Dyslipidemia is an abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood. Dyslipidemia is a risk factor for the development of atherosclerotic cardiovascular disease (ASCVD). ASCVD includes coronary artery disease, cerbrovascular disease, and peripheral artery disease. Although dyslipidemia is a risk factor for ASCVD, abnormal levels doesn't mean that lipid lowering agents need to be started. Other factors, such as comorbid conditions and lifestyle in addition to dyslipidemia, is considered in a cardiovascular risk assessment. 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. Likewise, increased levels of O-GlcNAc transferase (OGT) may cause dyslipidemia.
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). The other way is due to the underlying cause for the condition (genetic, or secondary to another condition). This classification can be problematic, because most conditions involve the intersection of genetics and lifestyle issues. However, there are a few well-defined genetic conditions that are usually easy to identify.
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). High triglyceride levels (>1.7 mmol/L fasting) can indicate dyslipidemia. Triglycerides are transported through the blood by using very low density lipoproteins (VLDL) as a carrier. 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. 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. Another blood level collected to assess dyslipidemia is HDL-C. HDL cholesterol is made up of very little lipids and a high amount of protein. It is beneficial in the body because it functions by going to the tissues and picking up extra cholestrol and fat. Due to the positive effects of HDL-C, it is named "good cholesterol" since it helps prevent plaque formation. 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. Due to the positive functions of HDL cholesterol, a low level indicates dyslipidemia and is a risk factor for complications. Another diagnostic test that is often reviewed is LDL cholesterol. Low density lipoproteins are made up of cholesterol, TG, phospholipids, and apolipoproteins. LDL-C molecules bind to the endothelium of blood vessels and cause plaque formation. Once plaques are formed, LDL-C floating in the bloodstream can attach to the plaques and cause further accumulation. In addition to plaque formation, LDL-C molecules can undergo oxidation. Oxidation can cause further accumulation of cholesterol and the release of inflammatory cytokines, which damages the blood vessels. Due to the damaging effects of LDL-C, high levels increase the risk for cardiovascular disease and indicate dyslipidemia.
Dyslipidemias can also be classified based on the underlying cause, whether it is primary, secondary, or a combination of both. Primary dyslipidemias are caused by genetic disorders that can cause abnormal lipid levels without any other obvious risk factors. Those with primary dyslipidemias are at higher risk of getting complications of dyslipidemias, such as atherosclerotic cardiovascular disease, at a younger age. Some common genetic disorders associated with primary dyslipidemias are homozygous or heterozygous hypercholesterolemia, familial hypertriglyceridemia, combined hyperlipidemia, and HDL-C metabolism disorders. 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. In combined hyperlipidemia, there is an overproduction of apoB-100 in the liver. This causes high amounts of LDL and VLDL molecules to form. 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. In contrast to primary dyslipidemias, secondary dyslipidemas are based on modifiable environmental or lifestyle factors. 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.  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. Some medications that may contribute to dyslipidemia are thiazide diuretics, beta blockers, oral contraceptives, atypical antipsychotics (clozapine, olanzapine), corticosteroids, tacrolimus, and cyclosporine. Other non-hereditary factors that increase the risk of dyslipidemias are smoking, pregnancy, and obesity.
|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. 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. Testing the general population under the age of 40 without symptoms is of unclear benefit. UpToDate suggests screening males at age 35 and females at age 45 in those without any risk of cardiovascular disease.
Management consists of:
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