Drugs List

Therapeutic Indications

Uses

Combined hyperlipidaemia: lipid lowering therapy adjunct to diet
Coronary heart disease: Reduce risk of morbidity/mortality
Diabetes mellitus: Reduce cardiovascular morbidity/mortality
Heterozygous familial hypercholesterolaemia: Adjunct to diet
Homozygous familial hypercholesterolaemia: reduction of cholesterol
Treatment of primary hypercholesterolaemia resistant to diet

Adjunctive treatment of primary hypercholesterolaemia or mixed dyslipidaemia with dietary measures when response to diet and other non-pharmacological treatments (e.g. exercise and weight reduction) is inadequate.

Adjunctive treatment of homozygous familial hypercholesterolaemia with diet and other lipid lowering treatments (e.g. LDL apheresis) or if such treatments are not appropriate.

Reduction of cardiovascular mortality and morbidity as an adjunct to correction of other risk factors and cardioprotective therapy, in patients with manifest atherosclerotic cardiovascular disease or diabetes mellitus with normal or increased cholesterol levels.

Contraindications

Children under 5 years
Creatine kinase levels over 5 times upper limit of normal
Within 7 days of discontinuing fusidic acid
Breastfeeding
Myopathy
Pregnancy
Serum transaminases above 3 times upper limit of normal
Severe hepatic impairment
Unexplained elevated serum transaminases

Precautions and Warnings

Asian ancestry
Children aged 5 to 10 years
Family history of hereditary muscular disorders
Females of childbearing potential
High alcohol intake
Major surgery
Patients over 65 years
Severe trauma
Galactosaemia
Glucose-galactose malabsorption syndrome
Hereditary muscular disorder
History of hepatic impairment
History of muscular toxicity secondary to fibrates
History of muscular toxicity secondary to HMG-CoA reductase inhibitors
History of non-traumatic rhabdomyolysis
Hypothyroidism
Lactose intolerance
Renal impairment - creatinine clearance below 30 ml/minute

Advise ability to drive/operate machinery may be affected by side effects
Correct hypothyroidism before treatment
Exclude secondary causes of hypercholesterolaemia before treatment
Not all available brands are licensed for all age groups
Not all available brands are licensed for all indications
Some formulations contain lactose
Measure creatine kinase levels prior to treatment if risk of rhabdomyolysis
Perform liver function tests before commencing therapy
Monitor blood glucose in high risk patients
Monitor creatine kinase levels in patients at risk of rhabdomyolysis
Monitor creatine kinase levels in patients reporting myalgia
Repeat liver function tests within 3 months and at 12 months
Advise patient to report any symptoms of interstitial lung disease
Advise patients to report muscle pain/tenderness/weakness
Advise patients to report signs of hepatic damage (malaise, jaundice etc.)
Discontinue if jaundice or other clinical symptoms of hepatic injury
Discontinue if myopathy is suspected
Advise patient to seek advice at first indications of pregnancy
Discontinue if ALT level exceed 3 times the upper limit of normal & persist
Discontinue if AST level exceed 3 times the upper limit of normal & persist
Discontinue if creatine kinase levels >5 times upper limit of normal
Discontinue if evidence of interstitial lung disease
Discontinue if muscular symptoms are severe
Discontinue prior to surgery
Advise patient grapefruit products may increase plasma level
Dietary restrictions should be maintained
Female: Contraception required during and for 3 months after treatment

Statin therapy has been associated with the development of myalgia, myopathy and rhabdomyolysis, which can rarely be fatal. Myopathy is dose related.
Routine monitoring of creatinine kinase is not necessary in asymptomatic patients.

Do not measure creatine kinase levels following strenuous exercise or in the presence of other factors affecting CK levels. If CK is greater than 5 times the upper limit of normal (ULN) levels prior to treatment, re-measure 5 to 7 days later.

If symptoms of myopathy resolve and levels of creatinine kinase reduce, treatment can be reinitiated at the lowest dose and with close monitoring.

Cases of interstitial lung disease have been reported with some statins, especially in long-term therapy. If the patient presents with signs or symptoms of interstitial lung disease including dyspnoea, non-productive cough, or deterioration of general health (fatigue, weight loss, fever), treatment should be discontinued.

Some evidence suggests that statins as a class raise blood glucose and in some patients, at a high risk of future diabetes, may produce a level of hyperglycaemia where formal diabetes care is appropriate. This risk, however, is outweighed by the reduction in vascular risk with statins and therefore should not be a reason for stopping statin treatment. Patients at risk (raised fasting glucose, raised body mass index at baseline, history of hypertension and raised triglycerides)should be monitored both clinically and biochemically according to national guidelines.

Rare cases of myopathy/rhabdomyolysis have been associated with concomitant administration of HMG-CoA reductase inhibitors and lipid-modifying doses (greater than or equal to 1g/day) of niacin (nicotinic acid), either of which can cause myopathy when given alone.

Coadministration of simvastatin with lipid-modifying doses (greater than or equal to 1g/day) of niacin (nicotinic acid) is not recommended in Asian patients.

There have been very rare reports of an immune mediated necrotizing myopathy (IMNM) during or after treatment with some statins. IMNM is clinically characterised by persistent proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment.

The risk of myopathy is greater on simvastatin 80mg and should only be used in patients with severe hypercholesterolaemia and at high risk for cardiovascular complications. If an interacting agent is needed, an alternative statin based regimen with less potential for drug-drug interactions should be used.

Patients carrying the SLC01B1 gene allele (c.521T>C) have an increased systemic exposure of simvastatin and increased risk of myopathy. Where available, genotyping for the presence of the C allele should be considered prior to prescribing high dose simvastatin and high doses avoided in patients with the CC genotype.

If serious liver injury with clinical symptoms and/or hyperbilirubinaemia or jaundice occurs during treatment with simvastatin, promptly interrupt therapy. If an alternate etiology is not found, do not restart treatment.

Pregnancy and Lactation

Pregnancy

Simvastatin is contraindicated during pregnancy.

A mixture of human malformations have been reported with the used of statins in the first trimester, these include; VATER-association, neural tube defects, holoprosencephaly, other CNS malformations and limb abnormalities (Schaefer, 2007). None of these malformations have occurred in significant enough quantities to enable causality to be concluded. However, the theoretical risks of reducing cholesterol availability during embryo development should be considered since simvastatin may reduce the foetal levels of mevalonate which is a precursor of cholesterol biosynthesis. The suspension of treatment throughout pregnancy is not considered likely to have a detrimental effect on the long term course of hyperlipidaemia. For these reasons simvastatin should not be used during pregnancy. Schaefer (2007) concludes that inadvertent treatment with a statin during pregnancy, does not require a termination of pregnancy, however, treatment should be stopped immediately and a detailed ultrasound examination should considered.

Advise female patients of child bearing potential to take adequate contraceptive measures during treatment and for three months after discontinuation (NICE guideline no.71).

The use of all medication in pregnancy should be avoided whenever possible; particularly in the first trimester. Non-drug treatments should also be considered. When essential, a medication with the best safety record over time should be chosen, employing the lowest effective dose for the shortest possible time. Polypharmacy should be avoided. Teratogens taken in the pre-embryonic period, often quoted as lasting until 14-17 days post-conception, are believed to have an all-or-nothing effect. Where drugs have a short half-life, and when the date of conception is certain, this may allow women to be reassured where drug exposure has occurred within this time frame. Further advice may be available from the UK National Teratology Information Service (NTIS) and through ToxBase, available via password on the internet ( www.toxbase.org ) or if this is unavailable at the backup site ( www.toxbasebackup.org ).

Licensed in pregnancy? - No, contraindicated

Recommended for use in pregnancy? - No

Effects on foetus - VATER-association, neural tube defects, holoprosencephaly, other CNS malformations and limb abnormalities have been reported following the use of statins.

Lactation

Simvastatin is contraindicated while breastfeeding.

At the time of writing, there is little published experience concerning the use of statins during breastfeeding. Due to the possible inhibition of cholesterol biosynthesis by statins, there is a theoretical risk posed to the neonate. The products of cholesterol biosynthesis, including cholesterol are essential for neonatal development. Therefore, the use of statins is contraindicated while breastfeeding. The suspension of treatment while breastfeeding is not considered likely to detrimentally affect the long term course of hyperlipidaemia, therefore simvastatin use during breastfeeding is not recommended.

Neonates, infants born prematurely, those with low birth weight, those with an unstable gastrointestinal function or who have serious illnesses may require special consideration. For any infant, if a drug is prescribed to the nursing mother, it should be at the lowest practical dose and for the shortest time. When drug administration is unavoidable and breastfeeding is to continue, minimisation of exposure of the infant to the drug may sometimes be achieved by timing the maternal doses to just after a feeding episode. Infants exposed to drugs via breast milk should be monitored for unusual signs or symptoms. Interactions between the drug received by the infant from the mother's milk and medication prescribed for the infant should also be considered, for example, when the drug given to the infant may prevent metabolism of the drug received via breast milk.
Specialist advice is available from the UK Drugs in Lactation Advisory Service at https://www.midlandsmedicines.nhs.uk/content.asp?section=6&subsection=17&pageIdx=1 is contraindicated while breastfeeding.

Side Effects

Abdominal pain
Accelerated erythrocyte sedimentation
Acute renal failure
Alopecia
Altered liver function tests
Amnesia
Anaemia
Anaphylaxis
Angioedema
Arthralgia
Arthritis
Asthenia
Confusion
Constipation
Cough
Creatine phosphokinase increased
Depression
Dermatomyositis
Diarrhoea
Dizziness
Dyspepsia
Dyspnoea
Eosinophilia
Erectile dysfunction
Fatigue
Fever
Flatulence
Flushing
Forgetfulness
Gastro-intestinal disturbances
Headache
Hepatic failure
Hepatitis
Hypersensitivity reactions
Immune mediated necrotizing myopathy
Impaired memory
Increase in alkaline phosphatase
Increase in serum ALT/AST
Increased fasting blood glucose
Increased glycated haemoglobin (HbA1c) levels
Insomnia
Interstitial lung disease
Jaundice
Lupus erythematosus-like syndrome
Malaise
Muscle weakness
Muscular cramps
Myalgia
Myopathy
Myositis
Nausea
Nightmares
Pancreatitis
Paraesthesia
Peripheral neuropathy
Photosensitivity
Polymyalgia rheumatica
Precipitation of diabetes
Pruritus
Rash
Rhabdomyolysis
Sexual dysfunction
Sleep disturbances
Tendinopathy
Tendon rupture
Thrombocytopenia
Urticaria
Vasculitis
Visual disturbances
Vomiting
Weight loss

Presentation

Oral formulations of simvastatin.

Drugs List

Therapeutic Indications

Uses

Combined hyperlipidaemia: lipid lowering therapy adjunct to diet
Coronary heart disease: Reduce risk of morbidity/mortality
Diabetes mellitus: Reduce cardiovascular morbidity/mortality
Heterozygous familial hypercholesterolaemia: Adjunct to diet
Homozygous familial hypercholesterolaemia: reduction of cholesterol
Treatment of primary hypercholesterolaemia resistant to diet

Adjunctive treatment of primary hypercholesterolaemia or mixed dyslipidaemia with dietary measures when response to diet and other non-pharmacological treatments (e.g. exercise and weight reduction) is inadequate.

Adjunctive treatment of homozygous familial hypercholesterolaemia with diet and other lipid lowering treatments (e.g. LDL apheresis) or if such treatments are not appropriate.

Reduction of cardiovascular mortality and morbidity as an adjunct to correction of other risk factors and cardioprotective therapy, in patients with manifest atherosclerotic cardiovascular disease or diabetes mellitus with normal or increased cholesterol levels.

Dosage

Patients should be placed on a standard cholesterol-lowering diet before receiving simvastatin and should continue on this diet during treatment.

Adults

Children

Patients with Renal Impairment

Patients with Hepatic Impairment

Contraindications

Children under 5 years
Creatine kinase levels over 5 times upper limit of normal
Within 7 days of discontinuing fusidic acid
Breastfeeding
Myopathy
Pregnancy
Serum transaminases above 3 times upper limit of normal
Severe hepatic impairment
Unexplained elevated serum transaminases

Precautions and Warnings

Asian ancestry
Children aged 5 to 10 years
Family history of hereditary muscular disorders
Females of childbearing potential
High alcohol intake
Major surgery
Patients over 65 years
Severe trauma
Galactosaemia
Glucose-galactose malabsorption syndrome
Hereditary muscular disorder
History of hepatic impairment
History of muscular toxicity secondary to fibrates
History of muscular toxicity secondary to HMG-CoA reductase inhibitors
History of non-traumatic rhabdomyolysis
Hypothyroidism
Lactose intolerance
Renal impairment - creatinine clearance below 30 ml/minute

Advise ability to drive/operate machinery may be affected by side effects
Correct hypothyroidism before treatment
Exclude secondary causes of hypercholesterolaemia before treatment
Not all available brands are licensed for all age groups
Not all available brands are licensed for all indications
Some formulations contain lactose
Measure creatine kinase levels prior to treatment if risk of rhabdomyolysis
Perform liver function tests before commencing therapy
Monitor blood glucose in high risk patients
Monitor creatine kinase levels in patients at risk of rhabdomyolysis
Monitor creatine kinase levels in patients reporting myalgia
Repeat liver function tests within 3 months and at 12 months
Advise patient to report any symptoms of interstitial lung disease
Advise patients to report muscle pain/tenderness/weakness
Advise patients to report signs of hepatic damage (malaise, jaundice etc.)
Discontinue if jaundice or other clinical symptoms of hepatic injury
Discontinue if myopathy is suspected
Advise patient to seek advice at first indications of pregnancy
Discontinue if ALT level exceed 3 times the upper limit of normal & persist
Discontinue if AST level exceed 3 times the upper limit of normal & persist
Discontinue if creatine kinase levels >5 times upper limit of normal
Discontinue if evidence of interstitial lung disease
Discontinue if muscular symptoms are severe
Discontinue prior to surgery
Advise patient grapefruit products may increase plasma level
Dietary restrictions should be maintained
Female: Contraception required during and for 3 months after treatment

Statin therapy has been associated with the development of myalgia, myopathy and rhabdomyolysis, which can rarely be fatal. Myopathy is dose related.
Routine monitoring of creatinine kinase is not necessary in asymptomatic patients.

Do not measure creatine kinase levels following strenuous exercise or in the presence of other factors affecting CK levels. If CK is greater than 5 times the upper limit of normal (ULN) levels prior to treatment, re-measure 5 to 7 days later.

If symptoms of myopathy resolve and levels of creatinine kinase reduce, treatment can be reinitiated at the lowest dose and with close monitoring.

Cases of interstitial lung disease have been reported with some statins, especially in long-term therapy. If the patient presents with signs or symptoms of interstitial lung disease including dyspnoea, non-productive cough, or deterioration of general health (fatigue, weight loss, fever), treatment should be discontinued.

Some evidence suggests that statins as a class raise blood glucose and in some patients, at a high risk of future diabetes, may produce a level of hyperglycaemia where formal diabetes care is appropriate. This risk, however, is outweighed by the reduction in vascular risk with statins and therefore should not be a reason for stopping statin treatment. Patients at risk (raised fasting glucose, raised body mass index at baseline, history of hypertension and raised triglycerides)should be monitored both clinically and biochemically according to national guidelines.

Rare cases of myopathy/rhabdomyolysis have been associated with concomitant administration of HMG-CoA reductase inhibitors and lipid-modifying doses (greater than or equal to 1g/day) of niacin (nicotinic acid), either of which can cause myopathy when given alone.

Coadministration of simvastatin with lipid-modifying doses (greater than or equal to 1g/day) of niacin (nicotinic acid) is not recommended in Asian patients.

There have been very rare reports of an immune mediated necrotizing myopathy (IMNM) during or after treatment with some statins. IMNM is clinically characterised by persistent proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment.

The risk of myopathy is greater on simvastatin 80mg and should only be used in patients with severe hypercholesterolaemia and at high risk for cardiovascular complications. If an interacting agent is needed, an alternative statin based regimen with less potential for drug-drug interactions should be used.

Patients carrying the SLC01B1 gene allele (c.521T>C) have an increased systemic exposure of simvastatin and increased risk of myopathy. Where available, genotyping for the presence of the C allele should be considered prior to prescribing high dose simvastatin and high doses avoided in patients with the CC genotype.

If serious liver injury with clinical symptoms and/or hyperbilirubinaemia or jaundice occurs during treatment with simvastatin, promptly interrupt therapy. If an alternate etiology is not found, do not restart treatment.

Pregnancy and Lactation

Pregnancy

Simvastatin is contraindicated during pregnancy.

A mixture of human malformations have been reported with the used of statins in the first trimester, these include; VATER-association, neural tube defects, holoprosencephaly, other CNS malformations and limb abnormalities (Schaefer, 2007). None of these malformations have occurred in significant enough quantities to enable causality to be concluded. However, the theoretical risks of reducing cholesterol availability during embryo development should be considered since simvastatin may reduce the foetal levels of mevalonate which is a precursor of cholesterol biosynthesis. The suspension of treatment throughout pregnancy is not considered likely to have a detrimental effect on the long term course of hyperlipidaemia. For these reasons simvastatin should not be used during pregnancy. Schaefer (2007) concludes that inadvertent treatment with a statin during pregnancy, does not require a termination of pregnancy, however, treatment should be stopped immediately and a detailed ultrasound examination should considered.

Advise female patients of child bearing potential to take adequate contraceptive measures during treatment and for three months after discontinuation (NICE guideline no.71).

The use of all medication in pregnancy should be avoided whenever possible; particularly in the first trimester. Non-drug treatments should also be considered. When essential, a medication with the best safety record over time should be chosen, employing the lowest effective dose for the shortest possible time. Polypharmacy should be avoided. Teratogens taken in the pre-embryonic period, often quoted as lasting until 14-17 days post-conception, are believed to have an all-or-nothing effect. Where drugs have a short half-life, and when the date of conception is certain, this may allow women to be reassured where drug exposure has occurred within this time frame. Further advice may be available from the UK National Teratology Information Service (NTIS) and through ToxBase, available via password on the internet ( www.toxbase.org ) or if this is unavailable at the backup site ( www.toxbasebackup.org ).

Licensed in pregnancy? - No, contraindicated

Recommended for use in pregnancy? - No

Effects on foetus - VATER-association, neural tube defects, holoprosencephaly, other CNS malformations and limb abnormalities have been reported following the use of statins.

Lactation

Simvastatin is contraindicated while breastfeeding.

At the time of writing, there is little published experience concerning the use of statins during breastfeeding. Due to the possible inhibition of cholesterol biosynthesis by statins, there is a theoretical risk posed to the neonate. The products of cholesterol biosynthesis, including cholesterol are essential for neonatal development. Therefore, the use of statins is contraindicated while breastfeeding. The suspension of treatment while breastfeeding is not considered likely to detrimentally affect the long term course of hyperlipidaemia, therefore simvastatin use during breastfeeding is not recommended.

Neonates, infants born prematurely, those with low birth weight, those with an unstable gastrointestinal function or who have serious illnesses may require special consideration. For any infant, if a drug is prescribed to the nursing mother, it should be at the lowest practical dose and for the shortest time. When drug administration is unavoidable and breastfeeding is to continue, minimisation of exposure of the infant to the drug may sometimes be achieved by timing the maternal doses to just after a feeding episode. Infants exposed to drugs via breast milk should be monitored for unusual signs or symptoms. Interactions between the drug received by the infant from the mother's milk and medication prescribed for the infant should also be considered, for example, when the drug given to the infant may prevent metabolism of the drug received via breast milk.
Specialist advice is available from the UK Drugs in Lactation Advisory Service at https://www.midlandsmedicines.nhs.uk/content.asp?section=6&subsection=17&pageIdx=1 is contraindicated while breastfeeding.

Side Effects

Abdominal pain
Accelerated erythrocyte sedimentation
Acute renal failure
Alopecia
Altered liver function tests
Amnesia
Anaemia
Anaphylaxis
Angioedema
Arthralgia
Arthritis
Asthenia
Confusion
Constipation
Cough
Creatine phosphokinase increased
Depression
Dermatomyositis
Diarrhoea
Dizziness
Dyspepsia
Dyspnoea
Eosinophilia
Erectile dysfunction
Fatigue
Fever
Flatulence
Flushing
Forgetfulness
Gastro-intestinal disturbances
Headache
Hepatic failure
Hepatitis
Hypersensitivity reactions
Immune mediated necrotizing myopathy
Impaired memory
Increase in alkaline phosphatase
Increase in serum ALT/AST
Increased fasting blood glucose
Increased glycated haemoglobin (HbA1c) levels
Insomnia
Interstitial lung disease
Jaundice
Lupus erythematosus-like syndrome
Malaise
Muscle weakness
Muscular cramps
Myalgia
Myopathy
Myositis
Nausea
Nightmares
Pancreatitis
Paraesthesia
Peripheral neuropathy
Photosensitivity
Polymyalgia rheumatica
Precipitation of diabetes
Pruritus
Rash
Rhabdomyolysis
Sexual dysfunction
Sleep disturbances
Tendinopathy
Tendon rupture
Thrombocytopenia
Urticaria
Vasculitis
Visual disturbances
Vomiting
Weight loss

Overdosage

It is strongly recommended that the UK National Poisons Information Service be consulted on cases of suspected or actual overdose where there is doubt over the degree of risk or about appropriate management.

The following number will direct the caller to the relevant local centre (0844) 892 0111

Information may be obtained if you have access to ToxBase the primary clinical toxicology database of the National Poisons Information Service. This is available via password on the internet ( www.toxbase.org ) or if this is unavailable at the backup site ( www.toxbasebackup.org ).

Further Information

Last Full Review Date: February 2013

Reference Sources

Drugs During Pregnancy and Lactation: Treatment Options and Risk Assessment, 2nd edition (2007) ed. Schaefer, C., Peters, P. and Miller, R. Elsevier, London.

Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk, 9th edition (2011) ed. Briggs, G., Freeman, R. and Yaffe, S. Lippincott Williams & Wilkins, Philadelphia.

Martindale: The Complete Drug Reference, 37th edition (2011) ed. Sweetman, S. Pharmaceutical Press, London.

Medications and Mothers' Milk, 14th Edition (2010) Hale, T. Hale Publishing, Amarillo, Texas.

Summary of Product Characteristics: Simvador 10mg. Discovery Pharmaceuticals Ltd. Revised April 2015.
Summary of Product Characteristics: Simvador 20mg. Discovery Pharmaceuticals Ltd. Revised April 2015.
Summary of Product Characteristics: Simvador 40mg. Discovery Pharmaceuticals Ltd. Revised April 2015.
Summary of Product Characteristics: Simvador 80mg. Discovery Pharmaceuticals Ltd. Revised April 2015.

Summary of Product Characteristics: Simvastatin 10mg film-coated tablets. Accord healthcare Ltd. Revised December 2011.
Summary of Product Characteristics: Simvastatin 20mg film-coated tablets. Accord healthcare Ltd. Revised December 2011.
Summary of Product Characteristics: Simvastatin 40mg film-coated tablets. Accord healthcare Ltd. Revised December 2011.
Summary of Product Characteristics: Simvastatin 80mg film-coated tablets. Accord healthcare Ltd. Revised December 2011.

Summary of Product Characteristics: Simvastatin 10mg tablets. Actavis UK Ltd. Revised June 2010.
Summary of Product Characteristics: Simvastatin 20mg tablets. Actavis UK Ltd. Revised June 2010.
Summary of Product Characteristics: Simvastatin 40mg tablets. Actavis UK Ltd. Revised June 2010.
Summary of Product Characteristics: Simvastatin 80mg tablets. Actavis UK Ltd. Revised September 2012.

Summary of Product Characteristics: Simvastatin 10mg tablets. Aurobindo Pharma - Milpharm Ltd. Revised October 2010.
Summary of Product Characteristics: Simvastatin 20mg tablets. Aurobindo Pharma - Milpharm Ltd. Revised October 2010.
Summary of Product Characteristics: Simvastatin 40mg tablets. Aurobindo Pharma - Milpharm Ltd. Revised October 2010.
Summary of Product Characteristics: Simvastatin 80mg tablets. Aurobindo Pharma - Milpharm Ltd. Revised July 2010.

Summary of Product Characteristics: Simvastatin 40mg tablets. Kent pharmaceuticals Ltd. Revised January 2013.

Summary of Product Characteristics: Simvastatin 20mg/5ml Oral suspension. Rosemont Pharmaceuticals Ltd. Revised May 2017.
Summary of Product Characteristics: Simvastatin 40mg/5ml Oral suspension. Rosemont Pharmaceuticals Ltd. Revised May 2017.

Summary of Product Characteristics: Simvastatin 10mg tablets. Sandoz Ltd. Revised July 2012.
Summary of Product Characteristics: Simvastatin 20mg tablets. Sandoz Ltd. Revised July 2012.
Summary of Product Characteristics: Simvastatin 40mg tablets. Sandoz Ltd. Revised July 2012.

Summary of Product Characteristics: Simvastatin 10mg film-coated tablets. Zentiva. Revised July 2012.
Summary of Product Characteristics: Simvastatin 20mg film-coated tablets. Zentiva. Revised July 2012.
Summary of Product Characteristics: Simvastatin 40mg film-coated tablets. Zentiva. Revised July 2012.

Summary of Product Characteristics: Zocor 10mg, 20mg, 40mg and 80mg film-coated tablets. Merck Sharp & Dohme Ltd. Revised May 2018.

The Renal Drug Handbook. 3rd edition. (2009) ed. Ashley, C and Currie, Radcliffe Publishing Ltd, Abingdon.

Drug Safety Update. MHRA Volume 1 issue 7 February 2008.
Available at https://www.mhra.gov.uk/Publications/Safetyguidance/DrugSafetyUpdate/CON2033917
Last accessed: February 14, 2013

Drug Safety Update. MHRA Volume 3, issue 10 May 2010.
Available at https://www.mhra.gov.uk/Publications/Safetyguidance/DrugSafetyUpdate/CON081863 NB this is for simvastatin only.
Last accessed: February 14, 2013

Drug Safety Update. MHRA Volume 5, issue 6 January 2012.
Available at https://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON140667
Last accessed: February 14, 2013

Drug Safety Update. MHRA Volume 6, issue 1 August 2012.
Available at https://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON180637
Last accessed: February 14, 2013

NAPOS, The Drug Database for Acute Porphyria.
Available at; https://www.drugs-porphyria.org/
Simvastatin last revised: October 1, 2004
Last accessed: February 14, 2013

NICE Evidence Services Available at: www.nice.org.uk Last accessed: 12 September 2017

FDA Drug safety Communication: Important safety label changes to cholesterol lowering statin drugs.
Available at https://www.fda.gov/Drugs/DrugSafety/ucm293101.htm
Last accessed: February 14, 2013

National Institute for Health and Clinical Excellence, NICE 71, Identification and management of familial hypercholesterolaemia, issued August 2008.
Available at: https://www.nice.org.uk/nicemedia/pdf/CG071NICEGuideline.pdf
Last accessed: February 14, 2013

US National Library of Medicine. Toxicology Data Network. Drugs and Lactation Database (LactMed).
Available at: https://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?LACT
Simvastatin Last revised: April 3, 2012
Last accessed: February 14, 2013