scholarly journals Effect of Lipoprotein(a) on the Diagnosis of Familial Hypercholesterolemia: Does It Make a Difference in the Clinic?

2019 ◽  
Vol 65 (10) ◽  
pp. 1258-1266 ◽  
Author(s):  
Dick C Chan ◽  
Jing Pang ◽  
Amanda J Hooper ◽  
Damon A Bell ◽  
John R Burnett ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Ldl Cholesterol ◽  
Cholesterol Content ◽  
Cholesterol Concentration ◽  
Diagnostic Tools ◽  
Lipoprotein A ◽  
Clinical Criteria ◽  
Lipid Clinic ◽  
Significant Difference ◽  
Before And After

Abstract BACKGROUND Diagnostic tools for familial hypercholesterolemia (FH) rely on estimation of LDL cholesterol concentration. However, routine measurement or calculation of LDL cholesterol concentration using the Friedewald equation contains a cholesterol contribution from lipoprotein(a) [Lp(a)]. We investigated whether Lp(a) influences the phenotypic diagnosis of FH by commonly used clinical criteria. METHODS A cohort of 907 adult index patients attending a clinic were studied. The Dutch Lipid Clinic Network (DLCN) and Simon Broome (SB) diagnostic criteria were estimated before and after adjusting LDL cholesterol concentration for the cholesterol content (30%) of Lp(a). Diagnostic reclassification rates and area under the ROC (AUROC) curves in predicting an FH mutation were also compared. RESULTS Seventy-four patients defined by DLCN criteria (8.2%) and 207 patients defined by SB criteria (22.8%) were reclassified to “unlikely” FH after adjusting LDL cholesterol for Lp(a) cholesterol. The proportion of FH patients defined by DLCN (probable/definite) and SB (possible/definite) criteria decreased significantly in patients with increased Lp(a) (>0.5 g/L; n = 330) after Lp(a) cholesterol adjustment (P < 0.01). The overall reclassification rate was significantly higher in patients with Lp(a) concentration >1.0 g/L (P < 0.001). The AUROC curve for LDL cholesterol concentration ≥191 mg/dL (≥5.0 mmol/L), DLCN criteria, and SB criteria in predicting an FH mutation increased significantly after adjustment (P < 0.001). There was no significant difference in AUROC curve before and after Lp(a) cholesterol adjustment at an LDL cholesterol concentration ≥251 mg/dL (≥6.5 mmol/L). CONCLUSIONS Adjusting LDL cholesterol concentration for Lp(a) cholesterol improves the diagnostic accuracy of DLCN and SB criteria, especially with Lp(a) >1.0 g/L and LDL cholesterol <251 mg/dL (<6.5 mmol/L). Lp(a) should be measured in all patients suspected of having FH.

scholarly journals Impact of Lipoprotein(a)-Cholesterol on Accurate Classification of Familial Hypercholesterolemia

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S3-S3
Author(s):  
Erica Fatica ◽  
Jeffrey W Meeusen ◽  
Leslie J Donato
Keyword(s):  
Familial Hypercholesterolemia ◽  
Density Lipoprotein ◽  
Cholesterol Content ◽  
Lipid Lowering ◽  
Lipoprotein A ◽  
Lipid Clinic ◽  
Diagnostic Threshold ◽  
Before And After ◽  
Lipid Testing

Abstract Lipoprotein(a) [Lp(a)] is a pro-atherogenic and pro-thrombotic LDL-like particle recognized as an independent risk factor for cardiovascular disease (CVD) that is resistant to typical lipid-lowering treatments. The cholesterol within Lp(a) (Lp(a)-C) contributes to the reported LDL-cholesterol (LDL-C) concentration by nearly all available methods including beta-quantification, direct homogenous assays, and all estimating equations. Accurate LDL-C measurements are critical for identification of genetic hyperlipidemia conditions such as familial hypercholesterolemia (FH). FH risk estimators such as the Dutch Lipid Clinic Network (DLCN) criteria utilize LDL-C concentration cut-offs and other clinical inputs to assess the likelihood of FH. Therefore, failure to adjust for Lp(a)-C can impact accurate FH classification, appropriate follow-up testing and treatments, and interpretation of cholesterol-lowering treatment efficacy. Lp(a)-C can be estimated from Lp(a) mass as measured by immunoassay using an average cholesterol content per particle. However, Lp(a)-C size and composition varies significantly within individuals resulting in inaccurate Lp(a)-C estimates. In this study, we use direct Lp(a)-C measurements to assess the potential misclassification of FH risk due to the contribution of Lp(a)-C to LDL-C in patient samples submitted for advanced lipoprotein profiling. A total of 28,200 samples submitted for lipoprotein profiling were included. The profiling included lipid testing in a CDC-certified laboratory on Roche cobas 501 (cholesterol and triglycerides by enzymatic method, high-density lipoprotein cholesterol by MgCl2/dextran sulfate precipitation). LDL-C was measured by beta-quantification, and Lp(a)-C by quantitative lipoprotein electrophoresis (SPIFE Vis Cholesterol, Helena Laboratories). The DLCN LDL-C cut-offs (155, 190, 250, and 330mg/dL) were applied to LDL-C results before and after accounting for Lp(a)-C contribution. Lp(a)-C was detected in 3,728 (13.2%) samples. The median (range) concentrations of Lp(a)-C and LDL-C were 11mg/dL (5-108mg/dL) and 121mg/dL (27-678mg/dL), respectively. Overall, subtracting Lp(a)-C would reclassify 6.5% of all samples into a lower LDL-C category within the DLCN algorithm. Within the LDL-C scoring categories, 7.0% (n=222) of subjects with LDL-C 155-189mg/dL, 5.6% (n=66) of subjects with LDL-C 190-249mg/dL, 5.2% (n=10) of subjects with LDL-C 250-329mg/dL, and 3.4% (n=4) of subjects with LDL-C >330mg/dL would be down-classified after adjusting for Lp(a)-C. Limiting to subjects with measurable Lp(a)-C, reclassification to a lower diagnostic threshold occurred in 47.4% of subjects with LDL-C 155-189mg/dL, 37.5% with LDL-C 190-249mg/dL, 41.6% with LDL-C 250-329mg/dL, and 33.3% with LDL-C >330mg/dL after adjustment. Current guidelines recommend screening for elevated Lp(a) in patients with family history of CVD. Our data show that a high percentage of samples evaluated for advanced lipid testing contain measurable Lp(a)-C that could cause mis-classification in FH prediction algorithms. If labeled high probability of FH, these mis-classifications could trigger inappropriate work-up for suspected FH. As clinical follow-up and therapeutic strategies differ between FH and elevated Lp(a), proper distinction between LDL-C and Lp(a)-C is needed to guide appropriate patient management.

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 ◽  
...  
Keyword(s):  
Total Cholesterol ◽  
Familial Hypercholesterolemia ◽  
Apolipoprotein B ◽  
Ldl Cholesterol ◽  
Clinical Chemistry ◽  
Hdl Cholesterol ◽  
Lipid Profiles ◽  
Apolipoprotein A1 ◽  
Lipoprotein A ◽  
Remnant Cholesterol

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.

scholarly journals Lipoprotein(a) Is an Independent Risk Factor for Cardiovascular Disease in Heterozygous Familial Hypercholesterolemia

2005 ◽  
Vol 51 (11) ◽  
pp. 2067-2073 ◽  
Author(s):  
Daniel T Holmes ◽  
Brian A Schick ◽  
Karin H Humphries ◽  
Jiri Frohlich
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Familial Hypercholesterolemia ◽  
Independent Risk Factor ◽  
Independent Predictor ◽  
Cvd Risk ◽  
Lipoprotein A ◽  
Heterozygous Familial Hypercholesterolemia ◽  
Lipid Clinic

Abstract Background: The role of lipoprotein(a) [Lp(a)] as a predictor of cardiovascular disease (CVD) in patients with heterozygous familial hypercholesterolemia (HFH) is unclear. We sought to examine the utility of this lipoprotein as a predictor of CVD outcomes in the HFH population at our lipid clinic. Methods: This was a retrospective analysis of clinical and laboratory data from a large multiethnic cohort of HFH patients at a single, large lipid clinic in Vancouver, Canada. Three hundred and eighty-eight patients were diagnosed with possible, probable, or definite HFH by strict clinical diagnostic criteria. Multivariate Cox regression analysis was used to study the relationship between several established CVD risk factors, Lp(a), and the age of first hard CVD event. Results: An Lp(a) concentration of 800 units/L (560 mg/L) or higher was a significant independent risk factor for CVD outcomes [hazard ratio (HR) = 2.59; 95% confidence interval (CI), 1.53–4.39; P <0.001]. Other significant risk factors were male sex [HR = 3.19 (1.79–5.69); P <0.001] and ratio of total to HDL-cholesterol [1.18 (1.07–1.30); P = 0.001]. A previous history of smoking or hypertension each produced HRs consistent with increased CVD risk [HR = 1.55 (0.92–2.61) and 1.57 (0.90–2.74), respectively], but neither reached statistical significance (both P = 0.10). LDL-cholesterol was not an independent predictor of CVD risk [HR = 0.85 (0.0.71–1.01); P = 0.07], nor was survival affected by the subcategory of HFH diagnosis (i.e., possible vs probable vs definite HFH). Conclusion: Lp(a) is an independent predictor of CVD risk in a multiethnic HFH population.

scholarly journals Compound Heterozygous Familial Hypercholesterolemia and Familial Defective Apolipoprotein B-100 Produce Exaggerated Hypercholesterolemia

2001 ◽  
Vol 47 (3) ◽  
pp. 438-443 ◽  
Author(s):  
E Shyong Tai ◽  
Evelyn S C Koay ◽  
Edmund Chan ◽  
Tzer Jing Seng ◽  
Lih Ming Loh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Genetic Analysis ◽  
Familial Hypercholesterolemia ◽  
Apolipoprotein B ◽  
Ldl Cholesterol ◽  
Index Case ◽  
Ldl Receptor ◽  
Cholesterol Concentration ◽  
Apo B ◽  
First Degree Relatives

Abstract Background: Familial hypercholesterolemia (FH) and familial defective apolipoprotein B-100 (FDB) represent ligand-receptor disorders that are complementary. Individuals with both FH and FDB are unusual. We report a family with both disorders and the impact of the mutations on the phenotypes of the family members. Methods: We used single strand conformation polymorphism (SSCP) and denaturing gradient gel electrophoresis (DGGE) for genetic analysis of all 18 exons and the promoter region of the LDL receptor and DGGE for genetic analysis of the apolipoprotein B-100 (apo B-100) gene. The functional significance of the apo B-100 mutation was studied using a U937 cell proliferation assay. Fasting serum lipid profiles were determined for the index case and seven first-degree relatives. Results: One of the patient’s sisters had a missense mutation (Asp407→Lys) in exon 9 of the LDL receptor and a serum LDL-cholesterol concentration of 4.07 mmol/L. Four other first-degree relatives had hyperlipidemia but no LDL-receptor mutation. However, these subjects had a mutation of the apo B-100 gene (Arg3500→Trp). The cell proliferation rate of U937 cells fed with LDL from other subjects with the same mutation was fourfold less than that of controls. The index case had both FH- and FDB-related mutations. Her serum LDL-cholesterol (9.47 mmol/L) was higher than all other relatives tested. Conclusions: Existence of both FH and FDB should be considered in families with LDL-receptor mutations in some but not all individuals with hypercholesterolemia or when some individuals in families with FH exhibit exaggerated hypercholesterolemia.

scholarly journals Imputation of Baseline LDL Cholesterol Concentration in Patients with Familial Hypercholesterolemia on Statins or Ezetimibe

2018 ◽  
Vol 64 (2) ◽  
pp. 355-362 ◽  
Author(s):  
Isabelle Ruel ◽  
Sumayah Aljenedil ◽  
Iman Sadri ◽  
Émilie de Varennes ◽  
Robert A Hegele ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Ldl Cholesterol ◽  
Genetic Disorder ◽  
Pathogenic Mutation ◽  
Pharmacological Therapy ◽  
Cholesterol Concentration ◽  
Atherosclerotic Cardiovascular Disease ◽  
Percent Reduction ◽  
The Mean ◽  
The Individual

Abstract BACKGROUND Familial hypercholesterolemia (FH) is the most frequent genetic disorder seen clinically and is characterized by increased LDL cholesterol (LDL-C) (>95th percentile), family history of increased LDL-C, premature atherosclerotic cardiovascular disease (ASCVD) in the patient or in first-degree relatives, presence of tendinous xanthomas or premature corneal arcus, or presence of a pathogenic mutation in the LDLR, PCSK9, or APOB genes. A diagnosis of FH has important clinical implications with respect to lifelong risk of ASCVD and requirement for intensive pharmacological therapy. The concentration of baseline LDL-C (untreated) is essential for the diagnosis of FH but is often not available because the individual is already on statin therapy. METHODS To validate a new algorithm to impute baseline LDL-C, we examined 1297 patients. The baseline LDL-C was compared with the imputed baseline obtained within 18 months of the initiation of therapy. We compared the percent reduction in LDL-C on treatment from baseline with the published percent reductions. RESULTS After eliminating individuals with missing data, nonstandard doses of statins, or medications other than statins or ezetimibe, we provide data on 951 patients. The mean ± SE baseline LDL-C was 243.0 (2.2) mg/dL [6.28 (0.06) mmol/L], and the mean ± SE imputed baseline LDL-C was 244.2 (2.6) mg/dL [6.31 (0.07) mmol/L] (P = 0.48). There was no difference in response according to the patient's sex or in percent reduction between observed and expected for individual doses or types of statin or ezetimibe. CONCLUSIONS We provide a validated estimation of baseline LDL-C for patients with FH that may help clinicians in making a diagnosis.

scholarly journals Evaluation of cardiomyopathy diagnosis in heart transplant recipients: comparison of echocardiographic and pathologic classification

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Neda Behzadnia ◽  
Babak Sharif-Kashani ◽  
Zargham Hossein Ahmadi ◽  
Farah Naghashzadeh ◽  
Atosa Dorudinia ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Heart Transplant ◽  
Disease Process ◽  
Diagnostic Tools ◽  
Definite Diagnosis ◽  
Cross Sectional ◽  
Pathologic Diagnosis ◽  
Significant Difference ◽  
Pathologic Classification ◽  
Before And After

Abstract Background Definite diagnosis of cardiomyopathy types can be challenging in end-stage disease process. New growing data have suggested that there is inconsistency between echocardiography and pathology in defining type of cardiomyopathy before and after heart transplantation. The aim of the present study was to compare the pre-heart transplant echocardiographic diagnosis of cardiomyopathy with the results of post-transplant pathologic diagnosis. Results In this retrospective cross-sectional clinicopathological study, 100 consecutive patients have undergone heart transplantation in Masih-Daneshvari hospital, Tehran, Iran, between 2010 and 2019. The mean age of patients was 40 ± 13 years and 79% of patients were male. The frequency of different types of cardiomyopathy was significantly different between two diagnostic tools (echocardiography versus pathology, P < 0.001). On the other hand, in 24 patients, the results of echocardiography as regard to the type of cardiomyopathy were inconsistent with pathologic findings. Conclusion Based on the findings of the present study, it could be concluded that there is a significant difference between echocardiographic and pathologic diagnosis of cardiomyopathy; therefore, it is necessary to use additional tools for definite diagnosis of cardiomyopathy like advanced cardiac imaging or even endomyocardial biopsy before heart transplantation to reach an appropriate treatment strategy.

scholarly journals Role of Lipoprotein (a) and TGF-β1 in Atherosclerosis of Hemodialysis Patients

2000 ◽  
Vol 11 (10) ◽  
pp. 1889-1895
Author(s):  
MASAHISA FUJISAWA ◽  
REIKO HARAMAKI ◽  
HIROSHI MIYAZAKI ◽  
TSUTOMU IMAIZUMI ◽  
SEIYA OKUDA
Keyword(s):  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Intima Media Thickness ◽  
Atherosclerotic Vascular Disease ◽  
Plaque Score ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Significant Difference ◽  
Before And After ◽  
Tgf Β1

Abstract. Atherosclerotic vascular disease is a major cause of death for uremic patients who are on hemodialysis (HD). Recent evidence suggests that lipoprotein (a) [Lp(a)] may aggravate atherosclerosis by inhibiting activation of transforming growth factor-β1 (TGF-β1). Plasma Lp(a) and plasma TGF-β1 activation in HD patients (n = 51), chronic renal failure patients not subjected to hemodialysis (non-HD-CRF; n = 12), and healthy volunteers (control; n = 13) were investigated. Plasma Lp(a) was significantly higher in HD (18.75 ± 1.62 mg/ml) and non-HD-CRF patients (25.0 ± 8.4 mg/ml) than in control subjects (10.9 ± 5.8 mg/ml). The degree of atherosclerosis in HD patients was assessed by measuring the intima-media thickness (IMT) and plaque score with the use of an ultrasound scanner. IMT and plaque score were higher in HD and non-HD-CRF patients than in controls. A significant positive correlation was found in HD patients between Lp(a) and IMT (r = 0.377, P < 0.01) as well as between Lp(a) and plaque score (r = 0.43, P < 0.01). Plasma total TGF-β1 significantly increased in HD (119.8 ± 53.5 ng/ml) and non-HD-CRF patients (93.2 ± 25.0 ng/ml) compared with control subjects (17.7 ± 6.4 ng/ml), whereas the plasma level of mature (active) TGF-β1 did not differ among the groups. When plasma TGF-β1 and supernatant TGF-β1 from cultured peripheral mononuclear cells were compared before and after an HD session, neither total nor mature TGF-β1 showed a significant difference between the values before and after an HD session. There were no significant relationships between plasma total TGF-β1 and IMT or plaque score, between mature TGF-β1 and IMT or plaque score, or between mature TGF-β1 and Lp(a). In conclusion, Lp(a) may be an important atherogenic factor in CRF patients. However, it was not clarified whether Lp(a) exerts its effect by inhibiting TGF-β1 activation in CRF patients.

scholarly journals ANGPTL3 Inhibition With Evinacumab Results in Faster Clearance of IDL and LDL apoB in Patients With Homozygous Familial Hypercholesterolemia

2021 ◽  
Author(s):  
Laurens F. Reeskamp ◽  
John S. Millar ◽  
Liya Wu ◽  
Hans Jansen ◽  
Dewi van Harskamp ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Human Monoclonal Antibody ◽  
Density Lipoprotein ◽  
Fractional Catabolic Rate ◽  
Homozygous Familial Hypercholesterolemia ◽  
Unique Identifier ◽  
Catabolic Rate ◽  
Before And After

Objective: The mechanism by which evinacumab, a fully human monoclonal antibody directed against ANGPTL3 (angiopoietin-like 3 protein) lowers plasma LDL (low-density lipoprotein) cholesterol levels in patients with homozygous familial hypercholesterolemia is unknown. We investigated apoB (apolipoprotein B) containing lipoprotein kinetic parameters in patients with homozygous familial hypercholesterolemia, before and after treatment with evinacumab. Approach and Results: Four patients with homozygous familial hypercholesterolemia underwent apoB kinetic analyses in 2 centers as part of a substudy of a trial evaluating the efficacy and safety of evinacumab in patients with homozygous familial hypercholesterolemia. The enrichment of apoB with the stable isotope (5,5,5- 2 H 3 )-Leucine was measured in VLDL (very LDL), IDL (intermediate-density lipoprotein), and LDL at different time points before and after intravenous administration of 15 mg/kg evinacumab. Evinacumab lowered LDL-cholesterol by 59±2% and increased IDL apoB and LDL apoB fractional catabolic rate in all 4 homozygous familial hypercholesterolemia subjects, by 616±504% and 113±14%, respectively. VLDL-apoB production rate decreased in 2 of the 4 subjects. Conclusions: In this small study, ANGPTL3 inhibition with evinacumab is associated with an increase in the fractional catabolic rate of IDL apoB and LDL apoB, suggesting that evinacumab lowers LDL-cholesterol predominantly by increasing apoB-containing lipoprotein clearance from the circulation. Additional studies are needed to unravel which factors are determinants in this biological pathway. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04722068.

Characteristics of Children Referred to a Lipid Clinic Before and After the Universal Screening Guidelines

2019 ◽  
Vol 58 (6) ◽  
pp. 656-664
Author(s):  
Kavitha Selvaraj ◽  
Alicia Olave-Pichon ◽  
Irwin Benuck ◽  
Adolfo J. Ariza ◽  
Helen J. Binns
Keyword(s):  
Universal Screening ◽  
Total Sample ◽  
Guideline Recommendation ◽  
Public Insurance ◽  
Chi Square ◽  
Screening Guidelines ◽  
Lipid Clinic ◽  
Significant Difference ◽  
Before And After ◽  
The Impact

In 2011, universal lipid screening was recommended for children aged 9 to 11 years; the impact of this recommendation on the lipid clinic setting is unknown. We examined the rate of primary and secondary dyslipidemia diagnoses in a lipid clinic before (2010-2011) and after (2012-2015) the guideline recommendation. We conducted a retrospective study of new clinic patients aged 0 to 20 years seen between April 2010 and April 2015. Chi-square testing was applied. The 345 subjects were 58% males; 48% ≥13 years; 56% Hispanic; and 59% obese. There was no difference in the rate of dyslipidemia diagnoses between periods (before: primary 23%, secondary 73%, no dyslipidemia 4% vs after: 22%, 72%, 6%, respectively; P = .616). There was no significant difference between periods in subject demographics for the total sample, but among those with primary dyslipidemia, pre- to post-guideline percentage of subjects with public insurance decreased (71% to 39%; P = .006). Additional strategies to increase identification of children with dyslipidemia are needed.

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