scholarly journals Validation of the Friedewald Formula in Patients with Metabolic Syndrome

Cholesterol ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
José Knopfholz ◽  
Caio César Diniz Disserol ◽  
Andressa Jardim Pierin ◽  
Fernanda Letícia Schirr ◽  
Larissa Streisky ◽  
...  

Currently, the Friedewald formula (FF) is the main method for evaluating low-density lipoprotein cholesterol (LDL-c). Recently, many limitations have emerged regarding its use, including patients with triglyceride levels ≥400 mg/dL, diabetes mellitus, and kidney or hepatic chronic diseases. We analyzed the use of the FF in patients with metabolic syndrome. We selected patients with known metabolic syndrome that fulfilled the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report and excluded patients with triglyceride levels ≥400 mg/dL and chronic liver and/or kidney disease. Using direct assays, we measured total cholesterol, high-density lipoprotein cholesterol, triglycerides, and LDL-c. Then, LDL-c was estimated using the FF and compared with the LDL-c by direct assay. The sample size was 135 patients. Using the FF, the mean LDL-c value was 124.4±42.1 mg/dL; it was 125.1±38.5 mg/dL by direct assay. The correlation coefficient between these two methods was 0.89, with statistical significance (P  value<0.001). There were no significant differences between the patients with triglyceride levels >150 mg/dL (P=0.618). In conclusion, FF is a good method for estimating LDL-c in patients with metabolic syndrome.

2020 ◽  
pp. 263246362097804
Author(s):  
Rejitha Jagesh ◽  
Mathew John ◽  
Manju Manoharan Nair Jalaja ◽  
Tittu Oommen ◽  
Deepa Gopinath

Objectives: The accurate and precise measurement of low-density lipoprotein-cholesterol (LDL-C) is important in the assessment of atherosclerotic cardiovascular disease risk (ASCVD) in people with diabetes mellitus. This study aimed at comparing directly measured LDL-C with Friedewald formula (FF)-calculated LDL-C (c-LDL-C) in people with type-2 diabetes. Methods: Fasting lipid profiles of 1905 people with type-2 diabetes, whose LDL-C was estimated by direct LDL assay, were chosen for the study. In the same group, LDL-C was calculated with FF. Correlation and agreement between these methods were analyzed at various strata of triglycerides (TGs). The possibility of misclassifying people at various levels of LDL-C targets proposed in literature was calculated. Results: The mean LDL-C levels were lower in the c-LDL-C group across various TG strata. A significant correlation was found between c-LDL-C and direct LDL-C for all the study samples ( r = 0.948, P < .001) and across all TG strata. Analysis of agreement showed a positive bias for direct LDL-C which increased at higher strata of TGs. c-LDL-C underestimated ASCVD by misclassifying people at various LDL-C target levels. Conclusion: There is a difference between direct LDL-C and c-LDL-C values in people with diabetes and this may result in misclassifying ASCVD especially at lower levels of LDL-C and higher levels of TGs.


Author(s):  
Agnieszka Ćwiklińska ◽  
Ewa Wieczorek ◽  
Anna Gliwińska ◽  
Marta Marcinkowska ◽  
Monika Czaplińska ◽  
...  

Abstract Objectives Low-density lipoprotein cholesterol (LDL-C) is the main laboratory parameter used for the management of cardiovascular disease. The aim of this study was to compare measured LDL-C with LDL-C as calculated by the Friedewald, Martin/Hopkins, Vujovic, and Sampson formulas with regard to triglyceride (TG), LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C)/TG ratio. Methods The 1,209 calculated LDL-C results were compared with LDL-C measured using ultracentrifugation-precipitation (first study) and direct (second study) methods. The Passing-Bablok regression was applied to compare the methods. The percentage difference between calculated and measured LDL-C (total error) and the number of results exceeding the total error goal of 12% were established. Results There was good correlation between the measurement and calculation methods (r 0.962–0.985). The median total error ranged from −2.7%/+1.4% (first/second study) for Vujovic formula to −6.7%/−4.3% for Friedewald formula. The numbers of underestimated results exceeding the total error goal of 12% were 67 (Vujovic), 134 (Martin/Hopkins), 157 (Samspon), and 239 (Friedewald). Less than 7% of those results were obtained for samples with TG >4.5 mmol/L. From 57% (Martin/Hopkins) to 81% (Vujovic) of underestimated results were obtained for samples with a non-HDL-C/TG ratio of <2.4. Conclusions The Martin/Hopkins, Vujovic and Sampson formulas appear to be more accurate than the Friedewald formula. To minimize the number of significantly underestimated LDL-C results, we propose the implementation of risk categories according to non-HDL-C/TG ratio and suggest that for samples with a non-HDL-C/TG ratio of <1.2, the LDL-C level should not be calculated but measured independently from TG level.


2005 ◽  
Vol 62 (11) ◽  
pp. 811-819
Author(s):  
Aleksandra Jovelic ◽  
Goran Radjen ◽  
Stojan Jovelic ◽  
Marica Markovic

Background/Aim. C-reactive protein is an independent predictor of the risk of cardiovascular events and diabetes mellitus in apparently healthy men. The relationship between C-reactive protein and the features of metabolic syndrome has not been fully elucidated. To assess the cross-sectional relationship between C-reactive protein and the features of metabolic syndrome in healthy people. Methods. We studied 161 military pilots (agee, 40?6 years) free of cardiovascular disease, diabetes mellitus and active inflammation on their regular annual medical control. Age, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, fasting glucose, glycosylated hemoglobin, blood pressure, smoking habit, waist circumference and body mass index were evaluated. Plasma C-reactive protein was measured by the immunonephelometry (Dade Behring) method. Metabolic syndrome was defined according to the National Cholesterol Education Program Expert Panel. Results. The mean C-reactive protein concentrations in the subjects grouped according to the presence of 0, 1, 2 and 3 or more features of the metabolic syndrome were 1.11, 1.89, 1.72 and 2.22 mg/L, respectively (p = 0.023) with a statistically, significant difference between those with 3, and without metabolic syndrome (p = 0.01). In the simple regression analyses C-reactive protein did not correlate with the total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, body mass index and blood pressure (p > 0.05). In the multiple regression analysis, waist circumference (? = 0.411, p = 0.000), triglycerides to high density lipoprotein cholesterol ratio (? = 0.774, p = 0.000), smoking habit (? = 0.236, p = 0.003) and triglycerides (? = 0.471, p = 0.027) were independent predictors of C-reactive protein. Conclusions. Our results suggested a cross-sectional independent correlation between the examined cardiovascular risk factors as the predominant features of metabolic syndrome and C-reactive protein in the group of apparently healthy subjects. The lack of correlation of C-reactive protein with the total cholesterol and low density lipoprotein cholesterol in our study may suggest their different role in the process of atherosclerosis and the possibility to determine C-reactive protein in order to identify high-risk subjects not identified with cholesterol screening.


2020 ◽  
Author(s):  
ling wu ◽  
Yazhen Di ◽  
Yuanling Chen ◽  
Yunyan Li ◽  
Jiapei Wang

Abstract Background Clinical findings reported that some cases of Juvenile Idiopathic Arthritis(JIA) gradually suffer from hyperuricemia(HUA) during the course of follow-up, followed by the detection of high urate crystal, gout, renal impairment, and other manifestations. And thoes patients would influence the prognosis. Methods This was a retrospective study of 60 patients diagnosed with JIA between October 2016 and March 2019 and followed up for > 1 year. Single-factor analyses of the clinical data, laboratory data, and the special drug used for JIA complicated with hyperuricemia (Group A, n = 18) and JIA without hyperuricemia (Group B, n = 42) were conducted. Results Comparison between Groups A and B revealed differences in sex; disease course; high disease activity; diastolic pressure; the levels of serum albumin (ALB), alanine aminotransferase (ALT), aspartate transaminase (AST), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), glucose (GLU), and urea nitrogen (BUN); NSAIDS application, systemic glucocorticoid application, MTX application, and tumor necrosis factor-alpha (TNF-α) inhibitors application were not statistically significant (P > 0.05). However, the differences in age, active sacroiliitis, body mass index (BMI), systolic pressure, serum creatinine (Scr) level, and salicylazosulfapyridine (SASP) application showed a statistical significance (P < 0.05). Conclusions JIA patients were obese ,with high systolic pressure, and after SASP treatment will be more likely to be complicated with hyperuricemia.


1988 ◽  
Vol 34 (12) ◽  
pp. 2456-2459 ◽  
Author(s):  
J S Cohn ◽  
J R McNamara ◽  
E J Schaefer

Abstract Lipoprotein cholesterol concentrations in plasma are routinely estimated by using the Friedewald formula, whereby very-low-density lipoprotein cholesterol (VLDL-C) is estimated to be one-fifth the plasma triglyceride concentration. Ordinarily, this formula is applied only to plasma sampled from patients in the fasted state. To determine whether lipoprotein cholesterol measurements are altered substantially in plasma sampled from nonfasting subjects, we obtained postprandial blood samples from 22 healthy subjects (nine men, 13 women, ages 22-79 years) fed a fat-rich meal (1 g fat per kilogram body wt.). The plasma triglyceride concentration increased postprandially in all subjects (233 +/- 16% of baseline at 3 h). The mean cholesterol concentration in plasma was essentially unchanged. High-density lipoprotein cholesterol (HDL-C) was significantly decreased (94 +/- 2% at 3 h, P less than 0.001). VLDL-C and low-density lipoprotein cholesterol (LDL-C), estimated by the Friedewald formula, were compared with measurements obtained by modified Lipid Research Clinics (LRC) methodology. As measured by either method, VLDL-C increased and LDL-C decreased significantly after the fat-rich meal. These postprandial changes were significantly greater (P less than 0.01) when estimated by the Friedewald formula than by LRC methodology. We conclude that (a) lipoprotein cholesterol concentrations measured in the fed subject differ significantly from those measured in the fasted subject, and (b) plasma must be obtained after at least a 12-h fast if an individual's risk of coronary heart disease is to be accurately assessed.


2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Prakash Chandra ◽  
Sukhdeep S. Basra ◽  
Tai C. Chen ◽  
Vin Tangpricha

Testosterone therapy in men and women results in decreased high-density lipoprotein cholesterol (HDL) and increased low-density lipoprotein cholesterol (LDL). We sought to determine whether testosterone therapy has this same effect on lipid parameters and adipocyte hormones in female-to-male (FTM) transsexuals. Twelve FTM transsexuals provided a fasting lipid profile including serum total cholesterol, HDL, LDL, and triglycerides prior to and after 1 year of testosterone therapy (testosterone enanthate or cypionate 50–125 mg IM every two weeks). Subjects experienced a significant decrease in mean serum HDL (52±11to40±7 mg/dL)(P<.001). The mean LDL(P=.316), triglyceride(P=.910), and total cholesterol(P=.769)levels remained unchanged. In a subset of subjects, we measured serum leptin levels which were reduced by 25% but did not reach statistical significance(P=.181)while resistin levels remained unchanged. We conclude that testosterone therapy in FTM transsexuals can promote an increased atherogenic lipid profile by lowering HDL and possibly reduce serum leptin levels. However, long-term studies are needed to determine whether decreases in HDL result in adverse cardiovascular outcomes.


Sign in / Sign up

Export Citation Format

Share Document