Measurement Of Lipoprotein Cholesterol Research Articles

Statin use and cardiovascular risk in young adults in the United States.

Atherosclerotic cardiovascular disease (ASCVD) pathogenesis begins in early adulthood, yet guidance on statin use for primary prevention in young adults is limited. This is a retrospective multi-center cohort study of adults aged 20-39 years receiving primary care within 87 U.S. health systems (2022-2023). The study included patients with at least 1 low-density lipoprotein cholesterol (LDL-C) measurement. The primary outcome was the measured the proportion of patients prescribed a statin within one month of LDL-C testing. The characteristics of those who were and were not prescribed statins were compared using standardized mean differences (SMD). Finally, the PREVENT 10- and 30-year ASCVD risk scores for the "average" patient (using the cohort mean values of risk score variables), a "lower-risk" patient, and a "higher-risk" patient were compared (using pooled values one standard deviation below and above the mean, respectively). Analyses were conducted in 2024-2025. Statins were initiated in 3,309 of 775,162 patients. Those who received statins were more likely to be older, male, and have higher mean LDL-C, systolic blood pressure, hemoglobin A1c, and body mass index (SMD>0.10). PREVENT 10-year risk scores were similar or higher among those prescribed statins compared to those not prescribed statins for the average (0.75% vs 0.76%), lower-risk (0.19% vs 0.35%), and higher-risk (8.87% vs 4.55%). In a multi-center cohort, 0.43% of young adults were prescribed a statin within one month of initial LDL-C measurement. The average patient would not have qualified for statin therapy based on their PREVENT risk percentile. Future studies should evaluate the cost effectiveness of statins for primary prevention in 20 to 39-year-old patients.

Baseline and cumulative Chinese visceral adiposity index and diabetic kidney disease: A prospective cohort study.

Diabetic kidney disease (DKD) makes up nearly half of all chronic kidney disease cases and is a major cause of mortality for people with diabetes. However, the study of the association of longitudinal Chinese visceral adiposity index (CVAI) with DKD is still missing. This prospective cohort study included 7874 diabetes patients from the Kailuan study. These participants had complete repeated waist circumference, body mass index, triglycerides and high-density lipoprotein cholesterol measurements that formed the continuous CVAI records. DKD was defined by increased proteinuria or decreased estimated glomerular filtration rate (eGFR), preceded by diabetes. Cox proportional hazard regression models were used to examine the associations between baseline and cumulative CVAI and the risk of DKD. There is a positive association between the CVAI level, whether baseline or cumulative, and the incidence of DKD among diabetic patients (p for log-rank tests <0.001). Compared to low CVAI level, the high baseline CVAI level was positively associated with the risk of DKD (HR: 1.24, 95% CI: 1.09-1.42), as well as the high cumulative CVAI level (HR: 1.62, 95% CI: 1.29-2.04). In addition, the assumption of linearity for the positive associations between both baseline (P-nonlinear = 0.264, p for overall <0.001) and cumulative (P-nonlinear = 0.765, p for overall <0.001) CVAI with incident DKD was satisfied. Higher baseline and cumulative CVAI are associated with a higher risk of DKD. This finding suggests the health benefits of low levels of CVAI and the importance of its regular surveillance among individuals with diabetes.

Clinical significance of small dense low-density lipoprotein cholesterol measurement in type 2 diabetes.

Low-density lipoprotein cholesterol (LDL-C) is known to be a causal substance of atherosclerosis, but its usefulness as a predictive biomarker for atherosclerotic cardiovascular disease (ASCVD) is limited. In patients with type 2 diabetes (T2D), LDL-C concentrations do not markedly increase, while triglycerides (TG) concentrations are usually elevated. Although TG is associated with ASCVD risk, they do not play a direct role in the formation of atheromatous plaques. TG changes the risk of ASCVD in a way that is dependent on LDL-C, and TG is the primary factor in reducing LDL particle size. Small dense (sd)LDL, a potent atherogenic LDL subfraction, best explains the "Atherogenic Duo" of TG and LDL-C. Although hypertriglyceridemia is associated with small-sized LDL, patients with severe hypertriglyceridemia and low LDL-C rarely develop ASCVD. This suggests that quantifying sdLDL is more clinically relevant than measuring LDL size. We developed a full-automated direct sdLDL-C assay, and it was proven that sdLDL-C is a better predictor of ASCVD than LDL-C. The sdLDL-C level is specifically elevated in patients with metabolic syndrome and T2D who have insulin resistance. Due to its clear link to metabolic dysfunction, sdLDL-C could be named "metabolic LDL-C." Insulin resistance/hyperinsulinemia promotes TG production in the liver, causing steatosis and overproduction of VLDL1, a precursor of sdLDL. sdLDL-C is closely associated with steatotic liver disease and chronic kidney disease, which are common complications in T2D. This review focuses on T2D and discusses the clinical significance of sdLDL-C including its composition, pathophysiology, measurements, association with ASCVD, and treatments.

Maximal Fat Oxidation During Exercise in Healthy Individuals: Lack of Genetic Association with the FTO rs9939609 Polymorphism.

Background/Objectives: Previous studies suggest that there is a genetically determined component of fat oxidation at rest and during exercise. To date, the FTO gene has been proposed as a candidate gene to affect fat oxidation during exercise because of the association of the "at-risk" A allele with different obesity-related factors such as increased body fat, higher appetite and elevated insulin and triglyceride levels. The A allele of the FTO gene may also be linked to obesity through a reduced capacity for fat oxidation during exercise, a topic that remains largely underexplored in the current literature. The aim of this study was to analyze the association between the FTO rs9939609 polymorphism with the rate of fat oxidation during exercise and metabolic syndrome criteria in healthy participants. Methods: A total of 80 healthy participants (41 men and 39 women) underwent comprehensive assessments, including measurements of anthropometric variables, blood pressure and blood measures of fasting glucose, triglycerides, low- and high-density lipoprotein cholesterol (LDL-c and HDL-c), insulin, interleukin-6 (IL-6) and C-reactive protein (CRP) concentrations. Additionally, the Homeostatic Model Assessment (HOMA-IR) was used to evaluate insulin resistance. Peak oxygen uptake (VO2peak) and maximal fat oxidation rate (MFO) were also measured during an incremental cycling test. FTO rs9939609 genotyping (TT, AT, AA) was performed using genomic DNA samples obtained from a buccal swab and measured with PCR. Results: There were 32 participants (40.0%) with the TT genotype; 31 (38.8%) with the AT genotype; and 17 (21.2%) with the AA genotype. Age, body characteristics, VO2peak, blood pressure and blood variables were similar across all three genotypes. However, serum insulin concentration and HOMA-IR were associated with the FTO rs9939609 genotype with higher values in AA with respect to AT and TT participants (p < 0.050). Still, MFO was similar in TT, AT and AA participants (0.35 ± 0.13, 0.37 ± 0.11, 0.33 ± 0.11 g/min, p = 0.702). In the dominant model, there was no statistical difference between TT and A allele carriers. However, the recessive model revealed that AA participants had higher values of body mass, body mass index, blood insulin concentration and HOMA-IR than T allele carriers (p < 0.050), with no differences in MFO. Conclusions: In our sample of healthy individuals, the FTO rs9939609 polymorphism was associated with several phenotypes associated with obesity and insulin resistance, particularly under the AA vs. T allele/recessive model. However, the FTO rs9939609 polymorphism was not associated with MFO during exercise as fat oxidation was similar across genotypes. This suggests that reduced fat oxidation during exercise is unlikely to be a cause of the obesogenic influence of the FTO AA genotype. Clinically, these findings suggest that the obesogenic effects of the FTO AA genotype are unlikely driven by impaired fat oxidation during exercise. Instead, attention should focus on mechanisms like appetite regulation and energy intake. Moreover, exercise interventions may still effectively mitigate obesity risk, as AA individuals retain normal fat oxidation capacity during exercise.

Triglyceride-Glucose Index and its Relationship to Erectile Dysfunction in Subjects without Heart Disease

ABSTRACT Aim: This study primarily focused on evaluating the triglyceride-glucose (TyG) index in patients experiencing erectile dysfunction (ED) and examining its potential role as a predictive tool in diagnosing ED. Materials and Methods: The study involved a cohort of 50 patients diagnosed with erectile dysfunction, forming the study group, alongside 50 individuals exhibiting normal sexual function, who served as the control group. The assessment of erectile function was conducted using the International Index of Erectile Function-5 (IIEF-5) questionnaire. All participants underwent the calculation of the TyG index. Results: The examination indicated that there were no notable disparities between the two groups regarding smoking rates, alcohol intake, or measurements of high-density lipoprotein cholesterol, haemoglobin, creatinine levels, and leukocyte and platelet counts. Individuals experiencing erectile dysfunction were found to be older and exhibited significantly higher levels of total cholesterol, low-density lipoprotein cholesterol, glucose, triglycerides, and the TyG index compared to the control group. Conclusion: I n patients with erectile dysfunction, the TyG index—a simple test for insulin resistance (IR) —was found to be predictive.

Comparison of low-density lipoprotein cholesterol (LDL-c) estimates by in-lab and point-of-care devices in the context of emerging LDL-c equations

Abstract Low-density lipoprotein cholesterol (LDL-c) and lipid measurements are used for hyperlipidemia diagnosis, cardiovascular disease risk classification, and medication management. Millions of lipid panels are performed annually. Given the widespread need for lipid testing, there are two CLIA-waived point-of-care (POC) lipid testing devices. These devices were FDA-approved using the Friedewald equation to estimate LDL-c based on measurements of (triglycerides (TG), high-density lipoprotein cholesterol (HDL-c), and total cholesterol (TC). By contrast, for laboratory-based LDL-c estimation, the Friedewald equation is being replaced by newer, more accurate equations such as the NIH-Sampson equation. These equations use the same lipid panel results to estimate LDL-c and only differ in the arithmetic of the estimation. This study evaluates how differences between the in-clinic POC machines and in-laboratory lipid measurements affect the estimated LDL-c results and are compounded by differences in the equations used for LDL-c estimation. This retrospective observational study collected deidentified lipid results (TG, HDL-c, TC, LDL-c) and demographic data (age, gender) for all samples that had lipid panel results from in-lab and POC within twenty-four hours of each other in a single hospital system between 2014 and 2023. Three hundred twenty samples were identified; samples with non-numerical values or results outside of the reportable range for TG, HDL-c, or TC were not included in subsequent LDL-c calculations using the Friedewald and NIH-Sampson equations (69 results). Patients under the age of 18 were excluded (2 results). Two hundred and forty-nine samples met inclusion criteria; this cohort showed non-significant differences in lipid, age, and gender distributions relative to all POC results tested in the same time frame. Consistent with prior reports, we observed discordance between POC and the in-lab lipid measurements, particularly for TG (Bland-Altman: bias:-23.04 mg/dL, standard deviation:61.3 mg/dL). These analytical differences may not change clinical management if the cardiovascular risk classification using estimated LDL-c is unchanged. However, the risk classification based on the in-lab versus in-clinic testing differed for 20% of patients. The most pronounced difference in LDL-c estimation occurred when the POC machine used Friedewald and in-lab testing used NIH-Sampson, and resulted in 5% more patients differentially classified. Regardless of testing platform, more patients are categorized as higher risk on an individual and population-based level with the NIH-Sampson equation. This study highlights the need for transparency in lipid panel reports regarding which LDL-c equation is used in both POC and in-lab testing formats, and the need for readily available tools for conversion between different LDL-c estimation equations.

A-213 Comparison of low-density lipoprotein cholesterol (LDL-c) estimates by in-lab and point-of-care devices in the context of emerging LDL-c equations

Abstract Background Low-density lipoprotein cholesterol (LDL-c) and lipid measurements are used for hyperlipidemia diagnosis, cardiovascular disease risk classification, and medication management. Millions of lipid panels are performed annually. Given the widespread need for lipid testing, there are two CLIA-waived point-of-care (POC) lipid testing devices. These devices were FDA-approved using the Friedewald equation to estimate LDL-c based on measurements of (triglycerides (TG), high-density lipoprotein cholesterol (HDL-c), and total cholesterol (TC). However, in laboratory-based testing, the Friedewald equation is being replaced by newer, more accurate equations such as the NIH-Sampson equation. These equations use the same lipid panel results to estimate LDL-c and only differ in the arithmetic of the estimation. The study objective is to evaluate how differences between the in-clinic POC machines and in-laboratory lipid measurements affect the estimated LDL-c results and are compounded by differences in the equations used for LDL-c estimation. Methods This retrospective observational study collected deidentified lipid results (TG, HDL-c, TC, LDL-c) and demographic data (age, gender) for all samples that had lipid panel results from in-lab and POC within twenty-four hours of each other in a single hospital system between 2014 and 2023. Three hundred twenty samples were identified; samples with non-numerical values or results outside of the reportable range for TG, HDL-c, or TC were not included in subsequent LDL-c calculations using the Friedewald and NIH-Sampson equations (69 results). Patients under the age of 18 were excluded (2 results). Two hundred and forty-nine samples met inclusion criteria; this cohort showed non-significant differences in lipid, age, and gender distributions relative to all POC results tested in the same time frame. Results Consistent with prior reports, we observed discordance between POC and the in-lab lipid measurements, particularly for TG (Bland-Altman: bias:-23.04 mg/dL, standard deviation:61.3 mg/dL). Regardless of the testing platform, LDL-c results are higher on an individual and population-based level with the NIH-Sampson equation. These analytical differences may not change clinical management if the cardiovascular risk classification using estimated LDL-c is unchanged. However, the risk classification based on the in-lab versus in-clinic testing differed for 20-30% of patients. The most pronounced difference in LDL-c estimation occurred when the POC machine used Friedewald and in-lab testing used NIH-Sampson, and resulted in 5% more patients differentially classified. Conclusions This study highlights the need for transparency in lipid panel reports regarding which LDL-c equation is used in both POC and in-lab testing formats, and the need for readily available tools for conversion between different LDL-c estimation equations.

Comparison of ten formulae for calculating low-density lipoprotein cholesterol with direct low-density lipoprotein cholesterol measurement

ABSTRACT Background: Accurate lipid profile assessment, mainly low-density lipoprotein cholesterol (LDL-C) measurement, is crucial for diagnosing and managing cardiovascular disease (CVD). The widely used Friedewald formula for LDL-C calculation has limitations, prompting the exploration of alternative equations. Aims: This study aims to compare ten LDL-C calculation formulas with direct measurement among study participants attending a tertiary care centre. Materials and Methods: Conducted from September 2021 to July 2022 at a tertiary healthcare centre in India, the study involved 114 participants aged 18 years or older. The exclusion criteria were high-serum triglyceride (TG) levels, renal failure, diabetes, liver diseases or unwillingness to participate. Blood samples were analysed for total cholesterol, TG, high-density lipoprotein cholesterol and LDL-C. The very-low-density lipoprotein cholesterol level was calculated. The LDL-C formulas evaluated were Friedewald, Anandaraja, De Cordova, Vujovic, Ahmadi, Puavillai, Chen, Hattori, Martin–Hopkin and Sampson. Results: Vujovic’s formula showed a negligible mean difference and strong correlation (r = 0.916, P &lt; 0.001) with direct LDL-C estimation across TG concentrations. Sampson’s formula performed best for TG &lt;150 mg/dL, whereas Vujovic’s formula excelled for 151–399 mg/dL TG concentrations. All formulas were highly correlated with direct LDL-C levels (P &lt; 0.001). Bland–Altman analysis indicated Vujovic’s formula as the closest match to direct measurement, with a mean bias of −1.42 ± 20.59 mg/dL. Conclusion: Vujovic’s formula demonstrated the slightest difference and strong correlation with direct LDL-C measurement, outperforming other formulas. This finding enhances the accuracy of LDL-C assessment and improves CVD risk management in clinical practice.

Prevention and Management of Cardiovascular Disease in Primary Care: A Comment on the PEER Simplified Lipid Guideline

BackgroundIn Canada, 2 guidelines provide guidance for the management of dyslipidemia. The Patients, Experience, Evidence, Research simplified lipid guidelines, intended for primary care practitioners, and the Canadian Cardiovascular Society guidelines, intended for all practitioners, are based on differing methodologies with distinct priorities and preferences. The disparate approaches may contribute to confusion among family practitioners and their co-managed patients, with the potential for compromised care, differing standards for training in the fundamentals of lipidology, and differing criteria that might be used in practice audits to evaluate quality of care. MethodsThe Patients, Experience, Evidence, Research (PEER) recommendations were considered by primary authors of the Canadian Cardiovascular Society guideline to identify areas of concordance, discordance, or agreement with qualifications. ResultsDiscordance between the guidelines is greatest with respect to interpretation of the cholesterol profile, the implications of elevated triglyceride, the utility of apolipoprotein B and non-high-density lipoprotein-cholesterol measurements, the role of nonstatin medications, and the importance of assuring adherence and avoiding undertreatment through follow-up measurement of lipid profiles. The disparate importance attached to identification of patients with enhanced risk due to an elevated lipoprotein (a) level is also apparent. ConclusionsThis comparison attempts to reconcile key principles of practice, to foster both high quality of care and fully informed patient-centred decision-making.

Sex-Specific Sarcopenia Prevalence and Risk Factors in the Korean Population: A Cross-Sectional Epidemiological Study.

Background and Objective: This study aimed to identify the incidence of sarcopenia and disease risk factors in Korean adults and to provide data for sarcopenia prevention. Materials and Methods: Based on the Korea National Health and Nutrition Survey, 2008-2011, we selected 14,185 adults over the age of 20 who participated in sarcopenia diagnostic tests and health surveys. We analyzed sarcopenia risk factors using complex sample multi-logistic regression analysis. Results: The prevalence of sarcopenia in Korea was 31.3%, with 20.2% in men and 40.4% in women. In men, there was a higher risk of sarcopenia in those of older age, without a spouse, with a low body mass index (BMI), who never engage in resistance exercise, or who do mid-level intensity resistance exercises. In women, sarcopenia risk was higher in those in their 20s compared to those in their 60s, and risk factors included a low BMI, high-density lipoprotein cholesterol and waist circumference measurements, alcohol consumption, aerobic exercise, and resistance exercise. Conclusions: Interventions and lifestyle improvements will help prevent the onset of sarcopenia in elderly men and young women with risk factors such as a low BMI.

Impact of Direct Measurement of Small Dense Low-Density Lipoprotein Cholesterol for Long-Term Secondary Prevention in Patients with Stable Coronary Artery Disease.

This study investigated whether directly measured small dense low-density lipoprotein cholesterol (D-sdLDL-C) can predict long-term coronary artery disease (CAD) events compared with low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B (apoB), and estimated small dense low-density lipoprotein cholesterol (E-sdLDL-C) determined by the Sampson equation in patients with stable CAD. D-sdLDL-C measured at Showa University between 2010 and 2022, and E-sdLDL-C were evaluated in 790 male and 244 female patients with stable CAD. CAD events, defined as sudden cardiac death, onset of acute coronary syndrome, and/or need for coronary revascularization, were monitored for 12 years. Cutoff lipid levels were determined by receiver operating characteristic curves. CAD events were observed in 238 male and 67 female patients. The Kaplan-Meier event-free survival curves showed that patients with D-sdLDL-C ≥32.1 mg/dL (0.83 mmol/L) had an increased risk for CAD events (P = 0.007), whereas risk in patients with E-sdLDL-C ≥36.2 mg/dL (0.94 mmol/L) was not increased. In the group with high D-sdLDL-C, the multivariable-adjusted hazard ratio (HR) was 1.47 (95% CI, 1.15-1.89), and it remained significant after adjustment for LDL-C, non-HDL-C, or apoB and in patients treated with statins. HRs for high LDL-C, non-HDL-C, or apoB were not statistically significant after adjustment for high D-sdLDL-C. Higher D-sdLDL-C was associated with enhanced risk of high LDL-C, non-HDL-C, and apoB (HR 1.73; 95% CI, 1.27-2.37). Higher D-sdLDL-C can predict long-term recurrence of CAD in stable CAD patients independently of apoB and non-HDL-C. D-sdLDL-C is an independent risk enhancer for secondary CAD prevention, whereas E-sdLDL-C is not.UMIN-CTR Clinical Trial Number: UMIN000027504.

An improved method for estimating low LDL-C based on the enhanced Sampson-NIH equation

BackgroundThe accurate measurement of Low-density lipoprotein cholesterol (LDL-C) is critical in the decision to utilize the new lipid-lowering therapies like PCSK9-inhibitors (PCSK9i) for high-risk cardiovascular disease patients that do not achieve sufficiently low LDL-C on statin therapy.ObjectiveTo improve the estimation of low LDL-C by developing a new equation that includes apolipoprotein B (apoB) as an independent variable, along with the standard lipid panel test results.MethodsUsing β-quantification (BQ) as the reference method, which was performed on a large dyslipidemic population (N = 24,406), the following enhanced Sampson-NIH equation (eS LDL-C) was developed by least-square regression analysis:eSLDL-C=TC1.15-HDL-C1.25-TG6.99-TG×NonHDL-C1120+TG28910+TG×ApoB1240+ApoB4.54-4.73\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$eS\\,LDL-C= \\frac{TC}{1.15}-\\frac{HDL-C}{1.25}-\\frac{TG}{6.99}-\\frac{\\left(TG\ imes NonHDL-C\\right)}{1120}+\\frac{{TG}^{2}}{8910}+\\frac{\\left(TG\ imes ApoB\\right)}{1240}+\\frac{ApoB}{4.54}-4.73$$\\end{document}ResultsThe eS LDL-C equation was the most accurate equation for a broad range of LDL-C values based on regression related parameters and the mean absolute difference (mg/dL) from the BQ reference method (eS LDL-C: 4.51, Sampson-NIH equation [S LDL-C]: 6.07; extended Martin equation [eM LDL-C]: 6.64; Friedewald equation [F LDL-C]: 8.3). It also had the best area-under-the-curve accuracy score by Regression Error Characteristic plots for LDL-C < 100 mg/dL (eS LDL-C: 0.953; S LDL-C: 0.920; eM LDL-C: 0.915; F LDL-C: 0.874) and was the best equation for categorizing patients as being below or above the 70 mg/dL LDL-C treatment threshold for adding new lipid-lowering drugs by kappa score analysis when compared to BQ LDL-C for TG < 800 mg/dL (eS LDL-C: 0.870 (0.853–0.887); S LDL-C:0.763 (0.749–0.776); eM LDL-C:0.706 (0.690–0.722); F LDL-C:0.687 (0.672–0.701). Approximately a third of patients with an F LDL-C < 70 mg/dL had falsely low test results, but about 80% were correctly reclassified as higher (≥ 70 mg/dL) by the eS LDL-C equation, making them potentially eligible for PCSK9i treatment. The M LDL-C and S LDL-C equations had less false low results below 70 mg/dL than the F LDL-C equation but reclassification by the eS LDL-C equation still also increased the net number of patients correctly classified.ConclusionsThe use of the eS LDL-C equation as a confirmatory test improves the identification of high-risk cardiovascular disease patients, who could benefit from new lipid-lowering therapies but have falsely low LDL-C, as determined by the standard LDL-C equations used in current practice.

The non-HDL-C to APOB ratio as a predictor of inaccurate LDL-C measurement in patients with chronic intrahepatic cholestasis and jaundice: a retrospective study.

Cholestasis is characterized by the accumulation of bile in the liver or biliary system due to obstruction or impaired flow, necessitating lipid profiling to assess lipid metabolism abnormalities. Intrahepatic cholestasis, being the most significant type of cholestasis, further complicates the assessment of lipid abnormalities. However, the accuracy of low-density lipoprotein cholesterol (LDL-C) measurement in intrahepatic cholestasis patients remains uncertain. This study aimed to evaluate the consistency of the homogeneous assay and the Friedewald formula in detecting LDL-C levels and identify factors influencing LDL-C test results in intrahepatic patients with cholestasis. Retrospective analysis of laboratory data was conducted on intrahepatic cholestatic patients. Correlations between LDL-C values obtained using the homogeneous method (LDL-C(D)) and the Friedewald formula (LDL-C(F)), as well as associations between high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A1 (ApoA1), LDL-C(D) and LDL-C(F), and apolipoprotein B (ApoB), were analyzed. Logistic regression analyses were employed to identify diagnostic indicators for inaccurate LDL-C measurements in intrahepatic cholestatic patients. Compared to patients with intrahepatic cholestasis without jaundice, the correlation between LDL-C(F) and LDL-C(D) was weaker in those with jaundice. Additionally, HDL-C exhibited a strong correlation with ApoA1 in both jaundice and non-jaundice cholestasis cases. Elevated non-HDL-C to APOB ratio (NH-C/B Ratio) levels (>4.5) were identified as a reliable predictor of inaccurate LDL-C measurements in patients with chronic intrahepatic cholestasis accompanied by jaundice. LDL-C measurement reliability is moderately weaker in patients with intrahepatic cholestasis accompanied by jaundice. Elevated levels of the NH-C/B ratio serve as a significant predictor of inaccurate LDL-C measurements in this chronic patient population, highlighting its clinical relevance for diagnostic assessments.

LIPID PROFILE CHANGES DURING DIFFERENT PHASES OF MENSTRUATED YOUNG AND PREMENOPAUSAL WOMEN

Background: Lipoprotein cholesterol measurements fluctuated across the menstrual cycle, corresponding to rising and declining concentrations of gonadotropins and ovarian steroid hormones levels in young women, whereas premenopausal women and those who inside the menopausal transition characterized by a poor ovarian response to high secretion of gonadotropin leading to low levels of ovarian steroids. Aims: To investigate the lipoprotein cholesterol changes and their interactions with sex steroid hormones during different phases of the menstrual cycle in menstruated young and old (premenopausal) women. Methods: The sample included thirty healthy women (aged 20-45 years) divided into two groups with 15 women /group according to their ages )20-25 years( (40-45 years). Blood samples were collected on the 8th, 16th, and 24th days of the menstrual cycle from both young and old menstruating women to compare the previous parameters between these days for each group and compare these parameters between similar days for the first and second groups. Lipid profile (Total cholesterol (TC), Triglyceride (TG), High density lipoprotein (HDL), Low density lipoprotein (LDL), and Very low density lipoprotein (VLDL) changes be assayed by Bio-Systems Kit components. Statistical analysis was carried out using one-way Analysis of Variance (ANOVA), followed by Duncan's test, and t-tests were used to assess differences between groups. Results: TC and TG levels did not significantly increase on the 8th day of the menstrual cycle, which represents the follicular phase, in comparison with the other days (16th and 24th days). However, LDL level increased significantly (p ? 0.05) on the 8th day compared to the other days. On the other hand, HDL and VLDL levels increased on the 16th day of the menstrual cycle, which represents the ovulatory phase. Discussion: TC, TG, and LDL levels increased during the follicular phase and were accompanied by high levels of FSH and estradiol, leading to a favorable lipid profile, whereas FSH and estradiol are considered regulators of cholesterol biosynthesis and a buffering capacity. HDL and VLDL levels rise during ovulation to meet the requirements of ovulation and ensure successful ovulation. Conclusions: Studying and evaluating changes in the lipid profile according to the menstrual cycle phase of the menstrual cycle represents an important issue in knowing the physiological and healthy woman state and preventing cardiovascular disease incidence.

The effect of hypertension on renal functions in patients with acute coronary syndrome

Objectives: In patients with acute coronary syndrome, age, ejection fraction, diabetes, hypertension, and chronic kidney disease (CKD) are regarded as independent risk factors for the development of acute kidney disease (ACD). This research evaluated the glomerular filtration rates (GFR) of acute coronary syndrome patient groups who were hypertensive and those who were not. Methods: This retrospective analysis comprised 764 patients with acute coronary syndrome who had applied to our institution before coronary angiography. There were two groups created from these patients. In the first group, there were 383 hypertensive patients; in the second group, there were 381 non-hypertensive patients. To assess how well these patients' kidneys were functioning, GFR was determined and compared. Results: The mean age of the two groups did not significantly differ from one another (p = 0.053). The standard lipid measures of total cholesterol, triglyceride, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol levels did not differ substantially between the two groups. The two groups had no discernible difference regarding high-sensitivity C-reactive protein, N-terminal fragment brain natriuretic peptides, creatinine, and thrombocyte levels. Systolic and diastolic blood pressure, as well as diabetes mellitus, were all considerably higher in the hypertensive patients’ group (p &amp;lt; 0.001). The GFR in hypertensive patients was substantially lower (64.83 ± 19.76 vs. 70.71 ± 19.19, p &amp;lt; 0.001) Conclusions: Our research revealed a strong link between hypertension and diminished renal function. This leads us to believe that hypertension may be a separate risk factor for the decline in renal function in acute coronary syndrome patients.

Standardization of Apolipoprotein B, LDL-Cholesterol, and Non-HDL-Cholesterol.

Concern continues about whether the measurement of apolipoprotein B (apoB) is adequately standardized, and therefore, whether apoB should be applied widely in clinical care. This concern is misplaced. Our objective is to explain why and what the term "standardization" means. To produce clinically valid results, a test must accurately, precisely, and selectively measure the marker of interest. That is, it must be standardized. Accuracy refers to how closely the result obtained with 1 method corresponds to the result obtained with the standard method, precision to how reproducible the result is on repeated testing, and selectivity to how susceptible the method is to error by inclusion of other classes of lipoprotein particles. Multiple expert groups have determined that the measurement of apoB is adequately standardized for clinical care, and that apoB can be measured inexpensively, using widely available automated methods, more accurately, precisely, and selectively than low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol. ApoB is a standard superior to low-density lipoprotein cholesterol and high-density lipoprotein cholesterol because it is a defined molecule, whereas the cholesterol markers are the mass of cholesterol within lipoprotein particles defined by their density, not by their molecular structure. Nevertheless, the standardization of apoB is being further improved by the application of mass spectrophotometric methods, whereas the limitations in the standardization and, therefore, the accurate, precise, and selective measurement of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol are unlikely to be overcome. We submit that greater accuracy, precision, and selectivity in measurement is a decisive advantage for apoB in the modern era of intensive lipid-lowering therapies.

Comparison of Anterior Segment Parameters in Obese Children And Healthy Control Group

Objective:: To evaluate anterior segment parameters in obese children&#x0D; Material and methods: 55 obese and 30 control group children subjects participated. All participants and the control group were examined and anthropometric measurements were made. The measurements of fasting blood glucose(FBG), triglyceride(TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and insulin values were performed. The homeostasis model assessment of insulin resistance (HOMA‑IR) was calculated. Each participant underwent a detailed ophthalmic examination and IOP, CCT, ACD and LT were measured.&#x0D; Results: The gender distribution of the groups was similar (p=0.893). The mean of CCT and LT were significantly higher in the obese group (572.9 ± 14.5 vs. 559.5 ± 10.1 µm, p=0.001; 3.6 ± 0.14 vs. 3.48 ± 0.25 mm, p=0.007) . No significant difference was found between the obese and control groups in terms of other parameters. BMI and WC had a significant negative correlation with LT control groups. The obese group showed a significant positive correlation between IOP and TG (r=0.276, p=0.042), and a significant negative correlation with HDL-C (r=-0.273, p=0.043). In the control group, there was a significant positive correlation between IOP and BMI (r=0.389, p=0.034), WC (r=0.497, p=0.005), HOMA-IR (r=0.384, p=0.036), Insulin (r=0.407, p=0.026), and a significant negative correlation with TC (r=-0.511, p=0.004). A significantly positive correlation between ACD and LDL-C (r=0.371, p=0.043) and a significantly negative correlation between HOMA-IR in the control group were detected (r=-0.682, p=0.000).&#x0D; Conclusion: The obese group had higher CCT and LT than the control groups.

Measurement of Serum Low Density Lipoprotein Cholesterol and Triglyceride-Rich Remnant Cholesterol as Independent Predictors of Atherosclerotic Cardiovascular Disease: Possibilities and Limitations

The serum low density lipoprotein cholesterol (LDL-C) concentration is the dominant clinical parameter to judge a patient’s risk of developing cardiovascular disease (CVD). Recent evidence supports the theory that cholesterol in serum triglyceride-rich lipoproteins (TRLs) contributes significantly to the atherogenic risk, independent of LDL-C. Therefore, combined analysis of both targets and adequate treatment may improve prevention of CVD. The validity of TRL-C calculation is solely dependent on the accuracy of the LDL-C measurement. Direct measurement of serum LDL- C is more accurate than established estimation procedures based upon Friedewald, Martin–Hopkins, or Sampson equations. TRL-C can be easily calculated as total C minus high density lipoprotein C (HDL-C) minus LDL-C. Enhanced serum LDL-C or TRL-C concentrations require different therapeutic approaches to lower the atherogenic lipoprotein C. This review describes the different atherogenic lipoproteins and their possible analytical properties and limitations.

تثبيط جملة الرينين-أنجيوتنسين يحسن الصيغة اللبيدية لدى مرضى الداء الكلوي المزمن

The aim of this study was to evaluate whether the blockade of renin-angiotensin system (RAS), achieved by angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs), could affect the plasma lipid profile in chronic kidney disease (CKD) patients. Ninety-four hypertensive patients with CKD (stage 3-5) were enrolled. Forty-nine patients were treated with either ACEIs or ARBs daily for 6 months, and forty-five patients were treated with other antihypertensive agents (calcium channel blockers (amlodipine), b blockers, diuretics) as positive control group. Creatinine, estimated glomerular filtration rate (eGFR), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), and triglyceride (TG) levels measurements were performed before and after the six-month treatment. An improvement in serum lipids levels in hypertensive patients with CKD resulted from RAS blocked therapy and other antihypertensive agents. Both treatment groups significantly decreased total cholesterol (TC), by 7.77% in ACEIs/ARBs group (p≤0.01) and 6.42% in other antihypertensive group (p≤0.05). In CKD patients treated with ACEIs/ARBs, levels of TG (3.29%), and LDL-C (3.15%) dropped more than with other antihypertensive medications (2.12%, and 1.19% respectively). RAS blocked therapy significantly increased HDL-C levels in CKD patients by 5.94% (p≤0.05). The results indicate that RAS blockade therapy with ACEIs or ARB positively affects lipid profile, which may improve the cardiovascular risks caused by CKD.

Association between lipid levels and all-cause and cause-specific mortality in critically ill patients

Extremely low lipid levels are considered a sign of debilitation and illness. The association between lipid levels and the risk of mortality in critically ill patients has not been well investigated. This study was designed to evaluate the association between lipid levels and all-cause and cause-specific mortality in critically ill patients using a large collaborative research database known as the eICU database. In total, 27,316 individuals with low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) and triglyceride (TG) measurements were analyzed. A J-shaped association was observed between LDL-C, HDL-C, and TC levels and all-cause and noncardiovascular mortality, with low concentrations associated with higher risk. LDL-C, HDL-C and TC levels in the first quintile were associated with higher all-cause and noncardiovascular mortality but not with cardiovascular mortality compared to the reference quintile. There was a marked synergistic effect between low LDL-C combined with low HDL-C on the risk of mortality. Individuals with LDL-C ≤ 96 mg/dL and HDL-C ≤ 27 mg/dL had an increased risk of all-cause mortality (OR 1.52, 95% CI: 1.26–1.82), cardiovascular mortality (OR 1.07, 95% CI: 1.37–1.76) and noncardiovascular mortality (OR 1.82, 95% CI: 1.37–2.43). The results of this observational cohort showed that low LDL-C, HDL-C and TC levels were independently associated with higher all-cause and noncardiovascular mortality in critically ill patients.