Hyperlipidemia refers to elevated levels of lipids in the blood, including triglycerides and cholesterol. There are several types of hyperlipidemia based on the elevated lipoprotein, including types I-V. Type I is caused by deficiencies of lipoprotein lipase or ApoC-II, resulting in an inability to remove chylomicrons from the blood. Type IIa, or familial hypercholesterolemia, is caused by mutations in the LDL receptor gene and results in markedly elevated LDL cholesterol. It can be either homozygous or heterozygous. Both forms increase the risk of premature cardiovascular disease if not properly treated.

1. Hyperlipidemia
Etiology, epidemiology and clinical features of hyperlipidemia

2. • lipoproteins
• cholesterol
• triglyceride
Hyperlipidemia
Hyperlipidemia: elevated levels of lipids, i.e. triglycerides and cholesterol in blood
Hyperlipoproteinemia: elevated levels of lipoproteins, especially VLDL, IDL and LDL
Hypercholesterolemia: elevated levels of cholesterol in blood
Hypertriglyceridemia: elevated levels of triglycerides in blood
Bays HE, et al. National Lipid Association Annual Summary of Clinical Lipidology 2016. J Clin Lipidol. 2016 Jan-Feb;10(1 Suppl):S1-S43.
Source: GUIDELINES FOR ADOLESCENT NUTRITION SERVICES. Stang J and story M. Chapter 10. Hyperlipidemia. Page 109-124. Adams LB. Http://www.Epi.Umn.Edu/let/pubs/adol_book.Shtm
VLDL: very low density lipoprotein
IDL: intermediate density lipoprotein
LDL: low density lipoprotein

3. Jacobson TA, et al. National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 1—Full Report. J Clin Lipidol. 2015 Mar-Apr;9(2):129-69.
Normal serum levels of cholesterol and triglycerides

4. Hyper-
lipoproteinemia
Name of the disease Increased
lipoprotein
Increased lipid
fraction
Type I Hyperchylomicronemia Chylomicrons Triglycerides
Type IIa Familial
hypercholesterolemia
LDL Cholesterol
Type IIb Familial combined
hypercholesterolemia
LDL and VLDL Cholesterol and
triglycerides
Type III Dysbetalipoprotenemia IDL Triglycerides and
cholesterol
Type IV Familial
hypertriglyceridemia
VLDL Triglycerides
Type V Familial lipoprotein
lipase deficiency
VLDL and
Chylomicrons
Triglycerides and
cholesterol
Fredrickson classification is still followed
Chandra KS, et al. Consensus statement on management of dyslipidemia in Indian subjects. Indian Heart J. 2014 Dec;66 Suppl 3:S1-51.
Levy RI, Fredrickson DS. Diagnosis and management of hyperlipoproteinemia. Am J Cardiol 1968;22:576-583.
Source: Classification of hyperlipidaemias and hyperlipoproteinaemias. Bull World Health Organ. 1970; 43(6): 891–915.

5. Main cause of
hypercholesterolemia
Primary disorders
Familial hypercholesterolemia
Familial combined hyperlipidemia
Polygenic hypercholesterolemia
Secondary disorders
Hyperthyroidism
Nephrotic syndrome
Dysproteinemias
Obstructive liver disease
Thiazide diuretics
Main cause of hypertriglyceridemia
Primary disorders
Familial hypertriglyceridemia
Familial combined hyperlipidemia
Congenital deficiency of lipoprotein lipase
Familial dysbetalipoproteinemia
Secondary disorders
Nephrotic syndrome
Dysproteinemias
Oral contraceptives
Thiazide diuretics
Beta-adrenergic blocking agents
Alcohol
Uncontrolled diabetes mellitus
Source: Clinical Methods: The history, physical, and laboratory examination. Chapter 31, Cholesterol, Triglycerides and Associated Lipoproteins. http://www.ncbi.nlm.nih.gov/books/NBK351/#!po=20.8333 Accessed on 04/22/2016
Looking at it at a different angle

6. White B. Dietary fatty acids. Am fam physician. 2009 aug 15;80(4):345-350.
Source: harrigan gg, et al. Metabolomics in alcohol research and drug development. Http://pubs.Niaaa.Nih.Gov/publications/arh311/26-35.Htm.
Accessed on 04/22/2016
Source: cholesterol esterase. Http://www.Worthington-biochem.Com/cepm/default.Html accessed on 04/22/2016
Source: Overweight & obesity. Http://www.Indiana.Edu/~k562/ob.Html accessed on 04/22/2016
Triglyceride
Fatty acid
Building blocks
Phospholipid
Cholesteryl esterCholesterol
+ Fatty acid =

7. Karasinska JM and Hayden MR. Cholesterol metabolism in Huntington disease. Nature Reviews Neurology 7, 561-572 (October 2011)
Cholesterol synthesis
Glucose
Pyruvate
Amino acid
Acetyl CoA
Fatty acids Ketone bodies
Source of Acetyl CoA
Acetyl CoA
Acetyl CoA
+
Source of Acetoacetyl CoA

8. Reaches back
into liver
Small percent
excreted
Walters JR. Bile acid diarrhoea and FGF19: new views on diagnosis, pathogenesis and therapy. Nat Rev Gastroenterol Hepatol. 2014 Jul;11(7):426-34
Ioannou YA.. Multidrug permeases and subcellular cholesterol transport. Nature Reviews Molecular Cell Biology 2, 657-668 (September 2001)
Bile acid synthesis, recirculation and excretion
Bile acid circulation

9. Chaves VE, et al. Glyceroneogenesis is reduced and glucose uptake is increased in adipose tissue from cafeteria diet-fed rats independently of tissue sympathetic innervation. J Nutr. 2006
Oct;136(10):2475-80.
Chen HC and Farese RV Jr. Inhibition of triglyceride synthesis as a treatment strategy for obesity: lessons from DGAT1-deficient mice. Arterioscler Thromb Vasc Biol. 2005 Mar;25(3):482-6.
Fung MA and Frohlich JJ. Common problems in the management of hypertriglyceridemia. CMAJ. 2002 November 26; 167(11): 1261–1266.
Triglyceride synthesis

10. Lipoproteins
Ridker PM. LDL cholesterol: controversies and future therapeutic directions. Lancet. 2014 Aug 16;384(9943):607-17.

11. Lipoprotein synthesis, transport and recycling
Source: Clinical Methods: The history, physical, and laboratory examination. Chapter 31, Cholesterol, Triglycerides and Associated Lipoproteins. http://www.ncbi.nlm.nih.gov/books/NBK351/#!po=20.8333 Accessed on 04/22/2016

12. VLDL synthesis
D Gruffat, D Durand, B Graulet, D Bauchart. Regulation of VLDL synthesis and secretion in the liver. Reproduction Nutrition Development, EDP Sciences, 1996, 36 (4), pp.375-389.
LDL

13. Source: Feingold KR, Grunfeld C. Introduction to Lipids and Lipoproteins. [Updated 2015 Jun 10]. In: De Groot LJ, Beck-Peccoz P, Chrousos G, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.
http://www.ncbi.nlm.nih.gov/books/NBK305896/?report=reader#_NBK305896_pubdet_ Accessed on 04/22/2016
Source: Lipids and lipoproteins: metabolism and its violations.
http://intranet.tdmu.edu.ua/data/kafedra/internal/distance/classes_stud/English/2%20course/Elective%20course%20(Modern%20Methods%20of%20Diagnosis)/08.%20Lipids%20and%20lipoproteins%20metabolis%20and%20its%20violatios.htm
Accessed on 04/22/2016
Vaverkova H. LDL-C or apoB as the Best Target for Reducing Coronary Heart Disease. Should Apob be Implemented into Clinical Practice? Clin Lipidology. 2011;6(1):35-48.
Composition of Lipoproteins

14. Rader DJ, Hoeg JM and Brewer HB Jr. Quantitation of plasma apolipoproteins in the primary and secondary prevention of coronary artery disease. Ann Intern Med. 1994 Jun 15;120(12):1012-25.
Lipoprotein Associated apolipoproteins
Chylomicron apoB-48, apoA, apoC, apoE, apoH
VLDL apoE, apoB-100, apoC
IDL apoE, apoB-100, apoC
LDL apoB-100, apoC, apoE
HDL apoA-1, apoC, apoD, apoE
The apolipoproteins that are in
bold are the major
apolipoprotein on the particular
lipoprotein
Lipoprotein synthesis, transport and recycling
Major
apolipoprotein
Function of the apolipoprotein
apoA-1 Structural protein - HDL
apoB-48 Structural protein - Chylomicron
apoB-100 Ligand for binding to LDL receptors
Structural protein in VLDL and LDL
apoE Ligand for binding to remnant apoE-receptor

15. Chylomicron
5%
90%
3%
2%
Protein Phospholipid
Triglycerides Cholesterol and esters
VLDL
20%
60%
15%
5%
Protein Phospholipid
Triglycerides Cholesterol and esters
LDL
50%
8%
22%
20%
Protein Phospholipid
Triglycerides Cholesterol and esters
HDL
25%
5%
30%
40%
Protein Phospholipid
Triglycerides Cholesterol and esters
Composition of Lipoproteins
Free fatty acids not
included in the above
diagrams

16. Hyper-
lipoproteinemia
Name of the disease Increased
lipoprotein
Increased lipid
fraction
Type I Hyperchylomicronemia Chylomicrons Triglycerides
Type IIa Familial
hypercholesterolemia
LDL Cholesterol
Type IIb Familial combined
hypercholesterolemia
LDL and VLDL Cholesterol and
triglycerides
Type III Dysbetalipoprotenemia IDL, chylomicron
remnants
Triglycerides and
cholesterol
Type IV Familial
hypertriglyceridemia
VLDL Triglycerides
Type V Familial lipoprotein
lipase deficiency
VLDL and
Chylomicrons
Triglycerides and
cholesterol
Fredrickson classification is still followed
Chandra KS, et al. Consensus statement on management of dyslipidemia in Indian subjects. Indian Heart J. 2014 Dec;66 Suppl 3:S1-51.
Levy RI, Fredrickson DS. Diagnosis and management of hyperlipoproteinemia. Am J Cardiol 1968;22:576-583.
Source: Classification of hyperlipidaemias and hyperlipoproteinaemias. Bull World Health Organ. 1970; 43(6): 891–915.

17. Tall AR and Yvan-Charvet L. Cholesterol, inflammation and innate immunity. Nature Reviews Immunology 15, 104–116 (2015)
Source: LIPOPROTEINS – ROLE IN HEALTH AND DISEASES. Edited by sasa frank and gerhard kostner. Chapter 5. The apob/apoa-i ratio is a strong predictor of cardiovascular risk. Göran walldius. Http://www.Intechopen.Com/books/lipoproteins-role-in-health-
and-diseases/the-apob-apoa-i-ratio-is-a-strong-predictor-of-cardiovascular-risk accessed on 04/23/2016
LDL vs HDL

18. Jacobson TA, et al. National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 1—Full Report. J Clin Lipidol. 2015 Mar-Apr;9(2):129-69.
Normal serum levels of cholesterol and triglycerides

19. Type I Hyperlipoproteinemia or Hyperchylomicronemia
Chylomicron
5%
90%
3%
2%
Protein Phospholipid
Triglycerides Cholesterol and esters
• Inherited condition (1 in 1 million)
• Deficiency of lipoprotein lipase or apolipoprotien C-II (a lipase-
activating protein)
• Thus, inability to remove chylomicrons and triglycerides from
blood (i.e. hyperchilomicronemia and hypertriglyceridemia)
• Usually presents in childhood with eruptive xanthomata and
abdominal colic
• Development of lipemia retinalis
• Complications include retinal vein occlusion, acute pancreatitis,
steatosis and organomegaly (hepatosplenomegaly)
Ladizinski B, and Lee KC. Clinical Images: Eruptive
xanthomas in a patient with severe hypertriglyceridemia
and type 2 diabetes CMAJ 2013;185:1600
George Yuan et al.. Hypertriglyceridemia: its etiology,
effects and treatment CMAJ 2007;176:1113-1120
Eruptive
xanthomata
Lipemic
plasma
Lipemia
retinalis
Tuberous
xanthomas
Palmar
crease
xanthomas
Eruptive xanthomata
Merkel M, Eckel RH and Goldberg IJ. Lipoprotein lipase: genetics,
lipid uptake, and regulation. J. Lipid Res. 2002 43:(12) 1997-2006. Forte TM, Shu X and Ryan RO. The ins (cell) and outs (plasma) of apolipoprotein A-V. J Lipid Res. 2009 Apr;50 Suppl:S150-5.

20. Type IIa Hyperlipoproteinemia or Familial
hypercholesterolemia (increased LDL) LDL
50%
8%
22%
20%
Protein Phospholipid
Triglycerides Cholesterol and esters
Homozygous familial hypercholesterolaemia
• 1 in 1 000 000
• Life-threatening condition (first decade of life)
• Mutations in LDL receptor (LDLR) gene
• Parents are heterozygous for the mutations
• Markedly elevated circulating levels of low-density lipoprotein
cholesterol (LDL-C)
Source: Namrata C. Biochemistry for medics. Cholesterol metabolism (Subjective questions Set-4).
http://www.namrata.co/cholesterol-metabolism-subjective-questions-set-4/
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512
Modified from: Harisa GI and Alanazi FK. Low density
lipoprotein bionanoparticles: From cholesterol
transport to delivery of anti-cancer drugs. Saudi Pharm
J. 2014 Dec; 22(6): 504–515.
Cont. next slide

21. Type IIa Hyperlipoproteinemia or Familial
hypercholesterolemia (increased LDL)
• Leading to accelerated and premature atherosclerotic
cardiovascular disease
• Usually presents as cutaneous xanthomas in feet, hands, elbows,
Achilles tendons.
• Arcus senilis corneae
• Complications are mainly cardiovascular
Homozygous familial hypercholesterolaemia
Source: Corneal arcus (arcus senilis). Ophthalmic Atlas Images by
EyeRounds.org, The University of Iowa
http://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/Arcus/in
dex.htm Accessed on 04/25/2016
Goldstein JL, and Brown MS. The LDL Receptor. Arterioscler
Thromb Vasc Biol. 2009;29:431-438
Cuch el M, et al. Homozygous familial hypercholesterolaemia: new insights and guidance for clinicians to improve
detection and clinical management. A position paper from the Consensus Panel on Familial Hypercholesterolaemia of the
European Atherosclerosis Society. Eur Heart J 2014;eurheartj.ehu274
Source: PEIR Digital Library. HISTOLOGY: CARDIOVASCULAR:
VASCULATURE: coronary artery: atherosclerosis: micro low mag
hemorrhage into plaque and thrombosis.
http://peir.path.uab.edu/library/picture.php?/1964

22. Type IIa Hyperlipoproteinemia or Familial
hypercholesterolemia (increased LDL)
Heterozygous familial hypercholesterolaemia
• 1 in 500
• Treatable life-threatening condition (beyond adolescence)
• Heterozygous mutations in the LDLR gene
• Autosomal dominant inheritance
• Markedly elevated circulating levels of low-density lipoprotein
cholesterol (LDL-C)
• Clinical features similar to Homozygous condition
Yuan G, Wang J and Hegele RA. Heterozygous familial hypercholesterolemia: an underrecognized cause of early cardiovascular disease. CMAJ. 2006 Apr 11;
174(8): 1124–1129.
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512
LDL
50%
8%
22%
20%
Protein Phospholipid
Triglycerides Cholesterol and esters

23. Type IIb Hyperlipoproteinemia or combined
hyperlipidemia
(increased VLDL and LDL)
• 1 in 40
• Autosomal dominant inheritance
• But molecular basis is yet to be deciphered
• Leads to increased serum Triglycerides and LDL cholesterol
• No/rare cutaneous xanthomas
• Usually recognized during investigation of cardiovascular or
ceribrovascular accident
VLDL
20%
60%
15%
5%
Protein Phospholipid
Triglycerides Cholesterol and esters
LDL
50%
8%
22%
20%
Protein Phospholipid
Triglycerides Cholesterol and esters
Yuan G, and Hegele RA. Hypertriglyceridemia: its etiology, effects and treatment. CMAJ. 2007 Apr 10; 176(8): 1113–1120.
Brahm A and Hegele RA. Hypertriglyceridemia. Nutrients. 2013 Mar; 5(3): 981–1001.
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512

24. IDL
22%
36%
22%
20%
Protein Phospholipid
Triglycerides Cholesterol and esters
Type III Hyperlipoproteinemia or
Dysbetalipoproteinemia (increased IDL)
• 1 in 1 million
• Mutation in apoE apoprotein has been identified but not in all
patients
• Autosomal recessive
• Not all with the mutation have symptoms
• Elevated plasma triglycerides and cholesterol
• Manifests earlier in males and usually after menopause in
women
• When severe: symptoms in first year of life or in young
childhood
• growth delay, malabsorption, hepatomegaly, and neurological
and neuromuscular manifestations, diarrhea with steatorrhea
HSPG/LPR: Heparan sulfate proteoglycan (HSPG)/low density lipoprotein
(LDL) receptor- related protein (LRP)
Mahley WR, Huang Y and Rall SC Jr. Pathogenesis of type III hyperlipoproteinemia
(dysbetalipoproteinemia): questions, quandaries, and paradoxes. J Lipid Res. 1999 Nov;40(11):1933-49.
Kei A, et al. Dysbetalipoproteinemia: Two cases report and a diagnostic algorithm. World J Clin Cases. 2015 Apr 16;3(4):371-6.
Source: Abetalipoproteinemia. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Expert=14 Accessed on 04/25/2016
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512

25. VLDL
20%
60%
15%
5%
Protein Phospholipid
Triglycerides Cholesterol and esters
Type IV Hyperlipoproteinemia or Familial
hypertriglyceridemia (increased VLDL)
Levy RI, Fredrickson DS. Diagnosis and management of hyperlipoproteinemia. Am J Cardiol 1968;22:576-583.
Fung MA and Frohlich JJ. Common problems in the management of hypertriglyceridemia. CMAJ. 2002 November 26; 167(11): 1261–1266.
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512
• 1 in 100
• Autosomal dominant inheritance
• Mutations have been identified in Apolipoprotein C and
Lecithin:cholesterol acyltransferase
• Clinical features include eruptive xanthomas, lipemia retinalis
and hepatosplenomegaly.
• May present as acute pancreatitis
• Patients are at increased risk of coronary artery disease

26. Type V Hyperlipoproteinemia or Familial lipoprotein
lipase deficiency (increased VLDL and Chylomicron)
Chylomicron
5%
90%
3%
2%
Protein Phospholipid
Triglycerides Cholesterol and esters
VLDL
20%
60%
15%
5%
Protein Phospholipid
Triglycerides Cholesterol and esters
Brahm A and Hegele RA. Hypertriglyceridemia. Nutrients. 2013 Mar; 5(3): 981–1001
Ghiselli G, et al. Increased prevalence of apolipoprotein E4 in type V hyperlipoproteinemia. J Clin Invest. 1982 Aug; 70(2): 474–477
Dammerman M and Breslow JL. Genetic Basis of Lipoprotein Disorders Circulation. 1995; 91: 505-512.
• 1 in 600
• Mutation in the apoE apolipoprotein
• Patients overproduce triglycerides and defective clearance of
VLDL
• A fat free diet will convert the patients to express a Type IV
Hyperlipoproteinemia features
• Presents with hepatosplenomegaly, occasional eruptive
xanthomas, increased incidence of pancreatitis

27. Secondary hyperlipidemia
• Usually a “two hit phenomenon” is noticed
o “First hit” is the genetic predisposition
o “Second hit” are the secondary factors, which worsen lipid
levels
Bays HE, et al. National Lipid Association Annual Summary of Clinical Lipidology 2016. J Clin Lipidol. 2016 Jan-Feb;10(1 Suppl):S1-S43.
Source: GUIDELINES FOR ADOLESCENT NUTRITION SERVICES. Stang J and story M. Chapter 10. Hyperlipidemia. Page 109-124. Adams LB. Http://www.Epi.Umn.Edu/let/pubs/adol_book.Shtm

28. • Secondary causes of hyperlipidemia: metabolic syndrome, insulin resistance,
limited physical activity, cigarette smoking, substantial alcohol consumption,
pregnancy, anorexia narvosa, corticosteroid therapy.
• Endocrine diseases: inadequately controlled diabetes mellitus, untreated
hypothyroidism, polycystic ovarian syndrome.
• Kidney disease: chronic kidney disease, nephrotic syndrome.
• Liver disease: hepatitis with fatty liver, cholestasis, biliary cirrhosis, primary
sclerosing cholangitis.
• Pancreatic disease: acute pancreatitis.
• Infections: HIV infection especially when on highly active anti-retroviral therapy.
• Inflammatory diseases: systemic lupus erythematosus, rheumatoid arthritis.
• Storage diseases: glycogen storage disease, Gaucher’s disease, juvenile Tay-Sachs
disease, Niemann-Pick disease.
• Others: idiopathic hypercalcemia, Klinefelter syndrome, Kawasakis disease, acute
intermittent prophyria.
Secondary hyperlipidemia
Source: GUIDELINES FOR ADOLESCENT NUTRITION SERVICES. Stang J and story M. Chapter 10. Hyperlipidemia. Page 109-124. Adams LB. Http://www.Epi.Umn.Edu/let/pubs/adol_book.Shtm
Bays HE, et al. National Lipid Association Annual Summary of Clinical Lipidology 2016. J Clin Lipidol. 2016 Jan-Feb;10(1 Suppl):S1-S43.

29. Hyperlipidemia in pregnancy
In normal pregnancy
• Maternal hyperlipidemia is normal during pregnancy
• Especially in the third trimester
• Mainly triglycerides (TAG) and to a lesser extent cholesterol and phospholipids
• Increased VLDL production and decreased removal
• Increased levels of TAG in LDL and HDL
• The above is assisted by the insulin-resistant state in pregnancy
Source: Metabolism in normal pregnancy. Herrera E and Ortega H. In Textbook of Diabetes and Pregnancy”, second ed. , M.Hod, L.Jovanovich, G.C.Di Renzo, A. De Leiva, O. Langer, eds., Informa healthcare, London, pgs. 25-34, 2008.
http://dspace.ceu.es/bitstream/10637/2873/1/pag25_34.pdf Accessed on 04/27/2016
Source: Lipoproteins – The Importance of Lipid and Lipoprote in Ratios in Interpretetions of Hyperlipidaemia of Pregnancy. Meshelia DS and Kullima AA. Role in health and disease. Biochemistry, Genetics and Molecular Biology. Frank S and Kostner G.
http://www.intechopen.com/books/lipoproteins-role-in-health-and-diseases/the-importance-of-lipid-and-lipoprote-in-ratios-in-interpretetions-of-hyperlipidaemia-of-pregnancy Accessed on 04/27/2016

30. Lipid and
lipoprotein (mg/dl)
Third trimester
Non-pregnant
controls
HDL-C 81±17 69±10
LDL-C 136±33 99±23
TGs 245±73 77±34
TC 267±30 183±23
VLDL 109 (38-710) 23 (5-85)
IDL 124(79-157) 35(18-62)
LDL 353(244-534) 207(150-363)
In normal pregnancy
Source: Lipoproteins – The Importance of Lipid and Lipoprote in Ratios in Interpretetions of Hyperlipidaemia of Pregnancy. Meshelia DS and Kullima AA. Role in health and disease. Biochemistry, Genetics and Molecular Biology. Frank S and Kostner G.
http://www.intechopen.com/books/lipoproteins-role-in-health-and-diseases/the-importance-of-lipid-and-lipoprote-in-ratios-in-interpretetions-of-hyperlipidaemia-of-pregnancy Accessed on 04/27/2016
Hyperlipidemia in pregnancy

31. Source: Lipoproteins – The Importance of Lipid and Lipoprote in Ratios in Interpretetions of Hyperlipidaemia of Pregnancy. Meshelia DS and Kullima AA. Role in health and disease. Biochemistry, Genetics and Molecular Biology. Frank S and Kostner G.
http://www.intechopen.com/books/lipoproteins-role-in-health-and-diseases/the-importance-of-lipid-and-lipoprote-in-ratios-in-interpretetions-of-hyperlipidaemia-of-pregnancy Accessed on 04/27/2016
Medical complications of pregnancy
Pre-eclampsia, Pregnancy-induced hypertension
Gestational diabetes mellitus, Prelipaemia
Intra-uterine growth restriction(retardation)
Co-existing medical conditions
Obesity, Types 1 and 2 diabetes mellitus
Hypothyroidism, Hypertension
Renal diseases, particularly nephritic syndrome
Others
Alcoholism, Medications, eg LMWt-heparin and
glucocorticoid
Other maternal factors
Obesity, Maternal weight gain, Maternal nutrition,
Pre-pregnancy lipid levels
Hyperlipidemia in pregnancy

32. Consequences
Consequences of hyperlipidemia in pregnancy on the mother
• Cholesterol gallstones
• Intrahepatic cholestasis
• Acute pancreatitis
• Endothelial dysfunction
• Preeclampsia
Consequences of hyperlipidemia in pregnancy on the child
• Intra-uterine growth retardation
• Future development of metabolic syndrome in affected fetus
• increased risk of cardiovascular disease later in life
• Preterm birth
• Large for gestational age
Vrijkotte TG, et al. Maternal lipid profile during early pregnancy and pregnancy complications and outcomes: the ABCD study. J Clin Endocrinol Metab. 2012 Nov;97(11):3917-25.
Clausen T, Djurovic S and Henriksen T. Dyslipidemia in early second trimester is mainly a feature of women with early onset pre-eclampsia. BJOG. 2001 Oct;108(10):1081-7.
Source: Mukherjee M. Dyslipidemia in Pregnancy. http://www.acc.org/latest-in-cardiology/articles/2014/07/18/16/08/dyslipidemia-in-pregnancy. Accessed on 04/27/2016
Source: Lipoproteins – The Importance of Lipid and Lipoprote in Ratios in Interpretetions of Hyperlipidaemia of Pregnancy. Meshelia DS and Kullima AA. Role in health and disease. Biochemistry, Genetics and Molecular Biology. Frank S and Kostner G.
http://www.intechopen.com/books/lipoproteins-role-in-health-and-diseases/the-importance-of-lipid-and-lipoprote-in-ratios-in-interpretetions-of-hyperlipidaemia-of-pregnancy Accessed on 04/27/2016
Hyperlipidemia in pregnancy

33. Hyperlipidemia
Conclusions
• Increased levels of lipids or lipoproteins
• Primary/Familial and secondary causes
• Fredrickson classification of familial causes of 1968 is still mainly followed
• Mainly concerned with cholesterol and triglyceride levels in blood
• Genetic mutations in the genes of apolipoprotein or its receptors or lipoprotein
lipase is the cause of familial diseases
• Secondary causes uncover the primary causes
• Pregnancy is, even normally, a hyperlipidemic condition
• Primary causes can get uncovered during pregnancy
• Hyperlipidemia can complicate pregnancy