Type of test Blood

Normal findings

 HDL

 Male: > 45 mg/dL or > 0.75 mmol/L (SI units) Female: > 55 mg/dL or > 0.91 mmol/L (SI units)

LDL

Adult: < 130 mg/dL Children: < 110 mg/dL

VLDL

7-32 mg/dL

Test explanation and related physiology

 Lipoproteins are considered to be an accurate predictor of heart disease. As part of the lipid profile, these tests are per formed to identify persons at risk for developing heart disease, to decide when to initiate statin therapy, and to monitor the response to statin therapy.

Lipoproteins are proteins that are used as markers indicating the levels of lipids within the bloodstream. The lipid pro file usually measures total cholesterol, triglycerides, HDL, LDL, and VLDL. HDLs (good cholesterol) are carriers of cholesterol. They are produced in the liver and, to a smaller degree, in the intestines. In general, the purpose of HDLs is believed to be removal of the cholesterol from the peripheral tissues and transportation to the liver for excretion. The function of removing lipids from the endothelium (reverse cholesterol transport) pro vides a protective effect against heart disease.

Total HDL cholesterol is an independent, inverse risk factor for coronary artery disease (CAD). Whereas low levels (< 35 mg/dL) are believed to increase a person’s risk for CAD, high levels (> 60 mg/dL) are considered protective. When HDL and total cholesterol measurements are combined in a ratio fashion, the accuracy of predicting CAD is increased. The total cholesterol/HDL ratio should be at least 5:1, with 3:1 being ideal.

Five subclasses of HDL (2a, 2b, 3a, 3b, and 3c) have been identified, but only 2b is cardioprotective. HDL 2b is the most efficient form of HDL in reverse cholesterol transport. Patients with low total HDL levels often have low levels of HDL 2b.

When levels of total HDL are between 40 and 60 mg/dL, cardioprotective levels of HDL 2b are minimal. However, when levels of total HDL are greater than 60 mg/dL, levels of HDL 2b predominate, and efficient reverse cholesterol transport takes place. This protects the coronary arteries from disease. The other subclasses of HDL are not capable of reverse cholesterol trans port and therefore are not cardioprotective.

LDLs (bad cholesterol) are also cholesterol rich. However, most cholesterol carried by LDLs can be deposited into the lining of the blood vessels and is associated with an increased risk of arteriosclerotic heart and peripheral vascular disease. Therefore high levels of LDLs are atherogenic. The LDL level should be less than 70 mg/dL in patients at high risk for heart disease. For patients at moderately high risk, the LDL should be less than or equal to 100 mg/dL (depending on other cardiac risk factors). LDL can be difficult to measure. Therefore the LDL level can be calculated using the Friedewald formula. In this formula, subtracting the HDL plus one-fifth of the triglycerides from the total cholesterol derives LDL level:

LDL = total cholesterol – ( HDL + [ triglycerides ÷ 5 ])

There are other formulas for deriving LDL, which may account for different sets of normal values. Furthermore, the formula is inaccurate if the triglycerides exceed 400 mg/dL.

LDL has been divided into seven classes based on particle size. These subclasses are (from largest to smallest) LDL I, LDL IIa, LDL IIb, LDL IIIa, LDL IIIb, LDL IVa, and LDL IVb. The most commonly elevated forms of LDL (IIIa and IIIb) are small enough to get between the endothelial cells and cause atheromatous disease. The larger LDL particles (LDL I, LDL IIa, and LDL IIb) cannot get into the endothelial layer and therefore are not associated with increased risk of disease. LDL IVa and IVb, however, are very small and are associated with aggressive arterial plaques that are particularly vulnerable to ulceration and vascular occlusion. Nearly all patients with levels of LDL IVa and IVb greater than 10% of total LDL have vascular events within months.

LDL patterns can be identified, and they are associated with variable risks of CAD. LDL pattern A is seen in patients with mostly large LDL particles and does not carry increased risks for CAD. LDL pattern B is seen in patients with mostly small LDL particles and is associated with an increased risk of CAD. An intermediate pattern is noted in a large number of patients; they have small and large LDL particles and experience an intermediate risk of CAD. LDL levels can be lowered with diet, exercise, and statins.

VLDLs, although carrying a small amount of cholesterol, are the predominant carriers of blood triglycerides. To a lesser degree, VLDLs are also associated with an increased risk of CAD by virtue of their capability to be converted to LDL by lipoprotein lipase in skeletal muscle. The VLDL value is sometimes expressed as a percentage of total cholesterol. Levels in excess of 25% to 50% are associated with increased risk of coronary disease.

 Interfering factors

 • Smoking and alcohol ingestion decrease HDL levels.

 • Binge eating can alter lipoprotein values.

 • HDL values are age and sex dependent.

 • HDL values, like cholesterol, tend to decrease significantly for as long as 3 months after MI.

 • HDL is elevated in hypothyroid patients and diminished in hyperthyroid patients.

• High triglyceride levels can make LDL calculations inaccurate.

* Drugs that may cause altered lipoprotein levels include alpha blockers, aspirin, beta-blockers, estrogens, phenothiazines, phenytoin, steroids, and sulfonamides.

Procedure and patient care

 • See inside front cover for Routine Blood Testing.

• Fasting: yes (12-14 hours)

• Blood tube commonly used: red

* Inform the patient that dietary indiscretion within the previous few weeks may influence lipoprotein levels.

* Instruct patients with high lipoprotein levels regarding diet, exercise, and appropriate body weight.

 Abnormal findings

 Increased HDL levels

- Familial HDL lipoproteinemia

- Excessive exercise

Decreased HDL levels

- Metabolic syndrome

- Familial low HDL

- Hepatocellular disease (e.g., hepatitis or cirrhosis)

- Hypoproteinemia (e.g., nephrotic syndrome or malnutrition)

Increased LDL and VLDL levels

- Familial LDL lipoproteinemia

- Nephrotic syndrome

- Glycogen storage diseases (e.g., von Gierke disease)

- Hypothyroidism

- Alcohol consumption

- Chronic liver disease (e.g., hepatitis or cirrhosis)

- Hepatoma

- Gammopathies (e.g., multiple myeloma)

- Familial hypercholesterolemia type IIa

- Cushing syndrome

- Apoprotein CII deficiency

Decreased LDL and VLDL levels

- Familial hypolipoproteinemia

- Hypoproteinemia (e.g., malabsorption, severe burns, or malnutrition)

- Hyperthyroidism

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مواضيع ذات صلة

liquid biopsy (Fluid biopsy, Fluid phase biopsy)

lipoprotein-associated phospholipase A2 (Lp-PLA2 PLAC test)

Hemolytic Anemias

Sickle Cell Anemia (Hemoglobinopathy S, Sickle Cell Disease)

Laboratory Diagnosis (Phenotypic) of Thalassemias

Pathophysiological and General Clinical Aspects of β-thalassemias

lipase (Pancreatic lipase, Lipoprotein lipase)

leucine aminopeptidase (LAP)

Legionnaires disease antibody test

Sideropenic and Assimilated Anemia

Automated Differential Count

Differential Leukocyte Count (Leukocyte Formula)