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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTI2NTY4LXRyZWF0bWVudA==\nDrugs & Diseases > Endocrinology\nHypertriglyceridemia Treatment & Management\nAuthor: Mary Ellen T Sweeney, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...\nHypertriglyceridemia\nSections Hypertriglyceridemia\nApproach Considerations\nLipid Analysis\nChylomicron Determination\nPharmacologic Therapy\nAdult Treatment Panel Guidelines\nPregnant Patients\nScreening and Prevention\nLong-Term Monitoring\nMedication Summary\nFibric Acid Agents\nOmega-3 Acids\nLipid-Lowering Agents, Other\nLipid-Lowering Agents, Statins\nEven without a definitive diagnosis from the workup, treatment of presumed dysbetalipoproteinemia may proceed, because other lipid disorders, such as type IIb hyperlipidemia produce similar elevations in cholesterol and triglyceride levels and will respond to the same medical interventions.\nIn general, lifestyle modifications (eg, smoking cessation, diet, exercise, weight reduction) are initiated before any pharmacologic therapy in the treatment of primary and secondary dyslipidemia, particularly in patients who are asymptomatic. [45, 34, 41, 46, 42] Weight reduction and a diet low in saturated fat and cholesterol are advocated. Patients should avoid alcohol and estrogen in certain types of hyperlipoproteinemias.\nThe patient’s low-density lipoprotein (LDL) cholesterol level response is measured in 6 weeks to 6 months, depending on the patient's cardiovascular risk factors. Consider an LDL cholesterol goal of less than 70 mg/dL in patients with established coronary artery disease (CAD) or CAD risk equivalents, including clinical manifestations of noncoronary forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and carotid artery disease, transient ischemic attacks or stroke of carotid origin or 50% obstruction of a carotid artery), diabetes, or a Framingham 10-year CAD risk score of greater than 20%. [47]\nConsider pharmacologic therapy if the LDL-C level remains above the following thresholds [47] :\nPatients with low risk, 190 mg/dL or greater\nPatients with moderate risk, 160 mg/dL or greater\nPatients with moderately high risk, 130 mg/dL (option 100 mg/dL) or greater\nPatients with high risk, 100 mg/dL (option 70 mg/dL) or greater\nBecause of the possibility of adverse effects and the question of whether the triglyceride level is an independent risk factor for atherosclerosis, many physicians use drugs to reduce the triglyceride level only when the level exceeds 500 mg/dL. Patients with triglyceride concentrations greater than 1000 mg/dL should receive diet and drug therapy and be closely monitored to prevent pancreatitis.\nPatients first should be treated for the metabolic condition that is causing or exacerbating their hyperlipidemia. If diabetes is present, glucose levels and glycosylated hemoglobin (HbA1c) should be normalized with treatment that meets or exceeds the guidelines of the American Diabetes Association (ADA), if possible. If hypothyroidism is diagnosed, thyroid stimulating hormone (TSH) should be normalized.\nIn managing secondary dyslipidemia, consider statin therapy for all patients, as these agents reduce mortality and coronary heart disease/atherosclerotic cardiovascular disease (CHD/ASCVD) endpoints. [45] High-potency statins (atorvastatin, rosuvastatin) at high doses have greater efficacy in reduction of cardiovascular events than low potency statins or high-potency statins at low doses. [45] However, patients treated with lipid-lowering medications should be carefully monitored for the development of myositis or liver disease. In addition, statin monotherapy is not recommended for severe or very severe hypertriglyceridemia. [42]\nA study by Shimabukuro et al found that the impact on lipoprotein subclass profiles varies between pitavastatin and atorvastatin. Determining the lipoprotein subclass profile and selecting the appropriate statin in patients with diabetes and an additional cardiovascular risk, such as low HDL cholesterol or hypertriglyceridemia may be beneficial. [48, 49, 50, 51]\nDo not start medications that may cause severe hypertriglyceridemia without first checking baseline triglycerides. These drugs may be used in patients with mildly elevated triglycerides and are not absolutely contraindicated in patients with significantly elevated triglycerides. Patients must be closely monitored, and a triglyceride-lowering medication should be instituted, if necessary.\nIleal bypass surgery and plasmapheresis to lower elevated serum lipids are used in selected cases of familial hypercholesterolemia. Only experienced physicians should use these therapies.\nNormally, in patients with acute pancreatitis secondary to severe hypertriglyceridemia, triglyceride levels rapidly decrease, often by 1000 mg/dL each day when treated with standard medical therapy: nothing by mouth (NPO), intravenous (IV) hydration, and if needed, parenteral insulin to reduce plasma glucose levels. If triglyceride levels do not decrease or, more ominously, if they increase, more aggressive intervention with plasmapheresis is probably warranted.\nIf 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. [52]\nOn March 1, 2012, the US Food and Drug Administration (FDA) issued updates to the prescribing information concerning interactions between protease inhibitors (such as those used to treat hepatitis C or human immunodeficiency virus infection) and certain statin drugs, notably that the combination of these agents taken together may raise the blood levels of statins and increase the risk for myopathy. [53] The most serious form of myopathy, rhabdomyolysis, can damage the kidneys and lead to kidney failure, which can be fatal. [53]\nTwo days earlier, on February 28, 2012, the FDA approved important safety label changes for statins, including removal of routine monitoring of liver enzymes from drug labels. [54] Information about the potential for generally nonserious and reversible cognitive side effects and reports of increased blood sugar and glycosylated hemoglobin (HbA1c) levels were added to the statin labels. In addition, the lovastatin label was extensively updated with new contraindications and dose limitations when this agent is taken with certain medicines that can increase the risk for myopathy. [54]\nOn June 8, 2011, the FDA recommended limiting the use of the highest approved dose of simvastatin (Zocor) (80 mg) due to the increased risk of myopathy. [55] The agency also required changes to the simvastatin label to add new contraindications (should not be used with certain medications) and dose limitations for using simvastatin with certain medicines. [55]\nHigh doses of a strong statin (simvastatin, atorvastatin, rosuvastatin) lower triglycerides, by as much as approximately 50%, and raise high-density lipoprotein (HDL) cholesterol. [41] The greater the baseline level of triglycerides the greater the percent triglyceride reduction will be with statin treatment. [56] In addition to statins, 3 classes of medications are appropriate for the management of major triglyceride elevations: fibric acid derivatives, niacin, and omega-3 fatty acids. [41, 46, 56]\nNicotinic acid combined with a statin generally improves low-density lipoprotein (LDL) cholesterol, HDL cholesterol, and triglyceride levels. However, the use of fibric acids has a variable effect on LDL cholesterol despite reducing triglyceride levels and increasing HDL cholesterol levels. [41, 56] In patients with diagnosed coronary artery disease (CAD) at very high risk of recurrent cardiovascular events, it may be necessary to use the combination of a cholesterol-lowering drug with a triglyceride-lowering drug to reach the non-HDL cholesterol goal. [41]\nFibrates\nCurrently, four fibrates are used clinically; two are available in the United States, both in generic formulations: gemfibrozil (Lopid) and fenofibrate (multiple brand names). Bezafibrate and ciprofibrate, available in Europe and elsewhere, have not been approved by the FDA.\nDelayed-release fenofibric acid was approved by the FDA for an indication in which it was coadministered with statin in patients with mixed dyslipidemia and CHD or a CHD risk equivalent in whom optimal statin therapy has been achieved. However, the FDA withdrew approval for this indication when the agency found that, in light of several large trials, \"scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events.\" [57, 58]\nA review of gemfibrozil, fenofibrate, and bezafibrate described their beneficial lipid effects and the association of these drugs with reductions in coronary morbidity and mortality (although no substantial effect on total mortality was found). [59]\nClinical trials have shown that some fibrates cause reversible increases in serum creatinine levels but either have no impact on or slightly decrease albumin excretion. [60] Moreover, the kidney is the primary route for elimination of most fibrates, and dose reductions are indicated for reduced creatinine clearance. The half-life of gemfibrozil is independent of renal function, and it is the drug of choice for patients with chronic kidney disease. [61]\nFenofibrate has been marketed in the United States under multiple brand names, each with different doses; generic fenofibrate is also available in different doses. In addition, micronized and nonmicronized formulations are produced; whether one formulation has any advantage over the other is not clear.\nAll manufacturers provide high- and low-dose fenofibrate tablets. The standard adult dose is always more than 100 mg/d; the lower dose is indicated for patients with renal dysfunction (creatinine clearance < 80). Fibrates are contraindicated in patients with creatine clearance of less than 30. The formulation known as fenofibric acid (Trilipix) was approved by the FDA for use with a statin in mixed dyslipidemia. [62, 63, 59, 60, 61] The older fenofibrate formulation also appears to be safe when combined with a statin.\nHigh-dose niacin (vitamin B-3) (1500 or more mg/d) decreases triglyceride levels by at least 40% and can raise HDL cholesterol levels by 40% or more. [42] Niacin also reliably and significantly lowers LDL cholesterol levels, which the other major triglyceride-lowering medications do not. In the Coronary Drug Project, niacin, in comparison with placebo, reduced coronary events. [64]\nAlthough extended-release niacin had been approved by the FDA for coadministration with statin for treatment of primary hyperlipidemia and mixed lipidemia, the FDA withdrew approval for this indication when the agency found that, in light of several large trials, \"scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events.\" [57, 58]\nNiacin 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. [65] 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.\nIf niacin is prescribed for patients with type 2 diabetes, glucose control should be carefully monitored, modest increases in insulin resistance can occur. [66] In addition, because uncontrolled diabetes can cause hypertriglyceridemia, patients with diabetes mellitus should be treated aggressively to reduce the HbA1c level to less than 7%. Niacin is the best available agent to increase HDL cholesterol. It also lowers lipoprotein (a).\nOmega acids\nOmega-3 fatty acids are attractive because of their low risk of major adverse effects or interaction with other medications. At high doses (≥4 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 acid (EPA) and docosahexaenoic acid (DHA) per capsule. A recent study of nonprescription fish and krill oil capsules available in the United States as dietary supplements showed that the content of DHA ranges from 0.05 to 0.22 mg/g and of EPA from 0.08 to 0.45 mg/g. The labels of the most common fish oil supplement capsules in the United States claim to provide 180 mg of EPA and 120 mg of DHA per capsule. Therefore, a minimum dose of 4 g of omega-3 fatty acids per day may require at least 8-12 capsules. [67]\nLow doses of EPA and DHA (750-1000 mg/d) that do not affect lipid levels have been demonstrated to lower the incidence of fatal coronary events, probably due primarily to its antiarrhythmic properties. [68]\nHowever, the role of omega-3 fatty acid supplements in coronary heart disease (CHD) prevention is controversial, with conflicting results derived from large trials of the fatty acids. For example, a meta-analysis by Aung et al indicated that in high-risk patients, daily supplements of marine-derived omega-3 fatty acids produce no significant reduction in the rate of fatal or nonfatal CHD or other major vascular events. However, a 2017 scientific statement update from the American Heart Association declared it reasonable for omega-3 fatty acid supplementation to be used in patients with prior CHD or heart failure with reduced ejection fraction, while European guidelines state that more evidence is required before use of these supplements can be justified. [69, 70]\nA retrospective study by Kim et al found that, using a baseline triglyceride level of 200-500 mg/dL, patients with hypertriglyceridemia who took omega-3 fatty acid experienced a greater reduction in triglyceride levels after 3 months than did those receiving statin monotherapy. However, the investigators found no significant difference in triglyceride decrease between those patients on omega-3 fatty acid monotherapy and those being administered a combination of omega-3 fatty acid and a statin. The study also found that at a baseline triglyceride level of 500 mg/dL or above, triglyceride reduction did not differ significantly between all the three groups. The study included 2071 patients. [71]\nA retrospective, observational cohort study by Tatachar et al found that even a suboptimal dose of over-the-counter (OTC) fish oil supplement can significantly lower triglyceride levels. The investigators found that in patients who were prescribed 2 g/day of fish oil supplements, triglycerides were reduced by 29%. However, patients in the study who were prescribed fenofibrate or gemfibrozil achieved greater triglyceride reduction, 48.5% and 49.8%, respectively. [72]\nSeveral prescription fish oil capsules have been approved by the FDA to treat triglyceride levels of more than 500 mg/dL. A report by Hilleman and Smer states that omega-3 fatty acid products available in prescription formulations have been found to significantly reduce triglycerides. In patients with baseline triglyceride levels of 500 mg/dL or greater taking 4 g/day of a prescription product, decreases compared with placebo ranged from 12.2% to 51.6%. Unlike the supplements, the prescription products are subject to FDA approval, and their safety and efficacy must be established prior to marketing. Currently, prescription capsules contain either a combination of EPA and DHA or EPA alone. [73] There is some concern regarding the use of DHA in patients with dyslipidemia, since high-dose omega-3 products containing DHA increase LDL cholesterol levels; the impact on HDL cholesterol levels varies.\nIcosapent ethyl (Vascepa), an ultra-pure prescription omega fatty acid, contains an ethyl ester of EPA; capsules have no DHA component. Past studies suggest that highly purified EPA can reduce TG levels without raising LDL cholesterol. [74, 75]\nServing as an adjunct to diet, icosapent has been indicated for lowering TG levels of at least 500 mg/dL. In December 2019, the drug gained FDA approval as adjunctive therapy for cardiovascular event risk reduction in adults whose TG levels are 150 mg/dL or higher and in whom established cardiovascular disease is present (or in whom, in the absence of established cardiovascular disease, diabetes exists, along with two or more additional cardiovascular disease risk factors).\nApproval was largely based on the REDUCE-IT (Reduction of Cardiovascular Events with Icosapent Ethyl - Intervention Trial). The study involved statin-treated patients, all with a history of atherosclerosis or diabetes, in whom TG levels between 135 to just under 500 mg/dL and LDL levels between just over 40 to 100 mg/dL were found. Of 3146 US patients, the primary endpoint—cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, or hospitalization for unstable angina—was reached by 24.7% of those on placebo, compared with 18.2% of patients treated with icosapent ethyl, by median 4.9-year follow-up. [76]\nOther examples of prescription products include Lovaza. A 1-g capsule contains at least 900 mg of ethyl esters of omega-3 fatty acids (~465 mg of EPA and 375 mg of DHA). Another prescription omega-3 fatty acid product, Omtryg, was approved by the FDA in 2014 and contains EPA and DHA in the same amounts as Lovaza. [77]\nThe Multi-center, plAcebo-controlled, Randomized, double-blINd, 12-week study with an open-label Extension (MARINE) trial randomized 229 diet-stable patients with fasting TG levels from 500-2000 mg/dL (with or without background statin therapy) to icosapent 4 g/day, icosapent 2 g/day, or placebo. Results showed that icosapent significantly reduced the TG levels and improved other lipid parameters without significantly increasing the LDL cholesterol levels. Icosapent 4 g/day reduced the placebo-corrected TG levels by 33.1% (n = 76; P< 0.0001) and icosapent 2 g/day by 19.7% (n = 73; P = 0.0051). For a baseline TG level >750 mg/dL, icosapent 4 g/day reduced the placebo-corrected TG levels by 45.4% (n = 28; P = 0.0001) and icosapent 2 g/day by 32.9% (n = 28; P = 0.0016). [78]\nAn omega-3 carboxylic acid product (Epanova) was approved by the FDA in May 2014. [79] It is the first prescription omega-3 product in free fatty acid form. It is indicated as an adjunct to diet to reduce triglyceride levels in adults with severe hypertriglyceridemia (TGs ≥500 mg/dL).\nApproval was based on data from the Phase III EVOLVE (EpanoVa fOr Lowering Very High triglyceridEs) trial. The trial showed a significant decrease in non-HCL-C, ratio of total cholesterol to HDL-C, VLDLs, Apo-C, phospholipase A2, and arachidonic acid with omega-3 carboxylic acids over a 12-week period compared with olive oil in patients with TGs ≥500 mg/dL. [80]\nVascazen, a medical food derived from fish oil, is also available. Each 1-g Vascazen capsule contains at least 900 mg of ethyl esters of omega-3 fatty acids sourced from fish oils and includes approximately 680 mg of EPA and approximately 110 mg of DHA.\nNote that although fatty fish (eg, salmon, tuna, trout, mackerel, sardines) are good sources of omega-3 fatty acids, they also usually contain high concentrations of mercury and polychlorinated biphenyls (PCBs). Fish oil supplements that can be obtained without a prescription have negligible amounts of mercury. [86] The advantage of prescription fish oil is that fewer capsules are necessary to achieve a therapeutic dose, facilitating adherence. Additionally, the prescription products have been thoroughly tested in phase 3 trials to show safety and efficacy (particularly for lowering very high TGs). [78, 80] [77, 79] Consistency of potency is ensured with the prescription fish oil products.\nHMG-CoA reductase inhibitors (statins)\nFor patients with mixed hyperlipidemias (elevations of both LDL cholesterol 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, and rosuvastatin, lower triglycerides approximately 40%, but such doses are not appropriate first-line therapy unless triglycerides are less than 500 mg/dL and LDL-C is elevated. [42, 81]\nIt is recommended that patients intolerant to one statin (eg, owing to myalgias) try the other statins before excluding the entire class, particularly in secondary prevention of dyslipidemias. [41] If the patients cannot take statins other agents suitable for management of mixed dyslipidemia may be tried, either alone or in combination therapy, including niacin, fibric acids, and ezetimibe. [41] Bile acid sequestrants can raise triglycerides and are contraindicated in patients with very high triglycerides. [56]\nNote the following [41] :\nStatins are more effective when taken at bedtime or in the evening\nAlthough lovastatin should be taken with food to maximize its absorption, the sustained-release formulation should be taken on an empty stomach\nA major reduction in HDL may occur in some patients on combined therapy with fibrates and thiazolidinediones (check HDL levels 1-2 mo following initiation of this combination therapy)\nDo not adjust dosing regimens more often than every 4 weeks after a fasting lipid panel has been obtained\nA study by Jun et al found that treatment with omega-3 fatty acid and atorvastatin more effectively lowered triglyceride levels in patients than did atorvastatin therapy alone. The report involved adults with fasting triglyceride levels of 200 mg/dL or above but less than 500 mg/dL, and low-density lipoprotein (LDL) cholesterol levels of below 110 mg/dL. Patients underwent 8 weeks of daily treatment consisting of either 4000 mg of omega-3 fatty acid and atorvastatin calcium 20 mg or atorvastatin calcium 20 mg plus placebo. The report found that 62.9% of individuals in the omega-3/atorvastatin group achieved triglyceride levels of less than 200 mg/dL, compared with 22.3% of the monotherapy group. [82]\nBile 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 fibrate.\nPatients with the metabolic syndrome are often treated with metformin, which improves impaired fasting glucose levels, frequently causes modest weight loss, and can lower triglyceride levels.\nEzetimibe (Zetia) is a selective cholesterol-absorption inhibitor that has been used as secondary therapy in the management of dyslipidemia, such as in the following clinical situations [41] :\nHigh LDL, low HDL (< 40 mg/dL), and high triglycerides (>200 mg/dL)\nHigh LDL, regardless of whether the HDL level is lower than 40 mg/dL or not\nThe Adult Treatment Panel guidelines (ATP III) were published in 2001 and reclassified serum triglycerides (TGs), as shown in Table 2 (below). An update to the ATP III guidelines (ATP IV) was published in 2013. [83]\nTable 2. Classification of Triglycerides (Open Table in a new window)\nTG level, mg/dL\nNormal triglyceride level\nBorderline-high triglyceride level\nVery high triglyceride level\nSource: National Cholesterol Education Program. Executive summary of the third report of The National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA. May 16 2001;285(19):2486-97. [14]\nIf triglycerides are 500 or above, their treatment takes priority over low-density lipoprotein (LDL) treatment to prevent pancreatitis, unless the patient has a high risk for an acute coronary artery disease (CAD) event, in which case simultaneous treatment for both conditions should be considered.\nIf the secondary conditions that raise triglyceride levels cannot be managed successfully and if triglycerides are 200-499 mg/dL, the non–high-density lipoprotein (HDL) cholesterol (total cholesterol – HDL) can be used as the initial target of using LDL-lowering medication (see Table 3, below). The non–HDL cholesterol is the sum of the cholesterol carried by the atherogenic lipoproteins, LDL, very low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL). The goals for non–HDL levels, similar to those for LDL levels, are dependent on risk and are 30 mg/dL higher than the corresponding LDL goals.\nTable 3. Classification of LDL Cholesterol and Non-HDL Cholesterol (Open Table in a new window)\nLDL Goal,\nmg/dL\nNon-HDL Goal,\nCHD and CHD risk equivalent, diabetes mellitus, and the following:\n10-year risk for CHD >20%\nTwo or more risk factors and the following:\n10-year risk < 20%\n0-1 risk factor\nCHD = coronary heart disease; LDL = low-density lipoprotein; HDL = high-density lipoprotein.\nWhen 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.\nThe 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. A dietitian or knowledgeable physician should counsel the patient. 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.\nIt is recommended that individuals consume less than 20% of calories as fat, with saturated fat reduced to less than 7% of calories, which may be achieved by avoiding trans fats, limiting dietary cholesterol to less than 200 mg/d. [41] Restrict refined carbohydrates, particularly sugar and liquid calories. In addition, lowering low-density lipoprotein (LDL) may be enhanced by adding dietary options such as 2 g/d of plant stanols/sterols and at least 5-10 g/d of viscous soluble fiber to the diet. [41]\nAlcohol consumption should also be severely limited or abstained; consuming more than 1 standard alcoholic drink per day may worsen hypertriglyceridemia. In March 2011, the American Dietetic Association published updated evidence-based guidelines for nutrition practice for disorders of lipid metabolism.\nTotal fat intake\nTotal 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.\nFat 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 lipoprotein lipase activity, a low-fat diet decreases chylomicron and very low-density lipoprotein (VLDL) production and improves the metabolism of these triglyceride-rich lipoproteins.\nHowever, in the setting of stable weight and moderately elevated triglycerides, a very low-fat diet increases triglycerides and may, in addition, decrease high-density lipoprotein (HDL) 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 level certainly will decrease. However, such a diet will, if anything, cause further deterioration in the HDL and triglyceride levels. If the patient has an isolated triglyceride elevation and does not lose weight on the diet, the triglyceride levels may increase. In such cases, addition of a healthy fat (monounsaturated or polyunsaturated fat) lowers levels of triglycerides, increases HDL, and sometimes decreases LDL.\nCarbohydrate intake\nIn 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 nondiet soda can increase triglycerides dramatically.\nAgain, alcohol should be eliminated or restricted to no more than 1 standard alcoholic beverage per day.\nOmega-3 (N-3) fatty acids\nThe 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.\nTo 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.\nExercise, particularly sustained aerobic activity, can have a dramatic impact on triglyceride levels and may increase HDL slightly. If patients have no known cardiovascular disease, they should be encouraged to begin an exercise program of graduated aerobics and toning.\nThe American Heart Association (AHA) recommends 30-60 minutes of aerobic exercise most days of the week and toning for 20-30 minutes twice a week. Frequent and sustained exercise lowers elevated triglyceride levels and may raise HDL cholesterol levels.\nBefore beginning an exercise program, consider giving a stress test to older patients and patients with multiple risk factors for coronary artery disease, as these patients are at increased risk for cardiovascular disease.\nExercise prescription also has substantial benefits beyond lipid effects as follows:\nReduced weight\nDecreased insulin resistance\nDecreased blood pressure\nImproved cardiovascular conditioning\nOverall 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.\nWomen with elevated triglycerides before conception may develop severe hypertriglyceridemia, with triglyceride levels well above 1000 mg/dL, and the concomitant risk of pancreatitis. These women should be counseled regarding diet, exercise, and weight management before becoming pregnant and must be monitored closely during their pregnancies. [84] All pregnancies require occasional triglyceride monitoring. Simple inspection to rule out lipemic serum is all that is necessary.\nThe use of lipid-lowering drugs in pregnant patients and pediatric patients has not been thoroughly investigated. Thus, most of the medications to treat hypertriglyceridemia are contraindicated during pregnancy, although treatment with gemfibrozil in a patient with severe hypertriglyceridemia and pancreatitis has been reported. [84] Omega-3 fatty acids may be a more acceptable intervention, but the safety of high-dose N-3 fatty acids has not been proven.\nTo decrease the risk of cardiovascular disease, patients should avoid smoking, obesity, and sedentary lifestyles. Moreover, pursue aggressive treatment of hypertension and diabetes.\nPrimary and secondary prevention\nPatients with hypertriglyceridemia, particularly if the high-density lipoprotein (HDL) level is low, are at risk for cardiovascular events. For primary prevention, it is recommended that men aged 35 and older—and those aged 20-35 if they are at increased risk—are screened for coronary heart disease (CHD) with a fasting lipid profile; screening for women is recommended only for those at increased risk for CHD. [45, 34] For patients who were screened with a nonfasting due to patient convenience, follow-up on abnormal nonfasting lipid levels with a fasting lipid profile. Screening should be repeated every 5 years in patients with normal lipid levels. [45]\nIn secondary prevention, all patients with CHD, other atherosclerotic cardiovascular disease (ASCVD), diabetes mellitus, or a Framingham 10-year risk of greater than 20% should be screened with a full lipid panel. [45] Evaluate the patient’s risk for cardiovascular events. Patients considered at high risk include those who have CHD without major risk factors or other risks associated with very high risk.\nPatients considered at very high risk include individuals with CHD or other atherosclerotic vascular disease as well as 1 or more of the following: major risk factors (eg, diabetes, hypertension, metabolic syndrome, active cigarette smoking) or acute coronary syndrome. [45, 47] Thus, these patients should be treated not only for their lipid disorder but also for other modifiable cardiovascular risk factors, such as hypertension, diabetes, smoking, sedentary lifestyle, and obesity. [85, 86]\nThe Endocrine Society’s 2012 guidelines in evaluating and treating hypertriglyceridemia included screening adults for this condition as part of a lipid panel at least at 5-year intervals. [42] For pediatric patients with dyslipidemia, the American Association of Clinical Endocrinologists (AACE) recommends early diagnosis and management to reduce LDL levels, thereby reducing the risk for cardiovascular events in adulthood. [68]\nAlthough the rare inherited disorders of severe hypertriglyceridemia require heroic restrictions in dietary fat, most elevated triglycerides can be controlled, at least partially, by a program of diet, exercise, and weight loss. Lifestyle modification can be more effective than a triglyceride-lowering medication if the habits are in need of intervention and the patient is willing and able to make significant changes. Therefore, prevention entails pursuing an active lifestyle with regular aerobic and toning exercise; adhering to a diet low in simple carbohydrates and alcohol and, if the triglycerides are well above 1000 mg/dL, low in fat; and maintaining a lean body habitus. These habits have the added benefit of reducing the probability of developing type 2 diabetes mellitus and hypertension.\nPatients with modest triglyceride elevations may develop severe hypertriglyceridemia and risk of pancreatitis if an aggravating agent is instituted. Drugs such as oral isotretinoin and unopposed oral estrogen replacement therapy should be used with caution.\nDuring 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.\nA specialist in lipid disorders may be helpful in treating the hyperlipidemia that develops in patients, which can be very severe and difficult to treat, often requiring multiple lipid-lowering agents.\nIn addition, patients should receive nutrition counseling and should be advised to restrict calories if they are overweight. These individuals also should reduce saturated and trans fats and cholesterol intake.\nFollow up with patients who are on diet and lipid-lowering therapy. Periodically monitor their blood cholesterol, triglyceride, and lipoprotein levels. If patients are taking lipid-lowering medications, obtain periodic liver function tests.\nIf patients are taking fibric acid derivatives or statins, advise them to report unexplained generalized muscle pain, tenderness, or weakness. Perform creatinine kinase determinations in these individuals.\nIn patients with diabetes, aggressive glucose control should be pursued with diet, oral hypoglycemic agents, or insulin.\nAlexopoulos AS, Qamar A, Hutchins K, Crowley MJ, Batch BC, Guyton JR. Triglycerides: Emerging Targets in Diabetes Care? Review of Moderate Hypertriglyceridemia in Diabetes. Curr Diab Rep. 2019 Feb 26. 19 (4):13. [Medline]. [Full Text].\nWu CW, Lin PY, Liu YF, Liu TC, Lin MW, Chen WM, et al. Central corneal mosaic opacities in Schnyder's crystalline dystrophy. Ophthalmology. 2005 Apr. 112(4):650-3. [Medline].\nFREDRICKSON DS, LEES RS. A SYSTEM FOR PHENOTYPING HYPERLIPOPROTEINEMIA. Circulation. 1965 Mar. 31:321-7. [Medline].\nMahley RW, Rall SC Jr. Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal metabolism. Scriver CR, Beaudet AR, Sly WS, Valle D, eds. The Metabolic and Molecular Bases of Inherited Disease. 8th ed. 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Safety: statins and HIV or hepatitis C drugs: drug safety communication - interaction increases risk of muscle injury. Posted: March 1, 2012. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm294294.htm. Accessed: November 1, 2013.\nUS Food and Drug Administration. Safety: statin drugs - drug safety. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm293670.htm. Accessed: November 1, 2013.\nUS Food and Drug Administration. Safety: Zocor (simvastatin): label change - new restrictions, contraindications, and dose limitations. Posted: June 8, 2011. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm258384.htm. Accessed: November 1, 2013.\nMaki KC, Bays HE, Dicklin MR. Treatment options for the management of hypertriglyceridemia: strategies based on the best-available evidence. J Clin Lipidol. 2012 Sep-Oct. 6(5):413-26. [Medline].\nFDA. AbbVie Inc. et al; Withdrawal of Approval of Indications Related to the Coadministration With Statins in Applications for Niacin Extended-Release Tablets and Fenofibric Acid Delayed-Release Capsules. Federal Register. 2016 Apr 18. [Full Text].\nWending P. FDA Pulls Approval of Niacin, Fibrate in Combo with Statins. Medscape. 2016 Apr 15. [Full Text].\nAbourbih S, Filion KB, Joseph L, Schiffrin EL, Rinfret S, Poirier P, et al. Effect of fibrates on lipid profiles and cardiovascular outcomes: a systematic review. Am J Med. 2009 Oct. 122(10):962.e1-8. [Medline].\nSica DA. Fibrate therapy and renal function. Curr Atheroscler Rep. 2009 Sep. 11(5):338-42. [Medline].\nHarper CR, Jacobson TA. Managing dyslipidemia in chronic kidney disease. J Am Coll Cardiol. 2008 Jun 24. 51(25):2375-84. [Medline].\nMohiuddin SM, Pepine CJ, Kelly MT, Buttler SM, Setze CM, Sleep DJ, et al. Efficacy and safety of ABT-335 (fenofibric acid) in combination with simvastatin in patients with mixed dyslipidemia: a phase 3, randomized, controlled study. Am Heart J. 2009 Jan. 157(1):195-203. [Medline].\nWu J, Song Y, Li H, Chen J. Rhabdomyolysis associated with fibrate therapy: review of 76 published cases and a new case report. Eur J Clin Pharmacol. 2009 Dec. 65(12):1169-74. [Medline].\nCanner PL, Berge KG, Wenger NK, Stamler J, Friedman L, Prineas RJ, et al. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol. 1986 Dec. 8(6):1245-55. [Medline].\nMcKenney JM, McCormick LS, Weiss S, Koren M, Kafonek S, Black DM. A randomized trial of the effects of atorvastatin and niacin in patients with combined hyperlipidemia or isolated hypertriglyceridemia. Collaborative Atorvastatin Study Group. Am J Med. 1998 Feb. 104(2):137-43. [Medline].\nGoldberg RB, Jacobson TA. Effects of niacin on glucose control in patients with dyslipidemia. Mayo Clin Proc. 2008 Apr. 83(4):470-8. [Medline].\nRoth EM, Bays HE, Forker AD, Maki KC, Carter R, Doyle RT, et al. Prescription omega-3 fatty acid as an adjunct to fenofibrate therapy in hypertriglyceridemic subjects. J Cardiovasc Pharmacol. 2009 Sep. 54(3):196-203. [Medline].\nLavie CJ, Milani RV, Mehra MR, Ventura HO. Omega-3 polyunsaturated fatty acids and cardiovascular diseases. J Am Coll Cardiol. 2009 Aug 11. 54(7):585-94. [Medline].\nWendling P. No CVD Benefit With Omega-3 Fatty Acids. Medscape Medical News. Feb 2, 2018. [Full Text].\nAung T, Halsey J, Kromhout D, et al. Associations of Omega-3 Fatty Acid Supplement Use With Cardiovascular Disease Risks: Meta-analysis of 10 Trials Involving 77 917 Individuals. JAMA Cardiol. 2018 Mar 1. 3 (3):225-34. [Medline]. [Full Text].\nKim HS, Kim H, Jeong YJ, et al. Comparative analysis of the efficacy of omega-3 fatty acids for hypertriglyceridaemia management in Korea. J Clin Pharm Ther. 2016 Jul 18. [Medline].\nTatachar A, Pio M, Yeung D, et al. Over-the-counter fish oil use in a county hospital: medication use evaluation and efficacy analysis. J Clin Lipidol. 2015 May-Jun. 9 (3):326-33. [Medline]. [Full Text].\nHilleman D, Smer A. Prescription Omega-3 Fatty Acid Products and Dietary Supplements Are Not Interchangeable. Manag Care. 2016 Jan. 25 (1):46-52. [Medline]. [Full Text].\nEgert S, Kannenberg F, Somoza V, Erbersdobler HF, Wahrburg U. Dietary alpha-linolenic acid, EPA, and DHA have differential effects on LDL fatty acid composition but similar effects on serum lipid profiles in normolipidemic humans. J Nutr 2009;139:861-68.\nBalk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P, Lau J. Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis 2006;189:19-30.\nBhatt DL, Miller M, Brinton EA, et al. REDUCE-IT USA: Results from the 3,146 Patients Randomized in the United States. Circulation. 2019 Nov 11. [Medline]. [Full Text].\nPrescribing information: Omtryg. FDA. Available at https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/204977s000lbl.pdf. 2014 Apr; Accessed: 2018 Jun 14.\nBays HE, Ballantyne CM, Kastelein JJ, Isaacsohn JL, Braeckman RA, Soni PN. Eicosapentaenoic acid ethyl ester (AMR101) therapy in patients with very high triglyceride levels (from the Multi-center, plAcebo-controlled, Randomized, double-blINd, 12-week study with an open-label Extension [MARINE] trial). Am J Cardiol. 2011 Sep 1. 108(5):682-90. [Medline].\nNainggolan L. FDA Approves Epanova for Severe Hypertriglyceridemia. Medscape. Available at http://www.medscape.com/viewarticle/824748. May 7, 2014; Accessed: June 14, 2014.\nKastelein JJ, Maki KC, Susekov A, Ezhov M, Nordestgaard BG, Machielse BN, et al. Omega-3 free fatty acids for the treatment of severe hypertriglyceridemia: the EpanoVa fOr Lowering Very high triglyceridEs (EVOLVE) trial. J Clin Lipidol. 2014 Jan-Feb. 8(1):94-106. [Medline].\nFletcher B, Berra K, Ades P, Braun LT, Burke LE, Durstine JL, et al. Managing abnormal blood lipids: a collaborative approach. Circulation. 2005 Nov 15. 112(20):3184-209. [Medline].\nJun JE, Jeong IK, Yu JM, et al. Efficacy and Safety of Omega-3 Fatty Acids in Patients Treated with Statins for Residual Hypertriglyceridemia: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial. Diabetes Metab J. 2019 Jun 20. [Medline]. [Full Text].\n[Guideline] Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 24. 129 (25 Suppl 2):S1-45. [Medline]. [Full Text].\nHsia SH, Connelly PW, Hegele RA. Successful outcome in severe pregnancy-associated hyperlipemia: a case report and literature review. Am J Med Sci. 1995 Apr. 309(4):213-8. [Medline].\nKuklina EV, Yoon PW, Keenan NL. Trends in high levels of low-density lipoprotein cholesterol in the United States, 1999-2006. JAMA. 2009 Nov 18. 302(19):2104-10. [Medline].\nHudgins LC, Kleinman B, Scheuer A, White S, Gordon BR. Long-term safety and efficacy of low-density lipoprotein apheresis in childhood for homozygous familial hypercholesterolemia. Am J Cardiol. 2008 Nov 1. 102(9):1199-204. [Medline].\nPharmacist's Letter. 2010; 26(1): 260101. Available at http://pharmacistsletter.therapeuticresearch.com/. Accessed: October 11, 2013.\nForan SE, Flood JG, Lewandrowski KB. Measurement of mercury levels in concentrated over-the-counter fish oil preparations: is fish oil healthier than fish?. Arch Pathol Lab Med. 2003 Dec. 127(12):1603-5. [Medline].\nEruptive xanthomas on the back of a patient admitted with a triglyceride level of 4600 mg/dL and acute pancreatitis.\nClose-up of eruptive xanthomas.\nComposition of triglyceride (TG)-rich lipoproteins. IDL = intermediate-density lipoprotein; VLDL = very low-density lipoprotein.\nLipoprotein lipase (LPL) releases free fatty acids (FFAs) from chylomicrons (chylo) and produces chylomicron remnants that are small enough to take part in the atherosclerotic process. Chol = cholesterol; TGs, TGS = triglycerides.\nOnce 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 low-density lipoprotein (LDL), or they can be taken up by the LDL receptor via either apolipoprotein B (apo B) or apo E. Chol = cholesterol; TGs = triglycerides.\nTable 1. Fredrickson Classification of Hyperlipidemia\nTable 2. Classification of Triglycerides\nTable 3. Classification of LDL Cholesterol and Non-HDL Cholesterol\nTable 4. Fibric Acid Agents, Omega Acid Ethyl Esters, and Niacin Drug Characteristics [87]\nTable 5. Statin Drug Characteristics [88]\nSerum Elevation\nLipoprotein Elevation\nCholesterol and triglycerides\nChylomicrons\nLDL, VLDL\nVLDL\nVLDL, chylomicrons\nIDL = intermediate-density lipoprotein; LDL = low-density lipoprotein; VLDL = very low-density lipoprotein.\nSource: Fredrickson DS, Lees RS. A system for phenotyping hyperlipidaemia. Circulation. Mar 1965;31:321-7. [3]\nLipid Effects\nLipid Effects in Combination with Statin\nOutcomes Data\nBezafibrate\nLDL decrease: 9.6-25% (400 mg)\nHDL increase: 15-24% (400 mg)\nTriglyceride decrease: 25-43% (400 mg)\nFurther LDL decrease: 1.1% (400 mg)\nFurther HDL increase: 22% (400 mg)\nFurther triglyceride decrease: 31.7% (400 mg)\nSecondary prevention: Prevents composite endpoint of MI and sudden death in a subgroup with triglycerides of 200 mg/dL or higher. No increase in non-CV death\nFirst-line option for triglyceride >10 mmol/L\nOption for triglyceride 5-10 mmol/L\nOption for low HDL\nReversible increase in serum creatinine\nRequires renal dose adjustment\nLimited data with statins\nLDL decrease: 18% (10 mg/day)\nHDL increase: 1% (10 mg/day)\nTriglyceride decrease: 8%\nFurther LDL decrease: 25%, as add-on\nFurther HDL increase: 3%, as add-on\nFurther triglyceride decrease: 14%, as add-on\nPrevention of CV events in post-acute coronary syndrome patient when added to statin showed a benefit of reducing the primary endpoint (composite of CV death, MI, unstable angina requiring rehospitalization, coronary revascularization or stroke) by 6.4% vs statin alone\nIn intermediate outcomes studies, ezetimibe did not reduce regression of carotid intima-media thickness (surrogate marker) when added to a statin\nEfficacy studied in combination with atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin\nRole as statin add-on to reduce LDL if HDL and triglyceride satisfactory\nLDL decrease: 20.6% (145 mg)\nHDL increase: 11% (145 mg)\nTriglyceride decrease: 23.5-50.6% (greatest drop in patients with highest triglycerides) (145 mg)\nFurther LDL decrease: 0-6% (200 mg)\nFurther HDL increase: 13-17% (200 mg)\nFurther triglyceride decrease: 20-32% (200 mg)\nPrevention of CV events in type 2 diabetes: Did not reduce primary composite outcome (nonfatal MI or CV death). Improved outcomes included nonfatal MI (24% decrease), coronary revascularization (21% decrease), progression to albuminuria, and reduced laser treatments for retinopathy. Nonsignificant increase in risk of CV death.\nFirst-line option for triglyceride >10 mmol/L (about 1000 mg/dL)\nOption for triglyceride >500 mg/dL or 5-10 mmol/L\nAssociated with reversible increase in serum creatinine\nLDL: No effect\nHDL increase: 6% (1200 mg/day)\nTriglyceride decrease: 33-50% (greatest drop in patients with highest triglycerides) (1200 mg/day)\nFurther triglyceride decrease: 41%\nFurther HDL increase: 9%\nPrimary prevention of coronary heart disease\nSecondary prevention of cardiac events in men with low HDL\nAvoid with statin\nIcosapent ethyl\nLDL decrease: 5%\nHDL decrease: 4%\nTriglyceride decrease: 27%\nFurther triglyceride decrease: 21.5% (4 g/day), 10.1% (2 g/day)\nFurther LDL decrease: 6.2% (4 g/day)\nSecondary CV risk prevention; REDUCE-IT trial showed primary endpoint (major CV events) occurred in 24.7% of placebo compared with 18.2% of icosapent ethyl treated patients (p = 0.000001) [76]\nOption for triglyceride >500 mg/dL\nSafe for use with statins\nUse caution with fish or shellfish allergy\nLDL decrease: 14-17% (Niaspan 2 g/day); 12% (niacin immediate-release 1.5 g/day and Niaspan 1.5 g/day)\nHDL increase: 22-26% (2 g/day Niaspan); 17% (niacin immediate release 1.5 g/day); 20-22% (Niaspan 1.5 g/day)\nTriglyceride decrease: 20-50%\nFurther LDL decrease: 1-5% (Niaspan 1 g/day); 10% (Niaspan 2 g/day)\nFurther HDL increase: 24% (Niaspan 2 g/day); 15-17% (Niaspan 1 g/day)\nFurther triglyceride decrease: 24% (Niaspan 2 g/day); 12-22% (Niaspan 1 g/day)\nSecondary MI prevention; in combination with a resin, slows progression or promotes regression of atherosclerosis; reduces mortality\nOption for triglyceride >500 mg/dL (about 5 mmol/L)\nRaises HDL more than any other agent\nDose-dependent risk of hyperglycemia (especially in patients with type 2 diabetes) and liver toxicity\nMay increase risk of statin myopathy\nOmega-3 ethyl esters\nLDL increase: 44.5% (4 g/day)\nHDL increase: 9.1% (4 g/day)\nTriglyceride decrease: 45% (4 g/day)\nLDL increase: 0.7% (4 g/day)\nFurther HDL increase: 3.4% (4 g/day)\nFurther triglyceride decrease: 29.5% (4 g/day)\nSecondary prevention: Reduces cardiovascular death; sudden death; and combined endpoint of death, nonfatal MI, and nonfatal stroke\nSecondary prevention in patients with, or at risk for, type 2 diabetes: did not reduce CV events\nAssociated with an increase in risk for recurrence of symptomatic atrial fibrillation or flutter within first 3 months of therapy\nUse with caution with fish or shellfish allergy\nPotency (average LDL decrease)\nRenal Considerations\nLiver Function Monitoring\n10 mg: 35-39%\n20 mg: 43%\nNo dose adjustment necessary for reduced renal function\nCheck liver function tests at baseline and when clinically indicated\n(as XL product)\nIn severe renal impairment, use daily doses >40 mg with caution\n(as 40 mg BID)\nIf CrCl < 30 mL/min, use daily doses over 20 mg with caution\n1 mg: 31-32%\nFor glomerular filtration rate 15-59 mL/min/1.73 m2, including hemodialysis, initial daily dose is 1 mg, not to exceed 2 mg/day\nIn significant renal impairment, start with 10 mg/day\n5 mg: 45%\nIf CrCl < 30 mL/min/1.73 m2 (but not on hemodialysis), starting dose is 5 mg/day, not exceed 10 mg/day\nRosuvastatin levels in hemodialysis patients are about 50% higher than levels in normal renal function\nIn severe renal impairment, starting dose is 5 mg daily with close monitoring\nMary Ellen T Sweeney, MD Associate Professor of Medicine (Endocrinology, Diabetes, and Metabolism), Department of Medicine, Emory University School of Medicine; Physician, Division of Endocrinology, Veterans Administration Medical Center; Physician, Lipid Metabolism Clinic, Emory Healthcare, The Emory Clinic\nMary Ellen T Sweeney, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, National Lipid Association\nRomesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School\nRomesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society\nHampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences\nHampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology\nSteve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong\nSteve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society\nDisclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting\nKaren E Friday, MD, FACP Clinical Core Director of Tulane Xavier National Center of Excellence, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Tulane University School of Medicine\nKaren E Friday, MD, FACP is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Heart Association, American Society for Clinical Nutrition, and Endocrine Society\nDisclosure: AstraZeneca own AstraZeneca stock None; Merck own Merck stock None; Schering Plough own Schering Plough stock None; Medco Health own Medco Health stock None\nRobert A Gabbay, MD, PhD Associate Professor of Medicine, Division of Endocrinology, Diabetes and Metabolism, Laurence M Demers Career Development Professor, Penn State College of Medicine; Director, Diabetes Program, Penn State Milton S Hershey Medical Center; Executive Director, Penn State Institute for Diabetes and Obesity\nRobert A Gabbay, MD, PhD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, and Endocrine Society\nDisclosure: Novo Nordisk Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching\nSteven 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\nSteven 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\nRomesh Khardori, MD, PhD Professor and Director, Division of Endocrinology, Metabolism, and Molecular Medicine, Southern Illinois University School of Medicine\nRomesh Khardori, MD, PhD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society of Andrology, Endocrine Society, and Illinois State Medical Society\nSimon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine\nSimon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology\nDisclosure: Medscape Salary Employment\nEmail Newsletters Manage My Account About You Professional Information Newsletters & Alerts\nencoded search term (Hypertriglyceridemia) and Hypertriglyceridemia\nLipid Management Guidelines\nDyslipidaemia: Recommendations on the Role of PCSK9 Inhibitors in Lipids Management\nFast Five Quiz: Do You Know Current Guidelines for Lipid Management?\nFast Five Quiz: Lipids Management: High HDL Cholesterol Levels (Hyperalphalipoproteinemia)\nTrending Clinical Topic: New Lipid Guidelines\nLocal Anesthetic Toxicity\nFast Five Quiz: How Much Do You Know About Hypertriglyceridemia?\nThe Year In Medicine 2014\nWhat Is the Role of SGLT2 Inhibitors in Patients With HFrEF?\nLarge Study Links Brown Fat With Lower Rates of Cardiometabolic Disease\nThe Top 10 Trending Clinical Topics of 2019\nAccording to Endocrinologists\n'Thyroid Diet': What's the Evidence?\nBlood Glucose on Admission Predicts COVID-19 Severity in All\nAssessing Thyroid Nodules: A Clinician's Guide\nFast Five Quiz: Metformin\nTo Fast or Not? The New Dieting Dilemma\n2010 /viewarticle/940625\nNonstatin Therapies and LDL-C Lowering: A Critical Analysis of the Data and Real-World Experiences 0.5 CME Credits\n0.5 CME\nNonstatin Therapies and LDL-C Lowering: A Critical Analysis of the Data and Real-World Experiences\n2002 2500032-overview Diseases & Conditions\nDiseases & Conditions Lipid Management Guidelines\n2001 http://www.medscape.com/resource/lipid-metabolic\nLipids Management"