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Guideline Summary
Guideline Title
Treatment of dyslipidaemias.
Bibliographic Source(s)
Finnish Medical Society Duodecim. Treatment of dyslipidaemias. In: 23958 [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2010 Aug 3 [Various].
Guideline Status

This is the current release of the guideline.

This guideline updates previous versions:

Finnish Medical Society Duodecim. Treatment of hyperlipidaemia: aims and selection. In: EBM Guidelines. Evidence-Based Medicine [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2007 Feb 9 [Various].

Finnish Medical Society Duodecim. Drug treatment for hyperlipidaemias. In: EBM Guidelines. Evidence-Based Medicine [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2008 Jan 3 [Various]. [3 references]

Scope

Disease/Condition(s)
  • Dyslipidemias
    • Hypercholesterolemia alone (including familial hypercholesterolemia)
    • Increased plasma triglycerides and cholesterol
    • Pure hypertriglyceridemia
    • Dyslipidemia secondary to hypothyroidism
  • Atherosclerotic arterial disease
Guideline Category
Evaluation
Prevention
Risk Assessment
Treatment
Clinical Specialty
Cardiology
Endocrinology
Family Practice
Internal Medicine
Intended Users
Health Care Providers
Physicians
Guideline Objective(s)

Evidence-Based Medicine Guidelines collect, summarize, and update the core clinical knowledge essential in general practice. The guidelines also describe the scientific evidence underlying the given recommendations.

Target Population
  • Patients with ischemic heart disease, other atherosclerotic diseases (cerebrovascular disease, peripheral arterial disease) or diabetes
  • Symptomless individuals with or at high risk for dyslipidemia
Interventions and Practices Considered

Evaluation/Risk Assessment

  1. Determination of age and living habits
  2. Assessment of risk for arterial disease based on standard risk calculators
  3. Ruling out secondary hypercholesterolemia

Treatment

  1. Lifestyle changes including smoking cessation, weight reduction, increased physical activity, reduced intake of saturated and trans fats
  2. Antihyperlipidemic agents
    • Statins (atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin)
    • Resins (cholestyramine, colesevelam)
    • Fibrates (bezafibrate, fenofibrate, and gemfibrozil)
    • Ezetimibe
    • Nicotinic acid
    • Fish oils
    • Thyroxine replacement therapy
  3. Follow-up
    • Lipid levels
    • Safety tests: serum alanine aminotransferase (ALT) concentration and creatine kinase in patients with myalgia
    • Referral for specialist consultation
Major Outcomes Considered
  • Reduction in lipid levels
  • Incidence of myocardial infarction, need for coronary surgery and mortality
  • Incidence of myopathy and other side effects

Methodology

Methods Used to Collect/Select the Evidence
Hand-searches of Published Literature (Primary Sources)
Hand-searches of Published Literature (Secondary Sources)
Searches of Electronic Databases
Description of Methods Used to Collect/Select the Evidence

The evidence reviewed was collected from the Cochrane database of systematic reviews and the Database of Abstracts of Reviews of Effectiveness (DARE). In addition, the Cochrane Library and medical journals were searched specifically for original publications.

Number of Source Documents

Not stated

Methods Used to Assess the Quality and Strength of the Evidence
Weighting According to a Rating Scheme (Scheme Given)
Rating Scheme for the Strength of the Evidence

Classification of the Quality of Evidence

Code Quality of Evidence Definition
A High Further research is very unlikely to change confidence in the estimate of effect.
  • Several high-quality studies with consistent results
  • In special cases: one large, high-quality multi-centre trial
B Moderate Further research is likely to have an important impact on confidence in the estimate of effect and may change the estimate.
  • One high-quality study
  • Several studies with some limitations
C Low Further research is very likely to have an important impact on confidence in the estimate of effect and is likely to change the estimate.
  • One or more studies with severe limitations
D Very Low Any estimate of effect is very uncertain.
  • Expert opinion
  • No direct research evidence
  • One or more studies with very severe limitations

GRADE (Grading of Recommendations Assessment, Development and Evaluation) Working Group (modified by the EBM Guidelines Editorial Team).

Methods Used to Analyze the Evidence
Systematic Review
Description of the Methods Used to Analyze the Evidence

Not stated

Methods Used to Formulate the Recommendations
Not stated
Rating Scheme for the Strength of the Recommendations

Not applicable

Cost Analysis

A formal cost analysis was not performed and published cost analyses were not reviewed.

Method of Guideline Validation
Peer Review
Description of Method of Guideline Validation

Not stated

Recommendations

Major Recommendations

The levels of evidence [A-D] supporting the recommendations are defined at the end of the "Major Recommendations" field.

Essentials

  • Goals
    • Preventing the progress of arterial disease in those already affected (the most important patient group to be treated)
    • Decreasing the risk of atherosclerotic arterial disease guided by the total risk (combined effect of risk factors). The assessment of the risk for arterial disease may be facilitated by the use of different risk calculators (e.g., Systematic Coronary Risk Evaluation [SCORE]).
      • Note that SCORE only gives the probability of death; the overall risk of arterial disease is significantly higher.
  • Changing living habits is the primary target in all patients.
  • Rule out secondary hypercholesterolaemia before starting drug treatment.
  • The general aim of treatment is to maintain ("5–4–3–2–1 rule")
    • Plasma cholesterol under 5.0 mmol/l (under 4.0 mmol/l in high-risk individuals, if possible)
    • Plasma low-density lipoprotein (LDL) cholesterol under 3.0 mmol/l (in high-risk individuals under 2.0 mmol/l, if possible). For calculation, see LDL calculator program in the original guideline document.
    • Plasma high-density lipoprotein (HDL) cholesterol over 1.0 mmol/l
    • Plasma triglycerides under 2.0 mmol/l
    • Plasma cholesterol/HDL cholesterol ratio under 4.0.
  • The treatment of a low HDL cholesterol concentration and a high serum triglyceride concentration in association with hypercholesterolaemia is probably beneficial at least in patients with type 2 diabetes.
  • In hypertriglyceridaemia, the serum triglyceride concentration should be under 10 mmol/l to minimize the risk of pancreatitis.

Treatment in Different Patient Groups

Patients with Ischaemic Heart Disease, Other Atherosclerotic Diseases (Cerebrovascular Disease, Peripheral Arterial Disease) or Diabetes

  • The risk of myocardial infarction or cardiac death increases sharply with rising serum cholesterol concentrations in patients with an arterial disease.
  • The effectiveness of drug treatment has been clearly shown in controlled studies (Scandinavian Simvastatin Survival Study Group, 1994) [A]. The target plasma cholesterol concentration is under 4.0 mmol/l (LDL cholesterol under 2.0 mmol/l); see table 1 below. There is evidence that especially patients with coronary heart disease or with diabetes benefit from intensive lowering of plasma LDL concentrations (well under 2 mmol/l) (Cannon et al., 2004).

Table 1. Dyslipidaemia in Patients with Arterial Disease

Plasma Cholesterol (mmol/l) LDL Cholesterol (mmol/l) Risk of Disease Progression Action
4.0-4.5 or higher 2.0-2.5 or higher Greatly increased Improve diet, change living habits, control cholesterol levels in 1-2 months. Reduce risk by modifying other risk factors. Drug therapy is usually always indicated if target levels are not reached.

Symptomless Individuals

  • The general target plasma cholesterol concentration is under 5.0 mmol/l (LDL cholesterol under 3.0 mmol/l). When considering indications for intervention the overall risk is taken into account (age, sex, smoking, blood pressure). Family history as well as HDL and triglyceride concentrations also reflect the risk (working age population is the most important group.) See table 2 below.
  • In high-risk symptomless individuals the target for plasma cholesterol is under 4.0 mmol/l (LDL cholesterol under 2.0 mmol/l) if possible.

Table 2. Dyslipidaemia in Asymptomatic Individuals (overall assessment is crucial in planning the treatment)

Plasma Cholesterol (mmol/l) LDL Cholesterol (mmol/l) Risk of Disease Progression Action
8.0 or higher 6.5 or higher Significantly increased Assess risk factors. Improve diet and change living habits. Control cholesterol levels in 1–2 months. Drug therapy is usually indicated if lifestyle changes are not sufficient. The probability of an inherited disorder is high. Relatives should be investigated.
6.5-7.9 5.0-6.4 Moderately increased Assess risk factors and start dietary therapy. Control treatment effect in 2–4 months. Further measures (drug treatment) according to outcome of dietary therapy and other risk factors. Hereditary disorders of lipid metabolism are possible (and should be treated in the same way as patients with serum cholesterol above 8 mmol/l).
5.0-6.4 3.0-4.9 Slightly increased Counselling on healthy diet and assessment of risk factors. Short-term measures according to other risk factors. Control of plasma cholesterol after 5 years at the latest.

Patients over 80 Years of Age

  • Treatment started at a younger age is continued.
  • There are no randomised prognostic studies on treatment started in this age group.
  • The biological age and the general prognosis are individually taken into account when deciding on treatment, especially in those with arterial disease.
  • The principles of treatment are the same as in younger patients.

Treatment of Dyslipidaemia by Lifestyle Changes

  • Smoking cessation
  • Weight reduction if needed
  • Increase of physical activity
  • Reduced intake of saturated fat (animal and dairy fat) and trans fats
  • Increased intake of polyunsaturated fats and monoenes (vegetable fats) instead of saturated fats (Clarke et al., 1997; Gardner & Kraemer, 1995) [A]. Rapeseed oil is to be recommended.
  • Reduced intake of cholesterol
  • Increased intake of dietary fibre (Brown et al., 1999; Olson et al., 1997) [A] (gel-forming fibre can be added if indicated)
  • Stanol/sterol margarine can be used (overweight individuals should use diet margarine [40% fat] or nothing).
  • If target serum lipid values are not reached with diet therapy, start drug treatment (instead of just ordering further control measurements).

Dietary Recommendations

  • The main principles of a "heart-friendly" diet have remained the same for decades and there is no essential new information that would affect them.
  • Fat <30 E% of total energy
    • Saturated <10 E%
    • Monoenes and polyunsaturated 20 E%
  • Dietary cholesterol 250–300 mg/day
  • Products containing plenty of soluble fibre (Brown et al., 1999; Olson et al., 1997) [A] instead of white carbohydrates (refined sugar, refined flour)
    • >20 g/1000 kcal (wholemeal bakery products, 500 g of vegetables and fruits per day)
  • Fish twice a week
  • Avoidance of boiled coffee
  • Reduction of alcohol consumption if the patient has
    • Overweight
    • High blood pressure
    • Hypertriglyceridaemia
  • Reduction of salt intake especially if the patient has high blood pressure.

Expected Effectiveness of Diet Therapy

  • The effectiveness of diet in the prevention of arterial diseases depends on its individual effect on plasma lipid concentrations.
  • Fasting serum cholesterol may decrease by 15% in some patients, but on the average the effect is only 3–6% (Tang et al., 1998) [A].
  • In some individuals the decrease in cholesterol level may exceed 30%.

Diet Therapy in Practice

  • A thorough diet history, preferably by diary, is the basis of diet counselling.
  • Reduce animal and dairy fat. Advise the patient to
    • Use fat-free milk or sour milk
    • Prefer other low fat milk products
    • Use vegetable margarine, diet margarine, or plant stanol/sterol margarine
    • Prefer low fat meat products, fish, skinless poultry, and sausages low in fat.
  • Avoid foods rich in cholesterol.
    • Meat products rich in fat and milk fat
    • Internal organs
    • Egg yolk
  • Hidden fats are often saturated.
    • Pizza
    • Fast food
    • Pastries
  • Reduce overweight by hypocaloric diet (or very-low-calorie diet, if necessary) and exercise.
  • Increase the intake of vegetable fibre (Brown et al., 1999; Olson et al., 1997) [A]. Prefer:
    • Vegetables, roots, leguminous plants
    • Berries and fruit
    • Whole-grain cereals.
  • Prepare food without adding fat or by using vegetable oils or vegetable margarines. Suitable oils include canola (most favourable content of fatty acids), olive, sunflower, soy, and maize oil.
  • Use filtered coffee instead of boiled.
  • As the proportion of fat as energy source is reduced it is substituted by carbohydrates: potatoes, cereals, rice, pasta, fruit, berries, vegetables and roots.

The Effect of Plant Stanol/Sterol Margarine on Cholesterol Concentrations

  • A daily 25 g dose of sitostanol margarine or 20–25 g of plant sterol margarine (2 g of sterol) decreases serum cholesterol by 10% and LDL cholesterol by 15% more than ordinary margarine. The concentrations of HDL cholesterol and triglycerides remain unchanged.
  • Plant stanol/sterol margarine may be suitable as the only treatment for mild hypercholesterolaemia in addition to other diet therapy. Patients that remain hypercholesterolaemic can be treated with a combination of sitostanol and statins.
  • Some patients with familial and other hypercholesterolaemia may be able to avoid hypocholesterolaemic drugs or reduce their doses by using plant stanol/sterol margarine.
  • Overweight persons should use low fat modifications where plant stanols/sterols are added.
  • Monitor the outcome and weight of the patient.

Drug Treatment for Dyslipidaemias

Principles

  • Make sure that an effective diet has been implemented, and start drug therapy without delay, if clearly indicated.
  • People with arterial disease or diabetes are important target groups.
  • Determine plasma cholesterol, triglycerides, HDL cholesterol and LDL cholesterol before commencing drug treatment.
  • Rule out secondary hypercholesterolaemia. If the cause of secondary hypercholesterolaemia cannot be managed treat the patient as if he had primary hypercholesterolaemia.
  • Identify patients with familial hypercholesterolaemia (plasma cholesterol usually above 8 mmol/L but may even be lower, xanthomas, family history) in order to screen family members.
  • Of the most commonly used drugs, statins (atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin), cholestyramine, fibrates (bezafibrate, fenofibrate, gemfibrozil) as well as ezetimibe in combination with simvastatin have been tested in long-term randomized clinical trials based on significant clinical endpoints.
  • A statin is the drug of choice (Baigent et al., 2005; Dale et al., 2006; Costa et al., 2006; Prospective Studies Collaboration et al., 2007) [A] unless the main abnormality is hypertriglyceridaemia or a low HDL cholesterol concentration. In these cases, even a fibrate may be considered.
  • If necessary, a statin can be combined with ezetimibe (which in selected cases can also be used as monotherapy).
  • Nicotinic acid may be combined with a statin if affecting HDL cholesterol concentration is a target.
  • Resins and guar gum are used as sole therapy in exceptional cases only. Because they are not absorbed from the intestine they are safe (e.g., during pregnancy and in children). Their adverse effects may cause problems.

Choice of Drug According to the Type of Dyslipidaemia

  • See Table 3 below

Table 3. Selection of Lipid Lowering Drug According to the Type of Dyslipidaemia

Dyslipidaemic (pheno)type Drug of Choice
Hypercholesterolaemia alone (familial hypercholesterolaemia) Statin or a combination of a statin and ezetimibe or a combination of a statin and a resin (the dose of resin <20 g to avoid adverse effects).
Both plasma cholesterol and triglycerides increased Statin if plasma triglycerides <4.5 mmol/L.
Fibrate + statin if increasing the dose of statin is not sufficient (the need for combination treatment should be evaluated by a specialist) or nicotinic acid + statin especially if HDL cholesterol concentration is small.
Pure hypertriglyceridaemia Reducing weight and limiting alcohol consumption is essential before drug treatment is considered. Control of diabetes should be improved. Fibrate.
Hypothyroidism Thyroxine substitution normalizes the lipid abnormality if it is caused by hypothyroidism.

Statins (Atorvastatin, Fluvastatin, Lovastatin, Pravastatin, Rosuvastatin, Simvastatin)

  • In practice the most important group of antilipidaemic agents (Bucher, Griffith, & Guyatt, 1999; Ross et al., 1999) [A]

Mechanism of Action

  • Based on the inhibition of the hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase resulting in the inhibition of cholesterol synthesis in hepatocytes. The number of LDL receptors on hepatocytes is increased, and the elimination of LDL from the blood is enhanced. Part of the action may be through very low-density lipoprotein (VLDL) or even other mechanisms.

Effectiveness

  • LDL is decreased by 30% to 40%.
  • HDL is increased by 5% to 15%.
  • Triglycerides are decreased by 10% to 30% or even more.
  • Combining statins with ezetimibe or resins (Schectman & Hiatt, 1996) [C] results in additive effects.

Adverse Effects

  • Statins are usually well tolerated, even by elderly patients.
  • Serum aminotransferase concentrations rise in about 2% of the patients. The clinical significance of this is unclear because the patients often have other concomitant factors that may increase the transaminase concentrations. There is no conclusive evidence that statin therapy would cause significant liver damage.
  • Muscle pains are the clinically most significant adverse effects.
  • Muscular symptoms are not necessarily caused by statins because such symptoms are also otherwise common in the age groups involved. It is, however, important to find out the cause of the muscular symptom because it may lead to unnecessary cessation of statin therapy.
  • The incidence of significant muscular adverse effects is <0.1%.
  • Serum creatine kinase need not be determined routinely. The test is indicated if the patient has unexplained myalgias or muscular symptoms (concentrations 10 times above the upper limit of the reference range are significant). However, statin-induced muscular symptoms are possible even without an increase in the creatine kinase (CK) concentration.
  • Factors apparently predisposing to myopathy include:
    • Concurrent use of agents increasing the concentration of statins (e.g., cyclosporine, fibrate, macrolide, or azole medication)
    • Predisposition, which can be investigated by gene testing
    • Very high age
    • Multiple concomitant diseases
    • Operations
    • Hypothyroidism
    • Vitamin D deficiency
  • Individual cases of other adverse effects (e.g., polyneuropathy) have been described in connection with statin treatment but true association has not been verified.

Dosage

  • Adjust the dose (Illingworth & Tobert, 1994; Hsu, Spinler, & Johnson, 1995) [A] according to response. Doubling the dose provides a further decrease of serum cholesterol by 7%.
  • Atorvastatin: 10 to 80 mg/day
  • Fluvastatin: (20) to 40 to 80 mg/day
  • Lovastatin: 20 to 80 mg/day
  • Pravastatin: 20 to 40 mg/day
  • Simvastatin: 10 to 80 mg/day
  • Rosuvastatin: 10 to 40 mg/day

Resins (Cholestyramine, Colesevelam)

Mechanism of Action

  • The resins absorb bile acids in the intestine, prevent their reabsorption, and increase their excretion in the faeces.
  • They do not increase the excretion of neutral steroids or cause fat malabsorption.
  • The enhanced excretion of bile acids results in increased metabolism of cholesterol into bile acids and further in an increase in the number of LDL receptors and intake of LDL cholesterol into hepatocytes.

Effectiveness

  • Total and LDL cholesterol concentrations decrease by 15% to 30%.
  • Plasma triglyceride concentration may increase.

Dosage

  • Cholestyramine 16 to 32 g/day
  • Colesevelam 625 mg tablets 4 to 6/day

Adverse Effects

  • Bowel symptoms: constipation, flatulence, nausea, epigastric pain
  • Deficiency of fat-soluble vitamins and folic acid because their absorption is impaired

Interactions

  • The absorption of the following drugs may be affected (these drugs should be taken at least 1 hour before or 4 hours after the resin):
    • Digoxin
    • Thyroxine
    • Warfarin
    • Thiazide diuretics

Fibrates (Bezafibrate, Fenofibrate, and Gemfibrozil)

Mechanism of Action

  • Fibrates act through the nuclear peroxisome proliferator-activated receptor (PPAR) system; the activity of lipoprotein lipase is increased in fat and muscular tissues and the elimination of triglyceride-containing lipoproteins is enhanced.

Effectiveness

  • Triglyceride concentration is decreased by 20% to 70%.
  • HDL cholesterol concentration is increased by 10% to 25%.
  • LDL cholesterol concentration is decreased if the initial concentration was high.

Adverse Effects

  • Mild abdominal and bowel irritation
  • Myalgia and an increase in serum creatine kinase concentration
  • Possible formation of gallstones
  • Increase in serum transaminase levels
  • Fluid retention, gynaecomastia, and impotence are rare.

Interactions

  • Protein-bound drugs are released and their concentrations are increased (warfarin, sulphonylureas).
  • Fenofibrate is the recommended choice in combination with statin therapy.

Contraindications

  • Severe renal or hepatic insufficiency, diseases of the gallbladder

Dosage

  • Bezafibrate: 400 mg x 1 at lunch
  • Fenofibrate: 200 mg x 1 with meal
  • Gemfibrozil: 600 to 1200 mg/day divided into 2 to 3 doses

Ezetimibe

  • For patients with hypercholesterolemia in whom statins are contraindicated or to be combined with a statin when the effect of statins alone is insufficient.

Mechanism of Action

  • Prevents cholesterol from being absorbed in the small intestine.
  • The effect is additive to statins which prevent cholesterol synthesis.

Effectiveness

  • When used alone diminishes the concentration of LDL cholesterol by 18% to 19 %, triglycerides by 4% to 11% and increases the concentration of HDL cholesterol by 2% to 3%.
  • Combining ezetimibe with a low dose of statin is additive and equals to a large dose of statin alone in reducing cholesterol concentrations.

Dosage

  • 10 mg/day

Adverse Effects

  • The studies conducted so far show little adverse effects.

Nicotinic Acid

  • Can usually be used in combination with a statin if triglyceride concentration is not sufficiently decreased or if the aim is to increase HDL cholesterol concentration.

Effectiveness

  • Nicotinic acid (2 g/day) increases HDL cholesterol concentration by 20% to 28% and decreases LDL cholesterol concentration by 15% to 20% and triglycerides by 20% to 30%.

Dosage

  • Gradually increased up to 1–2 g per day

Adverse Effects

  • Frequently flushing and feeling of heat. These adverse effects are less frequent when a slow-release drug form is used.
  • Combination of the prostaglandin D receptor antagonist laropiprant to nicotinic acid reduces the adverse effects.
  • May increase blood glucose concentrations.

Fish Oils

  • Fish oils (long-chain n-3-fatty acids) 2–4 g/day combined to statin therapy decrease elevated serum triglyceride concentrations.
  • The decreased rate of arterial events in association with fish oil intake is probably not due to the triglyceride-lowering effect.
  • When high doses of fish oils are consumed a possible increase in bleeding tendency should be borne in mind.

Thyroxine Replacement Therapy in Hypothyroidism

  • Thyroxine replacement therapy normalizes lipid disorders caused by hypothyroidism (Danese et al., 2000; Chu & Crapo, 2001) [C].

Follow-up of Drug Therapy

  • Lipid concentrations should initially be controlled after 1 to 2 months, then after 3 to 6 months if necessary, and thereafter annually.
  • Make sure that the target lipid levels are reached (see above). With statin therapy this is usually not a problem as long as the drug dosage is appropriately adjusted.

Safety Tests

Statins

  • Serum alanine transaminase (ALT) should be determined 1 to 2 months after the onset of therapy and thereafter usually once a year.
    • Concentrations greater than twice the upper limit of the reference range are clinically significant. A slight increase in serum ALT concentration is an indication for follow-up, not necessarily for discontinuation of the drug.
  • If unexplained myalgia should occur, serum creatine kinase should be determined if necessary.

Fibrates

  • Serum ALT is determined after 1 to 2 months, and thereafter at 6 to 12 month intervals. If used in combination with statins, ALT should be determined at 3 to 4 month intervals (when combined with a fibrate, the statin dosage should be only half of the normal).
  • If myalgia occurs serum creatine kinase should always be examined.

Indications for Specialist Consultation

  • Starting statin or fibrate therapy is contemplated.
  • A lipid disorder is associated with another complicated disease.
  • Serum triglyceride concentration is primarily above 10 mmol/l or remains above 5 mmol/l despite treatments.
  • Very high plasma cholesterol concentration (above 15 mmol/l)
  • Ischaemic heart disease or xanthomas occur in childhood or in adolescents or young adults.

Related Evidence

Refer to the original guideline document for related evidence, including Cochrane reviews and other evidence summaries.

Definitions:

Classification of the Quality of Evidence

Code Quality of Evidence Definition
A High Further research is very unlikely to change confidence in the estimate of effect.
  • Several high-quality studies with consistent results
  • In special cases: one large, high-quality multi-centre trial
B Moderate Further research is likely to have an important impact on confidence in the estimate of effect and may change the estimate.
  • One high-quality study
  • Several studies with some limitations
C Low Further research is very likely to have an important impact on confidence in the estimate of effect and is likely to change the estimate.
  • One or more studies with severe limitations
D Very Low Any estimate of effect is very uncertain.
  • Expert opinion
  • No direct research evidence
  • One or more studies with very severe limitations

GRADE (Grading of Recommendations Assessment, Development and Evaluation) Working Group (modified by the EBM Guidelines Editorial Team).

Clinical Algorithm(s)

None provided

Evidence Supporting the Recommendations

References Supporting the Recommendations
Type of Evidence Supporting the Recommendations

Concise summaries of scientific evidence attached to the individual guidelines are the unique feature of the Evidence-Based Medicine Guidelines. The evidence summaries allow the clinician to judge how well-founded the treatment recommendations are. The type of supporting evidence is identified and graded for select recommendations (see the "Major Recommendations" field).

Benefits/Harms of Implementing the Guideline Recommendations

Potential Benefits
  • Preventing the progress of arterial disease in those already affected (the most important patient group to be treated)
  • Decreasing the risk of atherosclerotic arterial disease guided by the total risk (combined effect of risk factors)
Potential Harms

Adverse Effects of Drug Treatment

See "Major Recommendations" section for specific adverse effects of the various drug classes.

Contraindications

Contraindications

The use of fibrates is contraindicated in patients with severe renal or hepatic dysfunction or diseases of the gallbladder.

Implementation of the Guideline

Description of Implementation Strategy

An implementation strategy was not provided.

Institute of Medicine (IOM) National Healthcare Quality Report Categories

IOM Care Need
Getting Better
Living with Illness
Staying Healthy
IOM Domain
Effectiveness
Patient-centeredness

Identifying Information and Availability

Bibliographic Source(s)
Finnish Medical Society Duodecim. Treatment of dyslipidaemias. In: 23958 [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2010 Aug 3 [Various].
Adaptation

Not applicable: The guideline was not adapted from another source.

Date Released
2001 Apr 4 (revised 2010 Aug 3)
Guideline Developer(s)
Finnish Medical Society Duodecim - Professional Association
Source(s) of Funding

Finnish Medical Society Duodecim

Guideline Committee

Editorial Team of EBM Guidelines

Composition of Group That Authored the Guideline

Primary Authors: Timo Strandberg; Hannu Vanhanen

Financial Disclosures/Conflicts of Interest

Not stated

Guideline Status

This is the current release of the guideline.

This guideline updates previous versions:

Finnish Medical Society Duodecim. Treatment of hyperlipidaemia: aims and selection. In: EBM Guidelines. Evidence-Based Medicine [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2007 Feb 9 [Various].

Finnish Medical Society Duodecim. Drug treatment for hyperlipidaemias. In: EBM Guidelines. Evidence-Based Medicine [Internet]. Helsinki, Finland: Wiley Interscience. John Wiley & Sons; 2008 Jan 3 [Various]. [3 references]

Guideline Availability

This guideline is included in "EBM Guidelines. Evidence-Based Medicine" available from Duodecim Medical Publications, Ltd, PO Box 713, 00101 Helsinki, Finland; e-mail: info@ebm-guidelines.com; Web site: www.ebm-guidelines.com External Web Site Policy.

Availability of Companion Documents

None available

Patient Resources

None available

NGC Status

This summary was completed by ECRI on March 16, 2001. The information was verified by the guideline developer as of June 15, 2001. The summary was updated by ECRI on August 17, 2001, December 9, 2002, December 29, 2003, and July 15, 2004. This summary was updated by ECRI on March 4, 2005, following the release of a public health advisory from the U.S. Food and Drug Administration regarding the use of revised labeling for the drug Crestor (rosuvastatin calcium). This summary was updated by ECRI Institute on September 25, 2008 and May 6, 2011. This summary was updated by ECRI Institute on November 22, 2011 following the U.S. Food and Drug Administration (FDA) advisory on Trilipix (fenofibric acid). This summary was updated by ECRI Institute on April 13, 2012 following the U.S. Food and Drug Administration advisories on Statin Drugs and Statins and HIV or Hepatitis C drugs.

Copyright Statement

This NGC summary is based on the original guideline, which is subject to the guideline developer's copyright restrictions.

Disclaimer

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