p.29 抽出テキスト

June 18/25, 2019 Circulation. 2019;139:e1082–e1143. DOI: 10.1161/CIR.0000000000000625 e1110

CLINICAL STATEMENTS AND GUIDELINES 3.	 Statins and nonstatins lower TC and LDL-C in children and adolescents with FH,S4.4.4.3-30 and other health conditions that put them at increased risk of CVD.S4.4.4.3-31,S4.4.4.3-32 Evidence from these RCTs demonstrates low short- and medium-term adverse event rates (abnormalities in liver function test, creatine kinase [CK] levels, and reported myopathy) with statin use in children and adolescents with FH.S4.4.4.3-30 Limited data show benefit from statins to subclinical atherosclerosis in FH. These data, coupled with the increased risk of CVD in untreated severe hypercholesterolemia, support the use of statins in children and adolescents at ages ≥10 years who have FHS4.4.4.3-33,S4.4.4.3-34 and have not responded to 3 to 6 months of lifestyle therapy. Statins may be considered at age 8 years in the presence of concerning family history, extremely elevated LDL-C level, or elevated Lp(a), in the context of informed shared decision-making and counseling with the patient and family. The intensity of treatment should be based on the severity of the hypercholesterolemia and should incorporate patient/ family preference. Scant data on the use of ezetimibe in children with severe hypercholesterolemia show reasonable LDL-C lowering with no significant adverse effects.S4.4.4.3-13 Nonsystemic bile acid sequestrants can be useful for LDL-C lowering, but tolerability is an issue.S4.4.4.3-13–S4.4.4.3-16

4.	 Lipid testing during childhood can identify the severe hypercholesterolemia phenotype.S4.4.4.3-35 Severe hypercholesterolemia, which includes FH, can be identified in children and adolescents with an LDL-C level ≥190 mg/dL (≥4.9 mmol/L). Moreover, children and adolescents with LDL-C ≥160 mg/dL (≥4.1 mmol/L) and a family history of early atherosclerosis or similarly elevated cholesterol in 1 parent likely are those with FH and related genetic disorders associated with accelerated ASCVD.S4.4.4.3-17–S4.4.4.3-21 Subclinical atherosclerosis data suggest divergence between affected and unaffected children and adolescents beginning at age 10 years,S4.4.4.3-28 which supports screening by this age, although this topic is still considered controversial.S4.4.4.3-36 Screening is advised beginning at age 2 years if a family history is suggestive of either early CVD or significant primary hypercholesterolemia. Identification of a child with severe hypercholesterolemia should prompt screening of extended family members (eg, reverse-cascade screening), according to studies outside the United States demonstrating efficacy of this approach.S4.4.4.3-37 Screening for severe hypercholesterolemia on the basis of family history includes an expanded group of family members (eg, grandparents, aunts, and uncles) in addition to parents and siblings because siblings of children are unlikely to have had cardiovascular events or been identified with significant cholesterol disorders.S4.4.4.3-38

5.	 One advantage of measuring lipids in children and adolescents is to identify genetic abnormalities in lipid metabolism that may be present in other family members. Regardless of the age at which abnormalities are detected, reverse-cascade screening in families is highly effective for the identification of family members at risk of ASCVD.S4.4.4.3-22–S4.4.4.3-24 6.	 Observational studies of children and adolescents show that obesity and other lifestyle-related behaviors and metabolic syndrome risk factors including lipid abnormalities,S4.4.4.3-25,S4.4.4.3-26 and with subclinical atherosclerosis into young adulthood,S4.4.4.3-38,S4.4.4.3-39 occur at higher rates than in lean and otherwise healthy children and adolescents. Longitudinal cohort data show moderate tracking of cardiovascular risk factors from childhood to adulthood in the general pediatric population,S4.4.4.3-40 suggesting some persistence of the underlying pathophysiology and potential benefit of identifying lipid disorders in childhood. 7.	 Selective screening for lipid disorders on the basis of family history (Recommendation 1) or lifestylerelated factors (Recommendation 2) identifies only a portion of childhood lipid abnormalitiesS4.4.4.3-19,

S4.4.4.3-21,S4.4.4.3-26 (Table 9). Therefore, concordant with the 2011 National Heart, Lung, and Blood Institute Expert Panel on Integrated Guidelines

Table 9.  Normal and Abnormal Lipid Values in Childhood*†

Acceptable,

mg/dL Borderline,

mg/dL Abnormal,

mg/dL

TC <170 (<4.3 mmol/L) 170–199 (4.3–5.1 mmol/L) ≥200 (≥5.1 mmol/L) Triglycerides (0-9 y) <75 (<0.8 mmol/L) 75–99 (0.8–1.1 mmol/L) ≥100 (≥1.1 mmol/L) Triglycerides (10-19 y) <90 (<1.0 mmol/L) 90–129 (1.0–1.5 mmol/L) ≥130 (≥1.4 mmol/L) HDL-C >45 (>1.2 mmol/L) 40–45 (1.0–1.2 mmol/L) <40 (<1.0 mmol/L) LDL-C <110 (<2.8 mmol/L) 110–129 (2.8–3.3 mmol/L) ≥130 (≥3.4 mmol/L) Non–HDL-C <120 (<3.1 mmol/L) 120–144 (3.1–3.7 mmol/L) ≥145 (≥3.7 mmol/L) Values given are in mg/dL. To convert to SI units, divide the results for TC, LDL-C, HDL-C, and non–HDL-C by 38.6; for triglycerides, divide by 88.6. *Values for plasma lipid and lipoprotein levels are from the NCEP Expert Panel on Cholesterol Levels in Children. Non–HDL-C values from the Bogalusa Heart Study are equivalent to the NCEP Pediatric Panel cutpoints for LDL-C. †The cutpoints for high and borderline high represent approximately the 95th and 75th percentiles, respectively. Low cutpoints for HDL-C represent approximately the 10th percentile. HDL-C indicates high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; NCEP, National Cholesterol Education Program; SI, Système international d’unités (International System of Units); and TC, total cholesterol.

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