Treatment Guideline Chart
Dyslipidemia is having an abnormal amount of lipids or fats in the blood.
Lipid profile is obtained from an individual with diabetes mellitus, coronary heart disease, cerebrovascular disease, peripheral arterial disease or other coronary heart disease risk factors or from an individual with family history or clinical evidence of familial hypercholesterolemia.
Plasma lipids are total cholesterol, high-density lipoprotein cholesterol, triglycerides, and low-density lipoprotein cholesterol.
Evaluation of lipid profile must be performed in parallel with the risk assessment of coronary heart disease.

Dyslipidemia Treatment


LDL-C-Lowering Pharmacological Therapy 

LDL-C is the primary target of lipid management 

  • The greater the LDL-C level is reduced, the more significant is the amount of CV risk reduction
  • Assess patient’s response to LDL-C-lowering therapy and lifestyle modifications with a repeat lipid profile 4-12 weeks after starting statin therapy or dose adjustment then every 3-12 months as needed

Statins (Beta-hydroxy-beta-methylglutaryl-Coenzyme A [HMG-CoA] Reductase Inhibitors) 

  • Reduce risk for acute coronary syndromes, coronary procedures and other coronary outcomes in both primary and secondary coronary heart disease prevention
  • Recommended for the following:
    • Adults ≥21 years old with clinical atherosclerotic cardiovascular disease (ASCVD)
    • Adults ≥21 years old with LDL-C ≥190 mg/dL
    • Adults 40-75 years of age without ASCVD but with diabetes mellitus (especially type 2 diabetes mellitus) and LDL-C levels of 70-189 mg/dL
    • Adults 40-75 years of age without ASCVD and diabetes mellitus but with LDL-C levels of 70-189 mg/dL and estimated 10-year risk of ≥7.5% for ASCVD
      • If decision to start statin therapy is uncertain, measure coronary artery calcium (CAC); statin therapy is favored with a CAC score of 1-99 and is indicated with a CAC score of ≥100 Agatston units or ≥75th percentile
    • Adults 40-75 years of age without diabetes mellitus but with risk-enhancing factors and estimated 10-year ASCVD risk of 7.5-19.9%
  • It is reasonable to initiate statin therapy in patients 20-39 years old with longstanding diabetes or to continue moderate- or high-intensity statin therapy in patients >75 years old with diabetes 
  • Effective in patients with nephrotic syndrome
  • Inhibit HMG-CoA reductase which is the rate-limiting step in cholesterol biosynthesis
  • Most effective class of drugs at lowering LDL-C levels, with moderate effects on lowering TG and elevating HDL-C: Decreases LDL-C in a dose-dependent manner by 20-55%, decreases TG by up to 35%, increases HDL-C by 2-10%
  • The drugs of choice for LDL lowering and in reducing CVD risk in high-risk patients (eg DM) with hypertriglyceridemia
    • Statin dose may be increased or a non-statin drug (eg Ezetimibe, fibrates, or Nicotinic acid) may be added if TG levels remain at >2 mmol/L (>200 mg/dL) after achieving the LDL-C target level
  • High-intensity statins: Atorvastatin (80 mg), Rosuvastatin (20 mg)
    • Statin regimen that helps lower LDL-C by ≥50%
    • Recommended to be given at the highest tolerated dose to achieve the LDL-C goals set for a specific risk group
    • Recommended as 1st-line treatment for patients ≤75 years old with clinical ASCVD
    • May be used for patients ≥21 years old with LDL-C ≥190 mg/dL or TG ≥500 mg/dL especially those trying to achieve at least 50% LDL-C level reduction
      • A non-statin drug may be added if LDL-C goal has not been achieved with high-intensity regimen
    • For ≥75-year-old patients with ASCVD without contraindications
    • For 40-75-year-old patients with diabetes mellitus with ≥7.5% 10-year ASCVD risk1
    • For 40-75-year-old patients with diabetes mellitus or LDL-C ≥190 mg/dL
  • Moderate-intensity statins: Atorvastatin (10 mg), Rosuvastatin (10 mg), Simvastatin (20-40 mg), Pravastatin (40 mg), Lovastatin (40 mg), Fluvastatin (40 mg 12 hourly), Pitavastatin (1-4 mg)
    • Daily dose helps lower LDL-C by 30-49% 
    • Alternative treatment for patients with clinical ASCVD with contraindications against high-intensity statins or with side effects from statin therapy
    • For ≥75-year-old patients with ASCVD with contraindications/intolerance to high-intensity statins
    • For 40-75-year-old patients with diabetes mellitus with or without 5-≤7.5% 10-year ASCVD risk
    • For 40-75-year-old patients with diabetes mellitus and LDL-C 70-189 mg/dL
    • For 40-75-year-old patients with diabetes mellitus or LDL-C ≥190 mg/dL with contraindications/intolerance to high-intensity statins
    • For 40-75-year-old patients without diabetes mellitus but LDL-C ≥70 mg/dL and ≥7.5% 10-year ASCVD risk
  • Low-intensity statins: Simvastatin (10 mg), Pravastatin (10-20 mg), Lovastatin (20 mg), Fluvastatin (20-40 mg)
    • Daily dose helps lower LDL-C by <30%
  • Treatment with statin is associated with the risk of developing statin-associated muscle symptoms (SAMS) or new-onset DM but benefits of statin therapy for CV risk reduction outweigh the risk
  • A non-statin drug may be added to a maximally tolerated statin therapy if LDL-C goal based on CVD risk has not been achieved

1Risk of developing a first ASCVD event, defined as nonfatal myocardial infarction or coronary heart disease (CHD) death or fatal or nonfatal stroke, over a 10-year period among people free from ASCVD at the beginning of the period.

Selective Cholesterol-Absorption Inhibitor

  • Eg Ezetimibe
  • Used as an adjunct to diet and exercise for the reduction of elevated TC, LDL-C, apo B and non-HDL-C in patients with primary hyperlipidemia alone or in combination with statin therapy, or in combination with Fenofibrate in patients with mixed hyperlipidemia
  • 1st optional non-statin to consider for patients with poor tolerance to statins
  • 1st option to add onto maximally tolerated statin therapy in patients who are less responsive to statins and failed to reach LDL-C goals
    • May be added to a maximally tolerated statin therapy in patients with high to very high-risk clinical ASCVD when LDL-C level remains ≥70 mg/dL
    • Combination is a strategy to prevent side effects associated with statin monotherapy
    • Combination products of selective cholesterol-absorption inhibitor + statin, eg Ezetimibe/Simvastatin, Ezetimibe/Atorvastatin, are available and may be used to reduce TC, LDL-C, apo B, TG and non-HDL-C and to increase HDL-C in patients with homozygous familial hypercholesterolemia
      • The IMPROVE-IT trial in patients with recent acute coronary syndrome showed further decrease in LDL-C and reduction in cardiovascular events with the addition of Ezetimibe to a moderate-intensity statin (Simvastatin) over 6 years of follow-up
      • The SHARP trial demonstrated reductions in LDL-C and primary endpoint of 1st major ASCVD event with Ezetimibe plus Simvastatin when compared to placebo over 4.9 years of follow-up
    • If the addition of Ezetimibe to a statin achieved therapy goals, the combination therapy may be continued with continuous monitoring of treatment response
  • Ezetimibe/statin combination is recommended in patients with CKD stage 3-5 not dependent on dialysis
  • Selective potent inhibitor of cholesterol absorption in the intestinal lumen and reduces the overall delivery of cholesterol to the liver
  • Causes moderate reduction in LDL-C levels
    • When used alone, Ezetimibe decreases LDL by 10-20% with favorable effects on HDL and TG
    • When used in combination with statins, there is an additional reduction in LDL-C by 18-25% with favorable effects on HDL and TG, with Fenofibrate 20-22% reduction in LDL-C

Proprotein Convertase Subtilisin/Kexin Type 9 Monoclonal Antibodies (PCSK9 mAbs) 

  • Eg Alirocumab, Evolocumab
  • May be given alone or in combination with other lipid-lowering therapies as an adjunct to diet to reduce LDL-C in patients with primary hyperlipidemia including heterozygous familial hypercholesterolemia
  • Recommended as adjunct to diet and maximally tolerated statin therapy plus Ezetimibe for the treatment of homozygous familial hypercholesterolemia with very high-risk clinical ASCVD that needs further reduction of LDL-C
  • Addition of a PCSK9 mAb is recommended to patients with high-risk clinical ASCVD or severe primary hypercholesterolemia with multiple risk factors for ASCVD events if the LDL-C level remains above goal on maximally tolerated statin and Ezetimibe therapy
  • Given also to patients with high and very high CV risk with intolerance to statin therapy  
  • May be preferred as the initial non-statin agent in addition to maximally tolerated statin therapy in patients with clinical ASCVD at very high risk that still require ≥25% LDL-C reduction  
  • As human monoclonal PCSK9 antibody, it binds to PCSK9 which then increases LDL receptor density to aid in clearing circulating LDL-C 
  • Lowers LDL-C levels by 48-71%, TC by 36-42%, apo B by 42-55%, and non-HDL-C by 49-58%

Anti-sense Apoliporotein B Oligonucleotides 

  • Eg Mipomersen
  • May be used for patients with homozygous familial hypercholesterolemia unresponsive to PCSK9 mAb therapy; may also be considered in patients with ASCVD and baseline LDL-C ≥190 mg/dL who had inadequate response to statin therapy (with or without Ezetimibe and PCSK9 mAbs)
  • Hybridization to mRNA results to RNase H-mediated degradation of mRNA used for translation of apo B-100
  • Lowers LDL-C levels by 21%, total cholesterol by 19%, apo B by 24%, and non-HDL-C by 22%

Bempedoic Acid

  • Indicated for the treatment of adults with heterozygous familial hypercholesterolemia or established ASCVD who require additional lowering of LDL-C 
  • Addition of Bempedoic acid may be considered if additional LDL-C lowering is needed in patients with clinical ASCVD at high or very high risk despite treatment with a maximally tolerated statin therapy with Ezetimibe and/or a PCSK9 mAb
  • Lowers LDL-C by inhibiting action of adenosine triphosphate-citrate lyase, which is an enzyme that works upstream of HMG-CoA reductase
  • May be used alone or in fixed combination with Ezetimibe
    • Has been shown to decrease LDL-C by 15-24% and in combination with Ezetimibe by 36% in clinical trials

Bile Acid Sequestrants

  • Eg Cholestyramine, Colesevelam, Colestipol  
  • Adjunct to diet for LDL-C reduction in patients with primary hyperlipidemia
  • Have been shown to reduce risk for CVD; considered in patients who have contraindications or intolerance to statin therapy
  • Also effective in LDL lowering in patients with diabetes mellitus
  • Bind bile acids in the intestine through anion exchange and impede their reabsorption 
  • Cause moderate reduction in LDL-C levels
    • LDL-lowering potential increases when combined with other agents (eg statins)
    • May raise TG levels in some patients
    • Decrease LDL-C by 15-25%; increase HDL-C by 4-11%


  • An add-on treatment for patients ≥12 years old with homozygous familial hypercholesterolemia 
  • May also be considered in patients without clinical ASCVD or with clinical ASCVD at very high risk and baseline LDL-C ≥190 mg/dL not from secondary causes who had inadequate response to maximal doses of statin with Ezetimibe and/or a PCSK9 mAb, Bempedoic acid or Inclisiran
  • A fully human monoclonal antibody that binds to angiopoietin-like protein 3 (ANGPTL3) which in turn inhibits lipoprotein and endothelial lipase 
  • Mean LDL-C reduction in combination with other lipid-lowering therapies has been shown to be 49%


  • Indicated for the treatment of adults with primary hypercholesterolemia (heterozygous familial and non-familial) or mixed dyslipidemia, or clinical ASCVD requiring additional lowering of LDL-C   
  • Given as an adjunct to diet in combination with a statin or statin with other lipid-lowering therapies in patients unable to reach LDL-C goals with max tolerated statin dose; or alone or in combination with other lipid-lowering therapies in patients who are statin intolerant or for whom a statin is contraindicated 
  • May be used in place of a PCSK9 mAb in patients with poor adherence to PCSK9 mAbs, adverse effects from both PCSK9 mAbs, or those who may be not be able to self-inject
  • It is a small-interfering RNA LDL-C-lowering treatment that targets hepatic PCSK9 synthesis which prolongs LDL receptor activity 
  • Dosing regimen is infrequent (initial dose is given subcutaneously which is repeated at 3 months then every 6 months) and side effects are acceptable
  • Mean LDL-C reduction has been shown to be 48-52% 

Microsomal Triglyceride Transfer Protein (MTP) Inhibitor

  • Eg Lomitapide
  • Used for patients with homozygous familial hypercholesterolemia as an adjunct to a low-fat diet and other lipid-lowering treatments including LDL apheresis  
  • May also be considered in patients without clinical ASCVD or with clinical ASCVD at very high risk and baseline LDL-C ≥190 mg/dL not from secondary causes who had inadequate response to maximally tolerated statin therapy with Ezetimibe and/or PCSK9 mAb, Bempedoic acid or Inclisiran  
  • Inhibits chylomicron and VLDL synthesis by direct binding and inhibition of MTP
  • Lowers LDL-C levels by 40%, TC by 36%, apo B by 39%, TG by 45%, and non-HDL-C by 40%

Nicotinic Acid

  • Favorably affects all lipid and lipoproteins when given in the proper dosage
    • Lower doses increase HDL-C
    • 2-3 g/day are needed to lower LDL-C
  • Moderate reduction in CVD risk
  • Alter lipid levels by inhibiting lipoprotein synthesis and decreasing the production of VLDL particles by the liver
  • Most effective at raising HDL levels among lipid-modifying drugs
    • Decrease LDL-C by 5-25%
    • Increase HDL-C by 10-35%
    • Decrease TG by 20-30% in a dose-dependent manner
  • May be combined with statins in managing DM patients with hypertriglyceridemia
  • May increase blood glucose levels

Intensified LDL-C-Lowering Pharmacotherapy

  • Dose increase; escalate intensity of statin therapy
  • Combination therapy eg statin with Ezetimibe with or without a PCSK9 mAb, statin with PCSK9 mAb, Ezetimibe with PCSK9 mAb, statin with bile acid sequestrant
  • LDL apheresis may be considered in patients with familial hypercholesterolemia unresponsive to dietary management and pharmacological therapy

Triglyceride-Lowering and HDL-C-Raising Pharmacological Therapy


  • Primary use is for lowering TG
    • Decrease TG by 20-50%
    • May be combined with statins in managing diabetes mellitus patients with hypertriglyceridemia and low HDL-C
    • If TG is not elevated, fibrates may lower LDL-C by 5-20%
  • Also useful in combined/mixed dyslipidemia and in increasing HDL-C by 6-35%
  • Recommended for patients with very high TG (>4.5 mmol/L) who are at risk for pancreatitis
  • Moderately reduce risk for CHD
  • Favorably lower LDL in patients with diabetes mellitus
  • Down-regulate the apolipoprotein C-III (apoC-III) gene and up-regulate genes for apolipoprotein A-1, fatty acid transport protein, fatty acid oxidation and possibly lipoprotein lipase
  • Primarily target atherogenic dyslipidemia including diabetic dyslipidemia
    • Fenofibrate with or without statin therapy reduces progression of diabetic retinopathy
  • When used in combination with LDL-lowering drugs, it improved the overall lipoprotein compared to either agent alone
    • In combination with statin, Fenofibrate is the preferred fibrate to use due to lower risk of myopathy and rhabdomyolysis
  • Provide an alternative treatment in statin-intolerant patients with mild to moderate hypercholesterolemia
  • In patients in whom a fibrate is recommended, Nicotinic acid can also be considered
  • Pemafibrate is a novel selective peroxisome proliferator-activated receptor alpha (PPARα) modulator with a favorable benefit-risk balance compared to conventional fibrates 
    • May be used to treat patients with hypertriglyceridemia and to prevent CV events in those with hypertriglyceridemia

Nicotinic Acid

  • Please see discussion under LDL-C-Lowering Pharmacological Therapy

Omega-3 Fatty Acids

  • Total eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) at dosages between 2 to 4 g/day can lower serum TG levels 
    • Studies showed EPA reduced serum TG levels by up to 45% in a dose-dependent manner 
  • Icosapent ethyl (IPE) is a highly purified, non-oxidized form of EPA and is indicated for patients with TG levels ≥150 mg/dL with established ASCVD or diabetes with ≥2 ASCVD risk factors and on maximally tolerated statins to prevent ASCVD morbidity and mortality


  • Clinical trials have shown its efficacy in the treatment of patients with elevated TG and familial chylomicronemia syndrome (FCS) 
    • Given to adult patients with FCS and at high risk for pancreatitis with inadequate response to a low-fat diet and TG-lowering therapy 
  • An antisense oligonucleotide that binds to apoC-III mRNA and prevents translation of apoC-III allowing for the metabolism and breakdown of TG and chylomicrons

Treatment of Specific Dyslipidemias

Very High LDL Cholesterol (≥4.9 mmol/L [≥190 mg/dL])

  • Usually caused by genetic forms of hypercholesterolemia
  • For patients at very high risk and with persistent high risk, use a maximally tolerated statin and, if necessary, Ezetimibe to lower LDL-C levels; if still not at treatment goal, a PCSK9 mAb may be added 
  • May consider addition of a bile acid sequestrant in patients 20-75 years old with an LDL-C level of ≥4.9 mmol/L (≥190 mg/dL) with <50% reduction in LDL-C and TG ≤3.4 mmol/L (≤300 mg/dL) while on maximally tolerated statin and Ezetimibe therapy

Elevated Triglycerides

  • Strong association between high TG levels and CHD risk
  • TG levels ≥2.3 mmol/L (≥200 mg/dL) indicate the need to identify non-HDL-C level, which is the secondary target of lipid-lowering therapy in these patients (LDL-C is still the primary goal of therapy)
    • Non-HDL-C is more representative of all atherogenic lipoproteins than LDL-C
      • Non-HDL-C (mmol/L) = TC-HDL-C; non-HDL-C levels can be calculated from non-fasting serum
  • Acquired causes: Obesity, physical inactivity, excess alcohol intake, high carbohydrate diet
    • Secondary causes (eg diabetes mellitus, chronic renal failure, nephrotic syndrome, chronic liver disease, hypothyroidism, Cushing’s disease, various medications, etc)
    • Genetic causes
  • Elevated TG can often be effectively treated through lifestyle changes; however, fibrates, Niacin, and combination therapy with statins may be appropriate options for many patients
  • Very high TG (>5.6 mmol/L [≥500 mg/dL])
    • Treatment should be likened to an emergency to avoid acute pancreatitis
      • Fibrate (preferably Fenofibrate), prescription omega-3 fatty acids, or Nicotinic acid should be started
    • Lifestyle modifications
      • Fish oils can replace some long-chain TG in diet
  • If LDL-C is still elevated despite a fibrate, consider adding a statin
    • Decision must be individualized
    • Must be started only when it is strongly indicated
    • The recommended fibrate to be combined with a statin is Fenofibrate
  • High TG (2.3-5.6 mmol/L [200-499 mg/dL])
    • Lifestyle modifications
    • If LDL-C or non-HDL-C levels are high or ASCVD risk ≥5%: Start statin
      • Consider combination therapy with Fenofibrate if LDL-C is at goal but TG level remains >200 mg/dL in primary prevention or high-risk patients 
      • Consider combination therapy with Icosapent ethyl if TG level is between 135-499 mg/dL despite statin therapy in patients at high risk (or above) 
  • Borderline high TG (1.7-2.2 mmol/L [150-199 mg/dL])
    • Lifestyle modifications
    • Medications are rarely required unless LDL-C is elevated above target level

Low HDL-C (1 mmol/L [<40 mg/dL])

  • Low HDL-C is a strong, independent predictor of CHD
  • Excluding secondary causes of low HDL-C and in the presence of other risk factors (eg borderline LDL-C, personal history of CAD, or a family history of premature CAD, HDL-C levels should be raised by as much as possible to levels of at least >40 mg/dL in both men and women
  • Raising HDL-C levels alone in patients without accompanying risk factors is not recommended

Low HDL-C without Hypertriglyceridemia

  • Causes: Obesity, physical inactivity, cigarette smoking, type 2 DM, certain drugs, etc
  • Treatment in patients with CHD or CHD-risk equivalents when lifestyle modifications fail to increase HDL include fibrates or Nicotinic acid

Low HDL-C with Hypertriglyceridemia

  • HDL-C is low and TG is high and LDL-C is not significantly elevated: Start fibrates or Nicotinic acid

Elevated Lipoprotein(a)

  • Aggressive reduction of LDL-C will help lower Lp(a)
  • Agents that have shown to reduce Lp(a) by approximately 20-30% include high-dose Niacin, PCSK9 mAbs, Estrogen and Aspirin
    • Niacin reduces Lp(a) by an average of 25% and may be given to patients with elevated Lp(a) and hypercholesterolemia with elevated LDL-C despite maximum tolerated statin therapy and Ezetimibe

Atherogenic Dyslipidemia (Triglycerides ≥1.7 mmol/L [≥150 mg/dL] and HDL-C <1 mmol/L [<40 mg/dL])

  • The patient likely has metabolic syndrome
  • Attempt adequate trial of lifestyle modification to meet LDL-C goals
    • Add LDL-lowering drug therapy if lifestyle modification fails to reach LDL-C goals
  • TG <2.3 mmol/L (<200 mg/dL): Drug therapy to lower TG is not necessary
    • If patient has CHD or CHD-risk equivalents, consider using drug therapy to raise HDL-C (eg fibrates or Nicotinic acid) 
  • TG 2.3-5.7 mmol/L (200-499 mg/dL): If non-HDL-C remains elevated after adequate LDL-C-lowering therapy: May consider higher dose of statin or statin + TG-lowering drug (fibrate or Nicotinic acid)


  • Target apo B level at <90 mg/dL for patients at risk of CAD, including those with diabetes mellitus 
  • Target apo B level at <80 mg/dL for patients with established CAD or DM plus ≥1 additional risk factor

Familial Hypercholesterolemia 

  • Common autosomal dominant genetic disease that causes LDL-C level elevation
  • Causes early-onset CHD
  • Dutch Lipid Clinic Network criteria are used for the diagnosis of heterozygous familial hypercholesterolaemia in adults and include the following:
    • Family history
      • 1st-degree relative with known premature* coronary or vascular disease, or 1st-degree relative with known LDL-C >95th percentile = 1 point
      • 1st-degree relative with tendinous xanthomata and/or arcus cornealis, or children <18 years old with LDL-C >95th percentile = 2 points
    • Clinical history 
      • Premature* coronary artery disease = 2 points
      • Premature* cerebral or peripheral vascular disease = 1 point
    • Physical examination
      • Presence of tendinous xanthomata = 6 points
      • Presence of arcus cornealis before 45 years old = 4 points
    • LDL-C levels (without treatment)
      • LDL-C ≥8.5 mmol/L (≥325 mg/dL) = 8 points
      • LDL-C 6.5-8.4 mmol/L (251-325 mg/dL) = 5 points
      • LDL-C 5.0-6.4 mmol/L (191-250 mg/dL) = 3 points
      • LDL-C 4.0-4.9 mmol/L (155-190 mg/dL) = 1 point
    • DNA analysis
      • Functional mutation in the LDLR, apoB, or PCSK9 genes = 8 points
    • Definite diagnosis of familial hypercholesterolemia can be made if the score is >8 points, probable if 6-8 points, possible if 3-5 points
  • Treatment of familial hypercholesterolemia includes the following:
    • Lifestyle modification that includes intervention on smoking, diet and physical activity
    • Initiation of cholesterol-lowering drugs that include statins (maximal potent dose), Ezetimibe, PCSK9 mAbs (Alirocumab, Evolocumab), bile acid-binding resins, Bempedoic acid or Evinacumab

*Premature = <55 years old in men, <60 years old in women

Pediatric Dyslipidemia

  • Benefits of developing healthy lifestyle habits in children have been recognized
  • Recommended first-line approach is intensive lifestyle modifications (with emphasis on improved dietary intake and normalization of body weight)
    • It is recommended that lifestyle changes in children should be implemented for at least 6-12 months prior to considering pharmacologic therapy
  • Studies have shown that high-fiber, low-fat diets are also beneficial in children by helping reduce cholesterol levels
    • However, monitoring of fat-soluble vitamin status in children on low-fat diet is recommended since this may reduce absorption of these vitamins
  • Avoid high carbohydrate diet in children with hypertriglyceridemia
  • Smoking cessation should also be implemented
  • Fish oil supplements are considered to have significant effects on TG levels in children, especially in those with end-stage renal insufficiency
  • Dietary supplementation with plant stanols and sterols (eg orange juice, yogurt drinks, cereal bars, margarines/ spreads, dietary supplements) may be considered for children with severe hypercholesterolemia or those who are at high risk
    • Above supplements may also reduce absorption of fat-soluble vitamins; monitoring of fat-soluble vitamin status is also recommended
  • Pharmacotherapy is generally reserved for those with severe dyslipidemia or those with genetic lipid disorders
  • Other candidates for pharmacotherapy include children and adolescents >8 years of age who satisfy the following criteria:
    • LDL-C level of ≥190 mg/dL or
    • LDL-C level of ≥160 mg/dL plus
      • Presence of ≥2 CAD risk factors
      • Family history of premature CAD (<55 years of age)
      • Being overweight or obese, or having other elements of insulin resistance syndrome
    • Pediatric diabetic patients with LDL level of ≥130 mg/dL
  • Pharmacotherapeutic options for pediatric dyslipidemia include the following:
    • Based on available evidence, statins are considered safe and effective 
      • Statin therapy can be initiated at 6-10 years of age for the treatment of children with familial hypercholesterolemia in addition to healthy lifestyle measures
    • Pediatric studies have demonstrated 15-20% reductions in LDL-C level with bile acid sequestrants
      • Cholestyramine is currently approved for hypercholesterolemia in children and should be initiated at <8 g daily
      • Safety and efficacy of Colestipol and Colesevelam have not yet been established in pediatric patients although Colestipol may be started at <10 g daily while Colesevelam is approved for children ≥8 years of age
      • Bile acid sequestrants may lead to folic acid and cholecalciferol depletion; multivitamins should therefore be used
      • Bile acid sequestrants should not be used in children with hypertriglyceridemia
    • Fibrates may be useful in children with severe hypertriglyceridemia and at increased risk of pancreatitis
      • Use of fibrates in children or adolescents with type I or V hyperlipoproteinemia warrants close monitoring
    • Ezetimibe may be used in children ≥10 years of age and adolescents with homozygous familial hypercholesterolemia or sitosterolemia
    • Evolocumab is used as an adjunct to diet and other LDL-C-lowering therapies in children ≥10 years of age and adolescents with heterozygous familial hypercholesterolemia
    • Experience with Niacin therapy in children is limited

COVID-19 and Lipid-lowering Therapy

  • Current evidence shows that lipid-lowering therapy is safe in patients with COVID-19 infection 
    • Lipid-lowering therapy should be continued in patients with confirmed COVID-19 diagnosis and abnormal liver function tests (LFTs) unless alanine transaminase (ALT) or aspartate transaminase (AST) progressively increases, a significant drug-drug interaction between the lipid-lowering agents and COVID-19 drugs has been identified, or patient is critically ill and/or cannot take oral medications 
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