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Dyslipidemia is a metabolic disorder characterized by abnormally high or low amounts of any or all (e.g. , , cholesterol, ) or in the blood. Dyslipidemia is a risk factor for the development of atherosclerotic cardiovascular diseases, which include coronary artery disease, cerebrovascular disease, and peripheral artery disease. Although dyslipidemia is a risk factor for cardiovascular disease, abnormal levels do not 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 ; 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.
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The three main blood levels collected to assess for dyslipidemia are (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 hypertriglyceridemia 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 cholesterol 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 . 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 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 on the skin, eyelids or around the cornea. In contrast to primary dyslipidemias, secondary dyslipidemias are based on modifiable environmental or lifestyle factors. Some diseases that are associated with a higher risk of dyslipidemia are uncontrolled Diabetes, 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, , oral contraceptives, atypical antipsychotics (clozapine, olanzapine), , tacrolimus, and Ciclosporin. Other non-hereditary factors that increase the risk of dyslipidemias are smoking, pregnancy, and obesity.
The Fredrickson Classification seen below classifies dyslipidemias into categories:Fredrickson DS, Lees RS. A system for phenotyping hyperlipoproteinemia. Circulation 1965;31:321-327.
An important non-pharmacological intervention in dyslipidemia is a diet aimed at reducing blood lipid levels and also weight loss if needed. These dietary changes should always be a part of treatment and the involvement of a dietician is recommended in the initial evaluation and also in follow-up as well. A 3-month trial of dietary changes is recommended in primary prevention before considering medication, but in secondary prevention and in individuals at high-risk, cholesterol-lowering medication is used in conjunction with diet modifications.
Recommended diets include the DASH diet, Mediterranean diet, low glycemic index diet, Portfolio diet, and vegetarian diet. Patients should reduce their intake of saturated fats, dietary cholesterol, and alcohol, and increase their intake of total fibre (≥30g/day), viscous soluble fibre (≥10g/day), and omega-3 (EPA and DHA 2-4g/d used to lower TG only). They should also increase the proportion of mono-and polyunsaturated fats that they intake.
Other lifestyle modifications include weight loss (5–10% of body weight loss) and reduction of abdominal obesity, 30–60 minutes per day of moderate-vigorous exercise, smoking cessation, stress management, and getting 6–8 hours of sleep at night.
Based on the Framingham Risk Scores, there are different thresholds that indicate whether treatment should be initiated. Individuals with a score of 20% are considered to have a high cardiovascular risk, a score of 10–19% indicates an intermediate risk, and patients with a score less than 10% are at low risk. Statin therapy and non-pharmacological interventions are indicated in those with high cardiovascular risk. In those at intermediate risk or low risk, the use of statin therapy depends on individual patient factors such as age, cholesterol levels, and risk factors.
Statins are considered the first-line agents but other drugs can be substituted if the lipid targets are not achieved with statin therapy or if they are not tolerated.
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