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- W2132959835 abstract "Future CardiologyVol. 6, No. 3 EditorialFree AccessCholesterol screening in children: makes sense but what is the impact?Anand RohatgiAnand RohatgiSearch for more papers by this authorPublished Online:12 May 2010https://doi.org/10.2217/fca.10.17AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInRedditEmail In July 2008, the American Academy of Pediatrics (AAP) published a revision of their 1998 policy on cholesterol in childhood, highlighting the need for targeted cholesterol screening in children given the obesity epidemic [1]. In addition, the revised policy statement recommended initiating statin therapy in children aged 8 years or older with elevated cholesterol levels resistant to lifestyle interventions, which received an incredible amount of attention from the lay media as well as stirring intense debate within the pediatric and adult medical communities.In the adult literature there is a large body of evidence supporting cholesterol screening, reflected in the National Cholesterol Educational Panel (NCEP) Adult Treatment Panel (ATP) III guidelines, which recommend periodic cholesterol screening in all persons over 20 years of age [2]. One in two men and one in three women over 40 years of age will die from coronary heart disease (CHD), making it the number one killer of adults in the USA [3]. Serum cholesterol is a necessary substrate for developing the atherosclerotic plaques that lead to clinically significant CHD. Reducing cholesterol levels through dietary and lifestyle measures, as well as pharmacologic therapies has been consistently shown to reduce CHD events and mortality in adults, both in primary and secondary prevention [2]. Given the rise in obesity, metabolic syndrome and diabetes in children [4], attention has turned toward cholesterol screening and potential treatment at even younger ages.Cholesterol screening in children would be rational only if several criteria are met: first, children with lipid abnormalities are at increased risk of developing accelerated atherosclerosis and CHD events; second, the cholesterol screening test and screening strategy can accurately identify those at increased risk; and finally, therapies currently exist that can modulate that risk safely and effectively in the pediatric population. This article will address each of these points in detail with regard to the feasibility of cholesterol screening in children.Background: atherosclerosis begins in early childhoodMuch of the information about atherosclerosis in children comes from autopsy studies of children dying from accidental causes. In the Bogalusa Heart Study [5], 50% of children aged 2–15 years had evidence of fatty streaks in the intima and 8% had raised fibrous plaques in the coronary arteries. The presence of both fatty streaks and fibrous plaques increased exponentially with more risk factors, including obesity, hypertension and dyslipidemia. Similarly, in 1443 autopsy subjects aged 15–34 years in the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study [6], fatty streaks and raised lesions in the coronary arteries were present in all age groups and increased primarily with age and serum cholesterol concentrations. In addition, noninvasive measurements have also shown increased prevalence of coronary lesions and increased carotid intima–media thickness in children associated with increasing cholesterol concentrations and other traditional CHD risk factors [7–9]. Based on these studies and others, the case can convincingly be made that the atherosclerosis process leading to CHD events and CHD death begins early in childhood and continues to progress with increasing age and CHD risk factors, including hypercholesterolemia.Children with lipid abnormalities have increased risk for CHDIn children, hypercholesterolemia is rare but usually occurs secondary to another disease state such as obesity, diabetes, chronic inflammatory disease or medications. Extreme elevations in low-density lipoprotein (LDL; >95th percentile for age and gender) are usually due to a primary genetic disorder, of which familial hypercholesterolemia (FH) is the most common and most studied [10]. FH is an autosomal dominant condition that is extremely rare in the homozygous form (1:1,000,000) presenting in the first decade of life with subsequent CHD events and death by the fourth decade of life without advanced lipid-lowering therapies such as LDL apheresis.Patients with homozygous FH have LDL levels above 500 mg/dl and have physical stigmata of hypercholesterolemia. Heterozygous FH is more common, occurring in one in 500 individuals. Children with heterozygous FH are usually asymptomatic with moderate elevations of LDL and identified only by cholesterol screening, which is usually prompted by a family history of premature CHD or hypercholesterolemia. One study of Dutch children who had parents with FH found that an LDL level greater than 135 mg/dl was associated with a 98% probability of having an LDL-receptor mutation [11]. Children with heterozygous FH have increased carotid intima-media thickness and abnormal arterial endothelial function, and adults with heterozygous FH have accelerated atherosclerosis and increased rates of CHD events [12,13]. Children with dyslipidemias secondary to high-risk conditions, including Kawasaki’s disease, diabetes mellitus, chronic kidney disease, HIV, transplant recipients, chronic inflammatory disease, post-cancer treatment survivors and congenital heart disease, are also at risk for developing CHD events, in part due to the accelerated lipid abnormalities [10]. These primary and secondary hyperlipidemic conditions form the basis of the current targeted cholesterol screening in children with the notable exception of obesity, which is a relatively new risk factor for hypercholesterolemia emphasized in the most recent 2008 AAP guideline statement [1].Obesity in children is associated with multiple lipid abnormalitiesBased on the US National Health and Nutrition Examination Surveys (NHANES), the prevalence of childhood obesity as defined by BMI >95th percentile) has markedly and steadily increased from 5 to 6% in the 1970s to 16% in 2006, with almost a third of all US children either overweight or obese [14]. These trends are concerning as overweight (BMI >85th percentile) and obese children (BMI >95th percentile) often have clusters of other CHD risk factors, including the metabolic syndrome and diabetes, are more likely to be obese as adults, and are at increased risk for CHD events and death [15].Overweight and obese children have an increased risk of both prevalent and incident hypercholesterolemia in adulthood [16]. In the Bogalusa Heart Study, the risk of any NCEP-defined lipid abnormality in children appears to increase after the 85th percentile for BMI (overweight) [17]. Data from the NHANES 2001–2006 study in children showed that cholesterol levels start to increase after the 80th percentile for BMI and, adjusted for other risk factors, the risk for high total cholesterol increased after the 80th percentile, and for high LDL after the 90th percentile [18]. Therefore, increasing BMI in children is certainly associated with hypercholesterolemia, but the optimal cutoff for screening is yet to be determined. Interestingly, childhood obesity is more robustly associated with high triglyceride levels and low high-density lipoprotein (HDL)-cholesterol [17,19], components of the metabolic syndrome that are not primary targets of current pediatric guidelines for screening or treatment. Another potential issue with using obesity for targeted cholesterol screening is that, despite a marked increases in childhood obesity over the past several decades, mean cholesterol levels in children have either remained stable or actually decreased, potentially dampening contemporary associations between obesity and hypercholesterolemia that have been seen in prior studies [20,21].Detecting high cholesterol levels in children: suboptimal performanceIn adults, a single nonfasting cholesterol determination can accurately measure total cholesterol and HDL, and help determine a person’s global CHD risk using the Framingham Risk Score as recommended in the NCEP ATP III guidelines [2].Lipoprotein testing in children is somewhat more complex. Based on the Lipids Research Clinic studies, cholesterol concentrations increase rapidly from birth and reach levels similar to young adults by 2 years of age [22]. In addition, cholesterol levels fluctuate by gender, ethnicity and developmental stage, so that a single cholesterol measurement may not accurately reflect the cholesterol exposure burden and may oscillate above and below recommended thresholds for therapy [21,23]. For example, only 41% of children aged 3–19 years with a total cholesterol level of 200 mg/dl or greater had a level that high 1 year later [24]. This variation is the main reason that an elevated cholesterol measurement in a child should be repeated, preferably in a fasting state to determine LDL levels, before initiating therapy. An LDL level greater than the 95th percentile for age and gender is recommended as the cut-off point for being abnormal [1]. The recommendation for fasting and the need for repeat cholesterol measurements significantly hinders the real-world feasibility and compliance of cholesterol screening, even in a targeted approach.Does the targeted cholesterol screening strategy in children actually work?Current recommendations from pediatric organizations do not include universal cholesterol screening in children given the lack of evidence of a convincing benefit. Instead, a targeted approach has been recommended to obtain fasting cholesterol measurements in children with a family history of premature CHD/hypercholesterolemia, BMI above the 85th percentile, blood pressure in the 95th percentile or greater, smoking or diabetes [1]. Current NHANES data show that up to 46% of all US children would be eligible for cholesterol screening based on these criteria [25]. However, up to 50% of children with elevated LDL would be missed by this targeted screening approach, which may be due to multiple reasons including variation in cholesterol concentration and a lack of full parental information regarding coronary disease and lipid status [26]. A cross-sectional study of mostly French–Canadian school-aged children in Quebec aged 9, 13 and 16 years (n = 2217) reported approximately a 25% prevalence of self-reported parental history of CHD/hypercholesterolemia [27]. The sensitivity of detecting a high LDL level above 130 mg/dl by parental history was only 50% with a false-positive rate of 30%. The positive predictive value of a self-reported parental history detecting high LDL was only 7.7%, only marginally higher than the population prevalence of high LDL of 4.8%. Including BMI above the 85th percentile did not improve these poor performance characteristics of the recommended targeted cholesterol screening strategy. The authors of this large study concluded that targeted screening based on parental history of CHD/hypercholesterolemia was no better than a random screening of the population.A recent study using NHANES 1999–2004 data show little to no benefit using current BMI thresholds in detecting hypercholesterolemia [28]. In this study, the investigators classified BMI thresholds of below the 5th percentile (underweight), in the 5th to 85th percentile (normal), 85–95th percentile (overweight), and equal to or above the 95th percentile (obese), and used area under the receiver-operating curves (auROC, analogous to the c-statistic) analysis to evaluate the ability of these BMI thresholds to detect NCEP-defined hypercholesterolemia. Overall, BMI thresholds only modestly detected total cholesterol greater than 200 mg/dl and LDL greater than 130mg/dl (auROC: 0.6 and 0.63, respectively). BMI thresholds tended to perform better in boys than girls and in detecting high triglycerides and low HDL versus total and LDL-cholesterol. Overall, given the poor performance characteristics in detecting high total cholesterol or LDL that would merit therapy, it is difficult to justify even a targeted cholesterol screening approach based on family history or BMI alone.Can existing therapies reduce the CHD risk associated with hypercholesterolemia in children?The AAP recommended in 1998 and 2008 a two-pronged approach to reducing CHD risk in children: first, a population-based approach to lower dietary saturated fat and cholesterol intake in children over 2 years of age; and second, an individual-based approach using targeted cholesterol screening to identify children who may benefit from lifestyle interventions and pharmacotherapies [1]. Low-fat diets only modesty reduce LDL (average LDL lowering 3.23 mg/dl in older children) [29] and are unlikely to reduce individual or population risk significantly. Moreover, compliance with the targeted cholesterol screening strategy and lifestyle interventions has been shown to be dismally low, further reducing effectiveness of any interventions [30].Statins have been the most studied class of lipid-lowering drugs in both adults and children. In adults, statins are associated with significant reductions in CHD events and mortality in both primary and secondary prevention settings [31]. The evidence supporting the use of statins in children is much more limited. Several randomized controlled trials have demonstrated the efficacy of statins in lowering total and LDL-cholesterol in children with FH above 8 years of age without adverse effects relating to sexual maturation, growth, muscle toxicity or liver damage [32–39]. A recently published study with rosuvastatin in patients with FH (eight children aged less than 18 years) also showed consistent cholesterol lowering [40]. This has led to pediatric labeling for lovastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin. However, these statin trials are limited primarily to children with homozygous or heterozygous FH over 8 years of age and do not report long-term clinical outcomes or long-term safety data beyond 4 years. In addition, based on the current recommended LDL thresholds for initiating pharmacologic lipid-lowering therapy in children, only 0.8% of US children would qualify for drug therapy (NHANES 1999–2006 survey: aged 12–17 years) [23]. Given the modest effects of low-fat diets, low compliance rates with lifestyle interventions and small number of children eligible for lipid-lowering drugs, there is no evidence to support the AAP recommended targeted cholesterol screening strategy in children for treatment purposes. Those rare children with homozygous FH and other high-risk conditions should be identified by history and targeted for aggressive treatment [10].ConclusionAtherosclerotic fatty streaks and plaques form early in life in coronary and carotid arteries, progress with age, and are accelerated in several chronic disease states including FH and diabetes, both of which are uncommon in children. These uncommon disease states, specifically FH, are characterized by high cholesterol levels in children and are associated with increased CHD events. The AAP and the American Heart Association recommend targeted cholesterol screening in children over 2 years of age and before 10 years of age in those who have a family history of premature CHD/hypercholesterolemia or are obese, but this strategy has not been shown to accurately detect children with LDL above the 95th percentile, the current recommended threshold for treatment (LDL >190 mg/dl with no risk factors). Furthermore, there are no reports on the impact of cholesterol screening in children on clinical outcomes later in life, a fact reflected by the inability of the US Preventive Services Task Force to recommend for or against cholesterol screening in children [41]. Although a third to a half of all children in the USA would be eligible for targeted cholesterol screening, less than 1% would meet criteria for therapy. Over 25% of all children tested using the recommended strategy would have a false positive result. This would translate into one in eight US children being inappropriately labeled as having hypercholesterolemia, which would potentially have major implications on the ability to obtain future medical and life insurance, job placement, and so on. Further efforts at a national level should concentrate on population-based strategies to reduce mean cholesterol levels and body weight, which could provide a much bigger impact on CHD risk reduction than targeted screening and individualized therapeutic options. For the individual pediatrician, aside from several uncommon high-risk conditions [10], efforts to reduce CHD risk should focus on optimizing lifestyle choices for all children and their families, and targeting weight loss in the 30% of US children that are overweight or obese.Financial & competing interests disclosureThe author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.Papers of special note have been highlighted as: ▪ of interest ▪▪ of considerable interestBibliography1 Daniels SR, Greer FR: Lipid screening and cardiovascular health in childhood. Pediatrics122(1),198–208 (2008).▪▪ 2008 updated American Academy of Pediatrics (AAP) guidelines on cholesterol screening in children, which is the focus of this editorial and stirred the current debate.Crossref, Medline, Google Scholar2 Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation106(25),3143–3421 (2002).Crossref, Medline, Google Scholar3 Lloyd-Jones D, Adams RJ, Brown TM et al.: Heart disease and stroke statistics – 2010 update: a report from the american heart association. Circulation121(7),e46–e215 (2010).Crossref, Medline, Google Scholar4 Weiss R, Dziura J, Burgert TS et al.: Obesity and the metabolic syndrome in children and adolescents. N. Engl. J. Med.350(23),2362–2374 (2004).Crossref, Medline, CAS, Google Scholar5 Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, Wattigney WA: Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. N. Engl. J. Med.338(23),1650–1656 (1998).Crossref, Medline, CAS, Google Scholar6 McGill HC Jr, McMahan CA, Malcom GT, Oalmann MC, Strong JP: Effects of serum lipoproteins and smoking on atherosclerosis in young men and women. The PDAY Research Group. Pathobiological determinants of atherosclerosis in youth. Arterioscler. Thromb. Vasc. Biol.17(1),95–106 (1997).Crossref, Medline, Google Scholar7 Davis PH, Dawson JD, Riley WA, Lauer RM: Carotid intimal–medial thickness is related to cardiovascular risk factors measured from childhood through middle age: The Muscatine Study. Circulation104(23),2815–2819 (2001).Crossref, Medline, CAS, Google Scholar8 Raitakari OT, Juonala M, Kahonen M et al.: Cardiovascular risk factors in childhood and carotid artery intima–media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA290(17),2277–2283 (2003).Crossref, Medline, CAS, Google Scholar9 Tuzcu EM, Kapadia SR, Tutar E et al.: High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound. Circulation103(22),2705–2710 (2001).Crossref, Medline, CAS, Google Scholar10 Kavey RE, Allada V, Daniels SR et al.: Cardiovascular risk reduction in high-risk pediatric patients: a scientific statement from the American Heart AssociationExpert Panel on Population and Prevention Science; the Councils on Cardiovascular Disease in the Young, Epidemiology and Prevention, Nutrition, Physical Activity and Metabolism, High Blood Pressure Research, Cardiovascular Nursing, and the Kidney in Heart Disease; and the Interdisciplinary Working Group on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation114(24),2710–2738 (2006).▪▪ American Heart Association (AHA) guideline statement on managing cardiovascular risk in several high-risk conditions in childhood, a must-read for every physician caring for children.Crossref, Medline, Google Scholar11 Wiegman A, Rodenburg J, de Jongh Set al.: Family history and cardiovascular risk in familial hypercholesterolemia: data in more than 1000 children. Circulation107(11),1473–1478 (2003).Crossref, Medline, Google Scholar12 Raitakari OT: Arterial abnormalities in children with familial hypercholesterolaemia. Lancet363(9406),342–343 (2004).Crossref, Medline, Google Scholar13 Jansen AC, van Aalst-Cohen ES, Tanck MW et al.: The contribution of classical risk factors to cardiovascular disease in familial hypercholesterolaemia: data in 2400 patients. J. Intern. Med.256(6),482–490 (2004).Crossref, Medline, CAS, Google Scholar14 Ogden CL, Carroll MD, Flegal KM: High body mass index for age among US children and adolescents, 2003–2006. JAMA299(20),2401–2405 (2008).Crossref, Medline, CAS, Google Scholar15 Daniels SR, Jacobson MS, McCrindle BW, Eckel RH, Sanner BM: American Heart Association Childhood Obesity Research Summit Report. Circulation119(15),e489–E517 (2009).▪▪ AHA statement on childhood obesityand its effects on risk factors, morbidity and mortality.Crossref, Medline, Google Scholar16 Lauer RM, Lee J, Clarke WR: Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine Study. Pediatrics82(3),309–318 (1988).▪▪ Documented the relationship between elevated cholesterol levels and obesity in childhood with elevated adult cholesterol levels in over 2400 subjects followed from childhood to young adulthood.Medline, CAS, Google Scholar17 Freedman DS, Dietz WH, Srinivasan SR, Berenson GS: The relation of overweight to cardiovascular risk factors among children and adolescents: the Bogalusa Heart Study. Pediatrics103(6 Pt 1),1175–1182 (1999).▪ Reported the cut-off BMI at which cholesterol levels began to increase in the Bogulasa Heart Study, one of the main studies on childhood cardiovascular disease.Crossref, Medline, CAS, Google Scholar18 Skinner AC, Mayer ML, Flower K, Perrin EM, Weinberger M: Using BMI to determine cardiovascular risk in childhood: how do the BMI cutoffs fare? Pediatrics124(5),E905–E912 (2009).Crossref, Medline, Google Scholar19 Harel Z, Riggs S, Vaz R, Flanagan P, Harel D: Isolated low HDL cholesterol emerges as the most common lipid abnormality among obese adolescents. Clin. Pediatr. (Phila.)49(1),29–34 (2010).Crossref, Medline, Google Scholar20 Ford ES, Mokdad AH, Ajani UA: Trends in risk factors for cardiovascular disease among children and adolescents in the United States. Pediatrics114(6),1534–1544 (2004).▪ Interesting report documenting the rise in childhood obesity, but flat trendin total and low-density lipoprotein (LDL)-cholesterol.Crossref, Medline, Google Scholar21 Hickman TB, Briefel RR, Carroll MD et al.: Distributions and trends of serum lipid levels among United States children and adolescents ages 4–19 years: data from the Third National Health and Nutrition Examination Survey. Prev. Med.27(6),879–890 (1998).Crossref, Medline, CAS, Google Scholar22 Tamir I, Heiss G, Glueck CJ, Christensen B, Kwiterovich P, Rifkind BM: Lipid and lipoprotein distributions in white children ages 6–19 yr. The Lipid Research Clinics Program Prevalence Study. J. Chronic Dis.34(1),27–39 (1981).Crossref, Medline, CAS, Google Scholar23 Ford ES, Li C, Zhao G, Mokdad AH: Concentrations of low-density lipoprotein cholesterol and total cholesterol among children and adolescents in the United States. Circulation119(8),1108–1115 (2009).▪▪ Reports on childhood data from US National Health and Nutrition Examination Surveys (NHANES) survey 1999–2006 and found that only 0.8% of children aged 12–17 years were eligibile for lipid-lowering therapy based on the AAP guidelines.Crossref, Medline, CAS, Google Scholar24 Benuck I, Gidding SS, Donovan M: Year-to-year variability of cholesterol levels in a pediatric practice. Arch. Pediatr. Adolesc. Med.149(3),292–296 (1995).Crossref, Medline, CAS, Google Scholar25 Bachman RP, Schoen EJ, Stembridge A, Jurecki ER, Imagire RS: Compliance with childhood cholesterol screening among members of a prepaid health plan. Am. J. Dis. Child.147(4),382–385 (1993).Medline, CAS, Google Scholar26 Griffin TC, Christoffel KK, Binns HJ, McGuire PA: Family history evaluation as a predictive screen for childhood hypercholesterolemia. Pediatric Practice Research Group. Pediatrics84(2),365–373 (1989).Medline, CAS, Google Scholar27 O’Loughlin J, Lauzon B, Paradis G et al.: Usefulness of the American Academy of Pediatrics recommendations for identifying youths with hypercholesterolemia. Pediatrics113(6),1723–1727 (2004).▪▪ This study of over 2400 Quebec children found that parental history of hypercholesterolemia or cardiovascular disease had a positive predictive value of only 7.7% for detecting highLDL-cholesterol in children. Adding obesity did improve detection of high LDL-cholesterol.Crossref, Medline, Google Scholar28 Lee JM, Gebremariam A, Card-Higginson P, Shaw JL, Thompson JW, Davis MM: Poor performance of body mass index as a marker for hypercholesterolemia in children and adolescents. Arch. Pediatr. Adolesc. Med.163(8),716–723 (2009).▪▪ This recent study was a response tothe 2008 AAP recommendation for targeted cholesterol screening. Using NHANES 1999–2004 data on children aged 3–18 years, the authors found that BMI percentiles poorly detected high total or LDL-cholesterol and modestly detected abnormal high-density lipoprotein and triglyceride levels, calling into serious question the current recommendations.Medline, Google Scholar29 Efficacy and safety of lowering dietary intake of fat and cholesterol in children with elevated low-density lipoprotein cholesterol. The Dietary Intervention Study in Children (DISC). The Writing Group for the DISC Collaborative Research Group. JAMA273(18),1429–1435 (1995).Crossref, Medline, Google Scholar30 Nader PR, Yang M, Luepker RV et al.: Parent and physician response to children’s cholesterol values of 200 mg/dl or greater: the Child and Adolescent Trial for Cardiovascular Health Experiment. Pediatrics99(5),E5 (1997).Crossref, Medline, CAS, Google Scholar31 Baigent C, Keech A, Kearney PM et al.: Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet366(9493),1267–1278 (2005).Crossref, Medline, CAS, Google Scholar32 Clauss SB, Holmes KW, Hopkins P et al.: Efficacy and safety of lovastatin therapy in adolescent girls with heterozygous familial hypercholesterolemia. Pediatrics116(3),682–688 (2005).Crossref, Medline, Google Scholar33 de Jongh S, Ose L, Szamosi T et al.: Efficacy and safety of statin therapy in children with familial hypercholesterolemia: a randomized, double-blind, placebo-controlled trial with simvastatin. Circulation106(17),2231–2237 (2002).Crossref, Medline, CAS, Google Scholar34 Knipscheer HC, Boelen CC, Kastelein JJ et al.: Short-term efficacy and safety of pravastatin in 72 children with familial hypercholesterolemia. Pediatr. Res.39(5),867–871 (1996).Crossref, Medline, CAS, Google Scholar35 Lambert M, Lupien PJ, Gagne C et al.: Treatment of familial hypercholesterolemia in children and adolescents: effect of lovastatin. Canadian Lovastatin in Children Study Group. Pediatrics97(5),619–628 (1996).Medline, CAS, Google Scholar36 McCrindle BW, Ose L, Marais AD: Efficacy and safety of atorvastatin in children and adolescents with familial hypercholesterolemia or severe hyperlipidemia: a multicenter, randomized, placebo-controlled trial. J. Pediatr.143(1),74–80 (2003).Crossref, Medline, CAS, Google Scholar37 O’Gorman CS, Higgins MF, O’Neill MB: Systematic review and metaanalysis of statins for heterozygous familial hypercholesterolemia in children: evaluation of cholesterol changes and side effects. Pediatr. Cardiol.30(4),482–489 (2009).▪ A nice meta-analysis of all randomized controlled trials of statins in childrenwith homozygous or heterozygous familial hypercholesterolemia.Crossref, Medline, Google Scholar38 Stein EA, Illingworth DR, Kwiterovich PO Jr et al.: Efficacy and safety of lovastatin in adolescent males with heterozygous familial hypercholesterolemia: a randomized controlled trial. JAMA281(2),137–144 (1999).Crossref, Medline, CAS, Google Scholar39 Wiegman A, Hutten BA, de Groot E et al.: Efficacy and safety of statin therapy in children with familial hypercholesterolemia: a randomized controlled trial. JAMA292(3),331–337 (2004).Crossref, Medline, CAS, Google Scholar40 Marais AD, Raal FJ, Stein EA et al.: A dose-titration and comparative study of rosuvastatin and atorvastatin in patients with homozygous familial hypercholesterolaemia. Atherosclerosis197(1),400–406 (2008).Crossref, Medline, CAS, Google Scholar41 Haney EM, Huffman LH, Bougatsos C, Freeman M, Steiner RD, Nelson HD: Screening and treatment for lipid disorders in children and adolescents: systematic evidence review for the US Preventive Services Task Force. Pediatrics120(1),E189–E214 (2007).▪▪ The US Preventive Services Task Force reviews available data on diagnostic testing for multiple disease states and provides the most conservative interpretations and conclusions. Their review of the available evidence resulted in no ability to recommend for or against cholesterol screening in children.Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited ByPrevalence of Cardiovascular Disease Risk Factors Among US Adolescents, 1999−20081 June 2012 | Pediatrics, Vol. 129, No. 6Improvement of the lipid profile with exercise in obese children: A systematic reviewPreventive Medicine, Vol. 54, No. 5 Vol. 6, No. 3 Follow us on social media for the latest updates Metrics History Published online 12 May 2010 Published in print May 2010 Information© Future Medicine LtdFinancial & competing interests disclosureThe author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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- W2132959835 cites W1934245552 @default.
- W2132959835 cites W1970072674 @default.
- W2132959835 cites W1986672491 @default.
- W2132959835 cites W1991965498 @default.
- W2132959835 cites W2001550141 @default.
- W2132959835 cites W2017464081 @default.
- W2132959835 cites W2022605831 @default.
- W2132959835 cites W2029349706 @default.
- W2132959835 cites W2036704981 @default.
- W2132959835 cites W2049170821 @default.
- W2132959835 cites W2063051821 @default.
- W2132959835 cites W2064524230 @default.
- W2132959835 cites W2079099510 @default.
- W2132959835 cites W2079699385 @default.
- W2132959835 cites W2079986890 @default.
- W2132959835 cites W2083240916 @default.
- W2132959835 cites W2090231128 @default.
- W2132959835 cites W2101976191 @default.
- W2132959835 cites W2105612671 @default.
- W2132959835 cites W2125639599 @default.
- W2132959835 cites W2126127706 @default.
- W2132959835 cites W2126184698 @default.
- W2132959835 cites W2126545477 @default.
- W2132959835 cites W2132629624 @default.
- W2132959835 cites W2133591735 @default.
- W2132959835 cites W2135545256 @default.
- W2132959835 cites W2155932961 @default.
- W2132959835 cites W2161453510 @default.
- W2132959835 cites W2166512947 @default.
- W2132959835 cites W2168680123 @default.
- W2132959835 cites W2169982919 @default.
- W2132959835 cites W2171262087 @default.
- W2132959835 cites W2172278218 @default.
- W2132959835 cites W2247997571 @default.
- W2132959835 cites W2315613231 @default.
- W2132959835 cites W2614781785 @default.
- W2132959835 cites W4230870013 @default.
- W2132959835 cites W4292539861 @default.
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