Hypertriglyceridemia Treatment & Management

  • Author: Elena Citkowitz, MD, PhD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: Jan 5, 2010
 

Medical Care

The latest Adult Treatment Panel guidelines (ATP III) have reclassified serum triglycerides as follows:

Table 2. Classification of Triglycerides (TG) (Open Table in a new window)

ClassificationTG level, mg/dL
Normal TG level< 150
Borderline-high TG level150-199
High TG level200-499
Very high TG level>500

If triglycerides are 500 or above, their treatment takes priority over LDL treatment to prevent pancreatitis, unless the patient has a high risk for an acute CAD event, in which case simultaneous treatment for both conditions should be considered.

If the secondary conditions that raise triglyceride levels cannot be managed successfully and if triglycerides are 200-499 mg/dL, the non–HDL-c (total cholesterol - HDLc) can be used as the initial target of using LDL-lowering medication. The non–HDL-c is the sum of the cholesterol carried by the atherogenic lipoproteins, LDL, VLDL, and IDL. The goals for non–HDL-c levels, similar to those for LDL-c levels, are dependent on risk and are 30 mg/dL higher than the corresponding LDL-c goals. The classification of LDL-c and non–HDL-c is as follows:

Table 3. Classification of LDL Cholesterol and Non-HDL Cholesterol (Open Table in a new window)

ClassificationLDL Goal,



mg/dL



Non-HDL Goal,



mg/dL



CHD* and CHD risk equivalent, diabetes mellitus, and the following:10-year risk for CHD >20%< 100< 130
Two or more risk factors and the following:10-year risk < 20%< 130< 160
0-1 risk factor< 160< 190
*Coronary heart disease

When hypertriglyceridemia is diagnosed, secondary causes should be sought out and controlled. If the triglyceride level is below 500 mg/dL, triglyceride-lowering medication may be withheld while secondary causes are managed. For example, lowering a substantially elevated HbA1c may normalize the triglycerides; or at least facilitate their treatment.

The importance of obesity, a sedentary lifestyle, very high fat diet, and intake of large concentrations of refined carbohydrates should not be underestimated as causes of severe hypertriglyceridemia. Instituting a program of progressive aerobic and toning exercise, weight loss, and dietary management can significantly lower triglyceride levels and, in some cases, normalize them.

During pregnancy, severe hypertriglyceridemia is an unusual complication and may cause pancreatitis.

  • Many case reports have been published describing interventions to manage this condition.
  • Most commonly, a very low-fat diet was sufficient to control triglycerides and prevent pancreatitis.
  • Intermittent and, in persistent cases, continuous total parenteral nutrition has been used—usually in the third trimester.
  • Reports also have been published describing plasma exchange or apheresis, as well as early third trimester termination of pregnancy by cesarean section.
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Consultations

If the primary care provider cannot control a patient's triglycerides, referral should be made to a lipidologist or endocrinologist with expertise in treating severe and difficult-to-manage lipid disorders.[10]

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Diet

  • Total fat intake should be restricted if this intervention assists in weight loss. If triglyceride levels are greater than 1000 mg/dL, allowing no more than 10% of total calories from fat will usually lower triglycerides promptly and dramatically.
    • Fat restriction is a 2-edged sword. Reducing fat intake causes needed weight loss, and triglycerides usually improve. When triglycerides are severely elevated (>1000 mg/dL), suggesting impaired or absent LPL activity, a low-fat diet decreases chylomicron and VLDL production and improves the metabolism of these triglyceride-rich lipoproteins.
    • On the other hand, in the setting of stable weight and moderately elevated triglycerides, a very low-fat diet increases triglycerides and may, in addition, decrease HDL-c levels. Patients who are extremely compliant and motivated may choose to follow such a diet in the hope of improving their cholesterol levels. If they have a mixed hyperlipidemia, their LDL-c certainly will decrease. However, such a diet will, if anything, cause further deterioration in the HDL-c and triglycerides. If the patient has an isolated triglyceride elevation and does not lose weight on the diet, the triglycerides may increase. In such cases, addition of a healthy fat (monounsaturated or polyunsaturated fat) lowers triglycerides, increases HDL-c, and sometimes decreases LDL-c.
  • In cases in which dietary intake of sugar and white flour products is substantial, restricting simple carbohydrates and increasing dietary fiber are important adjuncts that can lower triglycerides substantially.
  • Large quantities or fruit juice or non-diet soda can increase triglycerides dramatically.
  • Alcohol should be eliminated or restricted to no more than 1 standard alcoholic beverage per day.
  • Omega-3 (N-3) fatty acids
    • The class of polyunsaturated fats known as omega-3 fatty acids, which are derived mainly from fatty fish and some plant products (flax seed), has a unique impact on triglycerides.
    • In large amounts (10 or more g/d), N-3 fatty acids lower triglycerides 40% or more.
    • To achieve this dose, purified capsules are usually necessary, but some patients may prefer to eat large quantities of fatty fish. The fish highest in N-3 fatty acids are sardines, herring, and mackerel; daily servings of 1 pound or more may be necessary.
    • If weight gain ensues, triglyceride lowering will be compromised.
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Activity

  • Exercise, particularly sustained aerobic activity, can have a dramatic impact on triglyceride levels and may increase HDL-c slightly.
  • The American Heart Association recommends 30-60 minutes of aerobic exercise most days of the week and toning for 20-30 minutes twice a week. This prescription has substantial benefits beyond lipid effects as follows:
    • Reduced weight
    • Decreased insulin resistance
    • Decreased blood pressure
    • Improved cardiovascular conditioning
  • Overall reduction in acute cardiovascular events is also a likely benefit of regular exercise.
  • Toning of large muscles groups (abdomen, back, legs, arms) also improves metabolism of triglyceride-rich lipoproteins and lowers triglycerides.
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Contributor Information and Disclosures
Author

Elena Citkowitz, MD, PhD, FACP  Clinical Professor of Medicine, Yale University School of Medicine; Director, Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael

Elena Citkowitz, MD, PhD, FACP is a member of the following medical societies: American College of Physicians, American Heart Association, National Lipid Association, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Steven R Gambert, MD  Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric Medicine, University of Maryland Medical Center and R. Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Yoram Shenker, MD  Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison

Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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Eruptive xanthomas on the back of a patient admitted with a triglyceride level of 4600 mg/dL and acute pancreatitis.
Close-up of eruptive xanthomas.
Composition of triglyceride-rich lipoproteins.
Lipoprotein lipase (LPL) releases free fatty acids from chylomicrons and produces chylomicron remnants that are small enough to take part in the atherosclerotic process.
Once very low-density lipoprotein (VLDL) has been metabolized by lipoprotein lipase, VLDL remnants in the form of intermediate-density lipoprotein (IDL) can be metabolized by hepatic lipase, producing LDL, or they can be taken up by the LDL receptor via either apolipoprotein B (apo B) or apo E.
Table 1. Fredrickson Classification of Hyperlipoproteinemia
Type Serum elevation Lipoprotein elevation
ICholesterol and triglyceridesChylomicrons
IIaCholesterolLDL*
IIbCholesterol and triglyceridesLDL, VLDL**
IIICholesterol and triglyceridesIDL***
IVTriglyceridesVLDL
VCholesterol and triglyceridesVLDL, chylomicrons
*LDL (low-density lipoprotein)



**VLDL (very low-density lipoprotein)



***IDL (intermediate-density lipoprotein)



Table 2. Classification of Triglycerides (TG)
ClassificationTG level, mg/dL
Normal TG level< 150
Borderline-high TG level150-199
High TG level200-499
Very high TG level>500
Table 3. Classification of LDL Cholesterol and Non-HDL Cholesterol
ClassificationLDL Goal,



mg/dL



Non-HDL Goal,



mg/dL



CHD* and CHD risk equivalent, diabetes mellitus, and the following:10-year risk for CHD >20%< 100< 130
Two or more risk factors and the following:10-year risk < 20%< 130< 160
0-1 risk factor< 160< 190
*Coronary heart disease
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