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Hyperlipidemia, hyperlipoproteinemia, or hyperlipidaemia (British English) is abnormally elevated levels of any or all lipids and/or lipoproteins in the blood.^[1] It is the most common form of dyslipidemia (which includes any abnormal lipid levels).

Lipids (water-insoluble molecules) are transported in a protein capsule. The size of that capsule, or lipoprotein, determines its density. The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on metabolism.

Hyperlipidemias are divided into primary and secondary subtypes. Primary hyperlipidemia is usually due to genetic causes (such as a mutation in a receptor protein), while secondary hyperlipidemia arises due to other underlying causes such as diabetes. Lipid and lipoprotein abnormalities are common in the general population, and are regarded as a modifiable risk factor for cardiovascular disease due to their influence on atherosclerosis. In addition, some forms may predispose to acute pancreatitis.

1 Classification
- 1.1 Familial (primary)
  - 1.1.1 Hyperlipoproteinemia type I
  - 1.1.2 Hyperlipoproteinemia type II
    - 1.1.2.1 Type IIa
    - 1.1.2.2 Type IIb
  - 1.1.3 Hyperlipoproteinemia type III
  - 1.1.4 Hyperlipoproteinemia type IV
  - 1.1.5 Hyperlipoproteinemia type V
  - 1.1.6 Unclassified familial forms
- 1.2 Acquired (secondary)
2 Management
3 See also
4 References
5 External links

Classification

Hyperlipidemias may basically be classified as either familial (also called primary^[2]) caused by specific genetic abnormalities, or acquired (also called secondary)^[2] when resulting from another underlying disorder that leads to alterations in plasma lipid and lipoprotein metabolism.^[2] Also, hyperlipidemia may be idiopathic, that is, without known cause.

Hyperlipidemias are also classified according to which types of lipids are elevated, that is hypercholesterolemia, hypertriglyceridemia or both in combined hyperlipidemia. Elevated levels of Lipoprotein(a) may also be classified as a form of hyperlipidemia.

Familial (primary)

Familial hyperlipidemias are classified according to the Fredrickson classification, which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation.^[3] It was later adopted by the World Health Organization (WHO). It does not directly account for HDL, and it does not distinguish among the different genes that may be partially responsible for some of these conditions.

**Fredrickson classification of hyperlipidemias**
Hyperlipo- proteinemia		OMIM	Synonyms	Defect	Increased lipoprotein	Main symptoms	Treatment	Serum appearance	Estimated prevalence
Type I	a	238600	Buerger-Gruetz syndrome or familial hyperchylomicronemia	Decreased lipoprotein lipase (LPL)	Chylomicrons	Acute pancreatitis, lipemia retinalis, eruptive skin xanthomas, hepatosplenomegaly	Diet control	Creamy top layer	One in 1,000,000^[4]
	b	207750	Familial apoprotein CII deficiency	Altered ApoC2
	c	118830		LPL inhibitor in blood
Type II	a	143890	Familial hypercholesterolemia	LDL receptor deficiency	LDL	Xanthelasma, arcus senilis, tendon xanthomas	Bile acid sequestrants, statins, niacin	Clear	One in 500 for heterozygotes
Type II	b	144250	Familial combined hyperlipidemia	Decreased LDL receptor and increased ApoB	LDL and VLDL		Statins, niacin, fibrate	Turbid	1 in 100
Type III		107741	Familial dysbetalipoproteinemia	Defect in Apo E 2 synthesis	IDL	Tuboeruptive xanthomas and palmar xanthomas	Fibrate, statins	Turbid	One in 10,000^[5]
Type IV		144600	Familial hypertriglyceridemia	Increased VLDL production and decreased elimination	VLDL	Can cause pancreatitis at high triglyceride levels	Fibrate, niacin, statins	Turbid	One in 100
Type V		144650		Increased VLDL production and decreased LPL	VLDL and chylomicrons		Niacin, fibrate	Creamy top layer and turbid bottom

Relative prevalence of familial forms of hyperlipoproteinemia^[6]

Hyperlipoproteinemia type I

Type I hyperlipoproteinemia exists in several forms:

Lipoprotein lipase deficiency (type Ia), due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver
Familial apoprotein CII deficiency (type Ib),^[7]^[8] a condition caused by a lack of lipoprotein lipase activator.^[9]^:533
Chylomicronemia due to circulating inhibitor of lipoprotein lipase (type Ic)^[10]

Type I hyperlipoproteinemia usually presents in childhood with eruptive xanthomata and abdominal colic. Complications include retinal vein occlusion, acute pancreatitis, steatosis and organomegaly, and lipaemia retinalis.

Hyperlipoproteinemia type II

Hyperlipoproteinemia type II, by far the most common form, is further classified into types IIa and IIb, depending mainly on whether elevation in the triglyceride level occurs in addition to LDL cholesterol.

Type IIa

This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%). The familial form is characterized by tendon xanthoma, xanthelasma, and premature cardiovascular disease. The incidence of this disease is about one in 500 for heterozygotes, and one in 1,000,000 for homozygotes.

HLPIIa is a rare genetic disorder characterized by increased levels of LDL cholesterol in the blood due to the lack of uptake (no Apo B receptors) of LDL particles. This pathology, however, is the second-most common disorder of the various hyperlipoproteinemias, with individuals with a heterozygotic predisposition of one in every 500 and individuals with homozygotic predisposition of one in every million. These individuals may present with a unique set of physical characteristics such as: xanthelasmas (yellow deposits of fat underneath the skin often presenting in the nasal portion of the eye), tendon and tuberous xanthomas, arcus juvenilis (the graying of the eye often characterized in older individuals), arterial bruits, claudication, and of course atherosclerosis. Laboratory findings for these individuals are obvious and yet interesting because their serum cholesterol levels are two to three times greater than normal, as well as increased LDL cholesterol, but their triglycerides and VLDL values fall in the normal ranges. To manage persons with HLPIIa, drastic measures may need to be taken, especially if their HDL cholesterol levels are less than 30 mg/dl and their LDL levels are greater than 160 mg/dl. A proper diet for these individuals requires a decrease in total fat to less than 30% of total calories with a ratio of monounsaturated:polyunsaturated:saturated fat of 1:1:1. Cholesterol should be reduced to less than 300 mg/day, thus the avoidance of animal products and to increase fiber intake to more than 20 g/day with 6g of soluble fiber/day.^{[citation needed]} Exercise should be promoted, as it can increase HDL. The overall prognosis for these individuals is in the worst-case scenario if uncontrolled and untreated individuals may die before the age of 20, but if one seeks a prudent diet with correct medical intervention, the individual may see an increased incidence of xanthomas with each decade, and Achilles tendinitis and accelerated atherosclerosis will occur.

Type IIb

The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%.

Familial combined hyperlipoproteinemia (FCH)
Lysosomal acid lipase deficiency, often called (Cholesteryl ester storage disease)
Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome, for which it is a diagnostic criterion)

Hyperlipoproteinemia type III

This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia, the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (β-VLDL). Its prevalence has been estimated to be approximately 1 in 10,000.^[5]

It is associated with hypercholesterolaemia (typically 8-12 mmol/L), hypertriglyceridaemia (typically 5-20 mmol/L), a normal ApoB concentration, and two types of skin signs (palmar xanthomata or orange discoloration of skin creases, and tuberoeruptive xanthomata on the elbows and knees). It is characterized by the early onset of cardiovascular disease and peripheral vascular disease. Remnant hyperlipidaemia occurs as a result of abnormal function of the ApoE receptor, which is normally required for clearance of chylomicron remnants and IDL from the circulation. The receptor defect causes levels of chylomicron remnants and IDL to be higher than normal in the blood stream. The receptor defect is an autosomal recessive mutation or polymorphism.

Hyperlipoproteinemia type IV

Familial hypertriglyceridemia is an autosomal dominant condition occurring in approximately 1% of the population.^[11]

This form is due to high triglyceride level. Other lipoprotein levels are normal or increased a little.

Treatment include diet control, fibrates and niacins. Statins are not better than fibrates when lowering triglyceride level.

Hyperlipoproteinemia type V

Hyperlipoproteinemia type V, also known as mixed hyperlipoproteinemia familial or mixed hyperlipidemia,^[12] is very similar to type I, but with high VLDL in addition to chylomicrons.

It is also associated with glucose intolerance and hyperuricemia

In medicine, combined hyperlipidemia (or -aemia) (also known as "multiple-type hyperlipoproteinemia") is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterised by increased LDL and triglyceride concentrations, often accompanied by decreased HDL.^[13] On lipoprotein electrophoresis (a test now rarely performed) it shows as a hyperlipoproteinemia type IIB. It is the most common inherited lipid disorder, occurring in about one in 200 persons. In fact, almost one in five individuals who develop coronary heart disease before the age of 60 have this disorder. The elevated triglyceride levels (>5 mmol/l) are generally due to an increase in very low density lipoprotein (VLDL), a class of lipoprotein prone to cause atherosclerosis.

Types

Familial combined hyperlipidemia (FCH) is the familial occurrence of this disorder, probably caused by decreased LDL receptor and increased ApoB.
FCH is extremely common in patients who suffer from other diseases from the metabolic syndrome ("syndrome X", incorporating diabetes mellitus type II, hypertension, central obesity and CH). Excessive free fatty acid production by various tissues leads to increased VLDL synthesis by the liver. Initially, most VLDL is converted into LDL until this mechanism is saturated, after which VLDL levels elevate.

Both conditions are treated with fibrate drugs, which act on the peroxisome proliferator-activated receptors (PPARs), specifically PPARα, to decrease free fatty acid production. Statin drugs, especially the synthetic statins (atorvastatin and rosuvastatin) can decrease LDL levels by increasing hepatic reuptake of LDL due to increased LDL-receptor expression.

Unclassified familial forms

These unclassified forms are extremely rare:

Hyperalphalipoproteinemia
Polygenic hypercholesterolemia

Acquired (secondary)

Acquired hyperlipidemias (also called secondary dyslipoproteinemias) often mimic primary forms of hyperlipidemia and can have similar consequences.^[2] They may result in increased risk of premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to pancreatitis and other complications of the chylomicronemia syndrome.^[2] The most common causes of acquired hyperlipidemia are:

diabetes mellitus^[2]
Use of drugs such as thiazide diuretics,^[2] beta blockers,^[2] and estrogens^[2]

Other conditions leading to acquired hyperlipidemia include:

Hypothyroidism^[2]
Renal failure^[2]
Nephrotic syndrome^[2]
Alcohol consumption^[2]
Some rare endocrine disorders^[2] and metabolic disorders^[2]

Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.^{[citation needed]}

Another acquired cause of hyperlipidemia, although not always included in this category, is postprandial hyperlipidemia, a normal increase following ingestion of food.^[13]^[14]

Management

For treatment of type II, dietary modification is the initial approach, but many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates (peroxisome proliferator-activated receptor-alpha agonists) may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis, so is only done under close supervision. Other agents commonly added to statins are ezetimibe, niacin, and bile acid sequestrants. Dietary supplementation with fish oil is also used to reduce elevated triglycerides, with the greatest effect occurring in patients with the greatest severity.^[15] Some evidence exists for benefit of plant sterol-containing products and omega-3 fatty acids.^[16]

References

^ thefreedictionary.com > hyperlipidemia Citing:
- Dorland's Medical Dictionary for Health Consumers. 2007 by Saunders, an imprint of Elsevier
- The American Heritage Medical Dictionary. 2007, 2004 by Houghton Mifflin Company.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o Chait A, Brunzell JD (June 1990). "Acquired hyperlipidemia (secondary dyslipoproteinemias)". Endocrinol. Metab. Clin. North Am. 19 (2): 259–78. PMID 2192873.
^ Fredrickson, DS; Lees, RS (1965). "A system for phenotyping hyperlipoproteinemia" (PDF). Circulation 31 (3): 321–7. doi:10.1161/01.CIR.31.3.321. PMID 14262568.
^ Hyperlipoproteinemia, Type I from Centre for Arab Genomic Studies. Retrieved July 2011. Citing: "About 1:1,000,000 people are affected with Hyperlipoproteinemia type I worldwide with a higher prevalence in some regions of Canada."
^ ^a ^b Fung, M.; Hill, J.; Cook, D.; Frohlich, J. (2011). "Case series of type III hyperlipoproteinemia in children". Case Reports 2011: bcr0220113895. doi:10.1136/bcr.02.2011.3895.
^ New Product Bulletin on Crestor® (rosuvastatin)
^ OMIM entry 207750 last updated 02/10/2009
^ Yamamura, T.; Sudo, H.; Ishikawa, K.; Yamamoto, A. (1979). "Familial type I hyperlipoproteinemia caused by apolipoprotein C-II deficiency". Atherosclerosis 34 (1): 53–65. doi:10.1016/0021-9150(79)90106-0. PMID 227429.
^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
^ OMIM entry 118830 updated 03/18/2004
^ Boman H, Hazzard WR, AlbersJJ, et ah Frequency of monogenic forms of hyperlipidemia in a normal population. AmJ ttum Genet 27:19A,1975. [1]
^ "Medical Definition Search For 'Type 5 Hyperlipidemia". medilexicon. Retrieved 1 November 2013.
^ ^a ^b thefreedictionary.com > hyperlipidemia Citing:
- Saunders Comprehensive Veterinary Dictionary, 3 ed. 2007 by Elsevier
^ Sameer Ansar; Juraj Koska; Peter D Reaven. "Postprandial hyperlipidemia, endothelial dysfunction and cardiovascular risk: Role of Incretins". Cardiovascular Diabetology
^ Mattar M, Obeid O. Fish oil and the management of hypertriglyceridemia. Nutr Health. 2009;20(1):41-9.
^ Thompson, GR (2004). "Management of dyslipidaemia". Heart (British Cardiac Society) 90 (8): 949–55. doi:10.1136/hrt.2003.021287. PMC 1768388. PMID 15253984.

External links

The Fredrickson papers (with photos from early lipoprotein research)
745209914 at GPnotebook

UpToDate Contents

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1. Hypertriglyceridemia
2. 高トリグリセリド血症による急性膵炎 hypertriglyceridemia induced acute pancreatitis
3. 脂肪異栄養症症候群 lipodystrophic syndromes

English Journal

Gene therapy to be authorised for first time in EU.

Watts G.
BMJ (Clinical research ed.).BMJ.2012 Jul 23;345:e5009. doi: 10.1136/bmj.e5009.
PMID 22826599

Resequencing CETP, LIPC and LIPG genes in Thai subjects with hyperalphalipoproteinemia.

Khovidhunkit W, Chartyingcharoen P, Siriwong S, Limumpornpetch P, Plengpanich W.SourceDepartment of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Bangkok, Thailand. wkhovid@gmail.com
The American journal of cardiology.Am J Cardiol.2012 Jul 1;110(1):62-6. Epub 2012 Mar 29.
Genetic factors associated with hyperalphalipoproteinemia (HALP; or high levels of high-density lipoprotein cholesterol) are incompletely understood. The aim of this study was to resequence 3 candidate genes, CETP, LIPC, and LIPG, which encode cholesteryl ester transfer protein, hepatic lipase, and
PMID 22464213

Japanese Journal

原発性高脂血症 (特集内分泌・代謝領域の「難病」とその克服に向けた取り組みの現状と展望)

山﨑久隆,大須賀淳一,石橋俊
内分泌・糖尿病・代謝内科 37(5), 487-494, 2013-11
NAID 40019890949

原発性高カイロミクロン血症 (特集高トリグリセライド血症 : 高トリグリセライド血症の最新知見) -- (高トリグリセライド血症 : 病因・病態および管理法)

山下静也
日本臨床 71(9), 1578-1583, 2013-09
NAID 40019788794

原発性高カイロミクロン血症を伴う1型高脂血症による小児網膜脂血症 (特集第63回日本臨床眼科学会講演集(6))

竹内智一,林孝彰,長谷川行洋 [他]
臨床眼科 64(8), 1383-1388, 2010-08
NAID 40017268244

★リンクテーブル★

リンク元	「脂質異常症」「高カイロミクロン血症」

「脂質異常症」

Hyperlipidemia
	A 4-ml sample of hyperlipidemic blood with lipids separated into the top fraction (Sample is in an EDTA collection tube.)
Classification and external resources
Specialty	Cardiology
ICD-10	E78
ICD-9-CM	272.0-272.4
DiseasesDB	6255
Patient UK	Hyperlipidemia
MeSH	D006949
	[edit on Wikidata]

　　[★]

英: dyslipidemia
同: 高脂血症 hyperlipidemia、脂質代謝異常 lipoprotein disorders
関: 高脂血症治療薬、リポ蛋白

定義

血清：~~Total-CHO≧220 mg/dl~~。LDL-C≧140 mg/dl。TG≧150 mg/dl。HDL-C＜40 mg/dl

病型

原発性

家族性
特発性

二次性

分類

原発性高脂血症のWHO分類

型分類			増加するリポ蛋白	血清脂質の変動	コレステロール (mg/dl)	トリグリセリド (mg/dl)
正常			-	-	<220	<150
I型高脂血症	高カイロミクロン血症	hyperchylomicronemia	カイロミクロン	中性脂肪著明増加	<260	>1000
IIa型高脂血症	高コレステロール血症	hypercholesterolemia	LDL	コレステロール増加	>220	>150
IIb型高脂血症	複合型高脂血症	combined hyperlipidemia	LDL, VLDL	コレステロールと中性脂肪増加	>220	150-300
III型高脂血症	異常βリポ蛋白血症	dysbetalipoproteinemia	IDL	電気泳動でbroad β	350-500	350-500
IV型高脂血症	高トリグリセリド血症	hypertriglyceridemia	VLDL	中性脂肪増加	<240	200-1000
V型高脂血症	複合型高トリグリセリド血症	mixed hypertriglyceridemia	カイロミクロン, VLDL	中性脂肪著明増加	<300	>1000

原発性高脂血症の型分類 (臨床検査法提要第32版 p.533)

		I型	II型		III型	IV型	V型
		I型	IIa型	IIb型	III型	IV型	V型
		高カイロミクロン血症	高コレステロール血症	複合型高脂血症	異常βリポ蛋白血症	高トリグリセリド血症	複合型高トリグリセリド血症
増加リポ蛋白	CM	＋＋					＋
	VLDL			＋		＋	＋
	IDL				＋
	LDL		＋	＋
血漿脂質	TC	＋	＋＋＋	＋＋	＋＋	/＋	＋
	TG	＋＋＋		＋＋	＋＋	＋＋	＋＋＋
	TC/TG	＜0.2	＞1.6	不定	≒	0.6-1.6	＜0.6
病因		・LPL欠損・アポCII欠損 (外因性高脂血症)	LDL受容体異常	不明	アポE異常 (E2/E2など)	不明 (内因性高脂血症)	LPL欠損へテロ(一部) (外因性高脂血症 and (内因性混合型高脂血症)
臨床所見	発症時期	小児期	小児期～成人		成人	成人	小児期～成人
	肝脾肥大	＋＋＋	－		＋	＋＋＋脾のみ	＋＋＋
	腹痛	＋				＋	＋
	膵炎	＋					＋
	網膜脂血症	＋					＋
	肥満					＋	＋
	角膜輪		＋		＋
	冠動脈疾患	まれ	最も高率		高率	中程度	比較的まれ
	黄色腫	発疹状	黄色板状結節状腱黄色腫		手掌線結節状発疹状		発疹状
	耐糖能	正常	正常		正常	異常多い	異常多い
	高尿酸血症	なし	なし		少ない	多い	多い
遺伝		劣性遺伝	優性遺伝		劣性遺伝	優性遺伝	不明
頻度		まれ	多い 500人中 1人(ヘテロ) 100万人中 1人(ホモ)	多い 200人中 1人	少ない 1万人中 2-3人	最も多い	まれ
血清静置試験		上層：乳濁	透明	わずかに混濁	混濁、時にミルク状	混濁	上層：乳濁
血清静置試験		下層：透明	透明	わずかに混濁	混濁、時にミルク状	混濁	下層：混濁
特徴				small dense LDL の存在	broad β

頻度：IIa > IIb > IV
遺伝(AR)I, III　(AD)その他
症状

動脈硬化：IIa,IIb,III
膵炎：TG多い：I,IV,V

TC優位に多いのがIIa, TG優位に多いのがIV
リポ蛋白のパターンは、IIa + IV = IIb　で　IIIはその中間(IDL)。I +　IV = V

原発性高脂血症

		血清TG	血清TC
内分泌代謝疾患	甲状腺機能低下症		+++
	クッシング症候群	+	++
	先端性肥大症	+
	糖尿病	+++	+～++
	痛風	+
	神経性食思不振症		++
	ウェルナー症候群		++
肝疾患	閉塞性肝・胆道疾患		+++
肝疾患	肝癌		++
腎疾患	ネフローゼ症候群	++	+++
腎疾患	慢性腎不全	+++
免疫異常	全身性エリテマトーデス	+++
免疫異常	骨髄腫	++	+
薬剤など	サイアザイド	+	+
	β遮断薬	+
	シクロスポリン		+
	経口避妊薬	+++

リスク別脂質管理目標値 (http://jas.umin.ac.jp/pdf/guideline_summary.pdf)

	治療方針の原則	カテゴリー			脂質管理目標値（mg/dL）
		リスク群		LDL-C以外の主要危険因子	LDL-C	HDL-C	TG
一次予防	まず生活習慣の改善を行った後、薬物治療の適応を考慮する	I	低リスク群	0	＜160	≧40	＜150
		II	中リスク群	1～2	＜140
		III	高リスク群	3以上	＜120
二次予防	生活習慣の改善とともに薬物治療を考慮する	冠動脈疾患の既往			＜100

LDL－C値以外の主要危険因子

加齢(男性≧４５歳、女性≧５５歳）、高血圧、糖尿病(耐糖能異常を含む）、喫煙、冠動脈疾患の家族歴、低HDL－C血症(＜４０mg/dL）
糖尿病、脳梗塞、閉塞性動脈硬化症の合併はカテゴリーIIIとする。

「高カイロミクロン血症」

　　[★]

英

高カイロミクロン血症 hyperchylomicronemia

同

I型高脂血症、高リポ蛋白血症I型 hyperlipoproteinemia type I

;同:高リポ蛋白血症1型、I型高リポ蛋白血症、1型高リポ蛋白血症

関: 脂質異常症

概念

病因

遺伝性

familial lipoprotein lipase deficiency (LPLの欠陥)
常染色体劣性

疫学

病変形成＆病理

カイロミクロンに含まれるトリグリセリドがLPLによって分解されない→血中TG↑

症状

診断

検査

治療

予後

予防

[DorlandAndAmericanHeritage-1] thefreedictionary.com > hyperlipidemia Citing:

Dorland's Medical Dictionary for Health Consumers. 2007 by Saunders, an imprint of Elsevier

The American Heritage Medical Dictionary. 2007, 2004 by Houghton Mifflin Company.

[2] Dorland's Medical Dictionary for Health Consumers. 2007 by Saunders, an imprint of Elsevier

[3] The American Heritage Medical Dictionary. 2007, 2004 by Houghton Mifflin Company.

[Chait-2] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o Chait A, Brunzell JD (June 1990). "Acquired hyperlipidemia (secondary dyslipoproteinemias)". Endocrinol. Metab. Clin. North Am. 19 (2): 259–78. PMID 2192873.

[3] Fredrickson, DS; Lees, RS (1965). "A system for phenotyping hyperlipoproteinemia" (PDF). Circulation 31 (3): 321–7. doi:10.1161/01.CIR.31.3.321. PMID 14262568.

[4] Hyperlipoproteinemia, Type I from Centre for Arab Genomic Studies. Retrieved July 2011. Citing: "About 1:1,000,000 people are affected with Hyperlipoproteinemia type I worldwide with a higher prevalence in some regions of Canada."

[fung2011-5] Fung, M.; Hill, J.; Cook, D.; Frohlich, J. (2011). "Case series of type III hyperlipoproteinemia in children". Case Reports 2011: bcr0220113895. doi:10.1136/bcr.02.2011.3895.

[6] New Product Bulletin on Crestor® (rosuvastatin)

[7] OMIM entry 207750 last updated 02/10/2009

[8] Yamamura, T.; Sudo, H.; Ishikawa, K.; Yamamoto, A. (1979). "Familial type I hyperlipoproteinemia caused by apolipoprotein C-II deficiency". Atherosclerosis 34 (1): 53–65. doi:10.1016/0021-9150(79)90106-0. PMID 227429.

[Andrews-9] James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.

[10] OMIM entry 118830 updated 03/18/2004

[Boman1975-11] Boman H, Hazzard WR, AlbersJJ, et ah Frequency of monogenic forms of hyperlipidemia in a normal population. AmJ ttum Genet 27:19A,1975. [1]

[12] "Medical Definition Search For 'Type 5 Hyperlipidemia". medilexicon. Retrieved 1 November 2013.

[Elsevier-13] thefreedictionary.com > hyperlipidemia Citing:

Saunders Comprehensive Veterinary Dictionary, 3 ed. 2007 by Elsevier

[16] Saunders Comprehensive Veterinary Dictionary, 3 ed. 2007 by Elsevier

[BioMed_Central-14] Sameer Ansar; Juraj Koska; Peter D Reaven. "Postprandial hyperlipidemia, endothelial dysfunction and cardiovascular risk: Role of Incretins". Cardiovascular Diabetology

[15] Mattar M, Obeid O. Fish oil and the management of hypertriglyceridemia. Nutr Health. 2009;20(1):41-9.

[16] Thompson, GR (2004). "Management of dyslipidaemia". Heart (British Cardiac Society) 90 (8): 949–55. doi:10.1136/hrt.2003.021287. PMC 1768388. PMID 15253984.

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hyperchylomicronemia