Hyperlipoproteinemia
(Redirected from Hyperlipidemias)
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Hyperlipoproteinemia Microchapters |
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ACC/AHA Guideline Recommendations |
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Intensity of statin therapy in primary and secondary prevention |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Tarek Nafee, M.D. [2]
Overview
Hyperlipoproteinemia (also known as hyperlipidemia or high lipoproteins) is defined as presence of high levels of one or more type of lipoproteins. Hyperlipoproteinemia may be caused by primary genetic disorders or as a secondary complications of underlying medical conditions. After ruling out common secondary causes of hyperlipoproteinemia, the clinician must begin the work-up for primary causes.
Patients with hyperlipoproteinemia may present with elevated LDL, HDL, or triglycerides. Hyperlipoproteinemias have a high clinical significance due to the increased risk of cardiovascular, cerebrovascular, and peripheral arterial disease which they confer. Other complications of long-standing hyperlipidemia (specifically hypertriglyceridemia) may include pancreatitis, and steatohepatitis.
Primary causes of hyperlipoproteinemia have been classified into 5 subtypes by Friedrickson. The exact genetic cause of these conditions is not clearly understood. Secondary causes of hyperlipoproteinemia are more common and workup must be targeted at excluding them prior to evaluating primary causes. Regardless of the underlying pathogenesis of the disease, management is targeted at normalizing the affected lipid or lipoproteins either pharmacologically or by lifestyle modifications. However, gene therapy has been a subject of several investigational therapies aiming to treat familial hyperlipoproteinemias at the genomic level.[1]
Causes
To view a full list of causes of hypercholesterolemia click here
To view a full list of causes of hypertriglyceridemia click here
The table below gives a synopsis of the lipid profile of the most common causes of secondary hyperlipidemias:
| Diseases | LDL | HDL | Triglycerides | Total Cholesterol | Diagnostic test(s) |
|---|---|---|---|---|---|
| Diabetes Mellitus[2][3] | ↑
|
↓
|
↑
|
↑
|
|
| Alcohol Abuse[4][5][6] | ↓
|
↓
|
↑
|
↑
|
|
| Estrogen Therapy[7] | ↓
|
↑
|
↑
|
↓
|
|
| Glucocorticoid therapy[8][9][10] | ↑
|
↑
|
↑ or N
|
↑
|
|
| Renal Disease[11][12] [12] [6] | ↑
|
↓ or N
|
↑
|
↑
|
|
| Obesity[13] | ↑
|
↓
|
↑
|
-
|
|
| Pregnancy[14] | ↑
|
↑
|
↑
|
↑
|
|
| Paraproteinemic disorders[15][16] | -
|
↓
|
↑
|
-
|
|
| Hypothyroidism[17][18] | ↑↑↑
|
↑ or N
|
↑
|
↑
|
|
Classification
Hyperlipoproteinemias are classified into primary and secondary based on the etiology. The following is the classification for primary hyperlipopoproteinemias by Friedrickson:
| Hyperlipoproteinemia | |||||||||||||||||||||||||||||||||||||||||
| Type I: Familial hyperchylomicronemia | Type II | Type III: Dysbetalipoproteinemia | Type IV: Primary hypertriglyceridemia | Type V: Mixed hyperlipoproteinemia | |||||||||||||||||||||||||||||||||||||
| Type A: Familial hypercholesterolemia | Type B: Familial combined hyperlipidemia | ||||||||||||||||||||||||||||||||||||||||
The following table is a brief description of the different types of hyperlipoproteinemias:
| Hyperlipoproteinemia | Disease Name | Pathophysiology | Notable Laboratory Findings | Mainstay of treatment |
|---|---|---|---|---|
| Type I | Familial hyperchylomicronemia | Decreased lipoprotein lipase (LPL) or altered ApoC2 | Elevated chylomicrons | Diet control |
| Type IIa | Familial hypercholesterolemia | LDL receptor deficiency | Elevated LDL only | Bile acid sequestrants, statins, niacin |
| Type IIb | Combined hyperlipidemia | Decreased LDL receptor and increased ApoB | Elevated LDL, VLDL and triglycerides | Statins, niacin, gemfibrozil |
| Type III | Familial Dysbetalipoproteinemia | Defect in ApoE synthesis | Increased IDL | Drug of choice: Gemfibrozil |
| Type IV | Familial Hypertriglyceridemia | Increased VLDL production and decreased elimination | Increased VLDL | Drug of choice: Niacin |
| Type V | Mixed hyperlipoproteinemia | Increased VLDL production and decreased LPL | Increased VLDL and chylomicrons | Niacin, gemfibrozil |
Differential Diagnosis
Hyperlipoproteinemia may be caused by primary genetic disorders or as secondary complications of underlying medical conditions. After ruling out common secondary causes of hyperlipoproteinemia, the clinician must begin the work-up for primary causes.
| Diseases | Mode of Inheritance | Laboratory Findings | Other Findings | Management | Complications | |||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Lipid Profile | Other Laboratory Findings | |||||||||||
| Total Cholesterol | LDL | HDL | Triglycerides | Plasma Appearance | Chylomicrons | VLDL | Genetic mutations | |||||
| Type I | Autosomal Recessive
& Autosomal Dominant(Rare) |
Normal or ↑ | ↓ | ↓↓↓ | ↑↑↑ | Milky | ↑↑↑ | ↓ | -LPL gene mutation | -Fat tolerance markedly abnormal
-Carbohydrate inducibility may be abnormal |
Treatment for hyperlipoproteinemia type 1 is intended to control blood triglyceride levels with a very low-fat diet | -Recurrent Pancreatitis
-Rarely life threatening |
| Type IIA | Autosomal Dominant & Autosomal Recessive(Rare) | ↑↑ | ↑↑↑ | Normal/↓ | Normal | Clear | - LDL recptor mutation
- Apolipoportein B gene mutation -Proprotein convertase subtilisin/kexin type 9 mutation. |
Lipid management with lifestyle modifications and pharmacotherapy | -Symptomatic coronary artery disease by 50-60 years and half of the men and 15%-30% of the women will have died | |||
| Type IIB | Mostly Dominant mode | ↑↑ | ↑↑ | ↓ | ↑↑ | Clear or turbid | ↑ | -Locus 1q21-q23
-APOAI/CIII/AIV cluster -Gene encoding upstream transcription factor 1 (USF1) |
Lipid management with lifestyle modifications and pharmacotherapy | -Coronary heart disease
-Gangrene of the extremities | ||
| Type III | Autosomal Recessive | ↑↑ | ↓ | Normal | ↑↑↑ | Clear, cloudy,or turbid | -Apo E mutations | -IDL is elevated | Lipid management with lifestyle modifications and pharmacotherapy | -Atherosclerotic complications (e.g., coronary artery disease) | ||
| Type IV | Autosomal Recessive
& Autosomal Dominant |
Normal or ↑ | ↓ | Prebeta-HDL ↑
& HDL-C ↓ |
↑↑ | Clear or Cloudy | Normal | ↑ | -LPL genes (Gly188Glu,Asp9Asn, Asn291Ser,Ser447Ter)
-APOA5 -LMF1 -GPIHBP1 |
Hyperglycemia, Pancytopneia and pseudo-Niemann
pick cells |
-Weight reduction
-Niacin or Fibrates -Gene therapy |
-Ischemic Heart Disease
-Recurrent Pancreatitis -NIDDM -NAFLD |
| Type V | Variable | ↑ to ↑↑
|
↓
|
↓↓↓
|
↑↑↑
|
Creamy supernatant and turbid infranatant | ↑
|
↑↑↑
|
❑ Apo E, Apo A5 mutations ❑ LPL gene mutation in 10% of western population patients |
❑ Restriction of dietary fat eliminates Chylomicrons and reverts to type IV HLP ❑ When triglyceride levels are >1000mg/dl given the rarity of type I it is almost always type V HLP |
- Weight reduction - Niacin or Fibrates or Strong statins - Low fat diet |
❑ Recurrent Pancreatitis |
The following algorithm describes the approach to a patient with hyperlipoproteinemia: [19]
| Hyperlipidemia | |||||||||||||||||||||||||||||||||||||||||
| Triglycerides > 75th Percentile | NO | Type IIa | |||||||||||||||||||||||||||||||||||||||
| YES | |||||||||||||||||||||||||||||||||||||||||
| Types I, IIb, IV, V | |||||||||||||||||||||||||||||||||||||||||
| Total Cholesterol/Apo B ratio ≥ 6.2 | NO | Types IIb, IV | |||||||||||||||||||||||||||||||||||||||
| YES | |||||||||||||||||||||||||||||||||||||||||
| Types I, III, V | |||||||||||||||||||||||||||||||||||||||||
| Triglycerides/Apo B ratio < 10.0 | NO | Types I, V | |||||||||||||||||||||||||||||||||||||||
| YES | |||||||||||||||||||||||||||||||||||||||||
| Type III | |||||||||||||||||||||||||||||||||||||||||
Screening
Screening in adults
In 2008, the United States Preventive Services Task Force recommended screening with total cholesterol and HDL-C[20].
In 2016, the [United States Preventive Services Task Force]] recommended treating based on the pooled cohort calculation of cardiac risk (example online calculator) which requires total cholesterol, LDL-C and HDL-C[21].
In 2017, the American Association of Clinical Endocrinologists and American College Of Endocrinology made joint recommendations for screening[22][23].
Screening in children and adolescents
Lipid screening recommendations vary by age and risk factors as shown below:[24][25] [26]
|
Pediatric dyslipidemia screening guidelines from the 2011 Expert Panel Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents | ||
|---|---|---|
| Age | Screening recommendation | Reommendation level |
| birth- <2years | No lipid screening | C |
| 2-8years ( No routine lipid screening,
however screen if one of the following is present using FLP two times) |
Parent, grandparent, aunt/uncle, or sibling with myocardial infarction (MI), angina, stroke, coronary artery bypass graft Strongly recommend (CABG)/stent/angioplasty at <55 years in males, <65 years in females | B |
| Parent with TC ≥ 240 mg/dL or known dyslipidemia | B | |
| Child has diabetes, hypertension, BMI ≥ 95th percentile or smokes cigarettes | B | |
| Child has a moderate- or high-risk medical condition (eg. Diabetes mellitus type 1 and type 2, chronic renal disease/end-stage renal disease/ postrenal transplant, Postorthotopic heart transplant, Kawasaki disease with current aneurysms) | B | |
| 9-11years (Universal Screening) | Universal screening with a non-FLP screening using non-HDL-C levels ( Non-HDL–C = TC – HDL–C) when Non-HDL ≥ 145 mg/dL, HDL < 40 mg/dL check FLP × 2 | B |
| Do further FLP if LDL–C ≥ 130 mg/dL, non-HDL–C ≥ 145 mg/dL HDL–C < 40 mg/dL, TG ≥ 100 mg/dL if < 10 years; ≥ 130 mg/dL if ≥ 10 years. Repeat FLP after 2 weeks but within 3 months | B | |
| 12-16years (Selective screening using FLP x 2) | Lipid screening is not recommended for those ages 12–16 years because of significantly decreased sensitivity and specificity for predicting adult LDL–C levels and significantly increased false-negative results in this age group. Selective screening ( Interval between FLP measurements: after 2 weeks but within 3 months) is recommended for those with the clinical indications outlined below: | B |
| Parent, grandparent, aunt/uncle or sibling with MI, angina, stroke, CABG/stent/ Strongly recommend angioplasty, sudden death at < 55 years in males, < 65 years in females | B | |
| • Parent with TC ≥ 240 mg/dL or known dyslipidemia | B | |
| Patient has diabetes, hypertension, BMI ≥ 85th pr\ercentile or smokes cigarettes | B | |
| Patient has a moderate- or high-risk medical condition (eg. Diabetes mellitus type 1 and type 2, chronic renal disease/end-stage renal disease/ postrenal transplant, Postorthotopic heart transplant, Kawasaki disease with current aneurysms) | B | |
| 17-19years | Universal screening once during this time period with a nonfasting lipid screening using non-HDL-C levels. If Non-HDL-C ≥ 145 mg/dL, HDL-C < 40 mg/dL do FLP × 2, Further screening with FLP if LDL-C ≥ 130 mg/dL, non-HDL-C ≥ 145 mg/dL HDL-C < 40 mg/dL, TG ≥ 130 mg/dL repeat FLP after 2 weeks but within 3 months | B |
| 17-21years | Universal screening once during this time period with a nonfasting lipid screening using non-HDL-C levels. If Non-HDL-C ≥ 190 mg/dL, HDL-C < 40 mg/dL do FLP × 2, Further screening with FLP when LDL-C ≥ 160 mg/dL, non-HDL-C ≥ 190 mg/dL, HDL-C < 40 mg/dL, TG ≥ 150 mg/dL repeat FLP after 2 weeks but within 3 months | B |
2018 AHA/ACC/ Guideline on the Management of Blood Cholesterol (Do not edit please) [27]
Measurements of LDL-C and Non–HDL-C:
| Class I |
| "1. In adults who are 20 years of age or older and not on lipid-lowering therapy, measurement of either a fasting or a nonfasting plasma lipid profile is effective in estimating ASCVD risk and documenting baseline LDL-C (Level of Evidence: B-NR) " |
| "2. In adults who are 20 years of age or older and in whom an initial nonfasting lipid profile reveals a triglycerides level of 400 mg/dL or higher (≥4.5 mmol/L), a repeat lipid profile in the fasting state should be performed for assessment of fasting triglyceride levels and baseline LDL-C(Level of Evidence: B-NR) " |
| Class IIa |
| "3. For adults with an LDL-C level less than 70 mg/dL (<1.8 mmol/L), measurement of direct LDL-C or modified LDL-C estimate is reasonable to improve accuracy over the Friedewald formula (Level of Evidence: C-LD) " |
| "4. In adults who are 20 years of age or older and without a personal history of ASCVD, but with a family history of premature ASCVD or genetic hyperlipidemia, measurement of a fasting plasma lipid profile is reasonable as part of an initial evaluation to aid in the understanding and identification of familial lipid disorders(Level of Evidence:C-LD) " |
Treatment and Management
Mendelian randomization studies suggest a linear relationship between LDL and cardiac event reduction[28].
Clinical practice guidelines direct treatment.
- American Heart Association et al[29]
- United States Preventive Services Task Force (USPSTF)[30]
- National Institutes for Clinical Excellence (NICE)[31]
Secondary ASCVD Prevention. 2018 AHA/ACC/ Guideline on the Management of Blood Cholesterol (Please, do not edit ) [27]
| Class I |
| "1. In patients who are 75 years of age or younger with clinical ASCVD,*high-intensity statin therapy should be initiated or continued with the aim of achieving a 50% or greater reduction in LDL-C levels (Level of Evidence: A) " |
| "2. In patients with clinical ASCVD in whom high-intensity statin therapy is contraindicated or who experience statin-associated side effects, moderate-intensity statin therapy should be initiated or continued with the aim of achieving a 30% to 49% reduction in LDL-C (Level of Evidence: A) " |
| "3. In patients with clinical ASCVD who are judged to be very high risk and considered for PCSK9 inhibitor therapy, maximally tolerated LDL-C lowering therapy should include maximally tolerated statin therapy and ezetimib (Level of evidence B-NR)'' |
| Class IIa |
| " 4. In patients with clinical ASCVD who are judged to be very high risk and who are on maximally tolerated LDL-C lowering therapy with LDL-C 70 mg/dL or higher (≥1.8 mmol/L) or a non–HDL-C level of 100 mg/dL or higher (≥2.6 mmol/L), it is reasonable to add a PCSK9 inhibitor following a clinician-patient discussion about the net benefit, safety, and cost. (Level of Evidence A)". |
| '' 5. In patients with clinical ASCVD who are on maximally tolerated statin therapy and are judged to be at very high risk and have an LDL-C level of 70 mg/dL or higher (≥1.8 mmol/L), it is reasonable to add ezetimibe therapy (Level of Evidence B-R)''. |
| 6. Value Statement: Low Value (LOE: B-NR). At mid-2018 list prices, PCSK9 inhibitors have a low cost value (>$150 000 per QALY) compared to good cost value (<$50 000 per QALY) (Section 7 provides a full discussion of the dynamic interaction of different prices and clinical benefit) |
| '' 7. In patients older than 75 years of age with clinical ASCVD, it is reasonable to initiate moderate- or high-intensity statin therapy after evaluation of the potential for ASCVD risk reduction, adverse effects, and drug–drug interactions, as well as patient frailty and patient preferences (Level of Evidence B- R)'' |
| ''8. In patients older than 75 years of age who are tolerating high-intensity statin therapy, it is reasonable to continue it after evaluating the potential for ASCVD risk reduction, adverse effects, and drug-drug interactions, as well as patient frailty and patient preferences. (Level of Evidence C-LD)'' |
| Class IIb |
| " 4. In patients with clinical ASCVD who are receiving maximally tolerated statin therapy and whose LDL-C level remains 70 mg/dL or higher (≥1.8 mmol/L), it may be reasonable to add ezetimibe (Level of Evidence B-R)". |
| '' 5. In patients with heart failure (HF) with reduced ejection fraction attributable to ischemic heart disease who have a reasonable life expectancy (3 to 5 years) and are not already on a statin because of ASCVD, clinicians may consider initiation of moderate-intensity statin therapy to reduce the occurrence of ASCVD events (Level of Evidence B-R)''. |
Severe Hypercholesterolemia (LDL-C ≥190 mg/dL [≥4.9 mmol/L]). Secondary ASCVD Prevention. 2018 AHA/ACC/ Guideline on the Management of Blood Cholesterol (Please, do not edit )
| Class I |
| "1. In patients 20 to 75 years of age with an LDL-C level of 190 mg/dL or higher (≥4.9 mmol/L), maximally tolerated statin therapy is recommended(Level of Evidence: B-R) " |
[27]
| Class IIa |
| " 2. In patients 20 to 75 years of age with an LDL-C level of 190 mg/dL or higher (≥4.9 mmol/L) who achieve less than a 50% reduction in LDL-C while receiving maximally tolerated statin therapy and/or have an LDL-C level of 100 mg/dL or higher (≥2.6 mmol/L), ezetimibe therapy is reasonable (Level of Evidence B-R)". |
[27]
| Class IIb |
| " 3. In patients 20 to 75 years of age with a baseline LDL-C level of 190 mg/dL or higher (≥4.9 mmol/L), who achieve less than a 50% reduction in LDL-C levels and have fasting triglycerides 300 mg/dL or lower (≤3.4 mmol/L), while taking maximally tolerated statin and ezetimibe therapy, the addition of a bile acid sequestrant may be considered(Level of Evidence B-R)". |
| '' 4. In patients, 30 to 75 years of age with heterozygous FH and with an LDL-C level of 100 mg/dL or higher (≥2.6 mmol/L) while taking maximally tolerated statin and ezetimibe therapy, the addition of a PCSK9 inhibitor may be considered. (Level of Evidence B-R)'' |
| ''5. In patients 40 to 75 years of age with a baseline LDL-C level of 220 mg/dL or higher (≥5.7 mmol/L) and who achieve an on-treatment LDL-C level of 130 mg/dL or higher (≥3.4 mmol/L) while receiving maximally tolerated statin and ezetimibe therapy, the addition of a PCSK9 inhibitor may be considered (Level of Evidence C-LD)'' |
| 6. Value Statement: Uncertain Value (B-NR). Among patients with FH without evidence of clinical ASCVD taking maximally tolerated statin and ezetimibe therapy, PCSK9 inhibitors provide uncertain value at mid-2018 US list prices. |
Diabetes Mellitus in Adults. 2018 AHA/ACC/ Guideline on the Management of Blood Cholesterol (Please, do not edit )
| Class I |
| "1. In adults 40 to 75 years of age with diabetes mellitus, regardless of estimated 10-year ASCVD risk, moderate-intensity statin therapy is indicated (Level of Evidence: A) " |
| Class IIa |
| " 2. In adults 40 to 75 years of age with diabetes mellitus and an LDL-C level of 70 to 189 mg/dL (1.7 to 4.8 mmol/L), it is reasonable to assess the 10-year risk of a first ASCVD event by using the race and sex-specific PCE to help stratify ASCVD risk(Level of Evidence B-NR)". |
| '' 3. In adults with diabetes mellitus who have multiple ASCVD risk factors, it is reasonable to prescribe high-intensity statin therapy with the aim to reduce LDL-C levels by 50% or more (Level of Evidence B-R)'' |
| ''4. In adults older than 75 years of age with diabetes mellitus and who are already on statin therapy, it is reasonable to continue statin therapy(Level of Evidence B-NR)'' |
| Class IIb |
| " 5. In adults with diabetes mellitus and a 10-year ASCVD risk of 20% or higher, it may be reasonable to add ezetimibe to maximally tolerated statin therapy to reduce LDL-C levels by 50% or more(Level of Evidence C-LD)". |
| '' 6. In adults older than 75 years with diabetes mellitus, it may be reasonable to initiate statin therapy after a clinician–patient discussion of potential benefits and risks (Level of Evidence C-LD)'' |
| ''7. In adults, 20 to 39 years of age with diabetes mellitus that is either of long duration (≥10 years of type 2 diabetes mellitus, ≥20 years of type 1 diabetes mellitus), albuminuria (≥30 mcg of albumin/mg creatinine), estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2, retinopathy, neuropathy, or ankle-brachial index (ABI; <0.9), it may be reasonable to initiate statin therapy(Level of Evidence B-NR)'' |
Barriers to treatment
Patient preference, especially among minority populations, is a barrier to treatment[32].
References
- ↑ Brahm AJ, Hegele RA (2016). "Lomitapide for the treatment of hypertriglyceridemia". Expert Opin Investig Drugs. 25 (12): 1457–1463. doi:10.1080/13543784.2016.1254187. PMID 27785928.
- ↑ Ozder A (2014). "Lipid profile abnormalities seen in T2DM patients in primary healthcare in Turkey: a cross-sectional study". Lipids Health Dis. 13: 183. doi:10.1186/1476-511X-13-183. PMC 4271485. PMID 25481115.
- ↑ Lindegaard ML, Damm P, Mathiesen ER, Nielsen LB (2006). "Placental triglyceride accumulation in maternal type 1 diabetes is associated with increased lipase gene expression". J Lipid Res. 47 (11): 2581–8. doi:10.1194/jlr.M600236-JLR200. PMID 16940551.
- ↑ Phukan JP, Sinha A, Deka JP (2013). "Serum lipid profile in alcoholic cirrhosis: A study in a teaching hospital of north-eastern India". Niger Med J. 54 (1): 5–9. doi:10.4103/0300-1652.108886. PMC 3644745. PMID 23661892.
- ↑ HENEGAR GC, TURNER JL (1950). "Medical progress in cholesterol metabolism in relation to diseases of the liver and the biliary tract". Calif Med. 73 (6): 489–93. PMC 1520771. PMID 14792338.
- ↑ 6.0 6.1 Yuan G, Al-Shali KZ, Hegele RA (2007). "Hypertriglyceridemia: its etiology, effects and treatment". CMAJ. 176 (8): 1113–20. doi:10.1503/cmaj.060963. PMC 1839776. PMID 17420495.
- ↑ Nanda S, Gupta N, Mehta HC, Sangwan K (2003). "Effect of oestrogen replacement therapy on serum lipid profile". Aust N Z J Obstet Gynaecol. 43 (3): 213–6. PMID 14712987.
- ↑ Quinkler M, Ekman B, Marelli C, Uddin S, Zelissen P, Murray R (2016). "Prednisolone is associtaed with a worse lipid profile than hydrocortisone in patients with adrenal insufficiency". Endocr Connect. doi:10.1530/EC-16-0081. PMID 27864317 Check
|pmid=value (help). zero width space character in|pmid=at position 9 (help) - ↑ Yadav A, Jahan A, Yadav TP, Sachdev N, Chitkara A, Asare R (2013). "Effect of glucocorticoids on serum lipid profile and endothelial function and arterial wall mechanics". Indian J Pediatr. 80 (12): 1007–14. doi:10.1007/s12098-013-1035-6. PMID 23696151.
- ↑ Zimmerman J, Fainaru M, Eisenberg S (1984). "The effects of prednisone therapy on plasma lipoproteins and apolipoproteins: a prospective study". Metabolism. 33 (6): 521–6. PMID 6727652.
- ↑ Trevisan R, Dodesini AR, Lepore G (2006). "Lipids and renal disease". J Am Soc Nephrol. 17 (4 Suppl 2): S145–7. doi:10.1681/ASN.2005121320. PMID 16565240.
- ↑ 12.0 12.1 Vaziri ND (2003). "Molecular mechanisms of lipid disorders in nephrotic syndrome". Kidney Int. 63 (5): 1964–76. doi:10.1046/j.1523-1755.2003.00941.x. PMID 12675893.
- ↑ Nishide R, Ando M, Funabashi H, Yoda Y, Nakano M, Shima M (2015). "Association of serum hs-CRP and lipids with obesity in school children in a 12-month follow-up study in Japan". Environ Health Prev Med. 20 (2): 116–22. doi:10.1007/s12199-014-0433-3. PMC 4597345. PMID 25511645.
- ↑ Geraghty AA, Alberdi G, O'Sullivan EJ, O'Brien EC, Crosbie B, Twomey PJ; et al. (2016). "Maternal Blood Lipid Profile during Pregnancy and Associations with Child Adiposity: Findings from the ROLO Study". PLoS One. 11 (8): e0161206. doi:10.1371/journal.pone.0161206. PMC 4999287. PMID 27560495.
- ↑ van Gorselen EO, Diekman T, Hessels J, Verhorst PM, von Birgelen C (2010). "Artifactual measurement of low serum HDL-cholesterol due to paraproteinemia". Clin Res Cardiol. 99 (9): 599–602. doi:10.1007/s00392-010-0186-y. PMC 2928922. PMID 20593189.
- ↑ Brahm A, Hegele RA (2013). "Hypertriglyceridemia". Nutrients. 5 (3): 981–1001. doi:10.3390/nu5030981. PMC 3705331. PMID 23525082.
- ↑ Duntas LH (2002). "Thyroid disease and lipids". Thyroid. 12 (4): 287–93. doi:10.1089/10507250252949405. PMID 12034052.
- ↑ Nikkilä EA, Kekki M (1972). "Plasma triglyceride metabolism in thyroid disease". J Clin Invest. 51 (8): 2103–14. doi:10.1172/JCI107017. PMC 292367. PMID 4341014.
- ↑ Sniderman A, Tremblay A, Bergeron J, Gagné C, Couture P (2007). "Diagnosis of type III hyperlipoproteinemia from plasma total cholesterol, triglyceride, and apolipoprotein B". Journal of Clinical Lipidology. 1 (4): 256–63. doi:10.1016/j.jacl.2007.07.006. PMID 21291689. Retrieved 2012-10-24. Unknown parameter
|month=ignored (help) - ↑ https://www.uspreventiveservicestaskforce.org/Page/Document/ClinicalSummaryFinal/lipid-disorders-in-adults-cholesterol-dyslipidemia-screening
- ↑ US Preventive Services Task Force. Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW; et al. (2016). "Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: US Preventive Services Task Force Recommendation Statement". JAMA. 316 (19): 1997–2007. doi:10.1001/jama.2016.15450. PMID 27838723. Review in: Ann Intern Med. 2017 Mar 21;166(6):JC26
- ↑ Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ; et al. (2017). "AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY GUIDELINES FOR MANAGEMENT OF DYSLIPIDEMIA AND PREVENTION OF CARDIOVASCULAR DISEASE". Endocr Pract. 23 (Suppl 2): 1–87. doi:10.4158/EP171764.APPGL. PMID 28437620.
- ↑ Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ; et al. (2017). "AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY GUIDELINES FOR MANAGEMENT OF DYSLIPIDEMIA AND PREVENTION OF CARDIOVASCULAR DISEASE - EXECUTIVE SUMMARYComplete Appendix to Guidelines available at http://journals.aace.com". Endocr Pract. 23 (4): 479–497. doi:10.4158/EP171764.GL. PMID 28156151.
- ↑ Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents. National Heart, Lung, and Blood Institute (2011). "Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report". Pediatrics. 128 Suppl 5: S213–56. doi:10.1542/peds.2009-2107C. PMC 4536582. PMID 22084329.
- ↑ Gooding HC, Rodday AM, Wong JB, Gillman MW, Lloyd-Jones DM, Leslie LK; et al. (2015). "Application of Pediatric and Adult Guidelines for Treatment of Lipid Levels Among US Adolescents Transitioning to Young Adulthood". JAMA Pediatr. 169 (6): 569–74. doi:10.1001/jamapediatrics.2015.0168. PMID 25845026.
- ↑ Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents http://www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf.
- ↑ 27.00 27.01 27.02 27.03 27.04 27.05 27.06 27.07 27.08 27.09 27.10 27.11 27.12 PMID 30586774 (PMID 30586774)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ Ference BA, Ginsberg HN, Graham I, Ray KK, Packard CJ, Bruckert E | display-authors=etal (2017) Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 38 (32):2459-2472. DOI:10.1093/eurheartj/ehx144 PMID: 28444290
- ↑ Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ; et al. (2019). "2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines". Circulation. 140 (11): e596–e646. doi:10.1161/CIR.0000000000000678. PMID 30879355.
- ↑ https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/statin-use-in-adults-preventive-medication
- ↑ <https://www.nice.org.uk/guidance/cg181
- ↑ Peng JA, Ancock BP, Conell C, Almers LM, Chau Q, Zaroff JG (2016). "Nonutilization of Statins in a Community-based Population with a History of Coronary Revascularization". Clin Ther. 38 (2): 288–296.e2. doi:10.1016/j.clinthera.2015.11.020. PMID 26730455.