We hear it everyday-Eat more fiber to reduce your cholesterol! Any modification of your cholesterol levels must begin with the laboratory testing. The laboratory testing for cholesterol has become increasingly complicated and is now a veritable alphabet soup of different fat proteins. Collectively, they are known as lipids. The lipid panel usually includes the following:
- Cholesterol
- HDL
- LDL
- Triglycerides
Additional tests may include:
- VLDL
- Apolipoprotein A-1 and B
- Homocysteine
- C-reactive protein
ANALYTICAL METHOD LDLMost methodes have derived this using the Friedewald formula wich depends upon the total cholesterol, HDL, and TG-use of this formula in postprandial samples may underestimate levels by as much as 20%-the reason is mobilization of cholesterol out of LDL and HDL and into chylomicrons and VLDL
Direct measurement should be able to measure non fasting samples
BIOCHEMICAL THEORY See below IDEAL TESTING STATE Nine hour fast but a 12-14 hour fast after a low-fat, low-calorie meal, with no intake of alcohol for 24 hours is preferable REFERNCE RANGE JAMA 2001;285:2486-2497
Current Recommendations for Adults from the National Cholesterol Education Program (NCEP) Third Report
Total Cholesterol (TC)>240 mg/dL
>6.2 mmol/L Low Density Lipoprotein (LDL-C)Optimal <100 mg/dL
Near or above optimal (100-129 mg/dL)
Borderline High (130-159 mg/dL)
High (160-189 mg/dL)
Very High (>/= 190 mg/dL) High Density Lipoprotein (HDL)>40 mg/dL Triglyceride (TG)>/=150 mg/dL borderline
>/=400 mg/dL (4.5 mmol/L) elevated
>/=1000 mg/dL (11.3 mmol/L) very elevated Additional PointsCurrent guidelines raises those with diabetes to an equivalent risk level for heart attack as those with coronary heart disease
Recommends treatment for beyond LDL lowering for those with TG >/= 200 mg/dL
Encourages use of plant stanols/sterols and viscous soluble fiber as a therapeutic dietary optionPOSSIBLE NEW TESTS Lipoprotein (a) JAMA 1996;276:544-548
JAMA 1994;271:999-1003Elevated levels associated with increased risk in many studies, but not all-independent from other lipoproteins
Composed of an LDL with an extra lipoprotein called apo(a) attached by a disulfide bond to apo B-100
Apo(a) is heterogenous in length because of a genetically variable repeating peptide sequence called kringles (MW varying from 185-650 kDa)
>75% homology to plasminogen suggesting that it interferes with plasminogen binding and disrupts the fibrinolytic cascade
Measurments are for apo(a) protein content which is then converted to total particle mass or for cholesterol concentration, similar to LDL or HDL
Assay uses the high degree of glycosylation by binding Lp(a) to lectin, eluting, then measuring cholesterol
Triglyceride rich lipoprotein remnants (TRL) Lipoproteins containing the greatest proportion of triglyceride including chylomicrons, chylomicron remnants, VLDL, VLDL remnants, and intermediate density lipoproteins (IDL) Homocysteine N Engl J Med 1998;338:1009-1015
Addition of folate reduced levels leading to decreased risk of CVD
C-reactive protein N Engl J Med 2000;342:836-843
Ultrasensitive measurment has revealed a very small rise may indicate higher levels of risk for CVD
CLINICAL UTILITY CHARACTERIZATION Veterans Affairs HDL Intervention Trial (VA-HIT) showed utility in raising HDL levels N Engl J Med 1999;341:410-418
2500 men with coronary artery disease and relatively normal baseline levels of LDL, cholesterol, TG, but low HDL levelsSignificant reduction in both primary and secondary endpoints in men with CAD when HDL was raised using gemfibrozil therpay
Raising HLD lowers risk without a change in LDL
7.5% increase in HDL and 24.5% decrease in TG associated with 22% decrease in coronary events and a 25% decrease in stroke
INTERFERING DISEASES OR SUBSTANCES THAT ELEVATE LEVELS CHARACTERIZATION Posture Ideally, patient should be sitting for at least 20 minutes before sample is taken Standing vs. lying down TC 10% higher
TG 12% higher
HDL 7% higher
INTERFERING DISEASES OR SUBSTANCES
THAT DECREASE LEVELSCHARACTERIZATION Postprandial levels HDL may be slightly lower Clinical Diagnosis and Management by Laboratory Methods. 20th Edition. Henry JB. WB Saunders 2001.
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