Dyslipidemia resident survival guide: Difference between revisions

Dyslipidemia resident survival guide
Overview
Classification
Causes
Screening
Complete Diagnostic Approach
Treatment
Do's
Don'ts

VisualWikitext

Latest revision as of 18:58, 17 December 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D., Javaria Anwer M.D.[2]
Synonyms and keywords: HDL, LDL, VLDL, hyperlipidemia, hypolipidemia, statin

Overview

Dyslipidemia is a metabolic abnormality that leads to an increase in the plasma concentrations of cholesterol and triglycerides. Lipoprotein abnormalities can be classified on the bases of the pattern of change in the lipoprotein levels, etiology, and the type of lipid that is increased. Dyslipidemia can be caused by endocrine disorders such as hypothyroidism, diabetes mellitus, medications such as protease inhibitors or antihypertensive, anabolic steroid use, cholestasis, and autoimmune disorders. While screening the disease it is important to identify the cardiovascular disease risk factors among patients. Framingham Risk Assessment Tool and Reynolds Risk Score are utilized to screen for CVD risk and follow-up screening varies with the diabetes mellitus status, patient age, and gender. Treatment involves setting the target cholesterol levels of < 200 mg/dL, and LDL-C levels of < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other patients. HDL should be as high as possible. Lifestyle recommendations is the first step in treatment before pharmacotherapy. Pharmacotherapy includes monotherapy such as statins (monitor AST, ALT, and CK); fibrates; niacin; and bile acid sequestrants. Uncontrolled dyslipidemia requires combination therapy. Regular follow up with labs to access drug side effects and monitoring patient health is vital.

Classification

There are several ways in which lipoprotein abnormalities are classified. Lipoprotein disorders can be classified according to:

The pattern of change in the lipoprotein levels, described as hyperlipidemia (increase in lipid levels) and hypolipidemia (decrease in lipid levels): However, this classification is problematic because the lipids and lipoproteins levels in some situation can be elevated in some types of lipoproteins and lipids and decreased in others.

Phenotype, or the specific type of lipid that is increased, as classified by Fredrickson: This classification is problematic because it does not include abnormalities in the level of HDL.

Etiology, as primary (genetic) or secondary to another condition: This classification can be problematic because most conditions involve the intersection of genetics and lifestyle issues. However, there are a few well defined genetic conditions that are usually easy to identify.

Levels of measured lipids (cholesterol and triglycerides), described as hypercholesterolemia and hypocholesterolemia or hypertriglyceridemia and hypotriglyceridemia: This distinction is not specific because it does not reflect the specific lipoprotein(s) that are abnormally high or low.

Fredrickson Classification of Hyperlipoproteinemia^[1]^[2]^[3]^[4]

Hyperlipoproteinemia

Type I:
Familial hyperchylomicronemia

Type II

Type III:
Dysbetalipoproteinemia

Type IV:
Primary hypertriglyceridemia

Type V:
Mixed hyperlipoproteinemia

Type A:
Familial hypercholesterolemia

Type B:
Familial combined hyperlipidemia

Type A

Type B

Type C

**Fredrickson classification of Hyperlipidemias**
Hyperlipoproteinemia	Synonyms	Pathogenesis	Labs description	Treatment
Type I	Buerger-Gruetz syndrome, primary hyperlipoproteinaemia, or familial hyperchylomicronemia	Decreased lipoprotein lipase (LPL) or altered ApoC2	Elevated chylomicrons	Diet control
Type IIa	Polygenic hypercholesterolaemia or familial hypercholesterolemia	LDL receptor deficiency	Elevated LDL only	Bile acid sequestrants, statins, niacin
Type IIb	Combined hyperlipidemia	Decreased LDL receptor and increased ApoB	Elevated LDL, VLDL and triglycerides	Statins, niacin, gemfibrozil
Type III	Familial Dysbetalipoproteinemia	Defect in ApoE synthesis	Increased IDL	Drug of choice: Gemfibrozil
Type IV	Endogenous Hyperlipemia	Increased VLDL production and decreased elimination	Increased VLDL	Drug of choice: Niacin
Type V	Familial Hypertriglyceridemia	Increased VLDL production and decreased LPL	Increased VLDL and chylomicrons	Niacin, gemfibrozil

Unclassified forms

Non-classified forms are extremely rare:

Hypo-alpha lipoproteinemia^[5]
Hypo-beta lipoproteinemia (prevalence 0.01-0.1%)^[6]^[7]

Classification According to Etiology^[4]

Lipoprotein Disorders

Primary
(Genetic)

Secondary

LDL

Chylomicron Remnants

Lipoproteins Rich in Triglyceride
(Chylomicrons, VLDL, IDL)

HDL

Multiple lipoproteins

Alcohol
Diabetes
Drugs
Liver disease
Obesity
Renal disease
Smoking
Thyroid

High LDL:
-Familial hypercholesterolemia
-Familial defective apo B 100
-Autosomal dominant hypercholesterolemia (PCSK9)
-Autosomal recessive hypercholesterolemia
-Familial sitosterolemia
-Familial lipoprotein a lipoproteinemia

Low LDL:
-Abetalipoproteinemia
-Hypobetalipoproteinemia
-PCSK 9 deficiency

-Deficiency in hepatic lipase
-Type III dysbetalipoproteinemia

-Deficiency in lipoprotein lipase
-Deficiency in Apo C-II
-Deficiency in Apo A-V
-Familial combined hyperlipidemia
-Familial hypertriglyceridemia
- Chylomicron retention disease

High LDL:
-Cholesteryl ester transferase protein deficiency

Low HDL:
-Deficiency in Apo A-I
-Deficiency in lecithin cholesterol acyltransferase (LCAT)
-Familial hypoalphalipoproteinemia
-Niemann-Pick disease
-Tangier disease

- Familial combined hypolipidemia (ANGPTL3)

Classification According to Laboratory Results^[8]^[9]^[10]

Lipid Laboratory Tests

Total cholesterol

LDL-C

HDL-C

Triglycerides

High total cholesterol

Low total cholesterol

Causes

Secondary causes of dyslipidemia may cause either an increase in total-cholesterol & low density lipoprotein-cholesterol (LDL-C) or an increase in total triglycerides & very low density lipoprotein cholesterol (VLDL-C). Common causes are listed below.

Increase in Total Cholesterol and LDL-C

Hypothyroidism^[11]
Nephrosis^[12]
Dysgammaglobulinemia (systemic lupus erythematosus, multiple myeloma)
Cholestatic hepatic diseases due to abnormal lipoproteins (e.g. primary biliary cirrhosis)^[13]
Administration of protease inhibitors (treatment for HIV infection)^[14]
Administration of progestin or anabolic steroids^[15]

Increase in Total Triglycerides and VLDL-C

Chronic kidney disease^[16]
Type 2 diabetes mellitus^[17]^[18]
Obesity^[19]
Excessive alcohol intake, poor diet^[18]
Hypothyroidism^[18]
Administration of anti-hypertensive therapy (thiazide diuretics or B-blockers)^[20]
Administration of corticosteroids, retinoids (depends on the duration of use and type of steroid)^[18]^[21]
Severe stress that increases endogenous corticosteroid concentration^[18]
Elevated concentrations of estrogen (administration of oral (not transdermal) estrogen therapy, oral contraceptives, or pregnancy)^[18]
Administration of protease inhibitors (treatment for HIV infection)

To view a comprehensive list of dyslipidemia causes, click here

Screening

The following algorithm explains the approach to screening for dyslipidemia patients.^[22]^[23]^[24]^[25]^[26]^[27]
Abbreviations: ASA: American society of anesthesiologists; BP: Blood Pressure; CCS: Canadian cardiovascular society; CrCl: Creatinine clearance; CXR: Chest X-ray; DNI: Do not intubate; DNR: Do not resuscitate; ECG: Electrocardiogram; eGFR: estimated glomerular filtration rate; HR:Heart rate; INR: International normalized ratio; LMWH: Low molecular weight heparin; LV: Left ventricle; LVED: Left ventricular ejection fraction; NOAC: Novel oral anticoagulant; NPO: Nothing per os; PMI: Point of maximal impulse; PT: Prothrombin time; RR: Respiratory rate; SpO2: Oxygen saturation; T: Temperature; VT: Ventricular tachycardia

Identify risk factors for CAD

Major risk factors:

❑ Advanced age

❑ ↑ total serum cholesterol

❑ ↑ non-HDL-C (calculated by: total cholesterol minus HDL-C)

❑ ↑ LDL-C (either measured or calculated by: total cholesterol minus HDL-c minus (total triglycerides/5))

❑ ↓ HDL-C

❑ Diabetes mellitus

❑ Hypertension

❑ Cigarette smoking

❑ Family history of CAD

Additional risk factors:

❑ Obesity, especially abdominal

❑ Family history of hyperlipidemia

❑ Small, dense LDL-C

❑ ↑ Apo-B

❑ ↑ LDL particle number (measured by ApoB)

❑ Fasting/postprandial hypertriglyceridemia

❑ Polycystic ovarian syndrome

❑ Dyslipidemic triad

Non-traditional risk factors:

❑ ↑ lipoprotein

❑ ↑ clotting factors

❑ Inflamamtory markers (e.g. hsCRP or Lipoprotein-associated phospholipase A2 (Lp-PLA2)

❑ Hyperhomocysteinemia

❑ ApoE4 isoform

❑ ↑ uric acid

Determine the 10-year risk of coronary event using ANY of the following assessment tools:

❑ Framingham Risk Assessment Tool (To be redirected to Framingham Risk Assessment Tool, click here)

❑ Reynolds Risk Score (To be redirected to Reynolds Risk Score website, click here)

High
(Framingham 10-year global risk > 20%)

Intermediate
(Framingham 10-year global risk between 10% and 20%)

Lower
(Framingham 10-year global risk < 10%)

Optimal
(Framingham 10-year global risk < 10% with optimal levels or risk factors and heart-healthy lifestyle)

Does the patient have type 2 diabetes mellitus?

Yes

No

Does the patient have ALL the following criteria for low-risk dyslipidemia during previous work-up?

❑ Low LDL-C < 100 mg/dL, AND

❑ HDL-C > 50 mg/dL, AND

❑ Triglycerides < 150 mg/dL

Adult patient

Pediatric patient (age at least 2 years)

Yes. The patient has ALL of the criteria for low-risk dyslipidemia

Either unknown history of lipid profile or No, the patient does not have ALL of the criteria for low-risk dyslipidemia (at least 1 criterion is not met)

Does that patient have risk factors for CAD (listed above)?

Does the patient have risk factors for CAD (listed above)?

Screen every 2 years

Screen annually

No

Yes

No

Screen patient more frequently than patients with no risk factors based on clinical judgement (unknown optimal interval)

Male patient

Female patient

Screen every 3 to 5 years

Do not screen patient for dyslipidemia

Age between 20 and 45 years

Age > 45 years to 65 years

Age > 65 years

Age between 20 years and 55 years

Age > 55 years to 65 years

Age > 65 years

Screen every 5 years

More frequent screening is recommended for patients with risk factors for CAD (shown above)

Screen every 1 to 2 years

More frequent screening is recommended for patients with risk factors for CAD (shown above)

Screen annually

Screen every 5 years

More frequent screening is recommended for patients with risk factors for CAD (shown above)

Screen every 1 to 2 years

More frequent screening is recommended for patients with risk factors for CAD (shown above)

Screen annually

Complete Diagnostic Approach

The algorithm explains the approach to the diagnosis of dyslipidemia.^[28]^[29]^[30]
Boxes in red signify that an urgent management is needed.

Abbreviations: ASA: American society of anesthesiologists; BP: Blood Pressure; CCS: Canadian cardiovascular society; CrCl: Creatinine clearance; CXR: Chest X-ray; DNI: Do not intubate; DNR: Do not resuscitate; ECG: Electrocardiogram; eGFR: estimated glomerular filtration rate; HR:Heart rate; INR: International normalized ratio; LMWH: Low molecular weight heparin; LV: Left ventricle; LVED: Left ventricular ejection fraction; NOAC: Novel oral anticoagulant; NPO: Nothing per os; PMI: Point of maximal impulse; PT: Prothrombin time; RR: Respiratory rate; SpO2: Oxygen saturation; T: Temperature; VT: Ventricular tachycardia

Obtain a Detailed History

History of present illness

❑ Address specific patient symptoms and complaints

❑ Obtain review of systems relevant to dyslipidemia and diseases associated with dyslipidemia

❑ Headache

❑ Dizziness

❑ Syncope/presyncope

❑ Blurry vision / double vision / reduced visual acuity

❑ Dysphagia

❑ Slurred speech

❑ Facial drooping

❑ Chest pain / Angina

❑ Palpitations

❑ Dyspnea

❑ Cough

❑ Abdominal pain

❑ Change in bowel movements

❑ Lower extremity pain, weakness, or tingling

❑ Peripheral edema

❑ Muscle pain

❑ Intake of dietary fat, saturated fat, fiber, and cholesterol intake

❑ Exercise patterns

❑ History of alcohol use

❑ History of smoking

Past Medical History
❑ History of previous medical diagnoses / past medical complaints/hospitalizations and surgeries

❑ History of CAD or myocardial infarction

❑ History of diabetes mellitus

❑ History of hypertension

❑ History of renal disease

❑ History of hepatic disease

❑ History of stroke (ischemic or hemorrhagic) or transient ischemic attack (TIA)

❑ History of hypothyroidism

Medications

❑ Currently prescribed medications

❑ List of over-the-counter drugs

❑ Previous intake of medications and reason for discontinuation

❑ History of drug adverse effects

❑ History of herbs and supplement use

❑ Compliance to medications

Allergies

❑ Known drug allergies

❑ Known environmental/food allergies

Family history
❑ Family history of dyslipidemia

❑ Family history of premature CAD (i.e. Established CAD in father or 1st-degree male relative before the age of 55 years OR established CAD in mother or 1st-degree female relative before the age of 65 years)

❑ Family history of hypothyroidism

❑ Family history of stroke/TIA

❑ Family history of peripheral vascular disease

Social History
❑ Overall living situation

❑ Occupation

❑ Exercise

❑ Diet (general)

❑ Smoking history

❑ Alcohol use

❑ Recreational drug use

❑ Stress

❑ Sexual lifestyle & contraceptive methods

Assess for CAD Risk Factors

Major risk factors:

❑ Advanced age

❑ ↑ total serum cholesterol

❑ ↑ non-HDL-C (calculated by: total cholesterol minus HDL-C)

❑ ↑ LDL-C (either measured or calculated by: total cholesterol minus HDL-c minus (total triglycerides/5))

❑ ↓ HDL-C

❑ Diabetes mellitus

❑ Hypertension

❑ Cigarette smoking

❑ Family history of CAD

Additional risk factors:

❑ Obesity, especially abdominal

❑ Family history of hyperlipidemia

❑ Small, dense LDL-C

❑ ↑ Apo-B

❑ ↑ LDL particle number (measured by ApoB)

❑ Fasting/postprandial hypertriglyceridemia

❑ Polycystic ovarian syndrome

❑ Dyslipidemic triad

Non-traditional risk factors:

❑ ↑ lipoprotein

❑ ↑ clotting factors

❑ Inflammatory markers (e.g. hsCRP or Lipoprotein-associated phospholipase A2 (Lp-PLA2)

❑ Hyperhomocysteinemia

❑ ApoE4 isoform

❑ ↑ uric acid

Evaluate possible causes of secondary dyslipidemia if suggested by findings during history-taking and physical examination
To view a complete list of dyslipidemia causes, click here

Determine the 10-year risk of coronary event using ANY of the following assessment tools:

❑ Framingham Risk Assessment Tool (To be redirected to Framingham Risk Assessment Tool, click here)

❑ Reynolds Risk Score (To be redirected to Reynolds Risk Score website, click here)

Examine the patient

Vital signs
❑ High blood pressure
Skin
❑ Xanthomas (eruptive, tuberous, tendinous)
❑ Xanthelesma
❑ Cool hairless extremities (suggestive of peripheral vascular disease)
❑ Other skin rashes that may be suggestive of secondary causes (e.g. systemic lupus erythematosus, drug eruptions, pregnancy rash)
HEENT
❑ Arcus senilis (corneal arcus)
Neck
❑ Carotid bruits
❑ Thyromegaly (when dyslipidemia is caused by [[]]thyroid disease)
Peripheral
❑ Diminished distal pulses

❑ Femoral bruits

Order tests to rule out secondary causes of dyslipidemia

Common causes include:

❑ Hypothyroidism

❑ Order TSH, FT4, and FT3

❑ Nephrosis

❑ Order serum creatinine and urinalysis with either spot urine for proteins or 24-hour urinary collection for proteins, urinary protein to creatinine ratio

❑ Dysgammaglobulinemia

❑ Order ANA, anti-dsDNA antibodies, plasma and urine electrophoresis

❑ Cholestatic hepatic diseases

❑ Order GGT, ALP, and bilirubins

❑ Chronic kidney disease

❑ Order serum creatinine, BUN, urinalysis, and renal ultrasound

❑ Type 2 diabetes mellitus

❑ Order glycemia and HbA1c

❑ Excessive alcohol intake
❑ Drugs

❑ Any of the following: estrogen, progestin, protease inhibitors, beta-blockers, corticosteroids, anabolic steroids, protease inhibitors

Order fasting lipid profile

Total cholesterol

❑ Optimal: < 200 mg/dL
❑ Borderline: 200-239 mg/dL
❑ High/very high risk: ≥ 240 mg/dL

LDL-C

May be either calculated or measured. Measured LDL-C is preferable, especially among certain high-risk populations (elevated triglycerides > 250 mg/dL, diabetes mellitus, peripheral vascular disease).
To calculate LDL-C, use the following equation: LDL-C=(total cholesterol-HDL-C)/(triglycerides/5). Do NOT calculate LDL-C when triglycerides > 200 mg/dL (low to no validity of the equation). Instead, use measured LDL-C.

❑ Optimal: < 100 mg/dL
❑ Borderline: 130-160 mg/dL
❑ High risk: 160-189 mg/dL
❑ Very high risk: ≥ 190 mg/dL

HDL-C

An optimal HDL-C concentration is a negative CAD risk factor in both genders (subtract 1 risk factor for CAD)

❑ Optimal: ≥ 60 mg/dL
❑ Borderline: 40-50 mg/dL (men) OR 50-59 mg/dL (women)
❑ High/very high risk: < 40 mg/dL (men) OR < 50 mg/dL (women)

Triglycerides

❑ Optimal: < 150 mg/dL
❑ Borderline: 150-199 mg/dL
❑ High risk: 200-499 mg/dL
❑ Very high risk: ≥ 500 mg/dL

Additional tests

❑ Non-HDL
non-HDL is calculated by the following equation: non-HDL=total cholesterol - HDL-C
non-HDL-C provides additional risk assessment information compared with LDL-C alone.
Calculate non-HDL-C only in the following cases: Either moderate elevation of triglyceride (between 200 to 500 mg/dL), diabetes mellitus, insulin resistance syndrome, or established CAD

❑ ApoB
ApoB reflects LDL-C particle number, which may be a more potent measure of CVD risk than either LDL-C or LDL-C particle size
Optimal: < 90 mg/dL for patients with at risk of CAD (including diabetes mellitus) OR < 80 mg/dL for patients with established CAD or diabetes mellitus plus at least 1 additional risk factor

❑ Ratio of ApoB/ApoAI
May be useful in evaluating residual risk (independent of LDL-C) in patients at high risk of CAD or patients with either established CAD, diabetes mellitus, or insulin resistance

❑ hsCRP
Order hsCRP for patients with borderline risk or patients with LDL-C < 130 mg/dL
hsCRP helps further stratify patient risk for CVD

❑ LP-PLA2
May provide more specificity than hsCRP and may be ordered for further stratification of CVD risk

Treatment

The algorithm demonstrates the treatment strategy for patients with confirmed dyslipidemia. ^[31]^[32]^[33]^[34]^[35]

Confirmed Dyslipidemia

Set lipid goals

❑ Total cholesterol target: < 200 mg/dL

❑ LDL-C target: < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other patients

❑ HDL-C target: As high as possible. At least > 40 mg/dL in both genders

❑ Non-HDL-C target: 30 mg/dL above LDL-C goal (target < 100 mg/dL for very high risk patients OR < 130 mg/dL for all other patients)

❑ Triglycerides target: < 150 mg/dL

❑ ApoB target: < 90 mg/dL for patients at risk of CAD (including patients with diabetes) or < 80 mg/dL for patients with established CAD or diabetes plus at least one additional CAD risk factor

Control modifiable CAD risk factors

❑ Hypertension

❑ Diabetes mellitus

❑ Obesity

❑ Cigarette smoking

Recommend lifestyle modification

❑ Recommend physical activity

❑ At least 30 minutes of moderate-intensity physical activity 4 to 6 times weekly

❑ Examples include brisk walking, riding a stationary bicycle, water aerobics, cleaning/scrubbing/ mowing lawn, and sporting activities

❑ Recommend medical nutrition therapy (reduced calorie intake)

❑ Advise patients to have at least 5 servings/day of vegetables and fruits

❑ Advise patients to have more than 6 servings/day of grains, at least 1/3 of which are whole grain

❑ Advise patients to limit intake of saturated fat, trans-fats, and cholesterol

❑ Smoking cessation

Lipid goal achieved with lifestyle modification alone?

Yes

No

Administer pharmacologic monotherapy
Table of available classes, generic names, recommended daily doses, and dose ranges also available below algorithm. Click here.

Statins
Administration of any of the following statins is recommended to manage dyslipidemia

❑ Lovastatin: Recommended starting daily dose 20 mg PO once daily at bedtime. Dose range: 10-80 mg

❑ Pravastatin: Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 10-80 mg

❑ Simvastatin: Recommended starting daily dose 20-40 mg PO once daily at bedtime. Dose range: 5-80 mg (80 mg not approved for therapy unless patient has been on treatment for more than 1 year without myopathy)

❑ Fluvastatin: Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 20-80 mg

❑ Atorvastatin: Recommended starting daily dose 10-20 mg PO once daily at bedtime. Dose range: 10-80 mg

❑ Rosuvastatin: Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 5-40 mg

❑ Pitavastatin: Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-4 mg

Safety Monitoring with Statins
If statin therapy is to be initiated, the following lab parameters should be monitored

❑ Liver transaminases (AST and ALT) should be measured among all patients (symptomatic and asymptomatic) as follows:

❑ Before initiation of statin therapy (baseline)

❑ At 3 months following initiation of statin therapy due to the high risk of hepatotoxicity within 3 months of therapy.

❑ Every 6 months thereafter

❑ Creatine kinase (CK) should be measured only among symptomatic patients who complain of muscle pain/weakness

Fibrates
Administration of any of the following fibrates is recommended to manage dyslipidemia
❑ Fenofibrate: Recommended starting daily dose 48-145 mg PO once daily. Dose range: 48-145 mg

❑ Gemfibrozil: Recommended starting daily dose 1200 mg PO once daily. Dose range: 1200 mg

❑ Fenofibric acid: Recommended starting daily dose 45-135 mg PO once daily. Dose range: 45-135 mg

Safety Monitoring with Fibric Acid
If fibric acid therapy is to be initiated, the following lab parameters should be monitored

❑ Liver transaminases (AST and ALT) measured as follows:

❑ Before initiation of statin therapy (baseline)

❑ At 3 months following initiation of fibric acid therapy due to the high risk of hepatotoxicity within 3 months of therapy.

❑ Every 6 months thereafter

Nacin

❑ Immediate release: Recommended starting daily dose 250 mg PO once daily at bedtime. Dose range: 250-3000 mg
❑ Extended release: Recommended starting daily dose 500 mg PO once daily at bedtime. Dose range: 50-2000 mg

Safety Monitoring with Niacin
If niacin therapy is to be initiated, the following lab parameters should be monitored

❑ Liver transaminases (AST and ALT) should be measured among asymptomatic patients as follows:

❑ Before initiation of niacin therapy (baseline)

❑ Every 3 months following initiation of niacin therapy for the first year

❑ Every 6 months thereafter

Bile acid sequestrants
Administration of any of the following bile acid sequestrants is recommended to manage dyslipidemia
❑ Cholestyramine: Recommended starting daily dose 8-16 mg PO once daily at bedtime. Dose range: 4-24 mg
❑ Colestipol: Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-16 mg
❑ Colesevelam: Recommended starting daily dose 3.8 mg PO once daily at bedtime. Dose range: 3.8-4.5 mg

Cholesterol absorption inhibitors

❑ Ezetimibe: Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 10 mg

Aim to reduce LDL

❑ Statin monotherapy at a recommended initial daily dose (LDL reduction: 21% to 55%)

❑ Fibrate monotherapy at a recommended initial daily dose (LDL reduction: 20% to 25%)

❑ Niacin monotherapy at a recommended initial daily dose (LDL reduction: 10% to 25%)

❑ Bile acid sequestrant monotherapy at a recommended initial daily dose (LDL reduction: 10% to 25%)

❑ Ezetimibe monotherapy at recommended initial daily dose (LDL reduction: 10% to 18%)

Aim to reduce triglycerides

❑ Fibrates monotherapy at a recommended initial daily dose with or without omega-3 fish oil (triglyceride reduction: 20% to 35%)

❑ Niacin monotherapy at recommended initial daily dose with or without omega-3 fish oil (triglyceride reduction: 20% to 30%)

Aim to increase HDL

❑ Niacin monotherapy at a recommended initial daily dose (HDL increase: 10% to 35%)

❑ Fibrates monotherapy at recommended initial daily dose (HDL increase: 6% to 18%)

❑ Statin monotherapy at recommended initial daily dose (HDL increase: 2% to 10%)

Lipid goal achieved with optimal administration of antilipidemic monotherapy?

Yes

No

Does the patient have ANY of the following criteria to initiate combination pharmacotherapy?

❑ Markedly elevated cholesterol concentration, OR

❑ Mixed dyslipidemia (e.g. Hypertriglyceridemia and reduced HDL-C), OR

❑ Patient developed or at high risk of developing drug-associated, dose-dependent adverse effects

No

Yes

❑ Consider changing drug class

❑ Reassess liver transaminase when changing drug class for statin, niacin, and fibrates

❑ Consider increasing dose of antilipidemic agent within dose range for each drug

❑ Reassess liver transaminase when increase dose for any of statin, niacin, or fibrates

Lipid goal achieved with optimal administration of antilipidemic monotherapy?

Yes

No

Administer combination therapy

Administer ANY of the following combination therapies:
❑ Ezetimibe/simvastatin (1 pill): Recommended starting daily dose 10/20 mg PO once daily at bedtime. Dose range: 10/10 to 10/80 mg, OR
❑ Extended-release niacin/simvastatin (1 pill): Recommended starting daily dose 500/20 mg PO once daily at bedtime. Dose range: 500/20 to 1000/20 mg

❑ Statin ± ezetimibe/ Alirocumab (a PCSK9 inhibitor)

Follow-up

❑ Reassess lipid profile at 6 weeks following initiation of management

❑ If the goal is not achieved following 6 weeks, reassess 6 weeks later. Continue 6-week interval until target lipid profile is achieved

❑ Once the target lipid profile is achieved, generally reassess lipid profile within 6 months to 12 months

❑ Consider more frequent lipid profile reassessments in the following conditions

❑ Deterioration of diabetic control

❑ Administration of a new drug that is known to affect the lipid profile

❑ Progression of atherothrombotic disease

❑ Considerable weight gain

❑ Unexpected adverse derangement in any parameter of the lipid profile

❑ Development of new risk factor for CAD

❑ For all patients (symptomatic or asymptomatic) receiving either statin, fibric acid, or niacin, assess liver tranaminases (AST and ALT) at 3 months

❑ For patients receiving either statin or fibric acid: Repeat liver transaminase reassessment every 6 months thereafter.

❑ For patients receiving niacin: Repeat liver transaminase reassessment every 3 months for the first year, then every 6 months thereafter.

❑ For patients receiving statin therapy who are complaining of significant myalgia or muscle weakness

❑ Assess creatine kinase (CK) to confirm or rule out myopathy

Do's

Treat pediatric patients who are older than 8 years of age with either LDL-C > 190 mg/dL or LDL > 160 mg/dL plus any of the following conditions: either ≥ 2 CV risk factors even after lifestyle intervention, family history of premature CAD, or overweight/obese/insulin resistance.^[36]

Don'ts

Do not routinely order homocysteine, uric acid, plasminogen activator inhibitor 1, or other inflammatory markers.
Do not routinely perform non-invasive measures of atherosclerosis (e.g. carotid intima media thickness).^[37]
Do not treat dyslipidemia among postmenopausal women with hormonal replacement therapy.^[38]

References

↑ Fredrickson, Donald S. (1971). "An International Classification of Hyperlipidemias and Hyperlipoproteinemias". Annals of Internal Medicine. 75 (3): 471. doi:10.7326/0003-4819-75-3-471. ISSN 0003-4819.
↑ Sánchez Fayos J, Prieto E, Chica Gullón E (April 1998). "[Chronic granulocytic leukemia (Ph+): among yesterday's myeloproliferative syndromes, today's chronic myeloid leukemias, and tomorrow's mature-element monocellular myelopathies]". Sangre (Barc) (in Spanish; Castilian). 43 (2): 121–6. PMID 9656773.
↑ Levy, Robert I.; Fredrigkson, Donald S. (1968). "Diagnoses and management of hyperlipoproteinemia". The American Journal of Cardiology. 22 (4): 576–583. doi:10.1016/0002-9149(68)90165-3. ISSN 0002-9149.
↑ ^4.0 ^4.1 Hegele RA, Ban MR, Hsueh N, Kennedy BA, Cao H, Zou GY, Anand S, Yusuf S, Huff MW, Wang J (November 2009). "A polygenic basis for four classical Fredrickson hyperlipoproteinemia phenotypes that are characterized by hypertriglyceridemia". Hum Mol Genet. 18 (21): 4189–94. doi:10.1093/hmg/ddp361. PMC 2758142. PMID 19656773.
↑ Pisciotta L, Calabresi L, Lupattelli G, Siepi D, Mannarino MR, Moleri E, Bellocchio A, Cantafora A, Tarugi P, Calandra S, Bertolini S (September 2005). "Combined monogenic hypercholesterolemia and hypoalphalipoproteinemia caused by mutations in LDL-R and LCAT genes". Atherosclerosis. 182 (1): 153–9. doi:10.1016/j.atherosclerosis.2005.01.048. PMID 16115486.
↑ Schonfeld G (May 2003). "Familial hypobetalipoproteinemia: a review". J Lipid Res. 44 (5): 878–83. doi:10.1194/jlr.R300002-JLR200. PMID 12639976.
↑ Garcia-Dorado, David (2012). Metabolomics in Cardiovascular Disease: Towards Clinical Application. City: INTECH Open Access Publisher. ISBN 978-953-51-0344-8.
↑ Herrmann W, Lackner KJ, Schmitz G (1994). "[Classification of hyperlipoproteinemias and interpretation of laboratory parameters]". Wien Med Wochenschr (in German). 144 (12–13): 292–9. PMID 8650932.
↑ Nelson RH (March 2013). "Hyperlipidemia as a risk factor for cardiovascular disease". Prim Care. 40 (1): 195–211. doi:10.1016/j.pop.2012.11.003. PMC 3572442. PMID 23402469.
↑ Al-Agha AE, Alnawab AM, Hejazi TM (November 2016). "Diverse etiology of hyperlipidemia among hospitalized children in Western region of Saudi Arabia". Saudi Med J. 37 (11): 1234–1238. doi:10.15537/smj.2016.11.16328. PMC 5303801. PMID 27761562.
↑ Rizos CV, Elisaf MS, Liberopoulos EN (2011). "Effects of thyroid dysfunction on lipid profile". Open Cardiovasc Med J. 5: 76–84. doi:10.2174/1874192401105010076. PMC 3109527. PMID 21660244.
↑ Agrawal S, Zaritsky JJ, Fornoni A, Smoyer WE (January 2018). "Dyslipidaemia in nephrotic syndrome: mechanisms and treatment". Nat Rev Nephrol. 14 (1): 57–70. doi:10.1038/nrneph.2017.155. PMC 5770189. PMID 29176657.
↑ Longo M, Crosignani A, Battezzati PM, Squarcia Giussani C, Invernizzi P, Zuin M, Podda M (August 2002). "Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis". Gut. 51 (2): 265–9. doi:10.1136/gut.51.2.265. PMC 1773333. PMID 12117892.
↑ Lo J (April 2011). "Dyslipidemia and lipid management in HIV-infected patients". Curr Opin Endocrinol Diabetes Obes. 18 (2): 144–7. doi:10.1097/MED.0b013e328344556e. PMC 3154840. PMID 21297466.
↑ Min, Li; Simon W, Rabkin (2018). "Extremely Low HDL Cholesterol and Increased LDL Cholesterol Induced by the use of Anabolic Steroids in a Body Builder: A Case Study". International Journal of Sports and Exercise Medicine. 4 (4). doi:10.23937/2469-5718/1510109. ISSN 2469-5718.
↑ Mikolasevic I, Žutelija M, Mavrinac V, Orlic L (2017). "Dyslipidemia in patients with chronic kidney disease: etiology and management". Int J Nephrol Renovasc Dis. 10: 35–45. doi:10.2147/IJNRD.S101808. PMC 5304971. PMID 28223836.
↑ Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, Shochat T, Rudich A (October 2008). "Changes in triglyceride levels over time and risk of type 2 diabetes in young men". Diabetes Care. 31 (10): 2032–7. doi:10.2337/dc08-0825. PMC 2551650. PMID 18591400.
↑ ^18.0 ^18.1 ^18.2 ^18.3 ^18.4 ^18.5 Brahm A, Hegele RA (March 2013). "Hypertriglyceridemia". Nutrients. 5 (3): 981–1001. doi:10.3390/nu5030981. PMC 3705331. PMID 23525082.
↑ Klop B, Elte JW, Cabezas MC (April 2013). "Dyslipidemia in obesity: mechanisms and potential targets". Nutrients. 5 (4): 1218–40. doi:10.3390/nu5041218. PMC 3705344. PMID 23584084.
↑ Dordain M, Chevrie Muller C, Guidet C (1978). "[Tachylalia: clinical and acoustic study of 149 subjects (author's transl)]". Acta Neurol Belg (in French). 78 (6): 354–72. PMID 34973.
↑ Vakhitov M, Al'bitskiĭ V (1971). "[Methods of calculating indices of child mortality]". Sov Zdravookhr (in Russian). 30 (4): 43–5. PMID 5155420. Vancouver style error: initials (help)
↑ "Assessing Cardiovascular Risk: Systematic Evidence Review from the Risk Assessment Work Group | NHLBI, NIH".
↑ "Reynolds Risk Score".
↑ Berry JD, Lloyd-Jones DM, Garside DB, Greenland P (July 2007). "Framingham risk score and prediction of coronary heart disease death in young men". Am Heart J. 154 (1): 80–6. doi:10.1016/j.ahj.2007.03.042. PMC 2279177. PMID 17584558.
↑ Jahangiry L, Farhangi MA, Rezaei F (November 2017). "Framingham risk score for estimation of 10-years of cardiovascular diseases risk in patients with metabolic syndrome". J Health Popul Nutr. 36 (1): 36. doi:10.1186/s41043-017-0114-0. PMC 5682637. PMID 29132438.
↑ Damkondwar DR, Raman R, Suganeswari G, Kulothungan V, Sharma T (2012). "Assessing Framingham cardiovascular risk scores in subjects with diabetes and their correlation with diabetic retinopathy". Indian J Ophthalmol. 60 (1): 45–8. doi:10.4103/0301-4738.91344. PMC 3263245. PMID 22218246.
↑ Awad AI, Alsaleh FM (2015). "10-year risk estimation for type 2 diabetes mellitus and coronary heart disease in Kuwait: a cross-sectional population-based study". PLoS One. 10 (1): e0116742. doi:10.1371/journal.pone.0116742. PMC 4309592. PMID 25629920.
↑ Hajar R (2017). "Risk Factors for Coronary Artery Disease: Historical Perspectives". Heart Views. 18 (3): 109–114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17. PMC 5686931. PMID 29184622.
↑ Nadeem M, Ahmed SS, Mansoor S, Farooq S (January 2013). "Risk factors for coronary heart disease in patients below 45 years of age". Pak J Med Sci. 29 (1): 91–6. doi:10.12669/pjms.291.2828. PMC 3809218. PMID 24353515.
↑ Ahsan SK (November 1997). "Dyslipidemia: clinical approaches, evaluation of methods and strategies for standardization". Indian J Med Sci. 51 (11): 420–5. PMID 9567502.
↑ Ahmed SM, Clasen ME, Donnelly JE (May 1998). "Management of dyslipidemia in adults". Am Fam Physician. 57 (9): 2192–2204, 2207–8. PMID 9606309.
↑ Tonkin A, Byrnes A (2014). "Treatment of dyslipidemia". F1000Prime Rep. 6: 17. doi:10.12703/P6-17. PMC 3944745. PMID 24669298.
↑ Zodda D, Giammona R, Schifilliti S (January 2018). "Treatment Strategy for Dyslipidemia in Cardiovascular Disease Prevention: Focus on Old and New Drugs". Pharmacy (Basel). 6 (1). doi:10.3390/pharmacy6010010. PMC 5874549. PMID 29361723.
↑ Rubba P, Marotta G, Gentile M (2009). "Efficacy and safety of rosuvastatin in the management of dyslipidemia". Vasc Health Risk Manag. 5 (1): 343–52. doi:10.2147/vhrm.s3662. PMC 2672446. PMID 19436657.
↑ Rhee EJ, Kim HC, Kim JH, Lee EY, Kim BJ, Kim EM, Song Y, Lim JH, Kim HJ, Choi S, Moon MK, Na JO, Park KY, Oh MS, Han SY, Noh J, Yi KH, Lee SH, Hong SC, Jeong IK (July 2019). "2018 Guidelines for the management of dyslipidemia". Korean J Intern Med. 34 (4): 723–771. doi:10.3904/kjim.2019.188. PMC 6610190 Check |pmc= value (help). PMID 31272142.
↑ Eiland LS, Luttrell PK (July 2010). "Use of statins for dyslipidemia in the pediatric population". J Pediatr Pharmacol Ther. 15 (3): 160–72. PMC 3018249. PMID 22477808.
↑ Zhang, Y.; Guallar, E.; Qiao, Y.; Wasserman, B. A. (2014). "Is Carotid Intima-Media Thickness as Predictive as Other Noninvasive Techniques for the Detection of Coronary Artery Disease?". Arteriosclerosis, Thrombosis, and Vascular Biology. 34 (7): 1341–1345. doi:10.1161/ATVBAHA.113.302075. ISSN 1079-5642.
↑ Phan BA, Toth PP (2014). "Dyslipidemia in women: etiology and management". Int J Womens Health. 6: 185–94. doi:10.2147/IJWH.S38133. PMC 3923614. PMID 24532973.

[Fredrickson1971-1] Fredrickson, Donald S. (1971). "An International Classification of Hyperlipidemias and Hyperlipoproteinemias". Annals of Internal Medicine. 75 (3): 471. doi:10.7326/0003-4819-75-3-471. ISSN 0003-4819.

[pmid9656773-2] Sánchez Fayos J, Prieto E, Chica Gullón E (April 1998). "[Chronic granulocytic leukemia (Ph+): among yesterday's myeloproliferative syndromes, today's chronic myeloid leukemias, and tomorrow's mature-element monocellular myelopathies]". Sangre (Barc) (in Spanish; Castilian). 43 (2): 121–6. PMID 9656773.

[LevyFredrigkson1968-3] Levy, Robert I.; Fredrigkson, Donald S. (1968). "Diagnoses and management of hyperlipoproteinemia". The American Journal of Cardiology. 22 (4): 576–583. doi:10.1016/0002-9149(68)90165-3. ISSN 0002-9149.

[pmid19656773-4] 4.0 ^4.1 Hegele RA, Ban MR, Hsueh N, Kennedy BA, Cao H, Zou GY, Anand S, Yusuf S, Huff MW, Wang J (November 2009). "A polygenic basis for four classical Fredrickson hyperlipoproteinemia phenotypes that are characterized by hypertriglyceridemia". Hum Mol Genet. 18 (21): 4189–94. doi:10.1093/hmg/ddp361. PMC 2758142. PMID 19656773.

[pmid16115486-5] Pisciotta L, Calabresi L, Lupattelli G, Siepi D, Mannarino MR, Moleri E, Bellocchio A, Cantafora A, Tarugi P, Calandra S, Bertolini S (September 2005). "Combined monogenic hypercholesterolemia and hypoalphalipoproteinemia caused by mutations in LDL-R and LCAT genes". Atherosclerosis. 182 (1): 153–9. doi:10.1016/j.atherosclerosis.2005.01.048. PMID 16115486.

[pmid12639976-6] Schonfeld G (May 2003). "Familial hypobetalipoproteinemia: a review". J Lipid Res. 44 (5): 878–83. doi:10.1194/jlr.R300002-JLR200. PMID 12639976.

[7] Garcia-Dorado, David (2012). Metabolomics in Cardiovascular Disease: Towards Clinical Application. City: INTECH Open Access Publisher. ISBN 978-953-51-0344-8.

[pmid8650932-8] Herrmann W, Lackner KJ, Schmitz G (1994). "[Classification of hyperlipoproteinemias and interpretation of laboratory parameters]". Wien Med Wochenschr (in German). 144 (12–13): 292–9. PMID 8650932.

[pmid23402469-9] Nelson RH (March 2013). "Hyperlipidemia as a risk factor for cardiovascular disease". Prim Care. 40 (1): 195–211. doi:10.1016/j.pop.2012.11.003. PMC 3572442. PMID 23402469.

[pmid27761562-10] Al-Agha AE, Alnawab AM, Hejazi TM (November 2016). "Diverse etiology of hyperlipidemia among hospitalized children in Western region of Saudi Arabia". Saudi Med J. 37 (11): 1234–1238. doi:10.15537/smj.2016.11.16328. PMC 5303801. PMID 27761562.

[pmid21660244-11] Rizos CV, Elisaf MS, Liberopoulos EN (2011). "Effects of thyroid dysfunction on lipid profile". Open Cardiovasc Med J. 5: 76–84. doi:10.2174/1874192401105010076. PMC 3109527. PMID 21660244.

[pmid29176657-12] Agrawal S, Zaritsky JJ, Fornoni A, Smoyer WE (January 2018). "Dyslipidaemia in nephrotic syndrome: mechanisms and treatment". Nat Rev Nephrol. 14 (1): 57–70. doi:10.1038/nrneph.2017.155. PMC 5770189. PMID 29176657.

[pmid12117892-13] Longo M, Crosignani A, Battezzati PM, Squarcia Giussani C, Invernizzi P, Zuin M, Podda M (August 2002). "Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis". Gut. 51 (2): 265–9. doi:10.1136/gut.51.2.265. PMC 1773333. PMID 12117892.

[pmid21297466-14] Lo J (April 2011). "Dyslipidemia and lipid management in HIV-infected patients". Curr Opin Endocrinol Diabetes Obes. 18 (2): 144–7. doi:10.1097/MED.0b013e328344556e. PMC 3154840. PMID 21297466.

[MinSimon_W_2018-15] Min, Li; Simon W, Rabkin (2018). "Extremely Low HDL Cholesterol and Increased LDL Cholesterol Induced by the use of Anabolic Steroids in a Body Builder: A Case Study". International Journal of Sports and Exercise Medicine. 4 (4). doi:10.23937/2469-5718/1510109. ISSN 2469-5718.

[pmid28223836-16] Mikolasevic I, Žutelija M, Mavrinac V, Orlic L (2017). "Dyslipidemia in patients with chronic kidney disease: etiology and management". Int J Nephrol Renovasc Dis. 10: 35–45. doi:10.2147/IJNRD.S101808. PMC 5304971. PMID 28223836.

[pmid18591400-17] Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, Shochat T, Rudich A (October 2008). "Changes in triglyceride levels over time and risk of type 2 diabetes in young men". Diabetes Care. 31 (10): 2032–7. doi:10.2337/dc08-0825. PMC 2551650. PMID 18591400.

[pmid23525082-18] 18.0 ^18.1 ^18.2 ^18.3 ^18.4 ^18.5 Brahm A, Hegele RA (March 2013). "Hypertriglyceridemia". Nutrients. 5 (3): 981–1001. doi:10.3390/nu5030981. PMC 3705331. PMID 23525082.

[pmid23584084-19] Klop B, Elte JW, Cabezas MC (April 2013). "Dyslipidemia in obesity: mechanisms and potential targets". Nutrients. 5 (4): 1218–40. doi:10.3390/nu5041218. PMC 3705344. PMID 23584084.

[pmid34973-20] Dordain M, Chevrie Muller C, Guidet C (1978). "[Tachylalia: clinical and acoustic study of 149 subjects (author's transl)]". Acta Neurol Belg (in French). 78 (6): 354–72. PMID 34973.

[pmid5155420-21] Vakhitov M, Al'bitskiĭ V (1971). "[Methods of calculating indices of child mortality]". Sov Zdravookhr (in Russian). 30 (4): 43–5. PMID 5155420. Vancouver style error: initials (help)

[urlAssessing_Cardiovascular_Risk:_Systematic_Evidence_Review_from_the_Risk_Assessment_Work_Group_|_NHLBI,_NIH-22] "Assessing Cardiovascular Risk: Systematic Evidence Review from the Risk Assessment Work Group | NHLBI, NIH".

[urlReynolds_Risk_Score-23] "Reynolds Risk Score".

[pmid17584558-24] Berry JD, Lloyd-Jones DM, Garside DB, Greenland P (July 2007). "Framingham risk score and prediction of coronary heart disease death in young men". Am Heart J. 154 (1): 80–6. doi:10.1016/j.ahj.2007.03.042. PMC 2279177. PMID 17584558.

[pmid29132438-25] Jahangiry L, Farhangi MA, Rezaei F (November 2017). "Framingham risk score for estimation of 10-years of cardiovascular diseases risk in patients with metabolic syndrome". J Health Popul Nutr. 36 (1): 36. doi:10.1186/s41043-017-0114-0. PMC 5682637. PMID 29132438.

[pmid22218246-26] Damkondwar DR, Raman R, Suganeswari G, Kulothungan V, Sharma T (2012). "Assessing Framingham cardiovascular risk scores in subjects with diabetes and their correlation with diabetic retinopathy". Indian J Ophthalmol. 60 (1): 45–8. doi:10.4103/0301-4738.91344. PMC 3263245. PMID 22218246.

[pmid25629920-27] Awad AI, Alsaleh FM (2015). "10-year risk estimation for type 2 diabetes mellitus and coronary heart disease in Kuwait: a cross-sectional population-based study". PLoS One. 10 (1): e0116742. doi:10.1371/journal.pone.0116742. PMC 4309592. PMID 25629920.

[pmid29184622-28] Hajar R (2017). "Risk Factors for Coronary Artery Disease: Historical Perspectives". Heart Views. 18 (3): 109–114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17. PMC 5686931. PMID 29184622.

[pmid24353515-29] Nadeem M, Ahmed SS, Mansoor S, Farooq S (January 2013). "Risk factors for coronary heart disease in patients below 45 years of age". Pak J Med Sci. 29 (1): 91–6. doi:10.12669/pjms.291.2828. PMC 3809218. PMID 24353515.

[pmid9567502-30] Ahsan SK (November 1997). "Dyslipidemia: clinical approaches, evaluation of methods and strategies for standardization". Indian J Med Sci. 51 (11): 420–5. PMID 9567502.

[pmid9606309-31] Ahmed SM, Clasen ME, Donnelly JE (May 1998). "Management of dyslipidemia in adults". Am Fam Physician. 57 (9): 2192–2204, 2207–8. PMID 9606309.

[pmid24669298-32] Tonkin A, Byrnes A (2014). "Treatment of dyslipidemia". F1000Prime Rep. 6: 17. doi:10.12703/P6-17. PMC 3944745. PMID 24669298.

[pmid29361723-33] Zodda D, Giammona R, Schifilliti S (January 2018). "Treatment Strategy for Dyslipidemia in Cardiovascular Disease Prevention: Focus on Old and New Drugs". Pharmacy (Basel). 6 (1). doi:10.3390/pharmacy6010010. PMC 5874549. PMID 29361723.

[pmid19436657-34] Rubba P, Marotta G, Gentile M (2009). "Efficacy and safety of rosuvastatin in the management of dyslipidemia". Vasc Health Risk Manag. 5 (1): 343–52. doi:10.2147/vhrm.s3662. PMC 2672446. PMID 19436657.

[pmid31272142-35] Rhee EJ, Kim HC, Kim JH, Lee EY, Kim BJ, Kim EM, Song Y, Lim JH, Kim HJ, Choi S, Moon MK, Na JO, Park KY, Oh MS, Han SY, Noh J, Yi KH, Lee SH, Hong SC, Jeong IK (July 2019). "2018 Guidelines for the management of dyslipidemia". Korean J Intern Med. 34 (4): 723–771. doi:10.3904/kjim.2019.188. PMC 6610190 Check |pmc= value (help). PMID 31272142.

[pmid22477808-36] Eiland LS, Luttrell PK (July 2010). "Use of statins for dyslipidemia in the pediatric population". J Pediatr Pharmacol Ther. 15 (3): 160–72. PMC 3018249. PMID 22477808.

[ZhangGuallar2014-37] Zhang, Y.; Guallar, E.; Qiao, Y.; Wasserman, B. A. (2014). "Is Carotid Intima-Media Thickness as Predictive as Other Noninvasive Techniques for the Detection of Coronary Artery Disease?". Arteriosclerosis, Thrombosis, and Vascular Biology. 34 (7): 1341–1345. doi:10.1161/ATVBAHA.113.302075. ISSN 1079-5642.

[pmid24532973-38] Phan BA, Toth PP (2014). "Dyslipidemia in women: etiology and management". Int J Womens Health. 6: 185–94. doi:10.2147/IJWH.S38133. PMC 3923614. PMID 24532973.

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@@ Line 1: / Line 1: @@
 __NOTOC__
-{{CMG}}; {{AE}} {{YD}}, {{JA}}
+{{Main article|Dyslipidemia}}
+{{CMG}}; {{AE}} {{YD}}, {{JA}}<br>
 {{SK}} [[HDL]], [[LDL]], [[VLDL]], [[hyperlipidemia]], [[hypolipidemia]], [[statin]]
+{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 100px; background: #A8A8A8; position: fixed; top: 250px; right: 21px; border-radius: 0 0 10px 10px;" cellpadding="0" cellspacing="0";
+|-
+! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align=center| {{fontcolor|#2B3B44|Dyslipidemia resident survival guide}}
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Overview|Overview]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Classification|Classification]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Causes|Causes]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Screening|Screening]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Complete Diagnostic Approach|Complete Diagnostic Approach]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Treatment|Treatment]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Do's|Do's]]
+|-
+! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Dyslipidemia resident survival guide#Don'ts|Don'ts]]
+|}
 ==Overview==
-Dyslipidemia is a metabolic abnormality that leads to an increase in the plasma concentrations of [[cholesterol]] and [[triglycerides]].
+Dyslipidemia is a metabolic abnormality that leads to an increase in the [[plasma]] concentrations of [[cholesterol]] and [[triglycerides]]. Lipoprotein abnormalities can be classified on the bases of the pattern of change in the [[lipoprotein]] levels, [[etiology]], and the type of [[lipid]] that is increased. Dyslipidemia can be caused by endocrine disorders such as [[hypothyroidism]], [[diabetes mellitus]], medications such as protease inhibitors or antihypertensive, anabolic [[steroid]] use, [[cholestasis]], and autoimmune disorders. While screening the [[disease]] it is important to identify the [[cardiovascular disease]] risk factors among [[patient]]s. Framingham Risk Assessment Tool and Reynolds Risk Score are utilized to screen for [[CVD]] risk and follow-up [[screening]] varies with the [[diabetes mellitus]] status, patient [[age]], and gender. Treatment involves setting the target [[cholesterol]] levels of < 200 mg/dL, and [[LDL-C]] levels of < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other [[patients]]. [[HDL]] should be as high as possible. Lifestyle recommendations is the first step in treatment before pharmacotherapy. Pharmacotherapy includes monotherapy such as [[statins]] (monitor [[AST]], [[ALT]], and [[Creatine kinase|CK]]); [[fibrates]]; [[niacin]]; and bile acid sequestrants. Uncontrolled dyslipidemia requires combination therapy. Regular follow up with labs to access drug side effects and monitoring [[patient]] health is vital.
 ==Classification==
 There are several ways in which lipoprotein abnormalities are classified. Lipoprotein disorders can be classified according to:
@@ Line 76: / Line 97: @@
 ====Unclassified forms====
 Non-classified forms are extremely rare:
-* Hypo-alpha lipoproteinemia
+* Hypo-alpha lipoproteinemia<ref name="pmid16115486">{{cite journal |vauthors=Pisciotta L, Calabresi L, Lupattelli G, Siepi D, Mannarino MR, Moleri E, Bellocchio A, Cantafora A, Tarugi P, Calandra S, Bertolini S |title=Combined monogenic hypercholesterolemia and hypoalphalipoproteinemia caused by mutations in LDL-R and LCAT genes |journal=Atherosclerosis |volume=182 |issue=1 |pages=153–9 |date=September 2005 |pmid=16115486 |doi=10.1016/j.atherosclerosis.2005.01.048 |url=}}</ref>
-* Hypo-beta lipoproteinemia (prevalence 0.01-0.1%)
+* Hypo-beta lipoproteinemia (prevalence 0.01-0.1%)<ref name="pmid12639976">{{cite journal |vauthors=Schonfeld G |title=Familial hypobetalipoproteinemia: a review |journal=J Lipid Res |volume=44 |issue=5 |pages=878–83 |date=May 2003 |pmid=12639976 |doi=10.1194/jlr.R300002-JLR200 |url=}}</ref><ref>{{cite book | last = Garcia-Dorado | first = David | title = Metabolomics in Cardiovascular Disease: Towards Clinical Application | publisher = INTECH Open Access Publisher | location = City | year = 2012 | isbn = 978-953-51-0344-8 }}</ref>
 ===Classification According to Etiology<ref name="pmid19656773">{{cite journal |vauthors=Hegele RA, Ban MR, Hsueh N, Kennedy BA, Cao H, Zou GY, Anand S, Yusuf S, Huff MW, Wang J |title=A polygenic basis for four classical Fredrickson hyperlipoproteinemia phenotypes that are characterized by hypertriglyceridemia |journal=Hum Mol Genet |volume=18 |issue=21 |pages=4189–94 |date=November 2009 |pmid=19656773 |pmc=2758142 |doi=10.1093/hmg/ddp361 |url=}}</ref>===
@@ Line 83: / Line 104: @@
 {{familytree | | | | | | | | | | | A01 | | | | | | | | A01= '''Lipoprotein Disorders'''}}
 {{familytree | | | | | |,|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|.| | | }}
-{{familytree | | | | | B01 | | | | | | | | | | | | | | B02 | B01= '''Primary'''<br>(Genetic)| B02= '''Secondary'''}}
+{{familytree | | | | | B01 | | | | | | | | | | | | | | B02 | B01= '''Primary'''<br>([[Genetic]])| B02= '''Secondary'''}}
 {{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|-|-|-|-|.| | | |!| | | | }}
-{{familytree | C01 | | C02 | | C03 | | C04 | | C05 | | C06 | C01= '''LDL'''| C02= '''Chylomicron Remnants'''| C03= '''Lipoproteins Rich in Triglyceride'''<br> '''(Chylomicrons, VLDL, IDL)'''| C04= '''HDL'''| C05='''Multiple lipoproteins'''| C06= [[Alcohol]] <br> [[Diabetes]] <br> [[Drug]]s <br> [[Liver disease]] <br> [[Obesity]] <br> [[Renal disease]] <br> [[Smoking]] <br> [[Thyroid]]}}
+{{familytree | C01 | | C02 | | C03 | | C04 | | C05 | | C06 | C01= '''LDL'''| C02= '''Chylomicron Remnants'''| C03= '''Lipoproteins Rich in Triglyceride'''<br> '''(Chylomicrons, VLDL, IDL)'''| C04= '''HDL'''| C05='''Multiple lipoproteins'''| C06=<div style="float: left; text-align: left; line-height: 150% "> [[Alcohol]] <br> [[Diabetes]] <br> [[Drug]]s <br> [[Liver disease]] <br> [[Obesity]] <br> [[Renal disease]] <br> [[Smoking]] <br> [[Thyroid]]}}
 {{familytree | |!| | | |!| | | |!| | | |!| | | |!| | }}
-{{familytree | D01 | | D02 | | D03 | | D04 | | D05 |  D01= '''High LDL:''' <br> -Familial hypercholesterolemia <br> -Familial defective apo B 100 <br> -Autosomal dominant hypercholesterolemia (PCSK9) <br> -Autosomal recessive hypercholesterolemia <br> -Familial sistosterolemia <br> -Familial lipoprotein a lipoproteinemia <br><br> '''Low LDL:''' <br> -Abetalipoproteinemia <br> -Hypobetalipoproteinemia <br> -PCSK 9 deficiency| D02= -Deficiency in hepatic lipase<br> -Type III dysbetalipoproteinemia| D03= -Deficiency in lipoprotein lipase<br> -Deficiency in Apo C-II <br> -Deficiency in Apo A-V <br> -Familial combined hyperlipidemia<br> -Familial hypertriglyceridemia<br> - [[Chylomicron retention disease]]| D04= '''High LDL''':<br> -Cholesteryl ester transferase protein deficiency <br><br>'''Low HDL:''' <br> -Deficiency in Apo A-I<br> -Deficiency in lecithin cholesterol acyltransferase (LCAT) <br>-Familial hypoalphalipoproteinemia<br> -Nieman-Pick disease<br> -Tangier disease| D05=- Familial combined hypolipidemia (ANGPTL3)}}
+{{familytree | D01 | | D02 | | D03 | | D04 | | D05 |  D01= <div style="float: left; text-align: left; line-height: 150% ">'''High LDL:''' <br> -Familial hypercholesterolemia <br> -[[Familial]] defective [[Lipoprotein|apo B 100]] <br> -[[Autosomal dominant]] hypercholesterolemia ([[PCSK9|PCSK9]]) <br> -[[Autosomal recessive]] hypercholesterolemia <br> -Familial [[sitosterolemia]] <br> -Familial lipoprotein a lipoproteinemia <br><br> '''Low [[LDL]]:''' <br> -[[Abetalipoproteinemia]] <br> -[[Hypobetalipoproteinemia]] <br> -[[PCSK9|PCSK 9]] deficiency| D02=<div style="float: left; text-align: left; line-height: 150% "> -Deficiency in hepatic [[lipase]]<br> -Type III [[dysbetalipoproteinemia]]| D03= <div style="float: left; text-align: left; line-height: 150% ">-Deficiency in [[lipoprotein lipase]]<br> -Deficiency in [[Apolipoprotein C2|Apo C-II]] <br> -Deficiency in Apo A-V <br> -[[Familial combined hyperlipidemia]]<br> -Familial [[hypertriglyceridemia]]<br> - [[Chylomicron retention disease]]| D04= <div style="float: left; text-align: left; line-height: 150% ">'''High LDL''':<br> -[[Cholesterylester transfer protein|Cholesteryl ester transferase protein]] deficiency <br><br>'''Low HDL:''' <br> -Deficiency in [[Apo A-I]]<br> -Deficiency in [[lecithin cholesterol acyltransferase]] (LCAT) <br>-Familial [[hypoalphalipoproteinemia]]<br> -[[Niemann-Pick disease]]<br> -[[Tangier disease]]| D05=<div style="float: left; text-align: left; line-height: 150% ">- [[Familial combined hypolipidemia]] (ANGPTL3)}}
 {{familytree/end}}
-===Classification According to Laboratory Results===
+===Classification According to Laboratory Results<ref name="pmid8650932">{{cite journal |vauthors=Herrmann W, Lackner KJ, Schmitz G |title=[Classification of hyperlipoproteinemias and interpretation of laboratory parameters] |language=German |journal=Wien Med Wochenschr |volume=144 |issue=12-13 |pages=292–9 |date=1994 |pmid=8650932 |doi= |url=}}</ref><ref name="pmid23402469">{{cite journal |vauthors=Nelson RH |title=Hyperlipidemia as a risk factor for cardiovascular disease |journal=Prim Care |volume=40 |issue=1 |pages=195–211 |date=March 2013 |pmid=23402469 |pmc=3572442 |doi=10.1016/j.pop.2012.11.003 |url=}}</ref><ref name="pmid27761562">{{cite journal |vauthors=Al-Agha AE, Alnawab AM, Hejazi TM |title=Diverse etiology of hyperlipidemia among hospitalized children in Western region of Saudi Arabia |journal=Saudi Med J |volume=37 |issue=11 |pages=1234–1238 |date=November 2016 |pmid=27761562 |pmc=5303801 |doi=10.15537/smj.2016.11.16328 |url=}}</ref>===
 {{familytree/start |summary= Lipid Laboratory Tests}}
 {{familytree | | | | | | | | | | | | | | | A01 | | | |  A01= '''Lipid Laboratory Tests'''}}
@@ Line 102: / Line 123: @@
 Secondary causes of dyslipidemia may cause either an increase in total-cholesterol & low density lipoprotein-cholesterol (LDL-C) or an increase in total triglycerides & very low density lipoprotein cholesterol (VLDL-C). Common causes are listed below.
 ===Increase in Total Cholesterol and LDL-C===
-*Hypothyroidism
+*[[Hypothyroidism]]<ref name="pmid21660244">{{cite journal |vauthors=Rizos CV, Elisaf MS, Liberopoulos EN |title=Effects of thyroid dysfunction on lipid profile |journal=Open Cardiovasc Med J |volume=5 |issue= |pages=76–84 |date=2011 |pmid=21660244 |pmc=3109527 |doi=10.2174/1874192401105010076 |url=}}</ref>
-*Nephrosis
+*[[Nephrosis]]<ref name="pmid29176657">{{cite journal |vauthors=Agrawal S, Zaritsky JJ, Fornoni A, Smoyer WE |title=Dyslipidaemia in nephrotic syndrome: mechanisms and treatment |journal=Nat Rev Nephrol |volume=14 |issue=1 |pages=57–70 |date=January 2018 |pmid=29176657 |pmc=5770189 |doi=10.1038/nrneph.2017.155 |url=}}</ref>
-*Dysgammaglobulinemia (systemic lupus erythematosus, multiple myeloma)
+*Dysgammaglobulinemia ([[SLE|systemic lupus erythematosus]], [[multiple myeloma]])
-*Cholestatic hepatic diseases due to abnormal lipoproteins (e.g. primary biliary cirrhosis)
+*Cholestatic hepatic diseases due to abnormal [[lipoproteins]] (e.g. [[primary biliary cirrhosis]])<ref name="pmid12117892">{{cite journal |vauthors=Longo M, Crosignani A, Battezzati PM, Squarcia Giussani C, Invernizzi P, Zuin M, Podda M |title=Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis |journal=Gut |volume=51 |issue=2 |pages=265–9 |date=August 2002 |pmid=12117892 |pmc=1773333 |doi=10.1136/gut.51.2.265 |url=}}</ref>
-*Administration of protease inhibitors (treatment for HIV infection)
+*Administration of protease inhibitors (treatment for [[HIV]] infection)<ref name="pmid21297466">{{cite journal |vauthors=Lo J |title=Dyslipidemia and lipid management in HIV-infected patients |journal=Curr Opin Endocrinol Diabetes Obes |volume=18 |issue=2 |pages=144–7 |date=April 2011 |pmid=21297466 |pmc=3154840 |doi=10.1097/MED.0b013e328344556e |url=}}</ref>
-*Administration of progestin or anabolic steroids
+*Administration of progestin or anabolic [[steroids]]<ref name="MinSimon W 2018">{{cite journal|last1=Min|first1=Li|last2=Simon W |first2=Rabkin|title=Extremely Low HDL Cholesterol and Increased LDL Cholesterol Induced by the use of Anabolic Steroids in a Body Builder: A Case Study|journal=International Journal of Sports and Exercise Medicine|volume=4|issue=4|year=2018|issn=24695718|doi=10.23937/2469-5718/1510109}}</ref>
 ===Increase in Total Triglycerides and VLDL-C===
-*Chronic kidney disease
+*[[Chronic kidney disease]]<ref name="pmid28223836">{{cite journal |vauthors=Mikolasevic I, Žutelija M, Mavrinac V, Orlic L |title=Dyslipidemia in patients with chronic kidney disease: etiology and management |journal=Int J Nephrol Renovasc Dis |volume=10 |issue= |pages=35–45 |date=2017 |pmid=28223836 |pmc=5304971 |doi=10.2147/IJNRD.S101808 |url=}}</ref>
-*Type 2 diabetes mellitus
+*[[Type 2 diabetes mellitus]]<ref name="pmid18591400">{{cite journal |vauthors=Tirosh A, Shai I, Bitzur R, Kochba I, Tekes-Manova D, Israeli E, Shochat T, Rudich A |title=Changes in triglyceride levels over time and risk of type 2 diabetes in young men |journal=Diabetes Care |volume=31 |issue=10 |pages=2032–7 |date=October 2008 |pmid=18591400 |pmc=2551650 |doi=10.2337/dc08-0825 |url=}}</ref><ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref>
-*Obesity
+*[[Obesity]]<ref name="pmid23584084">{{cite journal |vauthors=Klop B, Elte JW, Cabezas MC |title=Dyslipidemia in obesity: mechanisms and potential targets |journal=Nutrients |volume=5 |issue=4 |pages=1218–40 |date=April 2013 |pmid=23584084 |pmc=3705344 |doi=10.3390/nu5041218 |url=}}</ref>
-*Excessive alcohol intake
+*Excessive [[alcohol]] intake, poor diet<ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref>
-*Hypothyroidism
+*[[Hypothyroidism]]<ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref>
-*Administration of anti-hypertensive therapy (thiazide diuretics or B-blockers)
+*Administration of anti-hypertensive therapy ([[thiazide diuretics]] or [[B-blockers]])<ref name="pmid34973">{{cite journal |vauthors=Dordain M, Chevrie Muller C, Guidet C |title=[Tachylalia: clinical and acoustic study of 149 subjects (author's transl)] |language=French |journal=Acta Neurol Belg |volume=78 |issue=6 |pages=354–72 |date=1978 |pmid=34973 |doi= |url=}}</ref>
-*Administration of corticosteroids
+*Administration of [[corticosteroids]], [[retinoids]] (depends on the duration of use and type of steroid)<ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref><ref name="pmid5155420">{{cite journal |vauthors=Vakhitov MKh, Al'bitskiĭ VIu |title=[Methods of calculating indices of child mortality] |language=Russian |journal=Sov Zdravookhr |volume=30 |issue=4 |pages=43–5 |date=1971 |pmid=5155420 |doi= |url=}}</ref>
-*Severe stress that increases endogenous corticosteroid concentration
+*Severe stress that increases endogenous [[corticosteroid]] concentration<ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref>
-*Elevated concentrations of estrogen (administration of oral (not transdermal) estrogen therapy, oral contraceptives, or pregnancy)
+*Elevated concentrations of [[estrogen]] (administration of oral (not transdermal) estrogen therapy, [[oral contraceptives]], or [[pregnancy]])<ref name="pmid23525082">{{cite journal |vauthors=Brahm A, Hegele RA |title=Hypertriglyceridemia |journal=Nutrients |volume=5 |issue=3 |pages=981–1001 |date=March 2013 |pmid=23525082 |pmc=3705331 |doi=10.3390/nu5030981 |url=}}</ref>
-*Administration of protease inhibitors (treatment for HIV infection)
+*Administration of protease inhibitors (treatment for [[HIV]] infection)
 <br>
 '''To view a comprehensive list of dyslipidemia causes, click [[Lipoprotein disorders causes|here]]'''
 ==Screening==
+The following algorithm explains the approach to screening for dyslipidemia [[patient]]s.<ref name="urlAssessing Cardiovascular Risk: Systematic Evidence Review from the Risk Assessment Work Group | NHLBI, NIH">{{cite web |url=https://www.nhlbi.nih.gov/health-topics/assessing-cardiovascular-risk |title=Assessing Cardiovascular Risk: Systematic Evidence Review from the Risk Assessment Work Group &#124; NHLBI, NIH |format= |work= |accessdate=}}</ref><ref name="urlReynolds Risk Score">{{cite web |url=http://www.reynoldsriskscore.org/ |title=Reynolds Risk Score |format= |work= |accessdate=}}</ref><ref name="pmid17584558">{{cite journal |vauthors=Berry JD, Lloyd-Jones DM, Garside DB, Greenland P |title=Framingham risk score and prediction of coronary heart disease death in young men |journal=Am Heart J |volume=154 |issue=1 |pages=80–6 |date=July 2007 |pmid=17584558 |pmc=2279177 |doi=10.1016/j.ahj.2007.03.042 |url=}}</ref><ref name="pmid29132438">{{cite journal |vauthors=Jahangiry L, Farhangi MA, Rezaei F |title=Framingham risk score for estimation of 10-years of cardiovascular diseases risk in patients with metabolic syndrome |journal=J Health Popul Nutr |volume=36 |issue=1 |pages=36 |date=November 2017 |pmid=29132438 |pmc=5682637 |doi=10.1186/s41043-017-0114-0 |url=}}</ref><ref name="pmid22218246">{{cite journal |vauthors=Damkondwar DR, Raman R, Suganeswari G, Kulothungan V, Sharma T |title=Assessing Framingham cardiovascular risk scores in subjects with diabetes and their correlation with diabetic retinopathy |journal=Indian J Ophthalmol |volume=60 |issue=1 |pages=45–8 |date=2012 |pmid=22218246 |pmc=3263245 |doi=10.4103/0301-4738.91344 |url=}}</ref><ref name="pmid25629920">{{cite journal |vauthors=Awad AI, Alsaleh FM |title=10-year risk estimation for type 2 diabetes mellitus and coronary heart disease in Kuwait: a cross-sectional population-based study |journal=PLoS One |volume=10 |issue=1 |pages=e0116742 |date=2015 |pmid=25629920 |pmc=4309592 |doi=10.1371/journal.pone.0116742 |url=}}</ref><br>
 <span style="font-size:85%">'''Abbreviations:''' '''ASA:''' [[American society of anesthesiologists]]; '''BP:''' [[Blood Pressure]]; '''CCS:''' [[Canadian cardiovascular society]]; '''CrCl:''' [[Creatinine clearance]]; '''CXR:'''  [[Chest X-ray]]; '''DNI:''' [[Do not intubate]]; '''DNR:''' [[Do not resuscitate]]; '''ECG:''' [[Electrocardiogram]]; '''eGFR:''' [[estimated glomerular filtration rate]]; '''HR:'''[[Heart rate]]; '''INR:''' [[International normalized ratio]]; '''LMWH:''' [[Low molecular weight heparin]]; '''LV:''' [[Left ventricle]]; '''LVED:''' [[Left ventricular ejection fraction]]; '''NOAC:''' [[Novel oral anticoagulant]]; '''NPO:''' [[Nothing per os]]; '''PMI:''' [[Point of maximal impulse]]; '''PT:''' [[Prothrombin time]]; '''RR:''' [[Respiratory rate]];  '''SpO2:''' [[Oxygen saturation]]; '''T:''' [[Temperature]]; '''VT:''' [[Ventricular tachycardia]]</span>
@@ Line 149: / Line 173: @@
 '''''Additional risk factors:'''''<br>
-❑ [[Obesity]], especially abdominal<br>
+❑ [[Obesity]], especially [[abdomin]]al<br>
-❑ Family history of [[hyperlipidemia]]<br>
+❑ Family [[history]] of [[hyperlipidemia]]<br>
-❑ Small, dense LDL-C<br>
+❑ Small, dense [[LDL]]-C<br>
 ❑ ↑ Apo-B<br>
@@ Line 166: / Line 190: @@
 '''''Non-traditional risk factors:'''''<br>
-❑ ↑ lipoprotein<br>
+❑ ↑ [[lipoprotein]]<br>
 ❑ ↑ clotting factors<br>
-❑ Inflamamtory markers (e.g. hsCRP or Lipoprotein-associated phospholipase A2 (Lp-PLA2)<br>
+❑ Inflamamtory markers (e.g. hsCRP or [[Lipoprotein-associated phospholipase A2]] (Lp-PLA2)<br>
-❑ Hyperhomocysteinemia<br>
+❑ [[Hyperhomocysteinemia]]<br>
 ❑ ApoE4 isoform<br>
@@ Line 204: / Line 228: @@
 {{familytree | | | |,|-|^|-|.| | | | | | |!| | | | | | | | | | | | |!| | | | | | | | | | | | | | |}}
-{{familytree | | | G01 | | G02 | | | | | G03 | | | | | | | | | | | G04 | | | | | | | | | | | | | |G01=Yes. The patient has '''ALL''' of the criteria for low-risk dyslipidemia|G02=Either unknown history of lipid profile or No, the patient does not have ALL of the criteria for low-risk dyslipidemia (at least 1 criterion is not met)|G03=Does that patient have risk factors for CAD (listed above)?|G04=Does the patient have risk factors for CAD (listed above)?}}
+{{familytree | | | G01 | | G02 | | | | | G03 | | | | | | | | | | | G04 | | | | | | | | | | | | | |G01=Yes. The patient has '''ALL''' of the criteria for low-risk dyslipidemia|G02=Either unknown history of lipid profile or No, the patient does not have ALL of the criteria for low-risk dyslipidemia (at least 1 criterion is not met)|G03=Does that patient have risk factors for [[CAD]] (listed above)?|G04=Does the patient have risk factors for [[CAD]] (listed above)?}}
 {{familytree | | | |!| | | |!| | | |,|-|-|^|-|-|.| | | | | | | |,|-|^|-|.| | | | | | | | | | | | |}}
@@ Line 212: / Line 236: @@
 {{familytree | | | | | | | | | | | |!| | | | | |!| | | | | | | |!| | | |!| | | | | | | | | | | | |}}
-{{familytree | | | | | | | | | | | |)|-|-|-|-| I01 | | | | | | |!| | | |!| | | | | | | | | | | | |I01=Screen patient more frequently than patients with no risk factors based on clinical judgement (unknown optimal interval)}}
+{{familytree | | | | | | | | | | | |)|-|-|-|-| I01 | | | | | | |!| | | |!| | | | | | | | | | | | |I01=Screen [[patient]] more frequently than [[patient]]s with no risk factors based on clinical judgement (unknown optimal interval)}}
 {{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | |!| | | |!| | | | | | | | | | | | |}}
@@ Line 230: / Line 254: @@
 ==Complete Diagnostic Approach==
+The algorithm explains the approach to the diagnosis of dyslipidemia.<ref name="pmid29184622">{{cite journal |vauthors=Hajar R |title=Risk Factors for Coronary Artery Disease: Historical Perspectives |journal=Heart Views |volume=18 |issue=3 |pages=109–114 |date=2017 |pmid=29184622 |pmc=5686931 |doi=10.4103/HEARTVIEWS.HEARTVIEWS_106_17 |url=}}</ref><ref name="pmid24353515">{{cite journal |vauthors=Nadeem M, Ahmed SS, Mansoor S, Farooq S |title=Risk factors for coronary heart disease in patients below 45 years of age |journal=Pak J Med Sci |volume=29 |issue=1 |pages=91–6 |date=January 2013 |pmid=24353515 |pmc=3809218 |doi=10.12669/pjms.291.2828 |url=}}</ref><ref name="pmid9567502">{{cite journal |vauthors=Ahsan SK |title=Dyslipidemia: clinical approaches, evaluation of methods and strategies for standardization |journal=Indian J Med Sci |volume=51 |issue=11 |pages=420–5 |date=November 1997 |pmid=9567502 |doi= |url=}}</ref><br>
 <span style="font-size:85%">Boxes in red signify that an urgent management is needed.</span>
@@ Line 235: / Line 260: @@
 {{familytree/start}}
-{{familytree | | | | | | | | | | | A01 | | | | | | | | | | | | | | | |A01='''Obtain a Detailed History'''<br><br><div style="float: left; text-align: left; width: 18em; padding:1em;">'''''History of present illness'''''<br>
+{{familytree | | | | | | | | | | | A01 | | | | | | | | | | | | | | | |A01='''Obtain a Detailed History'''<br><br><div style="float: left; text-align: left; width: 18em; padding:1em;"><div class="mw-collapsible mw-collapsed">'''''History of present illness'''''<br>
-❑ Address specific patient symptoms and complaints<br>
+❑ Address specific [[patient]] symptoms and complaints<br>
-❑ Obtain review of systems relevant to dyslipidemia and diseases associated with dyslipidemia<br>
+❑ Obtain review of systems relevant to [[dyslipidemia]] and [[disease]]s associated with [[dyslipidemia]]<br>
-:❑ Headache
+:❑ [[Headache]]
-:❑ Dizziness
+:❑ [[Dizziness]]
-:❑ Syncope/presyncope
+:❑ [[Syncope]]/presyncope
-:❑ Blurry vision / double vision / reduced visual acquity
+:❑ Blurry [[vision]] / [[diplopia|double vision]] / reduced [[visual acuity]]
-:❑ Dysphagia
+:❑ [[Dysphagia]]
 :❑ Slurred speech
 :❑ Facial drooping
-:❑ Chest pain / Angina
+:❑ Chest pain / [[Angina]]
-:❑ Palpitations
+:❑ [[Palpitation]]s
-:❑ Dyspnea
+:❑ [[Dyspnea]]
-:❑ Cough
+:❑ [[Cough]]
-:❑ Abdominal pain
+:❑ [[Abdominal pain]]
 :❑ Change in bowel movements
-:❑ Lower extremity pain, weakness, or tingling
+:❑ Lower extremity [[pain]], [[muscle weakness|weakness]], or [[tingling]]
-:❑ Peripheral edema
+:❑ Peripheral [[edema]]
-:❑ Muscle pain
+:❑ [[Muscle pain]]
-❑ Intake of dietary fat, saturated fat, fiber, and cholesterol intake<br>
+❑ Intake of dietary fat, [[saturated fat]], fiber, and [[cholesterol]] intake<br>
-❑ Exercise patterns<br>
+❑ [[Exercise]] patterns<br>
-❑ History of alcohol use<br>
+❑ History of [[alcohol]] use<br>
-❑ History of smoking<br><br>
+❑ History of [[smoking]]<br><br>
 '''''Past Medical History'''''<br>
-❑ History of previous medical diagnoses / past medical complaints/hospitalizations and [[surgery|surgeries]]<br>
+❑ History of previous medical [[diagnosis|diagnoses]] / past medical complaints/hospitalizations and [[surgery|surgeries]]<br>
-❑ History of CAD or myocardial infarction<br>
+❑ History of [[CAD]] or [[myocardial infarction]]<br>
-❑ History of diabetes mellitus<br>
+❑ History of [[diabetes mellitus]]<br>
-❑ History of hypertension<br>
+❑ History of [[hypertension]]<br>
-❑ History of renal disease<br>
+❑ History of [[renal disease]]<br>
-❑ History of hepatic disease<br>
+❑ History of [[hepatic disease]]<br>
-❑ History of [[stroke]] (ischemic or hemorrhagic) or [[transient ischemic attack]] (TIA)<br>
+❑ History of [[stroke]] ([[ischemicstroke|ischemic]] or [[hemorrhagic stroke|hemorrhagic]]) or [[transient ischemic attack]] (TIA)<br>
-❑ History of hypothyroidism<br><br>
+❑ History of [[hypothyroidism]]<br><br>
 '''''Medications'''''<br>
@@ Line 298: / Line 323: @@
 ❑ Currently prescribed medications<br>
-❑ List of over-the-counter drugs<br>
+❑ List of [[over-the-counter drugs]]<br>
 ❑ Previous intake of medications and reason for discontinuation<br>
@@ Line 314: / Line 339: @@
 ❑ Known environmental/food allergies<br><br>
 '''''Family history'''''<br>
-❑ Family history of dyslipidemia<br>
+❑ Family history of [[dyslipidemia]]<br>
-❑ Family history of premature CAD (i.e. Established CAD in father or 1st-degree male relative before the age of 55 years OR established CAD in mother or 1st-degree female relative before the age of 65 years)<br>
+❑ Family history of premature [[CAD]] (i.e. Established [[CAD]] in father or 1st-degree male relative before the [[age]] of 55 years OR established [[CAD]] in mother or 1st-degree female relative before the [[age]] of 65 years)<br>
 ❑ Family history of [[hypothyroidism]]<br>
-❑ Family history of [[stroke]]/TIA<br>
+❑ Family history of [[stroke]]/[[TIA]]<br>
 ❑ Family history of peripheral vascular disease<br><br>
@@ Line 328: / Line 353: @@
 ❑ Occupation<br>
-❑ Exercise<br>
+❑ [[Exercise]]<br>
 ❑ Diet (general)<br>
-❑ Smoking history<br>
+❑ [[Smoking]] history<br>
-❑ Alcohol use<br>
+❑ [[Alcohol]] use<br>
 ❑ Recreational drug use<br>
-❑ Stress<br>
+❑ [[Stress]]<br>
 ❑ Sexual lifestyle & [[contraceptive]] methods <br>
@@ Line 344: / Line 369: @@
 }}
 {{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | | | | |}}
-{{familytree | | | | | | | | | | | B01 | | | | | | | | | | | | | | | |B01='''Assess for CAD Risk Factors'''<br><br><div style="float: left; text-align: left; width: 18em; padding:1em;">'''''Major risk factors:'''''<br>
+{{familytree | | | | | | | | | | | B01 | | | | | | | | | | | | | | | |B01='''Assess for CAD Risk Factors'''<br><br><div style="float: left; text-align: left; width: 18em; padding:1em;"><div class="mw-collapsible mw-collapsed">'''''Major risk factors:'''''<br>
-❑ Advanced age <br>
+❑ Advanced [[age]] <br>
-❑ ↑ total serum cholesterol <br>
+❑ ↑ [[total cholesterol|total serum cholesterol]] <br>
-❑ ↑ non-HDL-C (calculated by: total cholesterol minus HDL-C)<br>
+❑ ↑ non-[[HDL]]-C (calculated by: [[total cholesterol]] minus [[HDL]]-C)<br>
-❑ ↑ LDL-C (either measured or calculated by: total cholesterol minus HDL-c minus (total triglycerides/5))<br>
+❑ ↑ [[LDL]]-C (either measured or calculated by: [[total cholesterol]] minus [[HDL]]-c minus (total [[triglycerides]]/5))<br>
-❑ ↓ HDL-C<br>
+❑ ↓ [[HDL]]-C<br>
-❑ Diabetes mellitus<br>
+❑ [[Diabetes mellitus]]<br>
-❑ Hypertension<br>
+❑ [[Hypertension]]<br>
-❑ Cigarette smoking<br>
+❑ Cigarette [[smoking]]<br>
 ❑ Family history of CAD<br><br>
 '''''Additional risk factors:'''''<br>
-❑ Obesity, especially abdominal<br>
+❑ [[Obesity]], especially [[abdomen|abdominal]]<br>
-❑ Family history of hyperlipidemia<br>
+❑ Family history of [[hyperlipidemia]]<br>
-❑ Small, dense LDL-C<br>
+❑ Small, dense [[LDL]]-C<br>
-❑ ↑ Apo-B<br>
+❑ ↑ [[Apo-B]]<br>
-❑ ↑ LDL particle number (measured by ApoB)<br>
+❑ ↑ [[LDL]] particle number (measured by [[ApoB]])<br>
-❑ Fasting/postprandial hypertriglyceridemia<br>
+❑ Fasting/postprandial [[hypertriglyceridemia]]<br>
-❑ Polycystic ovarian syndrome<br>
+❑ [[Polycystic ovarian syndrome]]<br>
 ❑ Dyslipidemic triad<br><br>
 '''''Non-traditional risk factors:'''''<br>
-❑ ↑ lipoprotein<br>
+❑ ↑ [[lipoprotein]]<br>
-❑ ↑ clotting factors<br>
+❑ ↑ [[clotting factors]]<br>
-❑ Inflamamtory markers (e.g. hsCRP or Lipoprotein-associated phospholipase A2 (Lp-PLA2)<br>
+❑ [[inflammation|Inflammatory]] markers (e.g. hs[[CRP]] or [[Lipoprotein-associated phospholipase A2]] (Lp-PLA2)<br>
-❑ Hyperhomocysteinemia<br>
+❑ [[Hyperhomocysteinemia]]<br>
-❑ ApoE4 isoform<br>
+❑ [[Apolipoprotein E|ApoE]]4 isoform<br>
-❑ ↑ uric acid</div>
+❑ ↑ [[uric acid]]</div>
 }}
 {{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | | | | |}}
@@ Line 402: / Line 427: @@
 ❑ Reynolds Risk Score (To be redirected to Reynolds Risk Score website, click [http://www.reynoldsriskscore.org/ here])</div>}}
 {{familytree | | | | | | | | | | | |!| | | | | | | | | | | | | | | | |}}
-{{familytree | | | | | | | | | | | D01 | | | | | | | | | | | | | | | |D01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Examine the patient'''<br>
+{{familytree | | | | | | | | | | | D01 | | | | | | | | | | | | | | | |D01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Examine the patient'''<div class="mw-collapsible mw-collapsed"><br>
 '''''Vital signs'''''<br>
 ❑ High blood pressure<br>
 '''''Skin'''''<br>
-❑ Xanthomas (eruptive, tuberous, tendinous)<br>
+❑ [[Xanthoma]]s (eruptive, tuberous, tendinous)<br>
-❑ Xanthelesma<br>
+❑ [[Xanthelesma]]<br>
-❑ Cool hairless extremities (suggestive of peripheral vascular disease)<br>
+❑ Cool hairless extremities (suggestive of [[peripheral vascular disease]])<br>
-❑ Other skin rashes that may be suggestive of secondary causes (e.g. systemic lupus erythematosus, drug eruptions, pregnancy rash)<br>
+❑ Other skin [[rash]]es that may be suggestive of secondary causes (e.g. [[systemic lupus erythematosus]], drug eruptions, [[pregnancy]] rash)<br>
 '''''HEENT'''''<br>
 ❑ Arcus senilis (corneal arcus)<br>
-'''''Neck'''''<br>❑ Carotid bruits<br>
+'''''Neck'''''<br>❑ [[Carotid bruit]]s<br>
-❑ Thyromegaly (when dyslipidemia is caused by thyroid disease)<br>
+❑ [[Thyromegaly]] (when dyslipidemia is caused by [[]]thyroid disease)<br>
 '''''Peripheral'''''<br>
 ❑ Diminished distal pulses<br>
-❑ Femoral bruits<br></div>}}
+❑ [[Femoral bruit]]s<br></div>}}
 {{familytree | | | | | | | | | |,|-|^|-|.| | | | | | | | | | | | | | |}}
 {{familytree | | | | | | | | | |!| | | E02 | | | | | | | | | | | | | |E02='''Order tests to rule out secondary causes of dyslipidemia'''<br>
-<div style="float: left; text-align: left; width: 18em; padding:1em;">Common causes include:<br>
+<div style="float: left; text-align: left; width: 18em; padding:1em;">Common causes include:<div class="mw-collapsible mw-collapsed"><br>
-❑ Hypothyroidism <br>
+❑ [[Hypothyroidism]] <br>
-:❑ Order TSH, FT4, and FT3
+:❑ Order [[TSH]], [[FT4]], and [[FT3]]
-❑ Nephrosis<br>
+❑ [[Nephrosis]]<br>
-:❑ Order serum creatinine and urinalysis with either spot urine for proteins or 24-hour urinary collection for proteins, urinary protein to creatinine ratio
+:❑ Order serum [[creatinine]] and [[urinalysis]] with either spot urine for proteins or 24-hour urinary collection for [[proteins]], urinary protein to creatinine ratio
-❑ Dysgammaglobulinemia <br>
+❑ [[Dysgammaglobulinemia]] <br>
-:❑ Order ANA, anti-dsDNA antibodies, plasma and urine electrophoresis
+:❑ Order [[ANA]], [[Anti-dsDNA antibody|anti-dsDNA antibodies]], plasma and urine [[electrophoresis]]
 ❑ Cholestatic hepatic diseases <br>
-:❑ Order GGT, ALP, and bilirubins
+:❑ Order [[Gamma-glutamyltransferase|GGT]], [[Alkaline phosphatase|ALP]], and [[bilirubin]]s
-❑ Chronic kidney disease <br>
+❑ [[Chronic kidney disease]] <br>
 :❑ Order serum creatinine, BUN, urinalysis, and renal ultrasound
-❑ Type 2 diabetes mellitus <br>
+❑ [[Type 2 diabetes mellitus]] <br>
-:❑ Order glycemia and HbA1c
+:❑ Order glycemia and [[HbA1c]]
-❑ Excessive alcohol intake <br>
+❑ Excessive [[alcohol]] intake <br>
 ❑ Drugs <br>
+:❑ Any of the following: [[estrogen]], [[progestin]], [[protease inhibitors]], [[beta-blockers]], [[corticosteroids]], [[anabolic steroids]], [[protease inhibitor]]s<br><br></div>}}
-:❑ Any of the following: estrogen, progestin, protease inhibitors, beta-blockers, corticosteroids, anabolic steroids, protease inhibitors<br><br></div>}}
 {{familytree | | | | | | | | | E01 | | | | | | | | | | | | | | | | | |E01=Order '''''fasting''''' lipid profile}}
 {{familytree | |,|-|-|-|v|-|-|-|+|-|-|-|v|-|-|-|.| | | | | | | | | | |}}
-{{familytree | F01 | | F02 | | F03 | | F04 | | F05 | | | | | | | | | |F01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Total cholesterol'''<br>❑ ''Optimal'': < 200 mg/dL<br>❑ ''Borderline'': 200-239 mg/dL<br>❑ ''High/very high risk'': ≥ 240 mg/dL</div>|F02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''LDL-C'''<br>May be either calculated or measured. Measured LDL-C is preferable, especially among certain high-risk populations (elevated triglycerides > 250 mg/dL, diabetes mellitus, peripheral vascular disease).<br>To calculate LDL-C, use the following equation: LDL-C=(total cholesterol-HDL-C)/(triglycerides/5). Do NOT calculate LDL-C when triglycerides > 200 mg/dL (low to no validity of the equation). Instead, use measured LDL-C.<br><br>❑ ''Optimal'': < 100 mg/dL<br>❑ ''Borderline'': 130-160 mg/dL<br>❑ ''High risk'': 160-189 mg/dL<br>❑ ''Very high risk'': ≥ 190 mg/dL</div>|F03=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''HDL-C'''<br>An optimal HDL-C concentration is a negative CAD risk factor in both genders (subtract 1 risk factor for CAD)<br><br>❑ ''Optimal'': ≥ 60 mg/dL<br>❑ ''Borderline'': 40-50 mg/dL (men) OR 50-59 mg/dL (women)<br>❑ ''High/very high risk'': < 40 mg/dL (men) OR < 50 mg/dL (women)</div>|F04=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Triglycerides'''<br>❑ ''Optimal'': < 150 mg/dL<br>❑ ''Borderline'': 150-199 mg/dL<br>❑ ''High risk'': 200-499 mg/dL<br>❑ ''Very high risk'': ≥ 500 mg/dL</div>|F05=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Additional tests'''<br><br>❑ '''Non-HDL'''<br>non-HDL is calculated by the following equation: non-HDL=total cholesterol - HDL-C<br>non-HDL-C provides additional risk assessment information compared with LDL-C alone.<br>Calculate non-HDL-C only in the following cases: Either moderate elevation of triglyceride (between 200 to 500 mg/dL), diabetes mellitus, insulin resistance syndrome, or established CAD<br><br>❑ '''ApoB'''<br>ApoB reflects LDL-C particle number, which may be a more potent measure of CVD risk than either LDL-C or LDL-C particle size<br>''Optimal'': < 90 mg/dL for patients with at risk of CAD (including diabetes mellitus) OR < 80 mg/dL for patients with established CAD or diabetes mellitus plus at least 1 additional risk factor<br><br>❑ '''Ratio of ApoB/ApoAI'''<br>May be useful in evaluating residual risk (independent of LDL-C) in patients at high risk of CAD or patients with either established CAD, diabetes mellitus, or insulin resistance<br><br>❑ '''hsCRP'''<br>Order hsCRP for patients with borderline risk or patients with LDL-C < 130 mg/dL<br>hsCRP helps further stratify patient risk for CVD<br><br>❑ '''LP-PLA2'''<br>May provide more specificity than hsCRP and may be ordered for further stratification of CVD risk</div>}}
+{{familytree | F01 | | F02 | | F03 | | F04 | | F05 | | | | | | | | | |F01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Total cholesterol'''<div class="mw-collapsible mw-collapsed"><br>❑ ''Optimal'': < 200 mg/dL<br>❑ ''Borderline'': 200-239 mg/dL<br>❑ ''High/very high risk'': ≥ 240 mg/dL</div>|F02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''LDL-C'''<div class="mw-collapsible mw-collapsed"><br>May be either calculated or measured. Measured LDL-C is preferable, especially among certain high-risk populations (elevated triglycerides > 250 mg/dL, diabetes mellitus, peripheral vascular disease).<br>To calculate LDL-C, use the following equation: LDL-C=(total cholesterol-HDL-C)/(triglycerides/5). Do NOT calculate LDL-C when triglycerides > 200 mg/dL (low to no validity of the equation). Instead, use measured LDL-C.<br><br>❑ ''Optimal'': < 100 mg/dL<br>❑ ''Borderline'': 130-160 mg/dL<br>❑ ''High risk'': 160-189 mg/dL<br>❑ ''Very high risk'': ≥ 190 mg/dL</div>|F03=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''HDL-C'''<div class="mw-collapsible mw-collapsed"><br>An optimal HDL-C concentration is a negative CAD risk factor in both genders (subtract 1 risk factor for CAD)<br><br>❑ ''Optimal'': ≥ 60 mg/dL<br>❑ ''Borderline'': 40-50 mg/dL (men) OR 50-59 mg/dL (women)<br>❑ ''High/very high risk'': < 40 mg/dL (men) OR < 50 mg/dL (women)</div>|F04=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Triglycerides'''<div class="mw-collapsible mw-collapsed"><br>❑ ''Optimal'': < 150 mg/dL<br>❑ ''Borderline'': 150-199 mg/dL<br>❑ ''High risk'': 200-499 mg/dL<br>❑ ''Very high risk'': ≥ 500 mg/dL</div>|F05=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Additional tests'''<br><br><div class="mw-collapsible mw-collapsed">❑ '''Non-HDL'''<br>non-HDL is calculated by the following equation: non-HDL=total cholesterol - HDL-C<br>non-HDL-C provides additional risk assessment information compared with LDL-C alone.<br>Calculate non-HDL-C only in the following cases: Either moderate elevation of triglyceride (between 200 to 500 mg/dL), diabetes mellitus, insulin resistance syndrome, or established CAD<br><br>❑ '''ApoB'''<br>ApoB reflects LDL-C particle number, which may be a more potent measure of CVD risk than either LDL-C or LDL-C particle size<br>''Optimal'': < 90 mg/dL for patients with at risk of CAD (including diabetes mellitus) OR < 80 mg/dL for patients with established CAD or diabetes mellitus plus at least 1 additional risk factor<br><br>❑ '''Ratio of ApoB/ApoAI'''<br>May be useful in evaluating residual risk (independent of LDL-C) in patients at high risk of CAD or patients with either established CAD, diabetes mellitus, or insulin resistance<br><br>❑ '''hsCRP'''<br>Order hsCRP for patients with borderline risk or patients with LDL-C < 130 mg/dL<br>hsCRP helps further stratify patient risk for CVD<br><br>❑ '''LP-PLA2'''<br>May provide more specificity than hsCRP and may be ordered for further stratification of CVD risk</div>}}
 {{familytree/end}}
 ==Treatment==
+The algorithm demonstrates the treatment strategy for [[patient]]s with confirmed dyslipidemia.
+<ref name="pmid9606309">{{cite journal |vauthors=Ahmed SM, Clasen ME, Donnelly JE |title=Management of dyslipidemia in adults |journal=Am Fam Physician |volume=57 |issue=9 |pages=2192–2204, 2207–8 |date=May 1998 |pmid=9606309 |doi= |url=}}</ref><ref name="pmid24669298">{{cite journal |vauthors=Tonkin A, Byrnes A |title=Treatment of dyslipidemia |journal=F1000Prime Rep |volume=6 |issue= |pages=17 |date=2014 |pmid=24669298 |pmc=3944745 |doi=10.12703/P6-17 |url=}}</ref><ref name="pmid29361723">{{cite journal |vauthors=Zodda D, Giammona R, Schifilliti S |title=Treatment Strategy for Dyslipidemia in Cardiovascular Disease Prevention: Focus on Old and New Drugs |journal=Pharmacy (Basel) |volume=6 |issue=1 |pages= |date=January 2018 |pmid=29361723 |pmc=5874549 |doi=10.3390/pharmacy6010010 |url=}}</ref><ref name="pmid19436657">{{cite journal |vauthors=Rubba P, Marotta G, Gentile M |title=Efficacy and safety of rosuvastatin in the management of dyslipidemia |journal=Vasc Health Risk Manag |volume=5 |issue=1 |pages=343–52 |date=2009 |pmid=19436657 |pmc=2672446 |doi=10.2147/vhrm.s3662 |url=}}</ref><ref name="pmid31272142">{{cite journal |vauthors=Rhee EJ, Kim HC, Kim JH, Lee EY, Kim BJ, Kim EM, Song Y, Lim JH, Kim HJ, Choi S, Moon MK, Na JO, Park KY, Oh MS, Han SY, Noh J, Yi KH, Lee SH, Hong SC, Jeong IK |title=2018 Guidelines for the management of dyslipidemia |journal=Korean J Intern Med |volume=34 |issue=4 |pages=723–771 |date=July 2019 |pmid=31272142 |pmc=6610190 |doi=10.3904/kjim.2019.188 |url=}}</ref>
 {{familytree/start}}
 {{familytree | | | A01 | | | | | | | | | | | | | | | | | | | | A01=Confirmed Dyslipidemia}}
@@ Line 448: / Line 475: @@
 {{familytree | | | B01 | | | | | | | | | | | | | | | | | | | | B01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Set lipid goals'''<br>
-❑ Total cholesterol target: < 200 mg/dL<br>
+❑ Total [[cholesterol]] target: < 200 mg/dL<br>
-❑ LDL-C target: < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other patients<br>
+❑ [[LDL]]-C target: < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other patients<br>
-❑ HDL-C target: As high as possible. At least > 40 mg/dL in both genders<br>
+❑ [[HDL]]-C target: As high as possible. At least > 40 mg/dL in both genders<br>
 ❑ Non-HDL-C target: 30 mg/dL above LDL-C goal (target < 100 mg/dL for very high risk patients OR < 130 mg/dL for all other patients)<br>
-❑ Triglycerides target: < 150 mg/dL<br>
+❑ [[Triglycerides]] target: < 150 mg/dL<br>
-❑ ApoB target: < 90 mg/dL for patients at risk of CAD (including patients with diabetes) or < 80 mg/dL for patients with established CAD or diabetes plus at least one additional CAD risk factor<br></div>}}
+❑ [[ApoB]] target: < 90 mg/dL for patients at risk of [[CAD]] (including patients with diabetes) or < 80 mg/dL for patients with established [[CAD]] or [[diabetes]] plus at least one additional CAD risk factor<br></div>}}
 {{familytree | |,|-|^|-|.| | | | | | | | | | | | | | | | | | | }}
 {{familytree | C01 | | C02 | | | | | | | | | | | | | | | | | | C01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Control modifiable CAD risk factors'''<br>
-❑ Hypertension<br>
+❑ [[Hypertension]]<br>
-❑ Diabetes mellitus<br>
+❑ [[Diabetes mellitus]]<br>
-❑ Obesity<br>
+❑ [[Obesity]]<br>
-❑ Cigarette smoking</div>|C02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Recommend lifestyle modification'''<br>
+❑ Cigarette [[smoking]]</div>|C02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Recommend lifestyle modification'''<br><div class="mw-collapsible mw-collapsed">
 ❑ Recommend physical activity<br>
@@ Line 481: / Line 508: @@
 :❑ Advise patients to have more than 6 servings/day of grains, at least 1/3 of which are whole grain
-:❑ Advise patients to limit intake of saturated fat, trans-fats, and cholesterol
+:❑ Advise patients to limit intake of saturated fat, trans-fats, and [[cholesterol]]
 ❑ Smoking cessation<br></div>}}
@@ Line 489: / Line 516: @@
 {{familytree | | | X01 | | | X02 | | | | | | | | | | | | | | | X01=Yes|X02=No}}
 {{familytree | | |,|'| | | | |!| | | | | | | | | | | | | | | | | | | }}
-{{familytree | | |!| | | | | D01 | | | | | | | | | | | | | | | | | |D01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Administer pharmacologic monotherapy'''<br>Table of available classes, generic names, recommended daily doses, and dose ranges also available below algorithm. Click here. <br><br>
+{{familytree | | |!| | | | | D01 | | | | | | | | | | | | | | | | | |D01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Administer pharmacologic monotherapy'''<br>Table of available classes, generic names, recommended daily doses, and dose ranges also available below algorithm. Click here. <br><br><div class="mw-collapsible mw-collapsed">
-'''''Statins'''''<br>
+'''''[[Statins]]'''''<br>
 Administration of any of the following statins is recommended to manage dyslipidemia<br>
 ❑ ''<u>Lovastatin</u>'': Recommended starting daily dose 20 mg PO once daily at bedtime. Dose range: 10-80 mg<br>
-❑ ''<u>Pravastatin</u>'': Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 10-80 mg<br>
+❑ ''<u>[[Pravastatin]]</u>'': Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 10-80 mg<br>
-❑ ''<u>Simvastatin</u>'': Recommended starting daily dose 20-40 mg PO once daily at bedtime. Dose range: 5-80 mg (80 mg not approved for therapy unless patient has been on treatment for more than 1 year without myopathy)<br>
+❑ ''<u>[[Simvastatin]]</u>'': Recommended starting daily dose 20-40 mg PO once daily at bedtime. Dose range: 5-80 mg (80 mg not approved for therapy unless patient has been on treatment for more than 1 year without myopathy)<br>
-❑ ''<u>Fluvastatin</u>'': Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 20-80 mg<br>
+❑ ''<u>[[Fluvastatin]]</u>'': Recommended starting daily dose 40 mg PO once daily at bedtime. Dose range: 20-80 mg<br>
-❑ ''<u>Atorvastatin</u>'': Recommended starting daily dose 10-20 mg PO once daily at bedtime. Dose range: 10-80 mg<br>
+❑ ''<u>[[Atorvastatin]]</u>'': Recommended starting daily dose 10-20 mg PO once daily at bedtime. Dose range: 10-80 mg<br>
-❑ ''<u>Rosuvastatin</u>'': Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 5-40 mg<br>
+❑ ''<u>[[Rosuvastatin]]</u>'': Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 5-40 mg<br>
-❑ ''<u>Pitavastatin</u>'': Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-4 mg<br><br>
+❑ ''<u>[[Pitavastatin]]</u>'': Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-4 mg<br><br>
-''Safety Monitoring with Statins''<br>
+''Safety Monitoring with [[Statin]]s''<br>
 If statin therapy is to be initiated, the following lab parameters should be monitored<br>
-:❑ Liver transaminases (AST and ALT) should be measured among all patients (symptomatic and asymptomatic) as follows:
+:❑ Liver transaminases ([[AST]] and [[ALT]]) should be measured among all patients (symptomatic and asymptomatic) as follows:
 ::❑ Before initiation of statin therapy (baseline)
-::❑ At 3 months following initiation of statin therapy due to high risk of hepatotoxicity within 3 months of therapy.
+::❑ At 3 months following initiation of statin therapy due to the high risk of hepatotoxicity within 3 months of therapy.
 ::❑ Every 6 months thereafter<br>
-:❑ Creatine kinase (CK) should be measured only among symptomatic patients who complain of muscle pain/weakness<br><br>
+:❑ [[Creatine kinase]] (CK) should be measured only among symptomatic patients who complain of muscle pain/weakness<br><br>
 '''''Fibrates'''''<br>
 Administration of any of the following fibrates is recommended to manage dyslipidemia<br>
-❑ ''<u>Fenofibrate</u>'': Recommended starting daily dose 48-145 mg PO once daily. Dose range: 48-145 mg<br>
+❑ ''<u>[[Fenofibrate]]</u>'': Recommended starting daily dose 48-145 mg PO once daily. Dose range: 48-145 mg<br>
-❑ ''<u>Gemfibrozil</u>'': Recommended starting daily dose 1200 mg PO once daily. Dose range: 1200 mg<br>
+❑ ''<u>[[Gemfibrozil]]</u>'': Recommended starting daily dose 1200 mg PO once daily. Dose range: 1200 mg<br>
 ❑ ''<u>Fenofibric acid</u>'': Recommended starting daily dose 45-135 mg PO once daily. Dose range: 45-135 mg<br><br>
 ''Safety Monitoring with Fibric Acid''<br>
 If fibric acid therapy is to be initiated, the following lab parameters should be monitored<br>
-:❑ Liver transaminases (AST and ALT) measured as follows:
+:❑ Liver transaminases ([[AST]] and [[ALT]]) measured as follows:
 ::❑ Before initiation of statin therapy (baseline)
-::❑ At 3 months following initiation of fibric acid therapy due to high risk of hepatotoxicity within 3 months of therapy.
+::❑ At 3 months following initiation of fibric acid therapy due to the high risk of hepatotoxicity within 3 months of therapy.
 ::❑ Every 6 months thereafter<br><br>
 '''''Nacin'''''<br>
@@ Line 535: / Line 562: @@
 ❑ <u>''Immediate release:''</u> Recommended starting daily dose 250 mg PO once daily at bedtime. Dose range: 250-3000 mg<br>
 ❑ <u>''Extended release''</u>: Recommended starting daily dose 500 mg PO once daily at bedtime. Dose range: 50-2000 mg<br><br>
-''Safety Monitoring with Niacin''<br>
+''Safety Monitoring with [[Niacin]]''<br>
-If niacin therapy is to be initiated, the following lab parameters should be monitored<br>
+If [[niacin]] therapy is to be initiated, the following lab parameters should be monitored<br>
 :❑ Liver transaminases (AST and ALT) should be measured among asymptomatic patients as follows:
-::❑ Before initiation of niacin therapy (baseline)
+::❑ Before initiation of [[niacin]] therapy (baseline)
-::❑ Every 3 months following initiation of niacin therapy for the first year
+::❑ Every 3 months following initiation of [[niacin]] therapy for the first year
 ::❑ Every 6 months thereafter<br><br>
 '''''Bile acid sequestrants'''''<br>
 Administration of any of the following bile acid sequestrants is recommended to manage dyslipidemia<br>
-❑ <u>''Cholestyramine''</u>: Recommended starting daily dose 8-16 mg PO once daily at bedtime. Dose range: 4-24 mg<br>
+❑ <u>''[[Cholestyramine]]''</u>: Recommended starting daily dose 8-16 mg PO once daily at bedtime. Dose range: 4-24 mg<br>
-❑ <u>''Colestipol''</u>: Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-16 mg<br>
+❑ <u>''[[Colestipol]]''</u>: Recommended starting daily dose 2 mg PO once daily at bedtime. Dose range: 2-16 mg<br>
-❑ <u>''Colesevelam''</u>: Recommended starting daily dose 3.8 mg PO once daily at bedtime. Dose range: 3.8-4.5 mg<br><br>
+❑ <u>''C[[olesevelam]]''</u>: Recommended starting daily dose 3.8 mg PO once daily at bedtime. Dose range: 3.8-4.5 mg<br><br>
 '''''Cholesterol absorption inhibitors'''''<br>
-❑ <u>''Ezetimibe''</u>: Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 10 mg<br></div>
+❑ <u>''[[Ezetimibe]]''</u>: Recommended starting daily dose 10 mg PO once daily at bedtime. Dose range: 10 mg<br></div>
 }}
 {{familytree | | |!| |,|-|-|-|+|-|-|-|.| | | | | | | | | | | | | | | }}
-{{familytree | | |!| E01 | | E02 | | E03 | | | | | | | | | | | | | |E01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to reduce LDL'''<br>
+{{familytree | | |!| E01 | | E02 | | E03 | | | | | | | | | | | | | |E01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to reduce LDL'''<br><div class="mw-collapsible mw-collapsed">
-❑ Statin monotherapy at a recommended initial daily dose (LDL reduction: 21% to 55%)<br>
+❑ [[Statin]] monotherapy at a recommended initial daily dose (LDL reduction: 21% to 55%)<br>
-❑ Fibrate monotherapy at a recommended initial daily dose (LDL reduction: 20% to 25%)<br>
+❑ [[Fibrate]] monotherapy at a recommended initial daily dose (LDL reduction: 20% to 25%)<br>
-❑ Niacin monotherapy at a recommended initial daily dose (LDL reduction: 10% to 25%)<br>
+❑ [[Niacin]] monotherapy at a recommended initial daily dose (LDL reduction: 10% to 25%)<br>
-❑ Bile acid sequestrant monotherapy at a recommended initial daily dose (LDL reduction: 10% to 25%)<br>
+❑ [[Bile acid sequestrant]] monotherapy at a recommended initial daily dose ([[LDL]] reduction: 10% to 25%)<br>
-❑ Ezetimibe monotherapy at recommended initial daily dose (LDL reduction: 10% to 18%)</div>|E02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to reduce triglycerides'''<br>
+❑ [[Ezetimibe]] monotherapy at recommended initial daily dose ([[LDL]] reduction: 10% to 18%)</div>|E02=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to reduce triglycerides'''<br>
-❑ Fibrates monotherapy at a recommended initial daily dose with or without omega-3 fish oil (triglyceride reduction: 20% to 35%)<br>
+❑ [[Fibrates]] monotherapy at a recommended initial daily dose with or without omega-3 fish oil ([[triglyceride]] reduction: 20% to 35%)<br>
-❑ Niacin monotherapy at recommended initial daily dose with or without omega-3 fish oil (triglyceride reduction: 20% to 30%)<br></div>|E03=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to increase HDL''' <br>
+❑ [[Niacin]] monotherapy at recommended initial daily dose with or without omega-3 fish oil (triglyceride reduction: 20% to 30%)<br></div>|E03=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Aim to increase HDL''' <br>
-❑ Niacin monotherapy at recommended initial daily dose (HDL increase: 10% to 35%)<br>
+❑ [[Niacin]] monotherapy at a recommended initial daily dose (HDL increase: 10% to 35%)<br>
 ❑ Fibrates monotherapy at recommended initial daily dose (HDL increase: 6% to 18%)<br>
@@ Line 578: / Line 605: @@
 {{familytree | | |!| | | | | | | H01 | | | | | | | | | | | | | | | | H01=<div style="float: left; text-align: left; width: 18em; padding:1em;">Does the patient have '''ANY''' of the following criteria to initiate combination pharmacotherapy?<br>
-❑ Markedly elevated cholesterol concentration, '''OR'''<br>
+❑ Markedly elevated [[cholesterol]] concentration, '''OR'''<br>
 ❑ Mixed dyslipidemia (e.g. Hypertriglyceridemia and reduced HDL-C), '''OR'''<br>
@@ Line 587: / Line 614: @@
 {{familytree | | |!| | | |,|-|^|-|.| | |!| | | | | | | | | | | | | | }}
 {{familytree | | |!| | | J01 | | J02 | |!| | | | | | | | | | | | | | J01=<div style="float: left; text-align: left; width: 18em; padding:1em;">❑ Consider changing drug class<br>
-:❑ Reassess liver transaminase when changing drug class for statin, niacin, and fibrates</div>|J02=<div style="float: left; text-align: left; width: 18em; padding:1em;">❑ Consider increasing dose of antilipidemic agent within dose range for each drug<br>
+:❑ Reassess liver transaminase when changing drug class for [[statin]], [[niacin]], and [[fibrates]]</div>|J02=<div style="float: left; text-align: left; width: 18em; padding:1em;">❑ Consider increasing dose of antilipidemic agent within dose range for each drug<br>
-:❑ Reassess liver transaminase when increase dose for any of statin, niacin, or fibrates</div>}}
+:❑ Reassess liver transaminase when increase dose for any of [[statin]], [[niacin]], or [[fibrates]]</div>}}
 {{familytree | | |!| | | |`|-|v|-|'| | |!| | | | | | | | | | | | | | }}
 {{familytree | | |!| | | | | K01 | | | |!| | | | | | | | | | | | | | K01=Lipid goal achieved with optimal administration of antilipidemic monotherapy?}}
@@ Line 595: / Line 622: @@
 {{familytree | | |)|-|-| L01 | | L02 |-|(| | | | | | | | | | | | | | L01=Yes|L02=No}}
 {{familytree | | |!| | | | | | | | | | M01 | | | | | | | | | | | | | M01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Administer combination therapy'''<br>
-Administer '''ANY''' of the following combination therapies:
+Administer '''ANY''' of the following combination therapies:<br>
-❑ Ezetimibe/simvastatin (1 pill): Recommended starting daily dose 10/20 mg PO once daily at bedtime. Dose range: 10/10 to 10/80 mg, '''OR'''<br>
+❑ [[Ezetimibe]]/[[simvastatin]] (1 pill): Recommended starting daily dose 10/20 mg PO once daily at bedtime. Dose range: 10/10 to 10/80 mg, '''OR'''<br>
-❑ Extended-release niacin/simvastatin (1 pill): Recommended starting daily dose 500/20 mg PO once daily at bedtime. Dose range: 500/20 to 1000/20 mg</div> }}
+❑ Extended-release [[niacin]]/[[simvastatin]] (1 pill): Recommended starting daily dose 500/20 mg PO once daily at bedtime. Dose range: 500/20 to 1000/20 mg<br>
+❑ [[Statin]] ± [[ezetimibe]]/ [[Alirocumab]] (a [[PCSK9]] inhibitor)</div> }}
 {{familytree | | |)|-|-|-|-|-|-|-|-|-|-|'| | | | | | | | | | | | | | }}
-{{familytree | | N01 | | | | | | | | | | | | | | | | | | | | | | N01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Follow-up'''<br>
+{{familytree | | N01 | | | | | | | | | | | | | | | | | | | | | | N01=<div style="float: left; text-align: left; width: 18em; padding:1em;">'''Follow-up'''<br><div class="mw-collapsible mw-collapsed">
 ❑ Reassess lipid profile at 6 weeks following initiation of management<br>
@@ Line 605: / Line 633: @@
 ❑ If the goal is not achieved following 6 weeks, reassess 6 weeks later. Continue 6-week interval until target lipid profile is achieved<br>
-❑ Once the target lipid profile is achieved, generally reassess lipid profile within 6 months to 12 months
+❑ Once the target [[lipid profile]] is achieved, generally reassess lipid profile within 6 months to 12 months
 :❑ Consider more frequent lipid profile reassessments in the following conditions
-::❑ Deterioration of diabetic control
+::❑ Deterioration of [[diabetes|diabetic]] control
-::❑ Administration of a new drug that is known to affect the lipid profile
+::❑ Administration of a new drug that is known to affect the [[lipid profile]]
 ::❑ Progression of atherothrombotic disease
-::❑ Considerable weight gain
+::❑ Considerable [[weight gain]]
-::❑ Unexpected adverse derangement in any parameter of the lipid profile
+::❑ Unexpected adverse derangement in any parameter of the [[lipid profile]]
-::❑ Development of new risk factor for CAD
+::❑ Development of new risk factor for [[CAD]]
-:❑ For all patients (symptomatic or asymptomatic) receiving either statin, fibric acid, or niacin, assess liver tranaminases (AST and ALT) at 3 months
+:❑ For all patients (symptomatic or asymptomatic) receiving either [[statin]], [[fibric acid]], or [[niacin]], assess liver tranaminases ([[AST]] and [[ALT]]) at 3 months
-::❑ For patients receiving either statin or fibric acid: Repeat liver transaminase reassessment every 6 months thereafter.
+::❑ For patients receiving either statin or [[fibric acid]]: Repeat [[liver transaminase]] reassessment every 6 months thereafter.
-::❑ For patients receiving niacin: Repeat liver transaminase reassessment every 3 months for the first year, then every 6 months thereafter.
+::❑ For patients receiving [[niacin]]: Repeat liver transaminase reassessment every 3 months for the first year, then every 6 months thereafter.
 :❑ For patients receiving statin therapy who are complaining of significant myalgia or muscle weakness
-::❑ Assess creatine kinase (CK) to confirm or rule out myopathy</div>}}
+::❑ Assess [[creatine kinase]] (CK) to confirm or rule out [[myopathy]]</div>}}
 {{familytree/end}}
 ==Do's==
-*Treat pediatric patients who are older than 8 years of age with either LDL-C > 190 mg/dL or LDL > 160 mg/dL plus any of the following conditions: either ≥ 2 CV risk factors even after lifestyle intervention, family history of premature CAD, or overweight/obese/insulin resistance.
+*Treat [[pediatrics|pediatric]] patients who are older than 8 years of [[age]] with either LDL-C > 190 mg/dL or [[LDL]] > 160 mg/dL plus any of the following conditions: either ≥ 2 [[cardiovascular system|CV]] risk factors even after lifestyle intervention, family [[history]] of premature [[CAD]], or overweight/[[obesity|obese]]/[[insulin resistance]].<ref name="pmid22477808">{{cite journal |vauthors=Eiland LS, Luttrell PK |title=Use of statins for dyslipidemia in the pediatric population |journal=J Pediatr Pharmacol Ther |volume=15 |issue=3 |pages=160–72 |date=July 2010 |pmid=22477808 |pmc=3018249 |doi= |url=}}</ref>
 ==Don'ts==
-*Do not routinely order homocysteine, uric acid, plasminogen activator inhibitor 1, or other inflammatory markers.
+*Do not routinely order [[homocysteine]], [[uric acid]], [[plasminogen activator inhibitor 1]], or other inflammatory markers.
-*Do not routinely perform non-invasive measures of atherosclerosis (e.g. carotid intima media thickness).
+*Do not routinely perform non-invasive measures of [[atherosclerosis]] (e.g. [[carotid]] intima media thickness).<ref name="ZhangGuallar2014">{{cite journal|last1=Zhang|first1=Y.|last2=Guallar|first2=E.|last3=Qiao|first3=Y.|last4=Wasserman|first4=B. A.|title=Is Carotid Intima-Media Thickness as Predictive as Other Noninvasive Techniques for the Detection of Coronary Artery Disease?|journal=Arteriosclerosis, Thrombosis, and Vascular Biology|volume=34|issue=7|year=2014|pages=1341–1345|issn=1079-5642|doi=10.1161/ATVBAHA.113.302075}}</ref>
-*Do not treat dyslipidemia among post-menopausal women with hormonal replacement therapy.
+*Do not treat dyslipidemia among postmenopausal women with [[hormonal replacement therapy]].<ref name="pmid24532973">{{cite journal |vauthors=Phan BA, Toth PP |title=Dyslipidemia in women: etiology and management |journal=Int J Womens Health |volume=6 |issue= |pages=185–94 |date=2014 |pmid=24532973 |pmc=3923614 |doi=10.2147/IJWH.S38133 |url=}}</ref>
 ==References==
 {{Reflist|2}}

Dyslipidemia resident survival guide: Difference between revisions

Latest revision as of 18:58, 17 December 2020

Overview

Classification

Fredrickson Classification of Hyperlipoproteinemia[1][2][3][4]

Unclassified forms

Classification According to Etiology[4]

Classification According to Laboratory Results[8][9][10]

Causes

Increase in Total Cholesterol and LDL-C

Increase in Total Triglycerides and VLDL-C

Screening

Complete Diagnostic Approach

Treatment

Do's

Don'ts

References

Navigation menu

Fredrickson Classification of Hyperlipoproteinemia^[1]^[2]^[3]^[4]

Classification According to Etiology^[4]

Classification According to Laboratory Results^[8]^[9]^[10]