eMedicine Specialties > Endocrinology > Metabolic Disorders
Hypertriglyceridemia: Treatment & Medication
Updated: Jul 12, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
The latest Adult Treatment Panel guidelines (ATP III) have reclassified serum triglycerides as follows:
Table 1. Classification of Triglycerides (TG)
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Table
| Classification | TG Level, mg/dL |
|---|---|
| Normal TG level | <150 |
| Borderline-high TG level | 150-199 |
| High TG level | 200-499 |
| Very high TG level | >500 |
| Classification | TG Level, mg/dL |
|---|---|
| Normal TG level | <150 |
| Borderline-high TG level | 150-199 |
| High TG level | 200-499 |
| Very high TG level | >500 |
If triglycerides are 500 or above, their treatment takes priority over LDL treatment to prevent pancreatitis.
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 2. Classification of LDL Cholesterol and Non-HDL Cholesterol
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Table
| Classification | LDL 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 | |
| Classification | LDL 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.
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.
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.
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.
Medication
Three classes of medications are appropriate for major triglyceride elevations; fibric acid derivatives, niacin, and omega-3 fatty acids. High-doses of a strong statin (simvastatin, atorvastatin, rosuvastatin) also lower triglycerides as much as approximately 50%.
Currently 3 fibrates are used clinically; 2 are available in the United States, gemfibrozil (Lopid), which is now generic, and fenofibrate (multiple brand names). Bezafibrate, available in Europe and elsewhere, has not been approved by the U.S. Food and Drug Administration (FDA).8 The oldest fibrate, clofibrate, is no longer used because of increased morbidity or mortality rates in large placebo-controlled studies (the World Health Organization [WHO] study and the Coronary Drug Project). Moreover, tumorigenicity has been demonstrated in rodents.
Gemfibrozil has been used in 2 major randomized placebo-controlled clinical trials—the Helsinki Heart Study and the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT). In a subset of men in the Helsinki study with elevated LDL-c levels and mildly elevated triglycerides greater than 204 mg/dL, a 70% reduction in coronary events was found compared with men with triglycerides less than 204 mg/dL.9 The VA-HIT studied men with coronary heart disease with relatively normal LDL-c and triglyceride levels but with HDL-c levels less than 31 mg/dL. The LDL-c did not change in the treatment group or the control group, but the small increase in HDL-c and decrease in triglycerides experienced by the treatment group resulted in a significant reduction of coronary events compared with controls.10
Niacin (vitamin B-3) in large doses decreases triglycerides at least 40% and can raise HDL-c levels 40% or more. Niacin also reliably and significantly lowers LDL-c levels, and the other major triglyceride-lowering medications do not. In the Coronary Drug Project (a randomized placebo-controlled trial of secondary prevention in men), niacin reduced coronary events compared with placebo.
Niacin has multiple adverse effects, the worst of which is chemical hepatitis. However, at doses of 1.5-2 g/d, complications are unusual. Sustained-release niacin is more hepatotoxic than immediate-release niacin but is better tolerated.11 Flushing, itching, and rash are expected adverse effects that are less common with long-acting formulations. These symptoms are an annoyance but are not life threatening and may be minimized by starting at low doses and increasing slowly. Switching from immediate-release niacin to an equal dose of time-release preparation has been reported to cause severe hepatotoxicity. Niacinamide, also called vitamin B-3, has no lipid-lowering effects; nor does inositol hexanicotinate.
Omega-3 fatty acids are attractive because of their low risk of major adverse effects or interaction with other medications. At very high doses (4 or more g/d), triglycerides are reduced. The triglyceride-lowering impact of fish oils is entirely dependent on the omega-3 content, and, therefore, the number of capsules required for a total dose of 4 g/d requires determining the content of eicosapentaenoic (EPA) and docosahexaenoic (DHA) per capsule. Over the counter fish oil capsules vary in concentration from approximately 0.4 g to 1.0 g of EPA +DHA per capsule. Therefore, a minimum dose of 4 g of omega-3 fatty acids per day may require 8 or more capsules.
A prescription fish oil capsule was approved by the FDA for triglyceride levels greater than 400 mg/dL. Originally called Omacor, it was renamed Lovaza in 2007. One 1-g capsule contains approximately 465 mg of EPA and 375 mg of DHA. High-dose fish oil increases LDL-C levels; the impact on HDL-c levels is variable. The cost is substantially higher than that of over the counter fish oil and is usually not covered by insurance companies.
For patients with mixed hyperlipidemias (elevations of both LDL-c and triglycerides), a moderate dose of a hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitor may be appropriate if the amount of triglyceride lowering necessary is only about 20%. Maximum doses of the strongest statins, atorvastatin, simvastatin, rosuvastatin, or cerivastatin (recalled from US market 8/8/01), lower triglycerides approximately 40%, but such doses are not appropriate unless the LDL-c is at least 30% above the desired level.
Bile acid sequestrants (cholestyramine or colestipol) raise triglyceride levels and are not appropriate therapy for hypertriglyceridemia. However, in patients with a mixed hyperlipidemia, resins may be combined with niacin or a fibric acid derivative.
Patients with the metabolic syndrome are often treated with metformin, which not only improves impaired fasting glucose levels, but also lowers triglycerides.
Fibric acid derivatives
Fibric acid derivatives lower triglycerides approximately 40% and increase HDL-c about 20%. Fenofibrate is reported to lower LDL-c levels more reliably than either clofibrate or gemfibrozil, but none of the drugs in this class should be used for isolated LDL-c elevations. The fibrates are commonly used to treat hyperlipidemias types IV (high VLDL) and V (high VLDL and chylomicrons), as well as type III dysbetalipoproteinemia (IDL or VLDL remnant disease).
They can also be used to treat type IIb mixed hyperlipidemia if used in conjunction with an LDL-lowering medication such as a resin.
Gemfibrozil (Lopid)
Lowers TGs and raises HDL-c. LDL-c is usually is unaffected but may increase if initially low or decrease if initially high. Available in generic formulation, most cost-effective fibrate at this time. FDA-approved indications are for type IV and V hyperlipidemia, ie, elevations in VLDL only or both VLDL and chylomicrons.
Adult
600 mg PO bid, ideally 30 min ac
To limit side effects, begin with 300 mg bid for 1-2 wk before increasing to 600 mg bid
Pediatric
Not established
May potentiate effects of warfarin; monitor closely if coadministered with lovastatin therapy
Documented hypersensitivity; active liver or gall bladder disease; severe renal dysfunction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Possible dose adjustment may be necessary in elderly patients or people with decreased renal function; mild and, rarely, more severe decreases in RBC, WBC, or platelets have been observed; periodic monitoring of CBC during first year of therapy is recommended; no increased risk for hepatic carcinoma or cholelithiasis has been documented for gemfibrozil; risk of concomitant gemfibrozil and statins therapy may outweigh benefits, but numerous literature citations document safety of such treatment in patients with mixed hyperlipidemia and significant risk of CAD
Fenofibrate (Tricor)
Similar to other fibric acid derivatives in TG-lowering and HDL-raising effects. Differs in that modest LDL-lowering can be expected with greater frequency than with gemfibrozil. The FDA-approved indications are for hypertriglyceridemia and hypercholesterolemia, but this difference does not qualify fenofibrate for treatment of isolated LDL-c elevations. Taken once a day. May increase compliance.
Adult
200 mg capsule PO qd with meals or its equivalent, 160 mg tablet PO qd with meals
Pediatric
Not established
Instruct patients to report complaints of myalgia, tenderness, and myasthenia; perform creatine kinase determinations and renal function assessment, including serum creatinine
Documented hypersensitivity; active liver or gall bladder disease; severe renal dysfunction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Instruct patients to report complaints of myalgia, tenderness, and myasthenia; perform creatine kinase determinations and renal function assessment, including serum creatinine
Niacin (nicotinic acid)
At least 1.5 g/d decreases triglycerides as much as about 50%. Substantial HDL-c increases of 30% or more can be achieved, particularly at higher doses. LDL-c will decrease 15-25%. Whether OTC or by prescription, it costs less than any other lipid-lowering medication. For reasons not clearly understood, changing brands during treatment is more likely to cause hepatotoxicity, occurring more so with time-release than immediate-release niacin.
Sustained-release niacin (Vitamin B-3)
More hepatotoxic than immediate-release niacin. Patients strongly advised against switching formulations or brands during treatment. Both OTC and prescription formulas are available. OTC brands cost less, but only reliable manufacturers should be recommended. Slo-Niacin is OTC formulation available in 250-mg, 500-mg, and 750-mg tablets. Sundown is another manufacturer. Prescription SR niacin (Niaspan) is available in 375-mg, 500-mg, and 1000-mg tabs.
Adult
Niaspan dosage schedule:
500 mg PO qhs with a small snack for 1 mo
1000 mg PO qhs with a small snack for 1 mo
1500 mg PO qhs with a small snack for 1 mo
2000 mg PO qhs with a small snack for 1 mo
Other SR formulations of niacin usually require bid dosing beginning with smallest dose available and gradually increasing to total dose; not to exceed 3 g/d
Pediatric
Not established
Cutaneous vasodilation may be a problem if high dose is used with peripheral dilators, such as nitroglycerine; taking aspirin 30-60 min before first dose of the day may help alleviate prostaglandin-mediated adverse effects of niacin (eg, flushing, itching); clonidine may inhibit niacin-induced flushing
Documented hypersensitivity; active liver disease or unexplained, significant increases in AST and ALT; large doses of niacin, especially when administered in an SR form are associated with severe hepatotoxicity; in patients who have a definite and recent history of peptic ulcer disease, therapy can reactivate ulcers
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
A serious and life-threatening complication is chemical hepatitis; if AST/ALT levels increase to >3 times ULN, stop immediately; transaminase abnormalities resolve within a wk; frequent AST/ALT monitoring (quarterly) is mandatory at doses >1 g/d; if AST/ALT levels rise above 3 times ULN, stop and monitor until return to normal
More importantly than with IR niacin, patients should be strongly counseled to not change formulations or brands of SR niacin; if change is necessary, dose should be dropped back to initial recommended dose for SR niacin, with gradual titration over several weeks or months to former final dose; changing brands at a high dose (>1.5 g/d) has been reported to cause severe chemical hepatitis and even fulminant hepatic failure
Dyspepsia is most common adverse effect, more common with IR than SR (symptoms often are extremely bothersome and worrisome for patients); if initially started at small doses and gradually increased, symptoms often can be tolerated and eventually may resolve (tachyphylaxis); ethanol or hot drinks can exacerbate flushing; flushing may be minimized if taken after meals or if 325 mg of aspirin is taken 30-60 minutes before each dose; most serious complication is exacerbation of PUD
May cause variety of GI adverse effects, most frequently benign dyspepsia; patients with elevated uric acid levels or history of gout should be treated with caution; patients with gout whose uric acid levels have been normalized with allopurinol may be treated if uric acid levels are followed closely; advise to refrain from consumption of excess quantities of alcohol; can cause small increases in fasting glucose levels in some patients without and with diabetes (should be prescribed cautiously in patients with known type 2 diabetes mellitus)
Immediate-release niacin (Niacor and Nicolar)
Less hepatotoxic than SR niacin but less well tolerated by patients due to prostaglandin-mediated flushing, itching, and rash. Therapy started at a low dose, such as 100 mg tid pc, and increased gradually over several weeks will allow some patients to accommodate adverse effects. At high doses (4-6 g/d), it is less hepatotoxic than SR niacin. Changing formulation at high dose may increase risk of hepatotoxicity. Niacor and Nicolar are prescription formulations that, while more expensive than OTC brands, may have an advantage in making it less likely that the patient switches brands.
Adult
100 mg PO tid pc initially; at weekly intervals, increase by 100 mg tid; after the fourth week, at a dose of 500 mg tid, a 500-mg tab may be substituted for smaller tabs; after at least 2 mo, 500 mg tid, dose may be increased by 500 mg/d every 2 mo; usual daily dose is 1.5-3 g/d; not to exceed 6 g/d
Pediatric
Not established
Cutaneous vasodilation may be a problem if high dose is used with peripheral dilators, such as nitroglycerine; taking aspirin 30-60 min before first dose of the day may help alleviate prostaglandin-mediated adverse effects of niacin (flushing, itching, etc); clonidine may inhibit niacin-induced flushing
Documented hypersensitivity; active liver disease or unexplained, significant increases in AST/ALT; high-dose niacin, especially SR form, has been associated with severe hepatotoxicity; in patients with a definite and recent history of peptic ulcer disease, therapy can reactivate ulcers
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Serious and life-threatening complication is chemical hepatitis; if AST/ALT increase to >3 times ULN, stop immediately; transaminase abnormalities resolve within a week; frequent AST/ALT monitoring (quarterly) is mandatory at doses >1 g/d; if AST/ALT levels rise above 3 times ULN, stop and monitor until return to normal
More importantly than with IR niacin, patients should be strongly counseled to not change formulations or brands of SR niacin; if change is necessary, dose should be dropped back to initial recommended dose for SR niacin, with gradual titration over several weeks or months to former final dose; changing brands at a high dose (>1.5 g/d) has been reported to cause severe chemical hepatitis and even fulminant hepatic failure
Dyspepsia is most common adverse effect, more common with IR than SR (symptoms often are extremely bothersome and worrisome for patients); if initially started at small doses and gradually increased, symptoms often can be tolerated and eventually may resolve (tachyphylaxis); ethanol or hot drinks can exacerbate flushing; flushing may be minimized if taken after meals or if 325 mg of aspirin is taken 30-60 minutes before each dose; most serious complication is exacerbation of PUD
May cause variety of GI adverse effects, most frequently benign dyspepsia; patients with elevated uric acid levels or history of gout should be treated with caution; patients with gout whose uric acid levels have been normalized with allopurinol may be treated if uric acid levels are followed closely; advise patients to refrain from consumption of excess quantities of alcohol; can cause small increases in fasting glucose levels in some patients without and with diabetes (should be prescribed cautiously in patients with known type 2 diabetes mellitus)
Omega-3 fatty acids
These agents reduce triglyceride biosynthesis.
Omega-3-acid ethyl esters (Lovaza)
First prescription omega-3-acid. Each 1-g cap contains at least 900 mg of omega-3-acid ethyl esters, predominantly a combination of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Theorized to reduce triglyceride synthesis in the liver. EPA and DHA are poor enzyme substrates for triglyceride synthesis in the liver, and they inhibit esterification of other fatty acids. Potential mechanisms of action include acyl CoA:1,2-diacylglycerol acyltransferase inhibition, increased hepatic mitochondrial and peroxisomal beta-oxidation, decreased hepatic lipogenesis, and increased plasma lipoprotein lipase activity.
Clinical trials show significant reduction in non–high-density lipoprotein cholesterol (HDL-C), triglycerides, total cholesterol, very low-density lipoprotein cholesterol (VLDL-C), and apolipoprotein B levels from baseline when combined with simvastatin compared with simvastatin and placebo. Monotherapy with omega-3-acid ethyl esters reduce median triglyceride, VLDL-C, and non–HDL-C levels from baseline.
Indicated as adjunctive treatment to diet to reduce very high triglyceride levels (ie, >500 mg/dL).
Adult
4 g PO qd; alternatively, 2 g PO bid
Pediatric
<18 years: Not established
>18 years: Administer as in adults
May prolong bleeding time when coadministered with anticoagulants
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Confirm by laboratory studies that triglyceride levels are consistently abnormal; first attempt to decrease hypertriglyceridemia by diet, exercise, weight loss (if overweight), and control of medical problems (eg, diabetes mellitus, hypothyroidism); if possible, discontinue medications known to exacerbate hypertriglyceridemia (eg, beta-blockers, thiazides, estrogens); may elevate low-density lipoprotein cholesterol and non–HDL-C levels in some individuals
More on Hypertriglyceridemia |
| Overview: Hypertriglyceridemia |
| Differential Diagnoses & Workup: Hypertriglyceridemia |
 Treatment & Medication: Hypertriglyceridemia |
| Follow-up: Hypertriglyceridemia |
| Multimedia: Hypertriglyceridemia |
| References |
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Further Reading
Keywords
hTG, chylomicronemia, dysbetalipoproteinemia, familial combined hyperlipoproteinemia, hyperlipidemia, hyperlipoproteinemia, mixed hyperlipidemia, type I hyperlipoproteinemia, type IIb hyperlipoproteinemia, type III hyperlipoproteinemia, type IV hyperlipoproteinemia, type V hyperlipoproteinemia, triglycerides, diabetes mellitus, DM, coronary artery disease, CAD, cardiovascular disease, CVD
