A disorder of lipoprotein metabolism, including lipoprotein overproduction or deficiency. Dyslipidemias may be manifested by elevation of the total cholesterol, the “bad” low-density lipoprotein (LDL) cholesterol and the triglyceride concentrations, and a decrease in the “good” high-density lipoprotein (HDL) cholesterol concentration in the blood.
Dyslipidemia comes under consideration in many situations includingdiabetes, a common cause of lipidemia. For adults with diabetes, it has been recommended that the levels of LDL, HDL, and total cholesterol, and triglyceride be measured every year. Optimal LDL cholesterol levels for adults with diabetes are less than 100 mg/dL (2.60 mmol/L), optimal HDL cholesterol levels are e4qual to or greater than 40 mg/dL (1.02 mmol/L), and desirable triglyceride levels are less than 150 mg/dL (1.7 mmol/L).
From dys- + lipid (fat) + -emia (in the blood) = essentially, disordered lipids in the blood.
Causes are classified into two groups: the Primary and secondary causes
- Primary Causes. Overproduction and defective clearance of the cholesterols TG and LDL is the result of the mutations of single or multiple genes. The primary disorders are the common dyslipidemia causes to the children, although it may not affect in the most cases of adult dyslipidemia.
- Secondary Causes. Adults are the most affected ones when it comes to secondary causes. The causes contribute a lot on how an adult will be affected with dyslipidemia. The sedentary lifestyle is the most essential secondary cause. The lifestyle includes excessive dietary intake of cholesterol, trans fats and saturated fats. Trans fats are the fatty acids that are either polyunsaturated or monounsaturated, in which there are added hydrogen atoms. Trans fats are usually used in a lot of processed foods.
Other secondary causes are:
- Alcohol overuse
- Diabetes mellitus
- Chronic kidney disease,
- Other cholestatic liver diseases and primary biliary cirrhosis.
- Drugs like thiazides, retinoids, estrogens and glucocorticoids, among others.
The insulin resistance/metabolic syndrome is characterised by the variable coexistence of hyperinsulinaemia, obesity, dyslipidaemia, and hypertension. The pathogenesis of the syndrome has multiple origins, but obesity and sedentary lifestyle coupled with diet and still largely unknown genetic factors clearly interact to produce the syndrome. Dyslipidaemia, the hallmark of the metabolic syndrome, includes increased flux of free fatty acids, raised triglycerides, apolipoprotein B, and small dense low density lipoprotein, and decreased high density lipoprotein cholesterol. The widely prevalent nature of the metabolic syndrome emphasises the importance of its diagnosis and treatment. This review analyses the clinical and dynamic features of this syndrome in the aspect of dyslipidaemia and its management.
Dyslipidemia doesn’t have symptoms at all, but it can cause other symptomatic vascular disease, like coronary artery disease.
Eyelid xanthelasmas, tendinous xanthomas at the elbow, knee tendons and Achilles and arcus cornea are caused by high levels of LDL. Acute pancreatitis is caused by high levels of TGs.
Patients that have familial hypercholesterolemia in homozygous form can have the above findings with planar xanthomas. Patients that have elevation of TGs in severe condition can expect having eruptive xanthomas over their elbow, back, trunks, knees, buttocks, feet and hands. Those with rare dysbetalipoproteinemia can expect having palmar xanthomas and tuberous xanthomas.
Retinal arteries and veins can have a creamy white appearance due to the severe hypertriglyceridemia. You can also have a milky appearance in your blood plasma when you have high lipid levels. You can expect symptoms like paresthesias, confusion and dypsnea.
- Serum lipid profile (measured total cholesterol, TG, and HDL cholesterol and calculated LDL cholesterol and VLDL)
Dyslipidemia is suspected in patients with characteristic physical findings or complications of dyslipidemia (eg, atherosclerotic disease). Primary lipid disorders are suspected when patients have physical signs of dyslipidemia, onset of premature atherosclerotic disease (at <60 yr), a family history of atherosclerotic disease, or serum cholesterol > 240 mg/dL (> 6.2 mmol/L). Dyslipidemia is diagnosed by measuring serum lipids. Routine measurements (lipid profile) include total cholesterol (TC), TGs, HDL cholesterol, and LDL cholesterol.
LIPID PROFILE MEASUREMENT
TC, TGs, and HDL cholesterol are measured directly. TC and TG values reflect cholesterol and TGs in all circulating lipoproteins, including chylomicrons, VLDL, intermediate-density lipoprotein (IDL), LDL, and HDL. TC values can vary by 10% and TGs by up to 25% day-to-day even in the absence of a disorder. TC and HDL cholesterol can be measured in the nonfasting state, but most patients should have all lipids measured while fasting (usually for 12 h) for maximum accuracy and consistency.
Testing should be postponed until after resolution of acute illness because TG and lipoprotein(a) levels increase and cholesterol levels decrease in inflammatory states. Lipid profiles can vary for about 30 days after an acute MI; however, results obtained within 24 h after MI are usually reliable enough to guide initial lipid-lowering therapy.
LDL cholesterol values are most often calculated as the amount of cholesterol not contained in HDL and VLDL. VLDL is estimated by TG ÷ 5 because the cholesterol concentration in VLDL particles is usually one fifth of the total lipid in the particle. Thus,
CLINICAL CALCULATOR: VERY LOW DENSITY LIPOPROTEIN (VLDL)
This calculation is valid only when TGs are < 400 mg/dL and patients are fasting, because eating increases TGs. The calculated LDL cholesterol value incorporates measures of all non-HDL, nonchylomicron cholesterol, including that in IDL and lipoprotein (a) [Lp(a)].
LDL can also be measured directly using plasma ultracentrifugation, which separates chylomicrons and VLDL fractions from HDL and LDL, and by an immunoassay method. Direct measurement may be useful in some patients with elevated TGs, but these direct measurements are not routinely necessary. The role of apo B testing is under study because values reflect all non-HDL cholesterol (in VLDL, VLDL remnants, IDL, and LDL) and may be more predictive of CAD risk than LDL cholesterol. Non-HDL cholesterol (TC – HDL cholesterol) may also be more predictive of CAD risk than LDL cholesterol.
Patients with premature atherosclerotic cardiovascular disease, cardiovascular disease with normal or near-normal lipid levels, or high LDL levels refractory to drug therapy should probably have Lp(a) levels measured. Lp(a) levels may also be directly measured in patients with borderline high LDL cholesterol levels to determine whether drug therapy is warranted. C-reactive protein may be considered in the same populations. Measurements of LDL particle number or apoprotein B-100 (apo B) may be useful in patients with elevated TGs and the metabolic syndrome. Apo B provides similar information to LDL particle number because there is one apo B molecule for each LDL particle. Apo B measurement includes all atherogenic particles, including remnants and Lp(a).
Clinical Calculator: Friedewald Equation for Low Density Lipoprotein (LDL-C SI units)
Clinical Calculator: Friedewald Equation for Low Density Lipoprotein (LDL-C)
Tests for secondary causes of dyslipidemia—including measurements of fasting glucose, liver enzymes, creatinine, thyroid-stimulating hormone (TSH), and urinary protein—should be done in most patients with newly diagnosed dyslipidemia and when a component of the lipid profile has inexplicably changed for the worse.
Universal screening using a fasting lipid profile (TC, TGs, HDL cholesterol, and calculated LDL cholesterol) should be done in all children between age 9 and 11 (or at age 2 if children have a family history of severe hyperlipidemia or premature CAD). Adults are screened at age 20 yr and every 5 yr thereafter. Lipid measurement should be accompanied by assessment of other cardiovascular risk factors, defined as
- Diabetes mellitus
- Cigarette use
- Family history of CAD in a male 1st-degree relative before age 55 or a female 1st-degree relative before age 65
A definite age after which patients no longer require screening has not been established, but evidence supports screening of patients into their 80s, especially in the presence of atherosclerotic cardiovascular disease.
Patients with an extensive family history of heart disease should also be screened by measuring Lp(a) levels.
The treatment of dyslipidemia depends on the age, symptoms and overall health of the patient. The probability of the dyslipidemia to progress to heart disease is also considered. The most common treatment is having a well regulated diet and exercise. However, exercise can also be combined with medication and surgery for more serious conditions, just to prevent any complications.
The doctor will explain the whole treatment option to a patient who is first diagnosed to have this condition. In cases like high levels of cholesterol and triglycerides, it is recommended that lifestyle change is needed, rather than a medical intervention. The patient must commit in exercising and dieting, as they are the most essential part of dyslipidemia treatment. A patient with mild dyslipidemia is asked by the doctor to take some exercises and general dietary guidelines. Those with advanced conditions are also asked to meet with a nutritionist to have a well designed meal plans and to have an exercise routine.
The dyslipidemia diet plans include foods that are low in cholesterol and calories and trans-fat free. Foods that are sugary and fried must be avoided. Dairy products and red meat are taken in moderation. In order to lower their cholesterol level, it is recommended that patients should eat fish, vegetables, nuts and fruits. It is also important that doctors and nutritionists explain the essence of eating certain kinds of foods to patient. They also need to help patients eat in smaller portions and avoid their cravings.
Having regular exercises help the patients in losing weight, improve the functions of their lungs and heart and to stabilize their blood pressure. Patients should always follow the instructions of their doctors for them to achieve their desired results. Exercise routines are adjusted to fit in the patient’s ability level. If the patient is physically able, they are encouraged to take walk regularly and ride bicycles. Other activities like Pilates, Yoga, Workout classes and weightlifting are also suggested.
It is said that diet and exercise are not just the things that you need to do in order to prevent other health complications. Patients can be prescribed with medications to lower down their triglyceride and cholesterol levels. One medication prescribed by doctors is Statins. These are drugs that inhibit the liver enzyme, which synthesizes the lipids and can lead to fatty buildup. Fibrates are other drugs that are combines with Statins to raise the lipoprotein levels. Lipoproteins are good cholesterol that helps in preventing the sticking of fatty deposits to arterial walls.
It is important that patients follow the treatment regimen to avoid surgery and prevent it from progressing to a serious health problem.
DYSLIPIDEMIA IN DIABETES
Diabetics with dyslipidemia are diagnosed to have low HDL cholesterol and too many triglycerides. Patients of type 2 diabetes have higher risk of having this condition. The risk factors are having high blood glucose, being obese, and resistant to insulin. And with the combinatioin of these two conditions, there is a consequence of having poor control of their diabetes. Those diabetics with no dyslipidemia can develop one for no apparent reasons like kidney diseases and hypothyroidism. Patients with dyslipidemia can develop diabetes in the future, according to studies. Female patients that have diabetes can have higher risk of cardiac disease because of this form.