scholarly journals Fasting Is Not Routinely Required for Determination of a Lipid Profile: Clinical and Laboratory Implications Including Flagging at Desirable Concentration Cutpoints—A Joint Consensus Statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine

2016 ◽  
Vol 62 (7) ◽  
pp. 930-946 ◽  
Author(s):  
Børge G Nordestgaard ◽  
Anne Langsted ◽  
Samia Mora ◽  
Genovefa Kolovou ◽  
Hannsjörg Baum ◽  
...  

Abstract AIMS To critically evaluate the clinical implications of the use of non-fasting rather than fasting lipid profiles and to provide guidance for the laboratory reporting of abnormal non-fasting or fasting lipid profiles. METHODS AND RESULTS Extensive observational data, in which random non-fasting lipid profiles have been compared with those determined under fasting conditions, indicate that the maximal mean changes at 1–6 h after habitual meals are not clinically significant [+0.3 mmol/L (26 mg/dL) for triglycerides; −0.2 mmol/L (8 mg/dL) for total cholesterol; −0.2 mmol/L (8 mg/dL) for LDL cholesterol; +0.2 mmol/L (8 mg/dL) for calculated remnant cholesterol; −0.2 mmol/L (8 mg/dL) for calculated non-HDL cholesterol]; concentrations of HDL cholesterol, apolipoprotein A1, apolipoprotein B, and lipoprotein(a) are not affected by fasting/non-fasting status. In addition, non-fasting and fasting concentrations vary similarly over time and are comparable in the prediction of cardiovascular disease. To improve patient compliance with lipid testing, we therefore recommend the routine use of non-fasting lipid profiles, whereas fasting sampling may be considered when non-fasting triglycerides are >5 mmol/L (440 mg/dL). For non-fasting samples, laboratory reports should flag abnormal concentrations as triglycerides ≥2 mmol/L (175 mg/dL), total cholesterol ≥5 mmol/L (190 mg/dL), LDL cholesterol ≥3 mmol/L (115 mg/dL), calculated remnant cholesterol ≥0.9 mmol/L (35 mg/dL), calculated non-HDL cholesterol ≥3.9 mmol/L (150 mg/dL), HDL cholesterol ≤1 mmol/L (40 mg/dL), apolipoprotein A1 ≤1.25 g/L (125 mg/dL), apolipoprotein B ≥1.0 g/L (100 mg/dL), and lipoprotein(a) ≥50 mg/dL (80th percentile); for fasting samples, abnormal concentrations correspond to triglycerides ≥1.7 mmol/L (150 mg/dL). Life-threatening concentrations require separate referral for the risk of pancreatitis when triglycerides are >10 mmol/L (880 mg/dL), for homozygous familial hypercholesterolemia when LDL cholesterol is >13 mmol/L (500 mg/dL), for heterozygous familial hypercholesterolemia when LDL cholesterol is >5 mmol/L (190 mg/dL), and for very high cardiovascular risk when lipoprotein(a) >150 mg/dL (99th percentile). CONCLUSIONS We recommend that non-fasting blood samples be routinely used for the assessment of plasma lipid profiles. Laboratory reports should flag abnormal values on the basis of desirable concentration cutpoints. Non-fasting and fasting measurements should be complementary but not mutually exclusive.

1997 ◽  
Vol 82 (8) ◽  
pp. 2653-2659
Author(s):  
Kamal A. S. Al-Shoumer ◽  
Katharine H. Cox ◽  
Carol L. Hughes ◽  
William Richmond ◽  
Desmond G. Johnston

Hypopituitary patients, particularly women, have excess mortality, mostly due to vascular disease. We have studied circulating lipid and lipoprotein concentrations, fasting and over 24 h, in hypopituitary women and men and in matched controls. Firstly, 67 hypopituitary patients (36 women) and 87 normal controls (54 women) were studied after an overnight fast. Secondly, 12 patients (6 women) and 14 matched controls (7 women) were studied over 24 h of normal meals and activity. The patients were all GH deficient and were replaced with cortisol, T4, and sex hormones where appropriate, but not with GH. In the first study, circulating triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, and low density lipoprotein (LDL) cholesterol were measured after an overnight fast. In the second study, fasting levels of apolipoprotein B, apolipoprotein A1, and lipoprotein(a) were also measured, and then circulating triglyceride and total cholesterol concentrations were measured over 24 h. Fasting concentrations of triglyceride (mean ± sem, 1.73 ± 0.22 vs. 1.11 ± 0.09 mmol/L; P = 0.0025), total cholesterol (6.45 ± 0.25 vs. 5.59± 0.21 mmol/L; P = 0.002), LDL cholesterol (4.58 ± 0.24 vs. 3.80 ± 0.19 mmol/L; P = 0.007), and apolipoprotein B (135 ± 10 vs. 111 ± 9 mg/dL; P = 0.048) were elevated in hypopituitary compared to control women. The lipid alterations were observed in older and younger women and occurred independently of sex hormone or glucocorticoid replacement. Fasting values were not significantly different in hypopituitary and control men. Patients and controls (women and men) had similar fasting HDL cholesterol, apolipoprotein A1, and lipoprotein(a) concentrations. Although the differences that existed in fasting lipid values were most marked in women, the men were also abnormal in this respect, in that a higher proportion of hypopituitary than control men had total and LDL cholesterol above recommended values (≥6.2 and ≥4.1 mmol/L, respectively). In the postprandial period (0730–2030 h), the areas under the curve (AUC) for circulating triglyceride and total cholesterol were significantly higher in hypopituitary than control women (P = 0.0089 and P = 0.0016, respectively). The AUC for triglyceride and total cholesterol over 24 h were also significantly increased (P= 0.009 and P = 0.0004, respectively). No significant differences were observed for postprandial and 24-h AUC for triglyceride and total cholesterol concentrations in men. We conclude that hypopituitarism with conventional replacement therapy is associated with unfavorable fasting and postprandial lipid and lipoprotein concentrations, particularly in women. The changes may contribute to the observed increased vascular morbidity and mortality.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Tao-Chun Peng ◽  
Chung-Ching Wang ◽  
Tung-Wei Kao ◽  
James Yi-Hsin Chan ◽  
Ya-Hui Yang ◽  
...  

Background. Although the link between hyperuricemia and metabolic syndrome had been recognized, the association of the dyslipidemia among individuals with hyperuricemia remains not comprehensively assessed.Methods. Using NHANES III study, we examined the relation between serum lipid profiles and different serum uric acid levels, including serum total cholesterol, LDL cholesterol, triglycerides, HDL cholesterol, apolipoprotein-B, lipoprotein (a), apolipoprotein AI, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI.Results. After adjusting for potential confounders, average differences (95% confidence interval) comparing the top to the bottom (reference) serum uric acid were 0.29 (0.19, 0.39) mmol/L for total cholesterol, 0.33 (0.26, 0.41) mmol/L for triglycerides, 0.14 (0.01, 0.27) mmol/L for LDL cholesterol, −0.08 (−0.11, −0.05) mmol/L for HDL, and 0.09 (0.05, 0.12) g/L for serum apolipoprotein-B. Notably, ratios of triglycerides to HDL cholesterol and apolipoprotein-B to AI were also linearly associated with uric acid levels (Pfor trend < 0.001).Conclusions. This study suggested that serum LDL cholesterol, triglycerides, total cholesterol, apolipoprotein-B levels, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI are strongly associated with serum uric acid levels, whereas serum HDL cholesterol levels are significantly inversely associated. In the clinical practice, the more comprehensive strategic management to deal with dyslipidemia and hyperuricemia deserves further investigation.


2020 ◽  
Vol 150 (4) ◽  
pp. 818-825 ◽  
Author(s):  
Alyssa M Tindall ◽  
Penny M Kris-Etherton ◽  
Kristina S Petersen

ABSTRACT Background Walnuts have established lipid-/lipoprotein-lowering properties; however, their effect on lipoprotein subclasses has not been investigated. Furthermore, the mechanisms by which walnuts improve lipid/lipoprotein concentrations are incompletely understood. Objectives We aimed to examine, as exploratory outcomes of this trial, the effect of replacing SFAs with unsaturated fats from walnuts or vegetable oils on lipoprotein subclasses, cholesterol efflux, and proprotein convertase subtilisin/kexin type 9 (PCSK9). Methods A randomized, crossover, controlled-feeding study was conducted in individuals at risk of cardiovascular disease (CVD) (n = 34; 62% men; mean ± SD age 44 ± 10 y; BMI: 30.1 ± 4.9 kg/m2). After a 2-wk run-in diet (12% SFAs, 7% PUFAs, 12% MUFAs), subjects consumed the following diets, in randomized order, for 6 wk: 1) walnut diet (WD) [57–99 g/d walnuts, 7% SFAs, 16% PUFAs [2.7% α-linolenic acid (ALA)], 9% MUFAs]; 2) walnut fatty acid–matched diet [7% SFAs, 16% PUFAs (2.6% ALA), 9% MUFAs]; and 3) oleic acid replaces ALA diet (ORAD) [7% SFAs, 14% PUFAs (0.4% ALA); 12% MUFAs] (all percentages listed are of total kilocalories ). Serum collected after the run-in (baseline) and each diet period was analyzed for lipoprotein classes and subclasses (vertical auto profile), cholesterol efflux, and PCSK9. Linear mixed models were used for data analysis. Results Compared with the ORAD, total cholesterol (mean ± SEM −8.9± 2.3 mg/dL; −5.1%; P &lt; 0.001), non-HDL cholesterol (−7.4 ± 2.0 mg/dL; −5.4%; P = 0.001), and LDL cholesterol (−6.9 ± 1.9 mg/dL; −6.5%; P = 0.001) were lower after the WD; no other pairwise differences existed. There were no between-diet differences for HDL-cholesterol or LDL-cholesterol subclasses. Lipoprotein(a) [Lp(a)], cholesterol efflux, and PCSK9 were unchanged after the diets. Conclusions In individuals at risk of CVD, replacement of SFAs with unsaturated fats from walnuts or vegetable oils improved lipid/lipoprotein classes, including LDL-cholesterol, non-HDL cholesterol, and total cholesterol, without an increase in Lp(a). These improvements were not explained by changes in cholesterol efflux capacity or PCSK9. This trial was registered at clinicaltrials.gov as NCT01235832.


2014 ◽  
Vol 54 (4) ◽  
pp. 232
Author(s):  
Sigit Prastyanto ◽  
Mei Neni Sitaresmi ◽  
Madarina Julia

Background The prevalence of smoking in adolescentstends to increase. Smoking is associated with a higher risk ofdyslipidemia.Objective To compare the lipid profiles of tobacco-smoking andnon-tobacco-smoking male adolescents.Methods We performed a cross- sectional study in three vocationalhigh schools in Yogyakarta from January to April 2011. Dataon smoking status, duration of smoking and number cigarettesconsumed per day were collected by questionnaires. We randomlyselected 50 male smokers and 50 male non-smokers as the studysubjects.Results Mean differences between smokers and non-smokerswere 44.5 (95%CI 28. 7 to 60.1) mg/dL for triglyceride levels; 8.0(95% CI 1.0 to 14.9) mg/dL for low density lipoprotein (LDL)cholesterol; 11.8 (1.1 to 22.4) mg/dL for total cholesterol and -5.7mg/dL (95% CI -8.8 to -2.6) for high density lipoprotein (HDL)cholesterol. Mean differences (95% CI) between smokers whohad engaged in smoking for > 2 years and those who had smokedfor :S:2 years were -18.1 (95% CI -33 .9 to -2.3) mg/dL for totalcholesterol; -49.4 (95% CI -67.2 to -3 1.5) mg/dL for triglycerides.Mean differences between those who smoked > 5 cigarettes/dayand :s:5 cigarettes per day were -18 .4 (95% CI -32.8 to -4.1) mg/dL for total cholesterol and -29.1 (95% CI -53.6 to -4.6) mg/dLfor triglycerides.Conclusion Smoking more than 5 cigarettes/day significantlyincreases total cholesterol, LDL cholesterol, and triglyceridelevels, as well as reduces HDL cholesterol levels; while smokingmore than 2 years significantly increases total cholesterol andtriglyceride levels


2001 ◽  
Vol 86 (11) ◽  
pp. 5479-5484 ◽  
Author(s):  
Richard G. IJzerman ◽  
Coen D. A. Stehouwer ◽  
Mirjam M. van Weissenbruch ◽  
Eco J. de Geus ◽  
Dorret I. Boomsma

Recent studies have demonstrated an association between low weight at birth and an atherogenic lipid profile in later life. To examine the influences of intrauterine and genetic factors, we investigated 53 dizygotic and 61 monozygotic adolescent twin pairs. Regression analysis demonstrated that low birth weight was associated with high levels of total cholesterol, low-density lipoprotein (LDL) cholesterol and apolipoprotein B (−0.17 mmol/liter per kg, P = 0.07; −0.18 mmol/liter per kg, P = 0.04; and− 0.07 g/liter per kg, P = 0.02, respectively) and with low levels of high-density lipoprotein (HDL) cholesterol (+0.04 mmol/liter per kg, P = 0.1), after adjustment for age, sex, and body mass index. Intrapair differences in birth weight were significantly associated with differences in total cholesterol, LDL cholesterol, and apolipoprotein B in dizygotic twins after adjustment for differences in current body mass index (−0.49 mmol/liter per kg, P = 0.02; −0.51 mmol/liter per kg, P = 0.01; and −0.10 g/liter per kg, P = 0.04, respectively), demonstrating that the larger the difference in birth weight, the higher these risk factors in the twin with the lower birth weight, compared with the cotwin with the higher birth weight. In monozygotic twins, however, the associations between intrapair differences in birth weight and differences in total cholesterol, LDL cholesterol, and apolipoprotein B were in the opposite direction (+0.32 mmol/liter per kg, P = 0.03; +0.23 mmol/liter per kg, P = 0.08; and +0.06 g/liter per kg, P = 0.04, respectively). The association between intrapair differences in birth weight and differences in HDL cholesterol was not significant in dizygotic twins (+0.04 mmol/liter per kg, P = 0.6) and of borderline significance in monozygotic twins (+0.11 mmol/liter per kg, P = 0.05). These data suggest that genetic factors account for the association of low birth weight with high levels of total cholesterol, LDL cholesterol, and apolipoprotein B, whereas intrauterine factors possibly play a role in the association between birth weight and HDL cholesterol.


Jurnal BIOMA ◽  
2015 ◽  
Vol 11 (2) ◽  
pp. 131
Author(s):  
Pratiwi Widyamurti ◽  
Rusdi Rusdi ◽  
Sri Rahayu

ABSTRACT Increased blood pressure more than 140/90 mmHg taken from three measurement in 24 hours can be diagnosed as hypertension. Abnormality of lipid values condition was found at many hypertensive. Based on this reason examination of lipid profile in hypertensive and normotensive should be done. The aim of this research was to measure and compare lipid profile on blood serum in hypertensive    and normotensive. Lipid profile was measured by Konelab 20XT clinical chemistry analyzer. Ex     Post Facto used as method and Cross-sectional used as design. A total of 50 blood samples collected from Hypertensive (N1=25) and normotensive (N2=25) from June to August 2014. SPSS 16.0 was used to analyze the data, T-test was used to compare value of LDL cholesterol, HDL cholesterol and total cholesterol while U Mann-Whitney test was used to compare value of triglyceride. The result      of this research showed that the mean value of triglyceride was 146.56 mg/dL in hypertensive and 143.92 mg/dL in normotensive (p=0.11). The mean value of LDL cholesterol was 129.80 mg/dL in hypertensive and 136.72 mg/dL in normotensive (p=0.62). The mean value of HDL cholesterol was  38.80 mg/dL in hypertensive and 45.04 mg/dL in normotensive (p=0.1). The mean value of total cholesterol was 201.04 mg/dL in hypertensive and 221.88 mg/dL in normotensive (p=0.25). In conclusion, there was no different of lipid profile on blood serum in hypertensive and normotensive.  Keywords: hypertension, lipid profile, normotensive


2019 ◽  
Vol 77 (12) ◽  
pp. 890-902 ◽  
Author(s):  
Daniel T Dibaba

Abstract Context Vitamin D deficiency is highly prevalent across the world. The existing evidence suggests vitamin D may have beneficial effects on serum lipid profiles and thus cardiovascular health. Objective The objective of this systematic review and meta-analysis was to examine the effect of vitamin D supplementation on serum lipid profiles. Data Source Original randomized controlled trials (RCTs) examining the effect of vitamin D supplementation on serum lipid profiles and published before July 2018 were identified by searching online databases, including PubMed, Google Scholar, and ScienceDirect, using a combination of relevant keywords. Data Extraction Data on study characteristics, effect size, measure of variation, type of vitamin D supplementation, and duration of follow-up were extracted by the author. Data Analysis PRISMA guidelines for systematic reviews were followed. Random effects (DerSimonian and Laird [D-V)] models were used to pool standardized mean differences in total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides between the active and the placebo arms of RCT studies. Between-study heterogeneities were assessed using Cochrane Q and I2, and publication bias was assessed using Begg’s test, Egger’s test, and funnel plot. Results A total of 41 RCTs comprising 3434 participants (n = 1699 in the vitamin D supplementation arm and n = 1735 in the placebo arm) were identified and included in the meta-analysis. Approximately 63.4% of study participants were women, with 14 studies conducted entirely among women. Approximately 24% of the trials had follow-up duration >6 months, whereas the remaining 76% had follow-up duration of <6 months. The standardized mean differences (SMDs) and 95% confidence intervals (CIs) for comparing the change from baseline to follow-up between the vitamin D supplementation arm and the placebo (control) arm were as follows: total cholesterol = –0.17 (–0.28 to –0.06); LDL cholesterol = –0.12 (–0.23 to –0.01); triglycerides = –0.12 (–0.25 to 0.01); and HDL cholesterol = –0.19 (–0.44 to 0.06). After removing a trial that was an outlier based on the magnitude of the effect size, the SMD for triglycerides was –0.15 (–0.24 to –0.06) and that for HDL cholesterol was –0.10 (–0.28 to 0.09). The improvements in total cholesterol and triglycerides were more pronounced in participants with baseline vitamin D deficiency. Conclusions Vitamin D supplementation appeared to have a beneficial effect on reducing serum total cholesterol, LDL cholesterol, and triglyceride levels but not HDL cholesterol levels. Vitamin D supplementation may be useful in hypercholesterolemia patients with vitamin D insufficiency who are at high risk of cardiovascular diseases.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Enkhmaa Byambaa ◽  
Anuurad Erdembileg ◽  
Wei Zhang ◽  
Lars Berglund

Background: Lipoprotein(a), Lp(a), is a genetically regulated independent cardiovascular risk factor, where levels differ across ethnicity. The relationship between Lp(a) and apolipoprotein B (apoB)-containing atherogenic lipoproteins across ethnicity is not well understood. Objective: To investigate the associations of Lp(a) levels with other apoB-containing lipoproteins with a focus on ethnicity. Methods: Plasma lipid and lipoproteins were measured in 336 Caucasians and 224 African Americans undergoing coronary angiography. Lp(a) levels were determined using an apo(a) size insensitive sandwich ELISA. Values for Lp(a) and triglyceride (TG) were square root or logarithmically transformed before analyses. Total and low density lipoprotein (LDL) cholesterol, and apoB levels were corrected for contribution of Lp(a) using previously published algorithms. Values are given mean ± standard deviation or median (interquartile range) for normally or non-normally distributed variables, respectively. Results: Levels of total and LDL cholesterol and apoB-100 did not differ between Caucasians and African Americans. As expected, African Americans had significantly higher levels of Lp(a) [110 (60-180) nmol/l vs. 24 (7-79) nmol/l, p<0.001] and high density lipoprotein (HDL) cholesterol (49±17 mg/dl vs. 41±12 mg/dl, p<0.001), as well as significantly lower levels of TG [106 (80-144) mg/dl vs. 153 (114-222) mg/dl, p<0.001] compared to Caucasians. For both ethnic groups, Lp(a) levels were significantly and positively correlated with total cholesterol (p<0.005 for Caucasians and p<0.001 for African Americans), LDL cholesterol (p<0.001 for both groups), apoB100 (p<0.05 for Caucasians and p<0.001 for African Americans) and apoB/apoA-1 ratio (p<0.05 for Caucasians and p<0.001 for African Americans). However, when adjusted for the corresponding contribution of Lp(a) to the levels of these parameters, the associations remained significant in African Americans (p<0.05 for total cholesterol; p<0.05 for LDL cholesterol; p<0.001 for apoB100, respectively), but not in Caucasians. Conclusion: Although total and LDL cholesterol, and apoB100 levels were comparable in African Americans and Caucasians, the associations of these parameters with Lp(a) levels differed across ethnicity. For African Americans, but not for Caucasians, associations of all three parameters with Lp(a) remained significant after appropriate adjustments. The findings suggest an interethnic difference in the relation between Lp(a) and other plasma apoB-containing lipoprotein levels, with a closer relationship among African Americans.


Open Medicine ◽  
2008 ◽  
Vol 3 (4) ◽  
pp. 422-429
Author(s):  
Lucia Agoston-Coldea ◽  
Teodora Mocan ◽  
Marc Gatfossé ◽  
Dan Dumitrascu

AbstractRecent evidence shows that apolipoprotein (apo) B, apoB/apoA-I ratio and lipoprotein(a) are better indicators of coronary risk than the conventional lipid profile. The aim of this study was to evaluate the correlation of apoA-I and B, and lipoprotein(a) with myocardial infarction (MI). We performed a cross-sectional study including 208 patients (100 men and 108 women), with and without previous MI evaluated by coronary angiography. The severity of coronary heart disease was scored on the basis of the number and extent of lesions in the coronary arteries. Lipid levels were measured by the enzymatic method and apolipoprotein levels were measured by the immunoturbidimetric method. The MI group had higher plasmatic levels of lipoprotein(a) (0.37±0.28 vs. 0.29±0.23 g/L, p<0.05), apoB (1.13±0.40 vs. 0.84±0.28 g/L, p<0.05) and of the apoB/apoA-I ratio (0.77±0.37 vs. 0.68±0.20, p<0.05) compared to controls. The area under the receiver operating characteristic (ROC) curves (AUC) suggested a good reliability in the diagnose of coronary heart disease for the apoB/apoA-I ratio (0.756, p<0.05), apoB (0.664, p<0.05), lipoprotein(a) (0.652, p<0.05) and total cholesterol/HDL-cholesterol (0.688, p<0.05). Multivariate analysis performed with adjustments for cardiovascular risk factors, showed that the levels of lipoprotein(a), apoB and apoB/apoA-I ratio are significant independent cardiovascular risk factors. Our results indicate that there is an important relationship among high plasma apoB concentration, lipoprotein(a) concentration, the apoB/apoA-I ratio, and MI. We showed that the apoB/apoA-I ratio has a stronger correlation with MI than the total cholesterol/HDL cholesterol ratio. We therefore suggest using apoB/apoA-I ratio and lipoprotein(a) in clinical practice as a markers of MI risk.


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