Lipid Measurements Research Articles

A comprehensive systemic review and meta-analysis of the association between lipid profile and hidradenitis suppurativa.

While several studies have suggested a connection between Metabolic Syndrome (MetS) and Hidradenitis Suppurativa (HS), a definitive analysis confirming the association between lipid abnormalities and HS based on actual lipid values is lacking. Previous research, using odds ratios from ICD codes, indicates links between elevated triglycerides and low high-density lipoprotein levels with HS. However, these findings may not fully represent real-life situations, as no comprehensive analysis using actual lipid measurements has been performed. To examine the relationship between lipid profile values-total cholesterol, triglycerides (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL)-and HS. A comprehensive search of PubMed, Cochrane Library, and Embase was conducted to identify studies reporting lipid profiles in HS patients. A meta-analysis using standardized mean differences (SMDs) was performed to assess the association between lipid abnormalities and HS. The meta-analysis found that HS patients had significantly higher TG levels (SMD = 0.28, 95% CI: 0.09-0.47, P = 0.004) and lower HDL levels (95% CI: -0.53 to -0.16, P < 0.001) compared to healthy controls. No significant differences were observed in total cholesterol (SMD = 0.01, 95% CI: -0.19-0.21, P = 0.93) and LDL levels (SMD = 0.04, 95% CI: -0.10-0.17, P = 0.61). These results corroborate earlier studies linking HS with dyslipidemia, particularly hypertriglyceridemia and hypo-HDL cholesterolemia, with the added strength of using actual lipid values. This study confirms the association between hypertriglyceridemia and low HDL cholesterol in HS patients, highlighting the broader systemic association of the condition. Dermatologists should monitor lipid profiles in HS patients to mitigate potential cardiovascular risks through early detection and management.

Polymorphisms in the leptin gene and their role in adolescent obesity and metabolic health

The leptin (LEP) gene polymorphism is one of the most common polymorphisms and is believed to be associated with high circulating LEP levels that can occur in obese individuals. Thus, this study purposed to determine the relationship of LEP1 and LEP2 gene polymorphisms with overweight/obese and non-obese adolescents in Palembang and their correlation with various metabolic and anthropometric parameters. This research was an analytical and observational study. A total of 50 blood samples from adolescents (aged 10-18 years) were analyzed in this study. Standard laboratory protocols for serum lipid measurements, deoxyribonucleic acid (DNA) extraction, allele analysis by polymerase chain reaction (PCR), and LEP and insulin analysis by enzyme-linked immunosorbent assay (ELISA) were employed. The study revealed the allelic frequencies for gene LEP1: non-obese (G = 0.45, A = 0.55) and obese (G = 0.87, A = 0.13), and gene LEP2: non-obese (G = 0.54, A = 0.45) and obese (G = 0.67, A = 0.33). The frequencies of alleles in the LEP1 gene showed a statistically significant association with nutritional status (p = 0.011), while there was no significant association between genotypes in the LEP gene and nutritional status. The level of LEP was 6.39 + 1.12 in non-obese and 11.57 + 1.68 in obese, with p 0.000; and the triglyceride level was 82.56 ± 43.22 in non-obese and 113.72 ± 54.03 in obese, with p 0.029. In conclusion, this study shows that LEP levels and the polymorphism in the LEP1 gene are associated with obese adolescents.

Prioritizing protein targets for dyslipidaemia and cardiovascular diseases using Mendelian randomization in South Asians.

South Asians are at higher risk of dyslipidaemia-a modifiable risk factor for cardiovascular diseases (CVDs). We aimed to identify protein targets for dyslipidaemia and CVDs in this population. We used a two-sample Mendelian randomization (MR) approach, supplemented with MR-Egger, weighted median, colocalization, and generalized MR (GMR), to evaluate the effect of 2,800 plasma proteins on high/low/non-high-density lipoprotein cholesterol (HDL-C/LDL-C/nonHDL-C), total cholesterol, and triglycerides. Observational analyses were conducted on MR findings with strong colocalization (posterior probability≥ 80%) and GMR findings. Univariate MR assessed lipid-associated proteins' effect on CVDs. Finally, we compared the potential causal effects of plasma proteins on lipids in South Asians with those in Europeans to study heterogeneity in the MR effects. We identified 29 genetically proxied proteins potentially causal to at least one lipid measure, 12 of which showed strong colocalization and GMR evidence, including ANGPTL3 and PCSK9. Notably, PCSK9 demonstrated a stronger association with LDL-C in European compared to South Asian (βEuropean= 0.37; 95% Confidence Interval (CI)= (0.36, 0.38), βSouth Asian= 0.16; 95% CI= (0.11, 0.21)). Observational analysis suggested significant interaction between PCSK9 levels with LDL-C levels in South Asians with South Asians having a significantly lower effect compared to other ethnicities (PCSK9*South Asian; β= -0.14; 95% CI= (-0.174, -0.107)). Additionally, we showed that CELSR2 is also linked with CAD in South Asians. Our study highlighted potential causal links between plasma proteins, dyslipidaemia, and CVD in South Asians, with significant heterogeneity across genetic ancestry groups. Larger studies in South Asians are needed to validate these findings.

Independent Association of Individual Lipid Abnormalities with Cardiovascular All-cause Mortality: A Prospective Cohort Study.

Abnormalities in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) are each associated with increased cardiovascular risk, after adjusting for non-lipid risk factors. However, whether and to what extent the association for each lipid measure is confounded by other lipid measures is less understood. This study aims to investigate the association of each lipid measure with cardiovascular and all-cause mortality while precluding the confounding caused by abnormalities in other lipid measures. The study utilized data from the third National Health and Nutrition Examination Survey (NHANES III, 1988-1994) and ten cycles of continuous NHANES (1999-2018). The study cohort included 23,761 participants who were 20 years or older, not pregnant, not receiving lipid-lowering treatment, and had complete data on all four lipid measures and mortality status. Participants were categorized into seven subgroups based on their lipid profiles. Kaplan-Meier survival curves and Cox proportional hazards models were used to examine the association between lipid abnormalities and mortality. During a median follow-up of 140 months, 5,003 participants (14.1%) died, with 1,665 deaths (4.2%) attributable to cardiovascular causes. Compared with the reference group in which the four lipid measures were all normal, the subgroups with isolated high TC, two to three lipid abnormalities, and four lipid abnormalities were associated with increased risks for both cardiovascular and all-cause mortality in univariate analysis. However, only those with isolated high TC (for cardiovascular mortality, HR 1.52, 95% CI 1.13-2.06) and four lipid abnormalities (for all-cause mortality, HR 1.34, 95% CI 1.04-1.72) remained statistically significant after adjusting for non-lipid risk factors. Of note, compared with the reference group, the profile of non-lipid risk factors was apparently less favorable in the subgroup with two to three lipid abnormalities but similar (and some factors even more favorable) in the subgroup with isolated high TC. When the lipid measures were analyzed as continuous variables, a U-shaped relationship between HDL-C and mortality risk was observed for both cardiovascular and all-cause mortality, and very low LDL-C level was associated with increased mortality risk. No statistically significant association was found between TG levels and mortality risk. Isolated high TC, very low LDL-C, and concurrent abnormalities in all four lipid measures were associated with increased mortality risk, whereas isolated high TG was not. A U-shaped relationship may exist between HDL-C level and mortality. Overall, these findings underscore the need for integrated management of dyslipidemia that takes all four lipid measures as well as non-lipid cardiovascular risk factors into account, particularly for those with concurrent abnormalities in two or more lipid measures.

Validation and Epidemiologic Definition of the Novel Steatotic Liver Disease Nomenclature in a National United States Cohort With Cirrhosis.

Novel steatotic liver disease (SLD) definitions were introduced in 2023. Accurate and meaningful classifications using clinical data are needed to study interventions and outcomes. In a national cohort of Veterans with cirrhosis and imaging-confirmed steatosis, 7 algorithms differentially emphasizing cardiometabolic risk factors (CMRFs) and alcohol exposure were developed to define alcohol-associated liver disease (ALD), metabolic dysfunction associated SLD (MASLD), and MASLD with increased alcohol intake (MetALD). The primary outcome was classification of SLD, which was validated using hospitalizations for major acute cardiac events (MACE) and alcohol use disorder (AUD). Secondary outcomes included longitudinal Child-Turcotte-Pugh class, incident hepatocellular carcinoma, and all-cause mortality. In all, 31,514 patients with cirrhosis (median age 64 years) were included. CMRFs (98.8% ≥ 1) and hazardous alcohol use (65.3%) were highly prevalent. The distributions of MASLD, MetALD, and ALD varied substantially across classification methods with varying CMRF and alcohol criteria. For example, MetALD ranged from 4.7% to 47.2%. Using method 4, incidence rates of MACE hospitalizations in MASLD, MetALD, and ALD were 16.7, 14.5, and 8.4 per 100 person-years, respectively, and incidence rates of AUD hospitalizations were 2.0, 26.1, and 47.6 per 100 person-years, respectively. Hypertriglyceridemia and low high-density lipoprotein were common across SLD subtypes, including ALD (67.3% hypertriglyceridemia; 48.2% low high-density lipoprotein). Patients with ALD (hazard ratio, 1.41; 95% confidence interval, 1.34-1.48) had significantly higher hazards of mortality relative to MASLD. Classification of SLD is highly sensitive to relative weighting of CMRFs and alcohol use. Clinically relevant definitions should consider data availability on alcohol and the limitations of lipid measurements in distinguishing SLD subtypes.

Windows of Susceptibility to Air Pollution During and Surrounding Pregnancy in Relation to Longitudinal Maternal Measures of Adiposity and Lipid Profiles.

Pregnancy is a critical window for long-term metabolic programming of fetal effects stemming from airborne particulate matter ≤2.5μm (PM 2.5 ) exposure. Yet, little is known about long-term metabolic effects of PM 2.5 exposure during and surrounding pregnancy in mothers. We assessed potential critical windows of PM 2.5 exposure during and surrounding pregnancy with maternal adiposity and lipid measures later in life. We included 517 pregnant women from the PROGRESS cohort with adiposity [body mass index (BMI), waist circumference (WC), % body fat] and lipids [total cholesterol, high-density-lipoprotein (HDL), low-density-lipoprotein (LDL)] measured repeatedly at 4, 6 and 8 years post-delivery. Monthly average PM 2.5 exposure was estimated at each participant's address using a validated spatiotemporal model. We employed distributed lag interaction models (DLIMs) adjusting for socio-demographics and clinical covariates. We found that a 1 μg/m 3 increase in PM 2.5 exposure throughout mid-/late-pregnancy was associated with higher WC at 6-years post-delivery, peaking at 6 months of gestation: 0.04 cm (95%CI: 0.01, 0.06). We also identified critical windows of PM 2.5 exposure during and surrounding pregnancy associated with higher LDL and lower HDL both measured at 4 years post-delivery with peaks at pre-conception for LDL [0.17 mg/dL (95%CI: 0.00, 0.34)] and at the 11 th month after conception for HDL [-0.07 mg/dL (95%CI: -0.11, -0.02)]. Stratified analyses by fetal sex indicated stronger associations with adiposity measures in mothers carrying a male, whereas stronger associations were observed with lipids in mothers carrying a female fetus. Stratified analyses also indicated potential stronger deleterious lagged effects in women with folic acid intake lower than 600mcg/day during pregnancy.

No effects of high- v. low-protein breakfast on body composition and cardiometabolic health in young women with overweight: the NewStart randomised trial.

The aim of this randomised controlled trial was to investigate the effects of breakfast high or low in protein on body composition and cardiometabolic markers in young women with overweight. In total, fifty-six women aged 18-30 years consumed a breakfast containing either high protein (34 g protein, n 26) or low protein (6 g protein, n 30) for 12 weeks. Measurements of body composition by dual-energy X-ray absorptiometry, waist circumference, glucose tolerance, fasting glucose, insulin and lipid profile were performed before and after this period. The primary outcome was fat mass. Satiety and hunger were evaluated by self-reported Visual Analogue Scale (VAS) scores. Dietary intake was estimated by 4-d dietary records, and calcium intake was estimated by FFQ. At baseline, relative daily protein intake was 15·2 ± 2·8 E%, which increased to 19·3 ± 3·4 E% in high protein but was unchanged in low protein (P < 0·001 between groups). High protein reported higher satiety compared with low protein (P = 0·02). Yet, no group differences were observed in changes in energy intake, body composition, blood lipid profile or measures of glucose tolerance (all P > 0·10). However, bone mineral content tended to increase in high protein (P = 0·05) and decrease in low protein (P = 0·07, interaction effect: P = 0·01). Conclusively, a high v. low content of protein in breakfast increased satiety but did not affect body composition or cardiometabolic markers in young women with overweight. This study adds to the sparse evidence on the effects of breakfast with different macronutrient compositions on health parameters in women with overweight. Registered at clinicaltrials.gov: NCT04518605.

Impact of L-carnitine supplementation on gastric emptying and bowel function in pediatric ketogenic diet therapy: a clinical trial

Ketogenic diet (KD) is an excess fat, enough protein, and minimal carbohydrate diet. The high fat content in KD lowers the oesophageal sphincter tone, slows gastric emptying, and decreases intestinal transit time. The primary aim of the current clinical trial was to study the effect of L-carnitine supplementation on gastric emptying in children with drug resistant epilepsy (DRE) on KD. Assessment of the protective effect of L-carnitine on bowel function and habits in those patients was a secondary aim. The current study recruited 30 patients aged 12 months to 18 years newly diagnosed with DRE assigned to start KD who were following up at the Pediatric Clinical Nutrition and Neurology Outpatient Clinics or were admitted due to DRE at the Pediatric Neurology Inpatient Department, Children’s Hospital, Ain Shams University (Egypt). Participants were assigned randomly into 2 arms; arm I: received KD with L-carnitine supplementation, arm II: received KD only. Patients were assessed at baseline and after 3 months of starting KD, the assessments of children included: 24-hour dietary recall, Chalfont Seizures Severity Scale, gastrointestinal symptoms score and Bristol stool chart, frequency of defecation per week, anthropometric measurements assessment, fasting serum lipid profile and measurement of the antral length by ultrasound. There was significant increase in antral length in the patients who received KD with L-carnitine supplementation compared to the non-supplemented group. The antral length showed a significant negative correlation with GI symptoms score in all cases and the L-carnitine supplemented group. It also showed a significant positive correlation with Bristol stool score in all patients and a significant positive correlation with stool frequency in the L-carnitine supplemented group only. L-carnitine supplementation to children with DRE on KD has a significant role in improving gastric motility and it increases the frequency of defecation. Further studies are recommended to explore additional benefits, meanwhile it is prudent to advise L-carnitine supplementation for such patients.

Associations of Serum Lipid Traits With Fracture and Osteoporosis: A Prospective Cohort Study From the UK Biobank.

Previous studies reveal inconsistent associations between serum lipid traits and the risks of fractures and osteoporosis in the general population. This prospective cohort study analysed data from 414 302 UK Biobank participants (223 060 women and 191 242 men, aged 37-73 years) with serum lipid measurements: apolipoprotein A (Apo A), apolipoprotein B (Apo B), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and lipoprotein A (Lp(a)). Multivariable Cox proportional hazard models with penalized cubic splines were used to explore potential nonlinear associations of each lipid trait with the risks of fractures and osteoporosis. Subgroup analyses by age, sex, BMI categories and pre-existing cardiovascular disease were conducted. Mediation analyses using the g-formula were performed to quantify to which extent bone mineral density (BMD) may mediate the association between serum lipids and fracture risk. Over a median follow-up period of 13.8 years, 25 918 (6.8%) of the 383 530 participants without prior fracture had incident fracture cases, and 7591 (4.1%) of the 184 919 participants with primary care data and without baseline osteoporosis were diagnosed with osteoporosis. TG had nonlinear associations with fractures and osteoporosis, whereas Apo B, TC and LDL-C had linear associations. There were also nonlinear associations of Apo A and HDL-C with fractures. Individuals in the highest quintiles for Apo A (fracture: HR 1.15 [95% CI 1.10, 1.21]; osteoporosis: HR 1.13 [1.02, 1.25]) and HDL-C (fracture: HR 1.27 [1.20, 1.34]; osteoporosis: HR 1.31 [1.18, 1.46]) were associated with higher risks of fractures and osteoporosis. Conversely, those in the highest quintile for Apo B (fracture: HR 0.85 [0.81, 0.89]; osteoporosis: HR 0.86 [0.79, 0.94]), LDL-C (fracture: HR 0.89 [0.85, 0.93]; osteoporosis: HR 0.91 [0.83, 1.00]) and TG (fracture: HR 0.78 [0.74, 0.82]; osteoporosis: HR 0.75 [0.68, 0.82]) were associated with lower risks. The associations of Apo A (ratio of HR [RHR] 1.05 [1.02, 1.09]) and HDL-C (RHR 1.06 [1.03, 1.09]) with fracture risk were more pronounced in men compared to women. Except for TG and Lp(a), the associations between serum lipids and fractures appear to be partially mediated through BMD (mediation proportions: 5.30% to 40.30%), assuming causality. Our study reveals a complex interplay between different lipid markers and skeletal health, potentially partially mediated through BMD. Routine lipid profile assessments, including HDL-C and Apo A among other lipid traits, may be integrated into the strategies for fracture risk stratification.

Lipid changes across menopause status point to increased cardiovascular risk

Abstract Background While women develop cardiovascular disease (CVD) approximately ten years later than men, risk of CVD in women rises precipitously following menopause. The mechanisms underlying this acceleration in CVD risk are not well elucidated, but adverse changes in lipid measures are known to occur during the perimenopause period. Previous investigations have been largely restricted to traditional lipid measures and have not examined changes in lipoprotein particles including lipid subfractions and particle number. Purpose We sought to examine longitudinal changes in lipoprotein particles that occur during the menopause transition. Methods A total of 1305 participants in the Dallas Heart Study with known menopause status underwent measurement of LDL-P, HDL-P, sd-LDL, and ld-HDL by NMR LipoProfile LP4 algorithm (LabCorp, Raleigh Durham, NC, U.S.A.) at 2 examinations (between 7-8 years between DHS studies). We compared longitudinal changes in lipoprotein measures between pre-, peri-, post-menopausal women and men using multivariable adjusted linear regression models. For our analysis peri- is the group that was pre-menopause at DHS I and post-menopause at DHS 2, not to mean the period before menopause. Results There 1346 men (referent group) included in the study with a mean age of 43 ± 9.4 years. There was a total of 1246 women with a mean age of 42 ± 5.6 for peri-group, 54 ± 6.2 for post-group, and 34 ± 3.08 for the pre-group. Of the women 440 (35.3%) were pre-menopausal, 298 (23.9%) were peri-menopausal, and 508 (40.8%) were post-menopausal. Over a median follow-up time of 7 years. All three groups had an increase in LDL-P but the greatest percent change is between peri and post, 18.30 (SE 3.05, P&amp;lt;0.001). When compared to men the post-group has the greatest percent change of HDL-P with a negative change of 4.77 (SE 0.948 P&amp;lt;0.0001). Small-dense LDL had the highest percent change in the peri- group when compared to men with a change of 578.62 (SE 288.45, P&amp;lt;0.045). Large-dense HDL had greatest percent change in the post- group when compared to men with negative change of 37.84 (SE 12.83, P&amp;lt;0.0032). Conclusions We found that menopause is associated with adverse changes in lipoprotein profiles, with the most pronounced changes in LDL-particles and subfractions observed for peri-menopausal women. By contrast, post-menopausal women demonstrated the greatest reductions in HDL-particles and subfractions. Taken together, these changes suggest that menopause is associated with a transition to a more atherogenic lipoprotein profile. Further research is needed to investigate whether these adverse changes in lipoproteins translate to greater CV risk.

Lipid and brain volumetric measures in multiple sclerosis patients: findings from a large observational study

ObjectivesThis study aimed to investigate relationships between cholesterol profile, brain volumetric MRI, and clinical measures in a large observational cohort of multiple sclerosis (MS) patients.Materials and methodsWe included 1.505 patients with 4.966 time points including complete lipid, clinical, and imaging data. The time among lipid, brain MRI and clinical measures was under 90 days. Cross-sectional statistical analysis at baseline was performed using an adjusted linear regression and analysis of longitudinal lipid and MRI measures data was performed using adjusted linear mixed models.ResultsWe found associations between higher high-density lipoprotein cholesterol (HDL-C) and lower brain parenchymal fraction (BPF) at cross-sectional analysis at baseline (B = −0.43, CI 95%: −0.73, −0.12, p = 0.005), as well as in longitudinal analysis over follow-up (B = −0.32 ± 0.072, χ2 = 36.6; p = < 0.001). Higher HDL-C was also associated with higher T2-lesion volume in longitudinal analysis (B = 0.11 ± 0.023; χ2 = 23.04; p = < 0.001). We observed a weak negative association between low-density lipoprotein cholesterol (LDL-C) levels and BPF at baseline (B = −0.26, CI 95%: −0.4, −0.11, p = < 0.001) as well as in longitudinal analysis (B = −0.06 ± 0.03, χ2 = 4.46; p = 0.03). T2-LV did not show an association with LDL-C. We did not find any association between lipid measures and disability. The effect of lipid levels on MRI measures and disability was minimal (Cohen f2 < 0.02).ConclusionsOur results contradict the previously described exclusively positive effect of HDL-C on brain atrophy in patients with MS. Higher LDL-C was weakly associated with higher brain atrophy but not with higher lesion burden.

Lipid metabolism and hearing loss: association of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) with adolescent hearing health

BackgroundThe ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol (NHHR) is a novel lipid measure for assessing the risk of cardiovascular disease. Lipid metabolism disorders are reportedly associated with hearing impairment. This study aimed to investigate the potential association between NHHR and hearing.MethodsThe data used in this study were obtained from the National Health and Nutrition Examination Survey (NHANES) cycles of 2005–2010 and 2017–2018, including 4,296 participants aged 6–19 years. The NHHR was calculated from lipid profiles, and hearing was assessed using pure-tone audiometry. Weighted multivariate logistic regression analyses were used to investigate the association between the NHHR and hearing loss. Subgroup and sensitivity analyses were performed to verify the robustness of the results.ResultsUnivariate analysis revealed significant associations between the NHHR and hearing threshold at all categorized frequency (low, speech, or high-frequency) (P < 0.001). Three models were used: an unadjusted model, a model adjusted for age, sex, and race, and a model further adjusted for PIR, BMI, and diabetes. Multiple regression analysis confirmed these associations consistently across all models. When considered as a continuous variable, NHHR had a significant association with enhanced hearing thresholds at all categorized frequencies: low-frequency (β:0.56, 95% CI: 0.36–0.75), speech-frequency (β:0.55, 95% CI: 0.36–0.7), and high-frequency (β:0.55, 95% CI: 0.36–0.74). The adjusted models showed persistent positive correlations after controlling for covariates. The NHHR was consistently positively associated with hearing loss. The NHHR and auditory thresholds showed a general dose-response association across all frequencies.ConclusionsNHHR is a promising biomarker for predicting adolescent hearing threshold shifts and hearing loss. The study highlights the importance of early lipid monitoring and management as strategies to prevent or reduce hearing impairment.

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.

NMR Insights into Lipoprotein Particles: analyzing correlations with traditional lipid measurements

Abstract Introduction Lipid metabolism plays a crucial role in various physiological processes. Lipid molecules are transported by lipoproteins, and the intricate involvement of lipoproteins in cardiovascular disease (CVD) is well-established, given their diverse size, density, and lipid composition. The emergence of Nuclear Magnetic Resonance (NMR) spectroscopy, a high-resolution analytical technique, promotes the assessment of lipoprotein particle numbers and sizes. Studies suggest that the measurement of total low-density lipoprotein particle numbers (LDL-P), small LDL-P (SLDL-P), and total high-density lipoprotein particle numbers (HDL-P) provides better evaluation of risk of CVD than enzymatic-based measurements of LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C). Our study examined the correlation between NMR-derived lipoprotein profiles and traditional cholesterol measurements in control and patient populations. Methods Fasting serum samples were collected from healthy male and female donors (n=148), ages 21-64 years. The analysis also included the results from &amp;gt;20,000 patients’ samples submitted to our laboratory for NMR lipid testing. We assessed LDL-P, SLDL-P, HDL-P, large HDL (LHDL-P), and HDL size (HDL-S) by NMR. In addition, total cholesterol (TC) and HDL-C were measured using traditional automated enzymatic assays (Roche Diagnostics); LDL-C was calculated. Statistical analyses, including Spearman correlation, were performed using GraphPad Prism software. Spearman coefficient (r) ≥0.75 indicated a strong correlation, r &amp;lt;0.5 indicated a weak correlation. Results HDL-C only moderately correlated with total HDL-P in samples collected from controls (rcontrols=0.52) and patients (rpatients=0.68), while showing better correlation with LHDL-P (rcontrols=0.90, rpatients=0.89). Traditional LDL-C strongly correlated with total LDL-P (rcontrols=0.76, rpatients=0.81), but showed only weak correlation with SLDL-P (rcontrols=0.42, rpatients=0.28), which is considered more atherogenic and predictive of CVD risk than LDL-C or total LDL-P. Interestingly, among various lipoprotein parameters, SLDL-P correlated the strongest with HDL-S in both study populations (rcontrols=-0.87, rpatients=-0.84). Samples with higher number of SLDL-P also had smaller size of HDL-P, although the number of total HDL-P did not differ between high vs low SLDL-P samples. In contrast, only moderate negative correlation was observed between SLDL-P and traditional HDL-C (rcontrols=-0.74, rpatients=-0.68), suggesting that the size of HDL particles might add value in evaluating CVD risk. Conclusion The NMR technology has advantage over traditional measurements in stratifying an individual’s lipoprotein milieu. It provides insights into the number of small LDL particles and size of HDL particles, which are not included in standard lipid testing and may allow for more individualized patient care. Incorporation of lipoprotein size and particle number in clinical guidelines may help physicians with assessment CVD risk and treatment monitoring.

Predictors in Youth of Adult Cardiovascular Events.

Childhood risk factors are associated with cardiovascular events in adulthood. We compared the utility of a risk model based solely on nonlaboratory risk factors in adolescence versus a model that additionally included lipids to predict cardiovascular events in adulthood. The study comprised 11 550 participants from 7 longitudinal cohort studies in the United States, Australia, and Finland with risk factor measurements in adolescence and followed into adulthood. The adolescent risk factors were defined by using clinical standards including overweight or obesity, elevated blood pressure, smoking, and borderline high or high levels of total cholesterol and triglycerides. The main outcomes were medically adjudicated fatal or nonfatal cardiovascular disease events occurring after age 25. Of 11 550 participants (55.1% female, mean age 50.0 ± 7.7 years), 513 (4.4%) had confirmed cardiovascular events. In a multivariable model (hazard ratio [95% confidence interval]), elevated blood pressure (1.25 [1.03-1.52]), overweight (1.76 [1.42-2.18]), obesity (2.19 [1.62-2.98]), smoking (1.63 [1.37-1.95]), and high total cholesterol (1.79 [1.39-2.31]) were predictors of cardiovascular events (P < .05). The addition of lipids (total cholesterol and triglycerides) into the nonlaboratory model (age, sex, blood pressure, BMI, and smoking) did not improve discrimination in predicting cardiovascular events (C-statistics for the lipid model 0.75 [SD 0.07] and nonlaboratory model 0.75 [0.07], P = .82). Nonlaboratory-based risk factors and lipids measured in adolescence independently predicted adult cardiovascular events. The addition of lipid measurements to nonlaboratory risk factors did not improve the prediction of cardiovascular events.

Huge and Multiple Xanthomas Misdiagnosed as Rheumatoid Nodules and Mistreated with Multiple Surgical Excisions over 4 Years, A Case Report

Background: Xanthoma is the iceberg of familial hypercholesterolemia; it’s resemblance to other cutaneous lesions such as rheumatoid nodules might lead to misdiagnosis. We emphasize in this case report the importance of comprehensive clinical and investigatory approach to cutaneous lesions as they could be the only manifestation of systemic diseases, and this helps to avoid delayed management and unnecessary interventions. Aim: Xanthomas as a possible diagnosis for multiple skin nodules, as it can be easily supported by performing simple noninvasive blood tests; the lipid panel. Case report: Female patient, presented with multiple skin lesions and a strong family history of premature coronary artery disease. She was firstly managed with multiple surgical resections as having benign masses, and later was misdiagnosed as having rheumatoid nodules and referred to rheumatology clinic for evaluation, wherein a clinical suspicion of xanthomas originated, and was supported by the severely elevated serum LDL level and a tissue diagnosis of xanthoma. She has been started on statins with regular clinic. Conclusion: The purpose of this case study is to explain the importance of including xanthomas within the differential diagnosis of recurrent skin lesions. Whereas the tissue diagnosis is the gold-slandered investigation, simple noninvasive blood test, serum lipid measurement can be the clue for diagnosis of the hidden fatal but easily controllable disease; familial hypercholesterolemia.

A role for plasma membrane Ca2+ ATPases in regulation of cellular Ca2+ homeostasis by sphingosine kinase-1

Sphingosine-1-phosphate (S1P) is a ubiquitous lipid mediator, acting via specific G-protein-coupled receptors (GPCR) and intracellularly. Previous work has shown that deletion of S1P lyase caused a chronic elevation of cytosolic [Ca2+]i and enhanced Ca2+ storage in mouse embryonic fibroblasts. Here, we studied the role of sphingosine kinase (SphK)-1 in Ca2+ signaling, using two independently generated EA.hy926 cell lines with stable knockdown of SphK1 (SphK1-KD1/2). Resting [Ca2+]i and thapsigargin-induced [Ca2+]i increases were reduced in both SphK1-KD1 and -KD2 cells. Agonist-induced [Ca2+]i increases, measured in SphK1-KD1, were blunted. In the absence of extracellular Ca2+, thapsigargin-induced [Ca2+]i increases declined rapidly, indicating enhanced removal of Ca2+ from the cytosol. In agreement, plasma membrane Ca2+ ATPase (PMCA)-1 and -4 and their auxiliary subunit, basigin, were strongly upregulated. Activation of S1P-GPCR by specific agonists or extracellular S1P did not rescue the effects of SphK1 knockdown, indicating that S1P-GPCR were not involved. Lipid measurements indicated that not only S1P but also dihydro-sphingosine, ceramides, and lactosylceramides were markedly depleted in SphK1-KD2 cells. SphK2 and S1P lyase were upregulated, suggesting enhanced flux via the sphingolipid degradation pathway. Finally, histone acetylation was enhanced in SphK1-KD2 cells, and the histone deacetylase inhibitor, vorinostat, induced upregulation of PMCA1 and basigin on mRNA and protein levels in EA.hy926 cells. These data show for the first time a transcriptional regulation of PMCA1 and basigin by S1P metabolism. It is concluded that SphK1 knockdown in EA.hy926 cells caused long-term alterations in cellular Ca2+ homeostasis by upregulating PMCA via increased histone acetylation.

Inferring the feeding history of the castor bean tick, Ixodes ricinus from lipid and body measurements.

The ability to determine when ticks last fed and assign them to a specific feeding cohort is important in attempts to explain their population dynamics; the biochemical measurement of stored lipid, has been widely used for this purpose. However, when relating feeding history to behaviour or infection status, a non-destructive approach to its assessment would be of value and, to this end, previous studies have attempted to use morphometric indices. Within any instar, the sclerotised scutal components of the body will not vary with increasing starvation while the alloscutal components will, and the resulting ratio should provide a measure of time since feeding. Here, the aim was to determine whether such a morphological ratio (described here as the hunger index) changed predictably with starvation in Ixodes ricinus L. (Ixodida: Ixodidae). For this a cohort of 300 I. ricinus nymphs was collected from the field in February 2021 and starved in a humidified incubator at 15°C and 80% relative humidity (RH). Every 2 weeks, 50 nymphs selected at random were removed and killed by freezing; morphometric measurement was followed by the measurement of lipid using a standard spectrophotometric approach. Both hunger index and stored lipid changed significantly with increasing starvation and were positively correlated with each other. However, the change in morphometric ratio was relatively slight (11%) over 9 weeks and the variation was high. The data suggest therefore that morphological measurements could be used to provide, at best, only broad categorisation of the hunger status of individual I. ricinus ticks in the field.

Tracking the Risk of Cardiovascular Disease after Almond and Oat Milk Intervene or Statin Medication with a Powerful Reflex SH-SAW POCT Platform.

Cardiovascular disease (CVD) represents the leading cause of death worldwide. For individuals at elevated risk for cardiovascular disease, early detection and monitoring of lipid status is imperative. The majority of lipid measurements conducted in hospital settings employ optical detection, which necessitates the use of relatively large-sized detection machines. It is, therefore, necessary to develop point-of-care testing (POCT) for lipoprotein in order to monitor CVD. To enhance the management and surveillance of CVD, this study sought to develop a POCT approach for apolipoprotein B (ApoB) utilizing a shear horizontal surface acoustic wave (SH-SAW) platform to assess the risk of heart disease. The platform employs a reflective SH-SAW sensor to reduce the sensor size and enhance the phase-shifted signals. In this study, the platform was utilized to monitor the impact of a weekly almond and oat milk or statins intervention on alterations in CVD risk. The SH-SAW ApoB test exhibited a linear range of 0 to 212 mg/dL, and a coefficient correlation (R) of 0.9912. Following a four-week intervention period, both the almond and oat milk intervention (-23.3%, p < 0.05) and statin treatment (-53.1%, p < 0.01) were observed to significantly reduce ApoB levels. These findings suggest that the SH-SAW POCT device may prove a valuable tool for monitoring CVD risk, particularly during routine daily or weekly follow-up visits.

Application of multispectral optoacoustic tomography for lower limb musculoskeletal sports injuries in adults

Compositional changes in relation to musculoskeletal injuries are difficult to measure non-invasively. This study aims to use non-invasive label-free imaging with Multispectral Optoacoustic Tomography (MSOT) to evaluate compositional changes with injury. Five different patient groups were examined, covering diagnoses of Achilles or patellar tendinopathy, Achilles tendon rupture and gastrocnemius muscle strain injury. Injured and contralateral limbs were imaged using a commercial MSOT device. Hemoglobin, collagen, and lipid contents were estimated. Some patients were examined before and after exercise. Hemoglobin measures had high reproducibility and displayed systematic changes in response to exercise. The content and exercise response of hemoglobin was equal on both limbs. In contrast, collagen and lipid measures were inconsistent and did not display the expected distribution. In conclusion, MSOT is applicable to imaging of hemoglobin in musculoskeletal injuries, providing complimentary information to conventional ultrasound, but applicability to other components like collagen and lipids could not be shown.