Low-density Lipoprotein In Patients Research Articles

Oxidised low-density lipoprotein and antibodies against oxidised low-density lipoprotein in patients with antiphospholipid syndrome.

Recurrent thrombosis is one of the main clinical features of antiphospholipid syndrome (APS), and recent studies revealed that APS shares similar pathophysiological mechanisms with atherosclerosis. Oxidised low-density lipoprotein (OxLDL) and antibodies against OxLDL (anti-OxLDL) are involved in the development of atherosclerosis. This study aims to investigate the clinical significance of OxLDL and anti-OxLDL in APS patients. One hundred and seventy APS patients and 39 healthy controls (HC) were enrolled. Clinical and laboratory data were collected from Clinical Data Center of Peking University People's Hospital. OxLDL and anti-OxLDL were detected using enzyme-linked immunosorbent assay. Among the 170 APS patients, 106 had isolated thrombotic APS. Compared with HC, APS patients exhibited higher titres of OxLDL [413.86 (220.11-853.67) ng/mL vs. 45.54 (0-105.98) ng/mL, p<0.001] and anti-OxLDL [107.62 (75.68-174.18) U/L vs. 44.13 (18.44-79.76) U/L, p<0.001]. Also, APS patients exhibited a higher positivity rate for OxLDL (88.2% vs. 5.1%, p<0.001) and anti-OxLDL (84.1% vs. 36.5%, p<0.001) compared to HC. APS patients with elevated levels of OxLDL had a higher rate of LAC positivity (68.0% vs. 45.0%, p=0.042). Furthermore, APS patients with positive anti-OxLDL demonstrated a higher occurrence of venous thrombosis (46.2% vs. 18.5%, p=0.008) and a lower rate of Coomb's test positivity (52.6% vs. 76.2%, p=0.049). Multivariate logistic regression revealed that anti-OxLDL positivity (OR 12.424, 95%CI 1.108-139.330, p=0.041) were risk factors for venous thrombotic APS. This study indicates that the presence of anti-OxLDL may serve as potential markers for venous thrombosis in APS patients. OxLDL and anti-OxLDL may function as valuable biomarkers for monitoring APS.

Increased circulating levels of malondialdehyde-modified low-density lipoprotein in patients with coronary microvascular dysfunction

Coronary microvascular dysfunction (CMD) is associated with angina symptoms and adverse clinical outcomes in patients without obstructive coronary artery disease (CAD). Malondialdehyde-modified low-density lipoprotein (MDA-LDL) is reportedly a marker of the initiation and acceleration of epicardial coronary atherosclerosis. However, its impact on CMD remains unclear. We aimed to investigate the relationship between CMD and MDA-LDL levels. This study included 95 patients who did not receive lipid-lowering medications and had no obstructive CAD. Obstructive CAD was defined as >50 % diameter reduction on coronary angiography or fractional flow reserve of ≤0.80. We retrospectively analyzed coronary flow reserve (CFR), index of microcirculatory resistance (IMR), and MDA-LDL levels. CMD was defined as either CFR <2.0 or IMR ≥25. CMD was observed in 29 (31 %) patients. MDA-LDL levels were significantly higher in patients with CMD than in those without CMD (124.8 ± 37.6 vs. 95.3 ± 29.5 U/L; p < 0.01). Univariable logistic regression analysis indicated a significant relationship between CMD and MDA-LDL levels (odds ratio (OR): 1.03; p < 0.01). In the multivariable model, MDA-LDL levels were significantly associated with CMD (OR: 1.02; p < 0.01). Regression analysis showed a significant correlation between MDA-LDL levels and CFR (r = -0.42, p < 0.01) and IMR (r = 0.35, p < 0.01). In the multiple regression analysis, MDA-LDL levels were independently associated with CFR (β = -0.30, p < 0.01) and IMR (β = 0.26, p = 0.02). MDA-LDL levels were associated with CMD in patients without obstructive CAD.

Effects of traditional Chinese exercise on vascular function in patients with Alzheimer's disease: A protocol for systematic review and network meta-analysis of randomized controlled trials.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with an insidious onset, usually characterized by memory impairment, visual-spatial skill impairment, executive dysfunction and personality behavioral changes. Studies have confirmed that vascular dysfunction may precede AD pathological changes and can present as vascular malformations, atherosclerosis, and impaired self-regulation, and can affect oxidative stress and amyloidosis. Therefore, it is important to improve or prevent vascular dysfunction in AD patients. Regular exercise can effectively inhibit the production of reactive oxygen species during the occurrence of AD and can improve the reduction of cerebral blood flow due to AD. Previous studies have shown that exercise can achieve superior clinical results in improving vascular function in AD patients. Therefore, we hypothesize that traditional Chinese exercises (TCEs) may have a good clinical effect in improving vascular function in patients with AD. We will search "PubMed," "the Cochrane Library," "Embase," "Web of Science," "CINAHL," "ProQuest Dissertations and Theses," and "ProQuest-Health & Medical Collection," "CNKI," "SinoMed," "VIP," and "Wanfang Data" to find randomized controlled trials of the effects of TCEs on AD vascular function from the creation of the database to the present, including at least 1 indicator in carotid intima-media thickness (cIMT), middle cerebral artery mean flow velocity (MFV), blood indicators [Heme Oxidase-1 (HO-1), angiopoietin I (Ang I), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor, matrix metalloproteinase-9 (MMP-9)], and arterial stiffness [(Ankle Brachial Index (ABI), pulse wave velocity (PWV)]. For the included literature, Excel 2019 will be used for data extraction and collection. For the indicators that can be netted for network meta-analysis, Surface Under the Cumulative Ranking for each exercise modality will be calculated with the help of Stata 16.0 and rank, where the higher the SUCRA score, the higher the ranking. For the indicators that cannot be netted, Review Manager 5.4 will be used for meta-analysis will be performed to evaluate the improvement effect of TCEs on AD patients. This meta-analysis will further determine the efficacy and safety of TCEs on vascular function in AD patients. In this study, randomized controlled trials of the effects of TCEs on vascular function in AD patients will be selected to provide evidence-based medical evidence for promoting the application of TCEs by observing the order of advantages and disadvantages of various exercise modalities through network meta-analysis.

Клинико-лабораторные параллели изменений углеводного обмена при тиреопатиях

The number of people suffering from endocrine disorders is increasing. The interaction between diseases such as diabetes and various thyroid diseases is of some interest. This article presents the results of investigating the effect of different thyreopathies on carbohydrate metabolism and lipid profile, which may have some significance for the possible management tactics of these patients. Objective. To demonstrate clinical and laboratory features of carbohydrate metabolism disorders in different thyroid diseases. Patients and methods. Patients were examined during the period 2021–2022, among them were patients with thyroid diseases: hypothyroidism, thyrotoxicosis, endemic goiter without dysfunction. A total of 257 patients were examined, including 96 patients with hypothyroidism, 29 with thyrotoxicosis, and 93 with endemic goiter, as well as 38 patients without thyroid diseases (the control group). Results and discussion. When comparing the results of plasma glucose and glycated hemoglobin (HbA1c) tests for all groups, a significant increase in their levels was revealed. Patients with hypothyroidism were found to have higher cholesterol levels compared to the control group, and significant differences were also established in the evaluation of low-density lipoproteins in patients with endemic goiter. Conclusion. Various thyroid diseases lead to certain metabolic disorders, namely, deterioration of carbohydrate metabolism and a slight deterioration of lipid profile. Key words: thyroid gland, carbohydrate metabolism, endemic goiter, hypothyroidism, thyrotoxicosis, euthyroidism, lipid metabolism

Antibodies to oxidized low-density lipoproteins in patients with syphilis

Antibodies to oxidized low-density lipoproteins in patients with syphilis

Inflammasome activation mediated by oxidised low-density lipoprotein in patients with sleep apnoea and early subclinical atherosclerosis.

Atherosclerosis is a common comorbidity of obstructive sleep apnoea (OSA) patients, caused by the interaction of dyslipidaemia and systemic inflammation. The OSA pro-inflammatory response is mediated by NLRP3 inflammasome activation, which requires a priming signal mediated by intermittent hypoxia (IH) and an activation signal provided by soluble stimulus present in plasma. Our objectives were to study oxidised low-density lipoprotein (oxLDL) expression in OSA patients with or without early subclinical atherosclerosis (eSA) as well as its contribution to NLRP3 activation and tissue factor (TF) release. We analysed oxLDL, key components of the NLRP3 inflammasome cascade and TF in plasma and monocytes from OSA patients and non-apnoeic subjects, with or without eSA as determined by increased carotid intima-media thickness without the appearance of atherosclerotic plaques. The oxLDL contribution to NLRP3 inflammasome activation was assessed using in vitro models. High levels of oxLDL were identified in plasma from OSA patients, particularly in those with eSA, as well as an overexpression of NLRP3 cascade components and TF. Furthermore, in vitro models showed that both oxLDL and plasma from OSA patients with eSA act synergistically with IH as a priming and activation signal of NLRP3 that enhances the inflammatory response, pyroptosis and TF release. OSA patients with eSA exhibit NLRP3 activation by IH and the presence of oxLDL capable of releasing TF, constituting a pathway for the interaction between dyslipidaemia and systemic inflammation in the development of atherosclerotic lesions.

Effect of JAK inhibitors on high- and low-density lipoprotein in patients with rheumatoid arthritis: a systematic review and network meta-analysis.

Janus kinase (JAK) inhibitors are a new class of medication for treatment of rheumatoid arthritis (RA), and such inhibitors alter levels of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) in RA patients. However, the extent of such changes has not been systematically reviewed. A systematic review and network meta-analysis was performed on randomized trials in RA patients in response to JAKi identified from Pubmed, Medline, Embase, and Cochrane Controlled Trials Register. The primary outcome was mean change of HDL-C and LDL-C from baseline. Mean treatment differences and the rank of the effect of various JAKi on HDL-C and LDL-C were estimated. Based on data from 18 unique studies involving five approved JAK inhibitors and 6697 RA patients (JAKi = 3341, placebo = 3356), such inhibitors led to a mean increase of 8.11mg/dl (95% CI 6.65-9.58, I2 = 82%) in HDL levels from baseline, and a mean increase of 11.37mg/dl (95% CI 7.84-14.91, I2 = 88%) in LDL levels from baseline. Cardiovascular disease risk did not differ significantly between patients who received JAK inhibitors or those who received placebo or active agents. Our analysis suggests that, at their recommended doses, all five JAK inhibitors lead to an increase in HDL and LDL levels in RA patients. Further long-term research is required to extend these results and understand whether changes in lipid levels in RA patients can affect cardiovascular risk. Key Points • This is the first systematic review and NMA examining the effect of all five clinically approved JAK inhibitors on lipid levels in RA patients. • Recommended doses of JAK inhibitors used for the treatment of RA patients can induce a significant increase in HDL and LDL levels. • Indirect pairwise comparisons suggest that only upadacitinib and peficitinib have significantly different ability to induce LDL change in RA patients.

Pasta Supplemented with Opuntia ficus-indica Extract Improves Metabolic Parameters and Reduces Atherogenic Small Dense Low-Density Lipoproteins in Patients with Risk Factors for the Metabolic Syndrome: A Four-Week Intervention Study.

Food supplementation with Opuntia ficus-indica (OFI) has been associated with a significant reduction in total cholesterol, body fat, hyperglycemia and blood pressure. Since OFI may also have antioxidant and anti-atherogenic properties, we hypothesized that its supplementation might reduce atherogenic lipoproteins, including small, dense low-density lipoproteins (sdLDL). Forty-nine patients (13 men and 36 women, mean age: 56 ± 5 years) with one or two criteria for the metabolic syndrome weekly consumed 500 g of pasta supplemented with 3% OFI extract (30% of insoluble polysaccharides with high antioxidant power) for 1 month. The full LDL subclass profile was assessed by gel electrophoresis (Lipoprint, Quantimetrix, Redondo Beach, CA, USA). After 1 month of pasta supplementation, waist circumference (p = 0.0297), plasma glucose (p < 0.0001), triglycerides (p = 0.0137), plasma creatinine (p = 0.0244), urea and aspartate transaminase (p < 0.0001 for each) significantly decreased. A percentage increase in larger, less atherogenic LDL-1 (p = 0.0002), with a concomitant reduction in smaller, denser LDL-2 (p < 0.0001) and LDL-3 (p = 0.0004), were found. LDL-4 and-5 decreased, although not significantly. This is the first intervention study suggesting that pasta enriched with an OFI extract may have beneficial effects on some metabolic parameters and the LDL particle sizes, reducing atherogenic sdLDL. Future studies will help to establish if these findings impact cardiovascular outcomes.

Effects of Pitavastatin on Lipoprotein Subfractions and Oxidized Low-density Lipoprotein in Patients with Atherosclerosis.

It has been demonstrated that pitavastatin can significantly reduce low-density lipoprotein (LDL) cholesterol (LDL-C), but its impact on lipoprotein subfractions and oxidized low-density lipoprotein (oxLDL) has not been determined. The aim of the present study was to investigate the potential effects of pitavastatin on subfractions of LDL and high-density lipoprotein (HDL) as well as oxLDL in untreated patients with coronary atherosclerosis (AS). Thirty-six subjects were enrolled in this study. Of them, 18 patients with AS were administered pitavastatin 2 mg/day for 8 weeks and 18 healthy subjects without therapy served as controls. The plasma lipid profile, lipoprotein subfractions and circulating oxLDL were determined at baseline and 8 weeks respectively. The results showed that pitavastatin treatment indeed not only decreased LDL-C, total cholesterol (TC), triglycerides (TG) and apolipoprotein B (ApoB) levels, and increased HDL cholesterol (HDL-C), but also reduced the cholesterol concentration of all of the LDL subfractions and the percentage of intermediate and small LDL subfractions. Meanwhile, pitavastatin could decrease plasma oxLDL levels. Furthermore, a more close correlation was found between oxLDL and LDL-C as well as LDL subfractions after pitavastatin treatment. We concluded that a moderate dose of pitavastatin therapy not only decreases LDL-C and oxLDL concentrations but also improves LDL subfractions in patients with AS.

THU347 - The electronegative low-density lipoprotein in patients with chronic hepatitis C infection

THU347 - The electronegative low-density lipoprotein in patients with chronic hepatitis C infection

Circulating levels of oxidized low-density lipoprotein in patients with obstructive sleep apnea: a systematic review and meta-analysis.

Obstructive sleep apnea (OSA) is associated with an increased risk of developing atherosclerotic cardiovascular disease (ASCVD). Patients with OSA have increased levels of oxidative stress and several studies have shown higher levels of oxidative stress markers. Oxidized-LDL (Ox-LDL) is an important risk factor for ASCVD and a number of studies have measured its levels in patients with OSA, though results from these studies are conflicting. This meta-analysis aimed to reassess circulating levels of Ox-LDL in patients with OSA in comparison with controls. Studies evaluating Ox-LDL levels in patients with OSA and controls were explored in databases of PubMed, EMBASE, Scopus, and Web of Science. Two authors independently performed the search from January 1990 to February 2019. Two authors independently screened the studies according to title, abstract, and full text. In addition, the Newcastle-Ottawa Quality Assessment Scale was utilized to evaluate the quality of the studies. The impact of OSA on Ox-LDL levels was determined using the random effects model. Of 195 articles retrieved, 98 were duplicates, 49 were excluded by title, 20 excluded by abstract, and 22 by full texts. Six eligible studies were included in the meta-analysis. Pooled analysis demonstrated that Ox-LDL increased in patients with OSA compared with controls. In addition, subgroup analysis revealed that studies matching age or BMI between OSA patients and controls showed no significant difference between patients with OSA and healthy controls, while unmatched studies had higher levels of Ox-LDL in patients with OSA in comparison with controls. This study demonstrated higher circulating concentrations of Ox-LDL in patients with OSA. However, no significant difference was found in studies in which patients and controls were matched for age and BMI, suggesting the involvement of these two confounding factors as a cause for elevated concentrations of circulating Ox-LDL in patients with OSA.

Study of the correlations between serum iron and Hepcidin with some biochemical variables in hyperlipidemia of elderly males and females in Salah Al Deen Province

The present research was designed to investigate the role of the relationship between Iron and hepcidin hormon with some biochemical variables in patients with hyperlipidemia in both males and females elderly in Salah al-Din governorate. The study included 40 individuals distributed into two groups. The first group was the control group, which included 20 human males and females and the second group included 20 patients (10 males and 10 females) whose ages ranged between (60-79) years. Blood was collected to estimate the hepcidine hormone, iron, cholesterol, triglycerides, high-density lipoproteins, low-density lipoproteins, and very low-density lipoproteins. The results showed a significant increase in (P≥ 0.05) in the concentration of iron and hepcidin hormone, cholesterol, triglycerides, low-density lipoproteins and very low-density lipoproteins while showed a significant decrease in (P≥ 0.05) in the concentration high-density lipoproteins in patients Males and females hyperlipidemia compared to the control group. The results also indicated a direct correlation relationship between iron and hepcidine hormone and studied variables cholesterol, triglycerides, low-density lipoproteins and very low-density lipoproteins in patients compared to the control group. It is concluded through the results that iron and the hepcidin hormon may have an important role in the development of cardiovascular diseases in hypertensive patients in elderly both males and females.

IFN Regulatory Factor 1 Mediates Macrophage Pyroptosis Induced by Oxidized Low-Density Lipoprotein in Patients with Acute Coronary Syndrome.

Background Atherosclerosis (AS) is recognized as a chronic inflammatory disease. It is caused by the interaction between inflammatory cells such as macrophages, dendritic cells, and lipoproteins. Evidence has revealed that macrophage pyroptosis in lesion contributes to the formation of the necrotic core and thinning of the fibrous cap, which plays crucial roles in the onset of acute coronary syndrome (ACS). IFN regulatory factor 1 (IRF-1) is a pleiotropic transcription factor involved in various immune processes and cell death. We propose that IRF-1 may be implicated in macrophage pyroptosis in the pathogenesis of AS and ACS. Methods Patients with stable angina, unstable angina, acute myocardial infarction, and clinical presentation of chest pain were enrolled. The expression of IRF-1 in human PBMC-derived macrophages was analyzed. Then, overexpression and inhibition of IRF-1 was performed in macrophages from patients with ACS to explore the possible role and mechanism of IRF-1 involvement in macrophage pyroptosis. Results The expression of IRF-1 in macrophages was upregulated in ACS patients. The overexpression or inhibition of IRF-1 effectively modulated caspase-1 activation, as well as macrophage lysis, expression of gasdermin D-N (GSDMD-N), production of IL-1β and IL-18, and activation of NLRP3-ASC inflammasome, which were all inhibited by caspase-1 inhibitor. Further experiments revealed that pyroptosis and the downstream inflammatory response in AS induced by IRF-1 is a process that is dependent on reactive oxygen species (ROS) generation. Conclusion Our observations suggest that IRF-1 potently activates ox-LDL-induced macrophage pyroptosis and may play an important role in AS and ACS.

PCSK9 Inhibitor causes a decrease in the level of oxidatively modified low-density lipoproteins in patients with coronary artery diseases.

We study the dynamics of oxidatively modified low-density lipoprotein (ox-LDL) content in blood plasma, as well as changes in the activity of key antioxidant enzymes such as Se-containing glutathione peroxidase (GSH-Px) Cu,Zn-superoxide dismutase (SOD) and catalase in erythrocytes of patients with coronary artery disease during treatment with PCSK9 inhibitor (ewolocumab). The study included 9 men (59 ± 10 years) with coronary artery disease with atherosclerotic lesion at least one main coronary artery according to coronary angiography. Patients took standard therapy before taking the study, everyone took the maximum tolerated dose of statins. Since the target cholesterol levels of low-density lipoprotein cholesterol (LDL-C) were not achieved during the statin therapy, patients were prescribed lipid-lowering therapy with the inclusion of the inhibitor PCSK9-emocoucumab from Amgen 420 mg once a month. The content of lipid metabolism indices was determined by standard biochemical methods. The level of ox-LDL in the blood plasma was determined by the immunochemical method. The activity of antioxidant enzymes was determined in blood erythrocytes using biochemical techniques. Cholesterol-lowering drug of the new type - inhibitor protein convertase subtilisin/kexin type 9 (PCSK9) evolocumab (Amgen) not only effectively lowers the level of cholesterol in low density lipoprotein (LDL), but also significantly reduces the content of oxdatively modified LDL in blood plasma. Unlike statins, the inhibitor of PCSK9 does not cause a decrease in the activity of antioxidant enzymes of the blood. PCSK9 inhibitor has no effect on the parameters of oxidative stress.

Effect of Vitamin E and omega 3 fatty acids in type 2 diabetes mellitus patients.

Diabetes mellitus (DM) and its complications have been implicated in hyperglycemia-induced oxidative stress. Antioxidants can improve glycemic control, lipid profile, and cognitive functions. We assessed the effect of Vitamin E and omega 3 fatty acids (OFA) on the above parameters. One hundred patients with type 2 DM receiving metformin 500 mg and glimepiride 1 mg were randomized to receive add-on therapy of Vitamin E 400 mg or OFA once daily for 12 weeks and the third group served as control. Fasting blood sugar (FBS), postprandial blood sugar (PPBS), glycated hemoglobin (HbA1c), body mass index (BMI), waist-hip ratio (WHR), lipid profile, and mini-mental state examination were done at baseline and 12 weeks. Eighty-seven patients completed the study. A significant reduction in FBS, PPBS, and HbA1c was observed in all the three groups at 12 weeks. There was significant reduction in total cholesterol and triglycerides (TG) in patients receiving either of the antioxidants and also significant reduction in low-density lipoprotein in patients receiving OFA at 12 weeks compared to baseline. BMI and WHR were significantly increased in control group. Intergroup analysis showed that in patients receiving Vitamin E and OFA, the reduction of FBS, PPBS, and HbA1c were similar. The patients receiving OFA had significant reduction in TG compared to control. There was no significant effect on cognitive function. Vitamin E and OFA had beneficial effects on lipid profile and anthropometric measurements; however, the glycemic control was similar to the patients in control group.

Postprandial Clearance of Oxidized Low-Density Lipoprotein in Patients with Stroke Due to Atherosclerosis

Oxidized low-density lipoprotein (OxLDL) is a contributor to atherosclerosis development. OxLDL formation increases in the postprandial state due to oxidative stress in subjects with coronary artery disease (CAD) and diabetes, but has not been studied in patients with atherosclerotic stroke. We aimed to determine differences in postprandial OxLDL in patients with atherosclerotic stroke compared to stroke from other causes. Patients with ischemic stroke but no history of CAD (n = 42) were enrolled and categorized by stroke subtype as extracranial atherosclerosis (EC), n = 12; intracranial atherosclerosis (IC), n = 16; or other cause, n = 14. After fasting overnight, subjects consumed a standardized fat meal. OxLDL levels were measured at t = 0 and t = 4 hours postprandial using enzyme-linked immunosorbent assay. Comparisons between the mean changes in OxLDL between the groups were performed using the analysis of variance procedure. The IC group had the highest mean baseline level of OxLDL and the greatest decline during the postprandial period. There was a trend toward a difference in the mean change in OxLDL between the 3 groups (P = .0553). Subjects with atherosclerotic stroke (EC and IC groups) had higher fasting OxLDL and had a significant decline in OxLDL compared to those with stroke from other causes (P = .0164). Subjects with stroke due to atherosclerosis, particularly intracranially, demonstrated high fasting OxLDL and a decline in OxLDL during the postprandial period. This decline in OxLDL may indicate an accelerated clearance of OxLDL resulting from meal-induced oxidative stress.

Effects of supervised structured aerobic exercise training program on high and low density lipoprotein in patients with type II diabetes mellitus.

Background and Objective:Hyperlipidemia and dyslipidemia are very common conditions among patients with Type-2 diabetes mellitus (T2DM) and associated with increased risk of coronary heart diseases. Physical activity and exercises along with medical management and dietary plan are common strategies to use for the management of deranged lipid profile in patients with T2DM. We aimed to determine the effects of supervised structured aerobic exercise training (SSAET) program on high and low density lipoprotein in patients with T2DM.Methods:This randomized control trial study was conducted at Riphah Rehabilitation Research Centre (RRRC), Pakistan Railway General Hospital (PRGH) Rawalpindi from 1st January 2015 to 30th March 2016. The inclusion criteria was Type-2 diabetes patients of both gender aged between 40 to 70 years. Patients with severe complications like coronary artery diseases (CAD), and other serious complications like diabetic foot, and severe knee and hip osteoarthritis (OA) were excluded from the study. A total of 195 patients diagnosed with T2DM were screened out and 102 were selected for the study as per the inclusion criteria. All participants were randomly assigned into two groups, experimental ‘A’ (n=51) and control ‘B’ (n=51). Patients in group A were treated with SSAET program of 25 weeks at 3 days a week in addition to routine medical management, while patients in Group-B were on their routine medications and dietary plan. Serum LDL, and HDL were tested at baseline and after 25 weeks. The data was analysed through SPSS 20.Results:Mean and standard deviation of LDL in group A (n=51) was 118.56±19.17 (pre) and 102.64±13.33 (post), while the mean and standard deviation for Group-B (n=51) was 116.50±18.45 (Pre) and 109.88±17.13 (post). Both groups showed improvement but, Group-A treated with SSAET along with RMM showed significantly higher (P Value ≤ 0.05) improvement as compared with group B treated with RMM alone. Mean and standard deviation of HDL in Group-A was 42.70±8.06 (pre) and 47.47±7.16 (post), while the mean and standard deviation of group B is 43.37±8.15 (Pre) and 44.41±7.91 (post). Both groups showed improvement but Group-A treated with SSAET program along with RMM showed significantly higher (P Value ≤ 0.05) improvement than group B treated with RMM alone.Conclusion:SSAET program along with RMM is more effective strategy for the management of deranged lipid profile in patients with T2DM.

УРОВЕНЬ МЕМБРАНОСВЯЗАННОГО ГЕМОГЛОБИНА И БЕЛКИ МЕМБРАНЫ ЭРИТРОЦИТОВ У БОЛЬНЫХ ГИПЕРТОНИЧЕСКОЙ БОЛЕЗНЬЮ, ОСЛОЖНЁННОЙ И НЕ ОСЛОЖНЁННОЙ МЕТАБОЛИЧЕСКИМ СИНДРОМОМ

We studied the effect of different levels of membrane-bound hemoglobin on the level of red-cell membrane proteins and also their interrelation in patients with essential hypertension with and without metabolic syndrome. It was found that high membrane-bound hemoglobin is closely related to the low level of high-density lipoproteins and high level of low-density lipoproteins in patients with essential hypertension complicated with metabolic syndrome. In patients with essential hypertension not complicated with metabolic syndrome high membrane-bound hemoglobin is related to the increased prothrombin time and decreased blood urea nitrogen. In patients with essential hypertension com-plicated with metabolic syndrome high membrane-bound hemoglobin significantly influences the level of membrane contractile proteins (actin, tropomiosine). In patients with essential hypertension without metabolic syndrome high membrane-bound hemoglobin is accompanied by the decrease of structural and integral membrane proteins levels (anion-transport protein and protein 4.1). As the result of quantitative changes in these proteins and change in their interrelations in patients with ssential hypertension complicated with metabolic syndrome more intensive disorders of structural and functional organization of red-cell membrane can appear.

Vitamin A Decreases Cytotoxicity of Oxidized Low-Density Lipoprotein in Patients with Atherosclerosis

ABSTRACTBackground: Oxidized low-density lipoprotein (ox-LDL) is implicated in initiation and progression of atherosclerosis. Previously, we found that ox-LDL increases vulnerability of peripheral blood mononuclear cells (PBMCs) in atherosclerotic patients compared to controls. Vitamin A induces proliferation of PBMCs. The aim of this study was to determine the effect of vitamin A supplementation on PBMC survival against LDL and different doses of ox-LDL.Method: In this double-blind placebo-controlled trial, we recruited 35 atherosclerotic patients and 38 healthy controls and randomly allocated them into placebo and vitamin A groups, which received either placebo or 25,000 IU/day of vitamin A for 3 months. PBMCs were isolated, cultured, and stimulated by 1 µg/mL LDL as well as 1 µg/mL and 50 µg/mL ox-LDL. The stimulation indexes (SIs) of PBMCs were calculated to identify cell viability. Additionally, the circulating ox-LDL levels were measured by ELISA.Results: Viability of PBMCs stimulated by 50 µg/mL ox-LDL significantly increased following vitamin A supplementation in patients (p < 0.01). The levels of circulating ox-LDL were not changed by vitamin A treatment. Ox-LDL levels were strongly and positively correlated to SI of PBMCs stimulated by 1 µg/mL LDL and1 µg/mL ox-LDL in all groups.Conclusion: Vitamin A decreases cytotoxicity of high-dose ox-LDL and improves PBMC viability. The protective effect of vitamin A is not mediated by an antioxidative mechanism, but may instead have been due to intracellular protection of the apoptotic machinery or induction of proliferation of the cells. Higher levels of ox-LDL increase PBMC irritability in all participants.

Phenotype receptor gene mutations in low-density lipoprotein in patients with familial hypercholesterolemia in Karelia

Familial hypercholesterolemia (FHC) - hereditary dyslipidemia, which is based on mutations in the gene for low-density lipoprotein receptor.However, there is variability in the clinical manifestations of the disease difficult to assess individual risk.Materials and methods. Under our supervision for 10 years were 109 patients with FHC, 17 mutation in the receptor density lipoprotein. FHC diagnosis established by the criteria of the British leadership Simon Broom. To search for mutations in low-density lipoprotein receptor was performed automated fluorescent SSCP-analysis of exons of the gene analysis of restriction fragment length polymorphism and the direct sequencing of DNA on a gel sequencer ALFExpress-2 (Amersham Biosciences) using the program ALFwin Sequence Analyzer.The Results. We analyzed five clinical cases of patients with genetically confirmed diagnosis of FHC. Shows a wide phenotypic variability FHC: the possibility of early debut of coronary heart disease, coronary tropism for the pool some patients and cerebral - others, the possibility of a long asymptomatic disease.Conclusion. The absence of clinical manifestations of atherosclerosis and wide phenotypic variability at FHC require targeted screening for FHC, at least among patients with coronary heart disease in order to timely and adequate preventive measures, especially in cases where the mutation is set low density lipoprotein receptor.