Direct LDL Research Articles

8481 A 32 Year Old Male With Recurrent Acute Pancreatits and Severe Hypertriglyceridemia: Importance of Considering Genetic Variants

Abstract Disclosure: M.F. Salazar Zelaya: None. J.D. Sibaja Jiménez: None. Background : Hypertriglyceridemia is a common medical scenario in daily practice, causing a variety of symptoms including recurrent episodes of acute pancreatits, which can be severe. Multiple genetic variants can lead to different spectrums of the disease. CLINICAL CASE: A 32 year old male police officer presented to our Endocrinology Outpatient Clinic with a history of long standing hypertriglyceridemia and six previous episodes of acute pancreatits, two in the last twelve months. Familiy history was negative for lipid disorders. The patient had adecuate adherence to diet and exercise as well to prescribed medications, which included Fenofibrate 250 mgs/day and Rosuvastatin 40 mgs/day. The patient denied consumption of alcoholic beverages. Recent abdominal ultrasound was reported without abnormalities. His lipid panel reported elevated triglycerides at 5831 mg/dl (n<150 mg/dl), Total Cholesterol normal at 147 (n<200 mg/dl), low HDL levels at 12 mg/dl (range 12-92 mg/dl) and direct LDL Cholesterol at 120 mg/dl. His TSH value was normal at 1.02 uUI/mL (range 0.55-4.78 uUI/mL). Creatinine level was normal at 0.81 mg/dl (range 0.7-1.3 mg/dl). Liver function tests were normal with AST level at 25 IU/L (range 13-39 IU/L) ALT levels at 22 IU/L (range 7-52 IU/L) and alcaline phosphatase at 62 IU/L (range 34-104 IU/L).His fasting glucose level were normal at 82 mg/dl (n<100 mg/dl). Due to a high Familial Chylomicronemia Syndrome clinical score (13 points) we proceeded with genetic analysis of this patient. Next Generation Sequencing for genes related with chylomicronemia (APOA5, APOC2, GPIHBP1,LMFI, LPL) was performed to determine gene sequence plus copy number variation.Two heterocigote variants were reported, both in the LPL gene. The first one: LPL (NM 000237.3) c.644>A;p.Gly215Glu heterozygous is a missense variant already reported in the literature, registered in ClinVar (ID 1522) and the Leiden Open Variation Database. This variant is classified as pathogenic according to criteria PS3, PM1, PP3, PP5 of the American College of Medical Genetics and Genomics. The second one: LPL (nm 000237.3): c.383C>A;p.Thr128Asn;heterozygous is also a missense variant which to the extent of our knowledge has previously been reported only once in the literature: ClinVar (ID 1520537). This variant is classified currently as of unknown clinical significance according to PM2 criteria. There is however and entry reported (PMID: 8778602) of another variant affecting the same codon (p.Thr128AIa) that is associated to chylomicronemia syndrome. Conclusion: In cases of severe hypertriglyceridemia, suspicion and determination of gene variants are of great importance nowadays as they could eventually guide treatment, given the availability in some countries (and currently pending FDA approval) of new pharmacological therapies such as apo C-III inhibitors. Presentation: 6/2/2024

A-223 Direct LDL or not Direct-LDL, that is the question

Abstract Background Management of Cardiovascular Disease (CVD) risk is dependent on Low Density Lipoprotein Cholesterol (LDL-C) levels; therefore LDL-C serves as the marker for the assessment of CVD risk and the focus of lipid lowering treatment. The gold standard reference method for measurement of LDL-C is beta-quantification. We compared calculated LDL-C with Friedewald (F-LDL-C), Martin-Hopkins (M-LDL-C) and Sampson (S-LDL-C) equations versus LDL-C directly measured (D-LDL-C). In CVD management also cholesterol ratios are evaluated. TC/HDL is associated with morbidity and mortality in the general population. Furthermore, several studies have stated that high triglycerides (TG) levels and low HDL-C (TG/HDL ratio) could function as an atherogenic index. Methods 11399 samples were analyzed on Siemens Atellica Solution® for the lipid profile determination measuring Total Cholesterol (TC), D-LDL-C, HDL-C and TG. In the absence of additional clinical parameters, based on desirable levels for LDL-C recommended by guidelines, CVD risk was evaluated by assigning to LDL-C a cut-off of 100 mg/dL. In presence of misclassifications, we used two other parameters to assess LDL-C results: TG/HDL-C ratio and CT/HDL-C. Results Patients cohort had a mean age of 57.7 (±16.8) years of which 53% (age=58.6, ±15.9) were males and 47% (age=56.5, ±17.8 years) were females. Of these, the 57.7% were outpatients and 42.3% inpatients (42.1% of infectious diseases - 24.4% of the cardiovascular department). Data about LDL-C misclassification and ratio data parameters are shown in table 1. Discordant patients for D-LDL-C vs F-LDL-C are 8.5%, that of D-LDL-C vs M-LDL-C are 7.7% and D-LDL-C vs S-LDL-C are 7.2%. Conclusions Is known that LDL plays a central role in the pathogenesis of atherosclerosis. Accurate estimation of LDL-C is a fundamental point for the stratification of CVD risk and the achievement of the therapeutic goal; however, we are still uncertain about the best and accurate way to measure it.

Evaluation of remnant lipoprotein accumulation by measuring non-HDL-cholesterol minus direct LDL cholesterol level (non-HDL-C-dLDL-C) instead of measuring remnant cholesterol levels

Evaluation of remnant lipoprotein accumulation by measuring non-HDL-cholesterol minus direct LDL cholesterol level (non-HDL-C-dLDL-C) instead of measuring remnant cholesterol levels

Comparison of the Friedewald and Vujovic methods with the calculated LDL concentration in a biochemical auto-analyzer.

To compare the concentration of Low-Density Lipoprotein (LDL-c) obtained using the Friedewald formula with those obtained directly with the RAYTO CHEMRAY 120 autoanalyzer. Cross-sectional study. We evaluated outpatients with a medical request for a lipid profile study (total cholesterol, triglycerides, LDL, and HDL). The analyses were carried out in a RAYTO CHEMRAY 120 autoanalyzer under the principle of spectrophotometry. We obtained LDL-c using the Friedewald and Vujovic formulas. We evaluated 199 individuals whose direct LDL concentration averages were measured by the RAYTO CHEMRAY 120 equipment. Those calculated by the Friedewald and Vujovic formulas were 129.97 ± 32.66, 119.28 ± 30.44, and 127.01 ± 32.01, respectively, and in all cases, significant differences (P < 0.001) were observed with the RAYTO analyzer. In both cases a low positive bias was found with the RAYTO analyzer.. The Passing-Bablok and Deming's regressions showed a linear correlation between both methods (Friedewald and Vujovic) with the LDL values obtained with the Rayto autoanalyzer. Our study found that the Friedewald and Vujovic methods are good predictors of LDL cholesterol levels and have a low level of bias. Therefore, they could be used as potential predictors.

Calculated LDL cholesterol (freidwald, martin johns and Sampson) comparison of retrospective data with direct LDL cholesterol and hypertriglyceridaemia

Calculated LDL cholesterol (freidwald, martin johns and Sampson) comparison of retrospective data with direct LDL cholesterol and hypertriglyceridaemia

Comparison of Friedewald, Martin/Hopkins, and Sampson formulae with direct LDL measurement in hyperlipidaemic and normolipidaemic adults

&#x0D; ABSTRACT&#x0D; Objective: In our study, we aimed to compare and validate the performance of the Friedewald, Martin/Hopkins, and Sampson formulae with direct LDL-C measurement.&#x0D; Material and Methods: The study was a retrospective investigation which by the Department of Medical Biochemistry of the Ankara Training and Research Hospital between 1 January 2021 and 31 December 2022. Our study evaluated the results of 6297 patients aged 18-99 years who underwent cholesterol panel TC, TG, HDL-C and direct LDL-C in our laboratory. Estimated LDL-C calculated according to Friedewald, Martin/Hopkins, and Sampson formulae. &#x0D; Results: All three formulae showed a stronger positive correlation with d-LDL-C (0.905, 0.897, and 0.886, respectively, for all data, p&lt;0.001). In addition, when we compared the total median difference (1st-3rd quartile) of all formulae, it was it was -0.69 (-1.62-0.39) for Friedewald, 0.034 (-0.74 -1.14) for Martin/Hopkins and -0.40 (-1.19-0.55) for Sampson. According to Passing Bablok regression analyses, the intercept was determined as -0.97 (95% CI = -1.01 to -0.93), 0.41 (95%=0.37 to 0.44) and -0.05 (-0.08 to -0. 03) and slopes were calculated as 1.083 (95% CI = 1.07-1.09), 0.88 (0.88 to 0.89) and 0. 90 (95% = 0.89 to 0.90) for Friedewald, Martin/Hopkins and Sampson, respectively.&#x0D; Conclusions: Our findings suggest that Martin/Hopkins formula indicated a better performance than Friedewald and Sampson formulae. We figured out utilizing the Martin/Hopkins formula as a good alternative for estimated LDL-C in Turkish adults. &#x0D;

Does Fredrickson Friedewald’s formula and direct assay of LDL concentration in serum give varying results? - A pilot retrospective study in a tertiary care hospital

Background and Aims: The LDL-C levels guide the cardiovascular risk assessment under the National Cholesterol Education Program Adult Treatment Panel (NCEP) as well as used for the management of dyslipidemia. Traditionally, LDL-C level is calculated using the Friedewald formula i.e., cLDL, however, recently many of the laboratories have shifted to newer methods of direct LDL-C estimation, i.e., dLDL. With this transition, there is increased demand to compare and establish updated LDL-C level cutoffs for the risk assessments of cardiovascular events. Methods: A retrospective observational study, comprising 216 study participants, was conducted in the Department of Biochemistry, Lady Hardinge Medical College, and associated hospitals, in New Delhi for 12 months. Data was collected from 216 adult patients (&gt; 18 years) whose routine fasting lipid profile was done and documented in our clinical biochemistry lab. LDL-C levels done by direct method and calculated methods were compared using the Intraclass correlation coefficient (ICC). Appropriate statistical tests were used with a p-value &lt;0.05 taken as statistically significant. Results: When compared between dLDL-C and cLDL-C significant difference was seen with mean values as 104 ±38.8 and 85.5 ±35.6 mg/dl respectively. However, a strong positive correlation was seen between dLDL-C and cLDL-C, r=0.9, p&lt;0.01. The ICC showed good reliability for overall comparison between dLDL-C and cLDL-C, however, reliability was found to be poor for group 2. Conclusions: Friedewald and modified Friedewald equations can be used as a substitute for direct homogenous LDL estimation when resources are scarce.

A comparative analysis of direct LDL measurement and calculated LDL: Assessing accuracy and clinical implications

A comparative analysis of direct LDL measurement and calculated LDL: Assessing accuracy and clinical implications

Concordance of Friedewald Formula results with direct LDL examination in non-diabetic young subjects

Concordance of Friedewald Formula results with direct LDL examination in non-diabetic young subjects

Concordance between low density lipoprotein cholesterol concentration measurement by enzymatic method and calculation by Friedewald formula in cardiovascular risk classification

Accurate estimation of low-density lipoprotein cholesterol (LDL-C) is important for cardiovascular risk assessment and guiding cholesterol-lowering therapy. Due to the high cost of β-quantification (Gold standard) and time-consuming, direct measurement of LDL-C is an alternative method. However, unlike the calculation of LDL-C by Friedewald formula, there is an additional cost in terms of reagents for performing a direct LDL-C test. The current study aimed to compare direct LDL-C concentration determination to data calculated by Friedewald formula. 752 lipid profiles of 710 people with LDL-C estimated by direct LDL assay, in the Biochemistry laboratory of university hospital center of Angré, were included in the study. In the same group, LDL-C was calculated using Friedewald formula. Lin’s concordance correlation coefficient (ccc) and Passing-Bablok regression analysis using, MedCal software, were performed to assess the strength of concordance between the 2 methods, and identify any possible bias. The concordance between the two methods was moderate (ρc = 0.9466). Passing-Bablok regression analysis revealed a systematic bias between the two methods. The total error observed (TEobs) between the two methods was higher than allowable total error recommended by the NCEP-ATPIII when LDL-C values was less than 159 mg/dL (4.112 mmol/L). The Friedewald formula resulted in lower LDL-C concentration values. Despite its cost-effectiveness in the estimation of LDL-C, an underestimation of LDL-C levels could result in inaccurate cardiovascular diseases (CVD) risk assessments and potentially significant future societal costs due to inadequate prevention and treatment of CVD.

Correlations of Estimated Serum Small Dense Low-Density Lipoprotein and Isoprostane with Metabolic Syndrome Criteria between Metabolic Syndrome and Non-Metabolic Syndrome Subjects in Selangor

Introduction: Metabolic syndrome (MetS) is a global healthcare burden associated with increased risk of atherosclerosis (ATH). The relationship between atherogenic lipoprotein and oxidative stress biomarkers with clinical risk factors of MetS have not been fully explored. Therefore, the objective of this study is to determine the correlation between small dense low-density lipoprotein (sdLDL-c) and isoprostane (ISP) with MetS criteria and comparing these biomarkers between MetS and non-MetS. Materials and Methods: This was a cross sectional study involving 67 MetS and 43 non-MetS diagnosed by JIS criteria 2009. Demographic details and anthropometric measurements were recorded. Blood samples were collected to analyse serum plasma glucose, direct LDL, calculated sdLDL-c and ISP. Results: Mean serum sdLDL-c and ISP levels were significantly higher among those with MetS compared to non-MetS (1.14+0.44 mmol/L vs 0.87±0.38 mmol/L respectively, p=0.005). Similarly, mean serum ISP concentration was higher among MetS compared to non-MetS (884.40+602.69 ng/L vs 657.89±616.42 ng/L respectively, p= 0.054). sdLDL-c was positively correlated with TG in the MetS (Pearson correlation 0.501, p&lt;.001) whilst HDL-c was positively correlated with sdLDL-c among the non-MetS (Pearson Correlation 0.422, p&lt;.005). Conclusion: This study highlights the correlation between sdLDL-c and TG in among MetS, emphasizing the need to closely monitor and manage TG among this cohort to reduce the risk of ATH. It was also noted that HDL-c showed positive correlation with sdLDL-c among non-MetS. This discordant finding suggests that HDL-c itself may not be causally associated with cardiovascular benefits and that perhaps HDL-c subfractions may be a better approach to determine cardioprotective effects of HDL-c.

Measurement of small, dense lipoproteins. Usefulness of the Tg/HDL index compared to direct LDL measurement

Abstract Funding Acknowledgements Type of funding sources: None. Main funding source(s): Ninguna Introduction The Triglyceride/HDL (Tg/HDL) ratio when &amp;gt; 2 is translated into the presence of small, dense lipoproteins (sdLDL), which are more atherogenic and help us measure global lipid risk regardless of LDL levels. There is the possibility of measuring sdLDL directly, but it is not performed in routine clinical practice. The objective of our study was to analyze the correlation of the TG/HDL index with the direct measurement of sdLDL and cardiovascular risk (CVR). Materials and methods Patients who were treated in cardiology from July 1 – July to September 30, 2022 were analyzed consecutively and the determination of the lipid profile with direct measurement of sdLDL was requested. This measurement is considered risk when sdLDL&amp;gt; 50 mg/dl. Results n 75. Mean age 60 ± 15 years. 37.3% were women. 49.3% were hypertensive, 48% dyslipidemic, 22.7% diabetic, 32% smokers, 58.7% very high CVR and 54.7% with lipid-lowering treatment. Mean LDL levels were 84.3±37 mg/dl, non-HDL 110±39 mg/dl, triglycerides 139±75 mg/dl, remnant cholesterol 27.8 ±15 mg/dl, LDL-sd 34±20 mg/dl and Tg/HDL 3.5±±2. Patients with Tg/HDL&amp;gt;2 had mean sdLDL levels 36± 23 mg/dl vs 29.7 ± 14 mg/dl (p0.06) and those with Tg/HDL&amp;gt;3 39.8± 26 mg/dl vs 28.9± 12 mg/dl ±(p&amp;lt;0.02). All patients with LDL&amp;gt; 50 mg/dL levels had Tg/HDL&amp;gt;2, however 60% of patients with Tg/HDL&amp;gt;2 had LDL&amp;lt;50 mg/dL levels (p0.01), but only 37% Tg/HDL&amp;gt;3 (p&amp;lt;0.001). (Table 1. Relationship between lipid profile, Tg/HDl and LDL-SD) 20% of very high/high RCV patients had LDL&amp;gt;50 mg/dl, 9.1% moderate RCV and 12.5% low RCV. Conclusions The Tg/HDL index may be more useful in identifying patients with LDL&amp;gt; 50 mg/dl primarily when it is &amp;gt; 3.

Factors of local conversion of iodothyronines correlate with indicators of hormonal, biochemical, and hematological profiles in patients with spinal canal and dural sac stenosis of the lumbar spine

In order to find out the mechanisms of pathogenesis of degenerative-dystrophic diseases of the spine, it is of particular interest to search for body parameters which are directly or indirectly interrelated with the key factors of peripheral conversion of nidus iodothyronines and constitute a system of network interactions, affecting metabolic indicators at the local and systemic level.The aim. To search for correlations of local key factors of peripheral conversion of Ligamentum flavum iodothyronines with indicators of biochemical, hematological and hormonal blood profiles of patients with stenosing processes of the spinal canal and dural sac in the lumbar spine.Materials and methods. 33 patients (15 males, 18 females) with stenosing processes of the spinal canal and dural sac in the lumbar spine were examined (mean age – 45.73 ± 1.95 years). The expression of deiodinase genes and other candidate genes was determined in Ligamentum flavum biopsies collected during surgical treatment. Biochemical, hematological and hormonal parameters were determined in peripheral blood. The resulting data array was processed in order to find correlations between the parameters of systemic and local metabolism.Results. The relationships of deiodinases with the expression of GDF5, MMP1, MMP3 and TIMP1 in Ligamentum flavum (p &lt; 0.05) were found. Of the hormonal profile of the blood serum, the most significant indicators were thyreotropin, free triiodothyronine and thyroperoxidase antibodies. In the biochemical profile, levels of direct bilirubin, total cholesterol, HDL and LDL cholesterol and triglycerides changed along with the expression of deiodinases. Correlative relationships with the expression of deiodinases were found for the following hematological analytes of whole peripheral blood: hemoglobin, mean corpuscular hemoglobin concentration, numbers of granulocytes, lymphocytes, eosinophils, monocytes, band neutrophils, red cell distribution width and platelet crit. The data obtained indicate the involvement of peripheral conversion factors in the pathogenetic process and provide information to form a new view on the pathogenesis of degenerative-dystrophic processes in the Ligamentum flavum of patients with stenosing processes of the spinal canal and the dural sac in the lumbar spine.

PSUN267 New-Onset Type 1 Diabetes (T1D) In a Child Presenting With Diabetic Ketoacidosis (DKA) and Severe Hypertriglyceridemia Without Pancreatitis

Abstract Background Hypertriglyceridemia is a rare complication of DKA in children that can prolong hospital course. Case Report A 7-year-old boy with past medical history of autism spectrum disorder presented to an outside hospital with 1 day of abdominal pain and vomiting with "heavy breathing" in the setting of 5 months of weight loss, anorexia, and polyuria/polydipsia with secondary nocturnal enuresis. He had venous pH 6.87, bicarbonate 4.8 mmol/L, and glucose 385 mg/dL consistent with DKA in new onset T1D. He received 10 mL/kg normal saline bolus and regular insulin infusion was then initiated at 0.1 units/kg/hour. Abdominal ultrasound was notable for small bowel-small bowel intussusception. He was transferred to a tertiary care children's hospital. On arrival, labs were notable for pH 7.03, bicarbonate 3 mmol/L, potassium 6.19 mmol/L, glucose 274 mg/dL, beta hydroxybutyric acid 8.90 mmol/L (ref ≤0.29), amylase 20 unit/L (ref 40-220), lipase 10 unit/L (ref 7-60), and HbA1c 9.9%. His blood was noted to be lipemic which prompted lipid evaluation. Direct LDL was 8 mg/dL, HDL was 16.5 mg/dL, and triglycerides (run via dilution) were markedly elevated at 17,675 mg/dL (ref 0-100). Given risk for pancreatitis, triglyceride and lipase levels were trended twice daily. Insulin infusion of 0.1 units/kg/hour did not lead to improvement of acidosis. Infusion rate was increased to 0.15 units/kg/hour and acidosis resolved within 24 hours. He remained NPO and insulin infusion was continued to manage hypertriglyceridemia. Plasmapheresis was considered but given no end-organ dysfunction and down-trending triglycerides, this was not pursued. The insulin infusion rate was decreased to 0.05 units/kg/hour to avoid hypoglycemia. Lipase rose above the upper limit of normal only once to 68 unit/L, on hospital day (HD) 5. The infusion was discontinued on HD 6 with triglycerides 1,290 mg/dL. His appetite improved by HD 5 and, given absence of pancreatitis, he began enteral intake of a low-fat diet. Prior to diagnosis, he had a restrictive diet due to his autism and ate primarily high-fat foods (reportedly 50 breakfast sausages/day), so his diet was liberalized on HD 7 with no increase in triglycerides. One month later, triglycerides normalized to 75 mg/dL. Total cholesterol was elevated at 250, direct LDL 157 mg/dL, and HDL 83 mg/dL. He continues to eat a restrictive, high fat diet which is thought to contribute to his hyperlipidemia. There is no clear family history of hyperlipidemia, but genetic testing for lipid disorders may be obtained. GAD and ZnT8 antibodies were elevated, confirming T1D. Conclusion Hypertriglyceridemia can complicate DKA and require prolonged insulin infusion. Even severe hypertriglyceridemia does not always lead to end-organ dysfunction and can be managed with insulin infusion rather than plasmapheresis. Underlying pathophysiology of hypertriglyceridemia in this case remains incompletely understood. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Derivation of a Modified Friedewald's equation for LDL cholesterol estimation in Sub-Himalayan population: A comparative study.

ABSTRACTBackground:Despite the availability of alternative homogenous assays for LDL-C measurement, most of the laboratories still use Friedewald Equation (FE). However, various novel equations have shown better performance than FE specific to a particular population. Besides, no equation has been devised for use in Sub-Himalayan population.Methods:A cross-sectional laboratory data-based study was conducted by recruiting lipid profiles of 1851 samples to validate 10 different equations for calculating LDL and to devise a novel Modified Friedewald Equation (MFE) specific for Sub-Himalayan population.Results:The novel MFE is presented as: LDL-C = -2.421 + (0.752 × TC) - (0.047 × TG) - (0.350 × HDL). A significant difference was observed between direct LDL-C (118.84 ± 40.39 mg/dL) and all other equations except MFE (118.84 ± 37.96 mg/dl, P > 0.999) and Puavilai Equation (117.99 ± 49.05 mg/dL, P = 0.138). Additionally, MFE showed lowest mean percentage bias of 0.14% with 95% limits of agreement within ± 2SD on Bland-Altman analysis. On ROC analysis at cut-offs of clinical decision limits of 100 mg/dl, 130 mg/dl, 160 mg/dl, and 190 mg/dl, MFE outperformed all other equations with highest AUC (0.974, 0.978, 0.982, and 0.995) respectively with specificity >95% at higher levels. MFE also showed highest correlation (r = 0.954, P < 0.001) and least rMSE (13.8) with direct LDL although all the equations showed significant positive correlation with direct LDL (p < 0.001).Conclusion:MFE derived in this study showed a better diagnostic performance as compared to other 10 equations taking Direct LDL-C as gold standard for Sub-Himalayan Population and may be used as a substitute for FE in the study population.

Evaluation of toxicity, nephroprotective and hepatoprotective activities of Argan oil on CCl4-induced nephrotoxicity and hepatotoxicity in Wistar rats

In traditional therapy, Argania spinosa L. seeds oil used as a nephroprotective and hepatoprotective agent. The present work aims to investigate the acute toxicity of unroasted Argan oil, and studied the nephroprotective and the hepatoprotective activity of both oils Roasted (Roil) and unroasted Argan oil (UnRoil) on CCl 4 -induced liver and kidney damages in Wistar rats. Animals were divided into five equal groups; Control and CCl 4 groups are received only distilled water (10 mL/Kg/day). Control positive group received 50 mg/Kg/day of Silymarin. Roil and UnRoil groups treated with 2 mL/Kg/day of Roil and UnRoil. One week after each pretreatment, the rats are injected intraperitoneally with 1 mL/kg/week of CCl 4 . The treatment has lasted for 15 days. The body weight, urinary volume, water, and food intake were measured at the end of the treatment. Then, the animals are sacrificed; the blood and the liver samples were collected for determining the liver weight ratio and biochemical parameters. UnRoil did not show any sign of toxicity up to 5 mL/Kg. In Roil and UnRoil groups the water intake, ALT, AST, total and direct bilirubin, triglycerides, LDL, plasmatic creatinine, urea, uric acid, and MDA levels are reduced significantly as compared with the CCl 4 group. However, body weight,liver weight ratio, food intake, urine urea, urinary creatinine, hepatic glycogen, and GSH levels showed a significant increase compared to the CCl 4 group. Roil and UnRoil showed important nephroprotective and hepatoprotective effects against CCl 4 . Although, the roasting process does not influence the ability of Argan seed oils towards these activities. Keywords:

Aplicabilidade da fórmula Martin‐Hopkins e comparação com a fórmula Friedewald na estimativa do colesterol LDL na população do estudo e_COR

IntroductionLow‐density lipoprotein cholesterol (LDL) is essential in managing cardiovascular disease risk. Since 1972, the Friedewald formula has been used to estimate LDL concentration, although with some limitations. In 2013, Martin et al. proposed a similar but more accurate formula for calculating LDL. AimTo assess the applicability of the new formula, which we have named the Martin‐Hopkins formula, in the Portuguese population and compare it with the Friedewald formula using direct LDL. Material and methodsCross‐sectional study, including 1689 participants from the e_COR study. We applied the Martin‐Hopkins and Friedewald formulas for estimated LDL (LDL‐M and LDL‐F). The Friedewald formula was not applied in 12 cases due to triglycerides ≥400mg/dL. Direct LDL was measured and the accepted significance level was p<0.05. ResultsOf the total subjects, 50.2% were male and had a median age of 51 (34) years. LDL‐D was 117.0 (44.0) mg/dL, LDL‐M was 114.6 (43.7) mg/dL and LDL‐F was 113.8 (43.2) mg/dL. The Spearman coefficient (ρ) between LDL‐M/LDL‐D was 0.987 and between LDL‐F/LDL‐D was 0.983, p=0.001. This strong correlation was maintained in the group with diabetes (LDL‐M/LDL‐D ρ=0.987; LDL‐F/LDL‐D ρ=0.978, p=0.001) and hypertriglyceridemia (LDL‐M/LDL‐D ρ=0.983; LDL‐F/LDL‐D ρ=0.982, p=0.001). In terms of agreement, the highest value of κ=0.90 was obtained for LDL‐M when LDL‐D <100 mg/dL. ConclusionThe Martin‐Hopkins formula performed well and had good applicability, showing superiority in relation to the Friedewald formula, especially for LDL‐D values <100 mg/dL, diabetes, and hypertriglyceridemia.

Multivariate analysis by OPLS as a novel tool to identify cause of variation between assays for direct LDL measurement in frozen and fresh plasma samples

Background and Aims: Direct LDL-cholesterol (dLDL-C) assays are widely used instead of calculated LDL-C. Although theoretically more accurate, inter-assay differences still exist. This study aimed to investigate whether an OPLS multivariate model could identify the cause of discrepancy in dLDL assays in frozen and fresh plasma samples.

Comparing Calculated LDL with Direct Method: A Retrospective, Real-World Evidence Study on Diagnostic Lab Reports from A Single Center in India

Objective: To compare and validate the calculated LDL values from Friedewald and Anandaraja formulas with directly measured values in the Indian population. Material and Methods: The study was conducted on randomly selected 102 individuals of 16 to 88 years of age during December 2019. The direct LDL values were measured using selective solubilization assay, and Friedewald and Anandaraja formulas were used to calculate LDL for comparison. The correlations between direct and calculated methods were assessed using the linear regression method. Receiver operating characteristic analysis with nonparametric distribution was used to compare the sensitivity and specificity of the three methods. Results: The average LDL of direct method, 107.3 mg/dL, Friedewald formula, 89.7 mg/dL, and Anandaraja was 99.0 mg/dL. The relation between direct and calculated values assessed by linear regression showed 97% and 87% of correlation with Friedewald and Anandaraja, respectively. The ROC analysis inferred that direct (AUC 0.74; 95% CI 0.64-0.83) and Friedewald (AUC 0.71; 95% CI 0.61-0.81) methods had shown about 70% efficiency in predicting true positive and true negative dyslipidemia cases. In our dataset, the Anandaraja formula could not well differentiate positives from negative cases of dyslipidemia with merely 60% AUC. Conclusion: The underpredicted values from the Friedewald formula were associated with deranged cholesterol and HDL values, not triglycerides. Anandaraja formula overpredicted by 10 to 30 mg/dL when triglycerides were &lt;150 mg/dL and underpredicted by 10-43 mg/dL while non-HDL was &gt;140 mg/dL.

Which LDL Value Should Clinicians Look at?

Objectives LDL cholesterol is routinely estimated by the Friedewald formula to guide the treatment of dyslipidemia. However, Friedewald equation has certain limitations, especially with high triglyceride levels. Direct methods are available for LDL estimation but have received relatively little scrutiny in the Indian setting. This study was aimed at comparing the calculative and direct methods of LDL estimation in Indian hyperlipidemic patients. Materials and Methods In this observational study, data from 380 consecutive lipid profiles of patients visiting a tertiary care hospital in Mumbai were analyzed retrospectively. CHOD PAP method was used to estimate total cholesterol. Enzymatic colorimetric method was used to estimate triglycerides. Enzyme selective protection method was used to estimate HDL. Direct LDL was estimated by homogenous enzymatic colorimetric assay and very low-density lipoprotein was calculated, whereas Friedewald’s formula was used to derive calculated LDL. Results Total cholesterol values correlated positively with the LDL values measured by both methods. However, a statistically significant difference was noted between the correlation coefficients of both the methods. Triglyceride values correlated weakly with the LDL levels measured by both the methods. A weak negative correlation was observed with LDL by the calculated method, whereas a weak positive correlation existed between TG and LDL by the direct method. The difference between the correlation coefficients was statistically significant. Conclusion Both direct and calculated methods of LDL estimation have their limitations. A robust study with a larger sample size is needed to further investigate whether the differences in the different LDL estimation methods can translate to “clinical relevance” in the Indian setting.