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with Michael Richman, MD, FACS

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Thursday, June 10, 2010

Understanding and Treating Triglyceride Disorders (Part 1)

My good friend Tom Dayspring, MD, who is a noted lipidologist and co-author of my book, Lipid and Lipoprotein Disorders: Current Clinical Solutions, wrote this wonderful piece on triglycerides. I thought I would share it with everyone and in some areas, make some changes to make it more understandable to non-medical personnel.

Triglycerides (TG), the so-called forgotten lipid, are so very important to both human life and unfortunately, to atherogenesis (the formation of plaques in the artery walls). Of course, the correct term is triacylglycerol. Three acyl groups (fatty acids) are attached to a glycerol molecule. Triglycerides are an archaic term, which we all keep using. Serum TG refers to all of the TG trafficked within all of the lipoproteins that exist in a deciliter of plasma.

A physiologic TG level is 10-70 with a mean of 30 mg/dL. NCEP ATP-III (National Cholesterol Education Panel-Adult Treatment Panel III) stated that unless pathological conditions are present, the TG should be < 100 mg/dL. With respect to cardiovascular risk, they stated borderline risk is > 150 mg/dL, high risk > 200 mg/dL and very high risk > 500 mg/dL when pancreatitis enters the picture. There is no specific NCEP ATP-III TG goal of therapy, but it is suggested that non-HDL-C be normalized in patients with high TG or high TG and low HDL-C. Persons with significant TG abnormalities can have a multitude of genetic perturbations and many but not all have coexisting insulin resistance. NCEP ATP-III states that anyone with a TG > 100 mg/dL likely overeats, does not exercise, smokes, has diabetes, renal or other metabolic diseases, is on certain drugs or if the TG is >200 mg/dL has genetic forces at play.

Genetic Triglyceride disorders are classified as:

Moderate Hypertriglyceridemia

  • Familial combined hyperlipidemia (FCH – Fredrickson Type IIB, IV or V)
  • Familial Dysbetalipoproteinemia (Fredrickson Type III)
  • Familial Hypertriglyceridemia (FHTG): usually not associated with CV risk

Very High Hypertriglyceridemia

  • Severe chylomicronemia (deficiency of apoCII) (Fredrickson Type I)
  • Familial Lipoprotein Lipase Deficiency (Fredrickson Type V)

Persons with FCH (familial combined hyperlipidemia) often have coexisting elevations of cholesterol level due to high VLDL-C or chylomicron-C. FCH can meet the Fredrickson criteria for Types IIb, IV or V and familial hypertriglyceridemia can be classified as Type IV or V. In Types I and V, chylomicrons are present. An easy way to establish that is to let a red top tube with serum stand overnight: If there a thick dense white band floating on top, then chylomicrons are present. That is a quick way to distinguish Types I and V from IIb or IV.  With VLDL induced hypertriglyceridemia, the serum would be turbid or milky without the dense band on top. In Fredrickson Type III dyslipidemia, the elevated triglyceride is usually associated with higher levels of cholesterol. This disorder is due to increases in small VLDLs and IDL particles associated with the E2 phenotype (available from Berkeley Heart Lab).

Of course, it does not matter whether the person has Type III, IV or V dyslipidemia as the treatment is going to be the same. Other than severe fat restriction and use of dietary supplied medium chain triglycerides (contain fatty acids that can be absorbed directly into plasma without being incorporated into chylomicrons), there is no treatment for Type I. The pharmacologic approach of the other TG disorders is to reduce fatty acid absorption (orlistat), inhibit TG synthesis, enhance TG catabolism (fibrates, high dose N-3 fatty acids and high dose niacin) and to facilitate TG-rich lipoprotein removal through upregulation of LDL receptors (LDLr) (statins, especially high dose atorvastatin or rosuvastatin and ezetimibe). Patients with FHTG simply have very large TG-rich VLDL and/or chylomicron particles but do not have an excess number of such particles. Thus TG can be very high, but apoB is not elevated. The particles are too big to enter the arterial wall: pancreatic risk is present, but atherosclerosis is not a risk due to the normal apoB.

Under conditions of delayed breakdown, plasma (blood) residence time of TG-rich lipoproteins can be significantly extended causing both fasting and postprandial hypertriglyceridemia. TG-tolerance tests in normal humans shows maximal rise in TG at 4 hours with return to normal by 6 hours. A physiologic TG is 10-70 mg/dL with a mean of 30 mg/dL. Four hours after meals or a FA-load, the TG increases to 70 mg/dL with a one standard deviation being up to 170 mg/dL. Any postprandial TG higher than that is abnormal. The most common cause is insulin resistance, which also know as Metabolic Syndrome. Any physician seeing a TG > 170-200 mg/dL must realize the level is abnormal and repeating the TG fasting serves no purpose (other than to get an accurate calculated LDL-C). However if one uses non-HDL-C (total cholesterol-HDL cholesterol) then there is no need to know LDL-C, as non-HDL-C is a better surrogate of atherogenic lipoproteins and is the NCEP goal of therapy in patients with TG between 200-500 mg/dL.

I will be addressing more issues on this topic and the next blog post, Part 2 will deal with explaining the drugs used to treat high triglycerides. There is also considerable information on lipids in the professional and patient sections of my website.

Do you know your triglyceride numbers? Ask your questions and share your comments about this post with the Cholesterol Management Community.

Posted by: Michael Richman, MD, FACS at 1:49 pm

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