardial infarction. Since the inflammation-sensitive proteins are glycoproteins with SA residues, an increase in their levels due to some type of acute-phase reaction or inflammation could be responsible for the elevated TSA levels in acute myocardial infarction (AMI). Elevated serum SA levels might also be due to either shedding or secretion of free SA from the cell or cell membrane surface if neuraminidase levels are increased, or to the release of cellular SA-containing glycolipids and/or glycoproteins into plasma from myocardial cells after AMI. The aim of the present study was to investigate both the possible role of SA-rich inflammation-sensitive proteins and the cell damage due to elevated serum TSA levels in AMI. A possible role of serum LSA as an indicator of the shedding or secretion of SA from the cell or cell membrane surface in AMI was also evaluated. The study included 38 subjects with AMI and 32 healthy volunteers. Serum TSA and LSA were determined using the methods of Warren and Katopodis, respectively. The concentrations of serum SA-rich inflammation-sensitive proteins, namely alpha1-antitrypsin, alpha2-macroglobulin and ceruloplasmin were determined immunoturbidimetrically. Our data showed that: a) mean levels of serum TSA and LSA and SA-rich inflammation-sensitive proteins in patients with AMI were significantly increased; and b) there was a significant positive correlation between TSA and LSA and alpha1-antitrypsin in patients with AMI. Since the transfer of free SA to lipoproteins is required for an increase in serum LSA levels, and free SA for this transfer can be provided by the secretion of SA from the cell, it is obvious that the shedding or secretion of SA from the cell membrane surface or release of cellular SA from cells into the bloodstream due to cell damage after AMI also occur after AMI. As a result, we can report that either the shedding or secretion of SA from the cell or cell membrane surface and the increased output of SA-rich inflammation-sensitive proteins may together be responsible for the elevated TSA levels in AMI.