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Dyslipidemia is an abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood.[1] Dyslipidemia is a risk factor for the development of atherosclerotic cardiovascular disease (ASCVD).[1] ASCVD includes coronary artery disease, cerbrovascular disease, and peripheral artery disease.[1] Although dyslipidemia is a risk factor for ASCVD, abnormal levels doesn't mean that lipid lowering agents need to be started.[2] Other factors, such as comorbid conditions and lifestyle in addition to dyslipidemia, is considered in a cardiovascular risk assessment.[3] In developed countries, most dyslipidemias are hyperlipidemias; that is, an elevation of lipids in the blood. This is often due to diet and lifestyle. Prolonged elevation of insulin resistance can also lead to dyslipidemia.[1] Likewise, increased levels of O-GlcNAc transferase (OGT) may cause dyslipidemia.[citation needed]


Increases Decreases



Physicians and basic researchers classify dyslipidemias in two distinct ways. One way is its presentation in the body (including the specific type of lipid that is increased).[1] The other way is due to the underlying cause for the condition (genetic, or secondary to another condition).[1] This classification can be problematic, because most conditions involve the intersection of genetics and lifestyle issues.[1] However, there are a few well-defined genetic conditions that are usually easy to identify.[1]

The three main blood levels collected to assess for dyslipidemia is triglycerides(TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C).[4] High triglyceride levels (>1.7 mmol/L fasting) can indicate dyslipidemia.[2] Triglycerides are transported through the blood by using very low density lipoproteins (VLDL) as a carrier.[1] One thing to note when measuring triglyceride levels is that fasting for 8-12 hours is required to get an accurate result as non-fasting TG results may be falsely elevated.[4] If TG results are greater than 10 mmol/L, then this needs to be addressed since severe hypertriglceridemia is a risk factor for acute pancreatitis.[2] Another blood level collected to assess dyslipidemia is HDL-C.[4] HDL cholesterol is made up of very little lipids and a high amount of protein.[1] It is beneficial in the body because it functions by going to the tissues and picking up extra cholestrol and fat.[1] Due to the positive effects of HDL-C, it is named "good cholesterol" since it helps prevent plaque formation.[1] Other functions of HDL-C is promoting cardiovascular health such as antioxidation effects, protection against thrombosis, maintenance of endothelial function, and maintaining low blood viscosity.[1] Due to the positive functions of HDL cholesterol, a low level indicates dyslipidemia and is a risk factor for complications.[1] Another diagnostic test that is often reviewed is LDL cholesterol.[4] Low density lipoproteins are made up of cholesterol, TG, phospholipids, and apolipoproteins.[5] LDL-C molecules bind to the endothelium of blood vessels and cause plaque formation.[5] Once plaques are formed, LDL-C floating in the bloodstream can attach to the plaques and cause further accumulation.[5] In addition to plaque formation, LDL-C molecules can undergo oxidation.[1] Oxidation can cause further accumulation of cholesterol and the release of inflammatory cytokines, which damages the blood vessels.[1][5] Due to the damaging effects of LDL-C, high levels increase the risk for cardiovascular disease and indicate dyslipidemia.[1]

Dyslipidemias can also be classified based on the underlying cause, whether it is primary, secondary, or a combination of both.[1] Primary dyslipidemias are caused by genetic disorders that can cause abnormal lipid levels without any other obvious risk factors.[1] Those with primary dyslipidemias are at higher risk of getting complications of dyslipidemias, such as atherosclerotic cardiovascular disease, at a younger age.[1] Some common genetic disorders associated with primary dyslipidemias are homozygous or heterozygous hypercholesterolemia, familial hypertriglyceridemia, combined hyperlipidemia, and HDL-C metabolism disorders.[1] In familial hypercholesterolemia, a mutation in the LDLR, PCSK9, or APOB is usually the reason for this and these mutations result in high LDL cholesterol.[6] In combined hyperlipidemia, there is an overproduction of apoB-100 in the liver.[7] This causes high amounts of LDL and VLDL molecules to form.[7] A unique sign of primary dyslipidemias is that patients will often present with acute pancreatitis or xanthomas on the skin, eyelids or around the cornea.[1] In contrast to primary dyslipidemias, secondary dyslipidemas are based on modifiable environmental or lifestyle factors.[8] Some diseases that are associated with a higher risk of dyslipidemia are uncontrolled diabetes mellitus, cholestatic liver disease, chronic kidney disease, hypothyroidism, and polycystic ovarian syndrome.[1] [8] What people eat can also have an influence, with excessive alcohol use, too much carbohydrates, and diets high in saturated fats having a higher risk.[1] Some medications that may contribute to dyslipidemia are thiazide diuretics, beta blockers, oral contraceptives, atypical antipsychotics (clozapine, olanzapine), corticosteroids, tacrolimus, and cyclosporine.[1][8] Other non-hereditary factors that increase the risk of dyslipidemias are smoking, pregnancy, and obesity.[1][8]

 The Fredrickson Classification seen below classifies dyslipidemias into categories:[9][5]

Phenotype I IIa IIb III IV V
Elevated Lipoprotein Chylomicron LDL LDL and VLDL IDL VLDL VLDL and chylomicrons


There is no clear consensus of when screening for dyslipidemia should be initiated.[10] In general, those with a high risk of cardiovascular disease should be screened at a younger age with males between 25-30 years old and females between 30-35 years of age.[10] Testing the general population under the age of 40 without symptoms is of unclear benefit.[10] UpToDate suggests screening males at age 35 and females at age 45 in those without any risk of cardiovascular disease.[10]


Management consists of:[citation needed]


  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z Dixon, Dave L; Riche, Daniel M (April 21, 2021). "Dyslipidemia". Pharmacotherapy:A Pathophysiological Approach, 11e. Book authored by Joseph T. DiPiro, Gary C. Yee, L. Michael Posey, Stuart T. Haines, Thomas D. Nolin, Vicki Ellingrod.
  2. ^ a b c Rosenson, Robert S; Eckel, Robert H (April 9, 2021). "Hypertriglyceridemia". UpToDate. Retrieved April 21, 2021.
  3. ^ Wilson, Peter WF (March 29, 2020). "Cardiovascular disease risk assessment for primary prevention in adults: Our approach". UpToDate. Retrieved April 22, 2021.
  4. ^ a b c d Rosenson, Robert S (January 16, 2020). "Measurement of blood lipids and lipoproteins". UpToDate. Retrieved April 21, 2021.
  5. ^ a b c d e Rosenson, Robert S (August 3, 2020). "Lipoprotein classification, metabolism, and role in atherosclerosis". UpToDate. Retrieved April 21, 2021.
  6. ^ Rosenson, Robert S; Durrington, Paul (September 21, 2020). "Familial hypercholesterolemia in adults: Overview". UpToDate. Retrieved April 22, 2021.
  7. ^ a b Rosenson, Robert S; Durrington, Paul (July 1, 2020). "Inherited disorders of LDL-cholesterol metabolism other than familial hypercholesterolemia". UpToDate. Retrieved April 22, 2021.
  8. ^ a b c d Rosenson, Robert S (April 6, 2021). "Secondary causes of dyslipidemia". UpToDate. Retrieved April 22, 2021.
  9. ^ Fredrickson DS, Lees RS. A system for phenotyping hyperlipoproteinemia. Circulation 1965;31:321-327.
  10. ^ a b c d Vijan, Sandeep (February 28, 2020). "Screening for lipid disorders in adults". UpToDate. Retrieved April 22, 2021.