Drugs List

Therapeutic Indications

Uses

Stable coronary artery disease: Reduce risk of cardiovascular events
Symptomatic cardiac failure: treatment
Treatment of essential hypertension

Contraindications

Children under 18 years
Desensitisation therapy
Within 36 hours of discontinuing a sacubitril containing product
Breastfeeding
Galactosaemia
Haemodialysis with high flux membranes
Haemodynamic instability
Hereditary angioneurotic oedema
Idiopathic angioneurotic oedema
Pregnancy
Renal artery stenosis

Precautions and Warnings

Elderly
General anaesthesia
Immunosuppression
Aortic stenosis
Atherosclerosis
Cerebral ischaemia
Collagen vascular disease
Diabetes mellitus
Electrolyte depletion
Glucose-galactose malabsorption syndrome
Hepatic impairment
History of angioedema
Hyperkalaemia
Hypertrophic cardiomyopathy
Hyponatraemia
Hypotension
Hypovolaemia
Ischaemic heart disease
Lactose intolerance
Left ventricular outflow obstruction
Metabolic acidosis
Mitral stenosis
Peripheral vascular disease
Renal impairment
Renal impairment - creatinine clearance < 60ml/minute/1.73m sq
Renovascular disorder
Unstable cardiac disorder

Adjustment of hypoglycaemic therapy may be necessary in diabetes mellitus
Anaphylaxis possible with concomitant hyposensitisation to wasp/bee venom
Patients with primary aldosteronism may not benefit from this treatment
Advise ability to drive/operate machinery may be affected by side effects
Afro-Caribbean or black patients may show reduced response
Consider stopping diuretic 2-3 days prior to therapy if appropriate
Contains lactose
Place patient in supine position if severe hypotension occurs
Evaluate renal function before and during treatment
Monitor serum electrolytes before and during treatment
Consider monitoring white blood cell counts in collagen vascular disease
If unstable angina occurs during first month: re-evaluate therapy
Monitor blood pressure regularly
Monitor serum potassium regularly
Reduce dose/discontinue if serum creatinine or blood urea increases
Advise patients at risk of neutropenia to report any signs of infection
Higher incidence of angioedema in black patients
Increased risk of hyperkalaemia with K+ suppl. and K+ sparing diuretic
Discontinue treatment 24 hours prior to surgery
Withdraw before desensitisation
Withdraw for at least 24 hours before LDL apheresis
Discontinue at first signs of jaundice,cholestasis,hepatitis
Discontinue immediately if angioedema of the tongue/glottis/larynx occurs
Advise patient not to take NSAIDs unless advised by clinician
Advise on problems of salt substitutes/high intake of potassium-rich food
Female: Ensure adequate contraception during treatment

A marked water and sodium depletion (salt free diet and/or diuretic treatment) or stenosis of the renal arteries stimulate the renin-angiotensin system. Inhibition by an ACE inhibitor, especially during the first two weeks of treatment, may lead to an abrupt fall in blood pressure and/or to functional and possibly acute renal failure, although the latter is uncommon and the time interval variable. Discontinuation of perindopril or reduction of the diuretic may be required.

Elevated potassium levels may occur during ACE inhibitor therapy. Those especially at risk of hyperkalaemia include renal impairment, worsening of renal function, age (greater than 70 years), diabetes mellitus, inter-current events, in particular dehydration, acute cardiac decompensation and metabolic acidosis.
Concurrent use of potassium sparing diuretics, potassium supplements, or potassium-containing salt substitutes may lead to a significant increase in plasma potassium. Hyperkalaemia can cause serious, sometimes fatal arrhythmias. Where combination therapy is considered essential, it should be used with caution and with frequent monitoring of plasma potassium. Advise on problems of salt substitutes/high intake of potassium-rich food.

Use with extreme caution in patients with collagen vascular disease, treatment with allopurinol or procainamide and therapy with immunosuppressive agents, it may lead to increased risk of neutropenia. Monitor white blood cell counts.

Serious infections, unresponsive to antibiotic may develop. Periodic monitoring of white blood count is advised. Instruct patients to report signs of infection.

ACE inhibitors should be initiated under specialist supervision and with careful clinical monitoring in those with severe cardiac failure or in those receiving multiple or high-dose diuretic therapy (e.g. more than 80 mg of furosemide daily or its equivalent).

If renovascular hypertension is present there may be an increased risk of severe hypotension and renal impairment.

Consider stopping diuretic a few days before starting treatment to prevent symptomatic hypotension, if a diuretic is considered necessary the diuretic dose should be initiated at the lowest dose. Potassium
sparing diuretics should be avoided.
May cause first-dose hypotension and perindopril should subsequently be restarted cautiously titrating dose against blood pressure after correction of hypovolaemia and hypotension. In most instances symptoms are relieved by lying the patient down, but volume repletion with oral fluids or intravenous infusion with normal saline may be required.

Severe angioedema: angioedema of the extremities, face, lips, mucous membranes, tongue, glottis and/or larynx may occur during treatment with ACE inhibitors at any point during therapy. Treatment should be discontinued promptly and replaced by an agent belonging to another class of drugs. When confined to the face and lips, angioedema usually resolves without treatment. However antihistamines have been used. Angioedema involving the tongue, glottis or larynx may be fatal.

Appropriate emergency therapy should be given (e.g. adrenaline/maintenance of patent airway). The patient should be hospitalised and observed for at least 12 to 24 hours and should not be discharged until complete resolution of symptoms has occurred.
Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Intestinal angioedema can occur in patients treated with ACE inhibitors, and should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain.

Symptomatic hypotension is more likely to occur in patients who have been volume-depleted and salt-depleted e.g. by diuretic therapy, dietary salt restriction, dialysis, diarrhoea or vomiting, or who have severe renin-dependent hypertension. Patients at risk should be closely supervised during initiation of therapy and during dose adjustment. Similar considerations apply to patients with ischaemic heart or cerebrovascular disease in whom an excessive fall in blood pressure could result in a myocardial infarction or cerebrovascular accident.

An additional lowering of blood pressure is anticipated in patients with congestive heart failure and should not be the cause of discontinuation of perindopril therapy unless the hypotension becomes symptomatic.

A persistent, non-productive cough may occur which usually resolves itself after therapy is discontinued.

Pregnancy and Lactation

Pregnancy

Perindopril is contraindicated during the second and third trimesters of pregnancy and should be avoided during the first trimester. If a pregnancy is confirmed or planned, the switch to alternative medication should be made as soon as possible.

It is not known if perindopril or its metabolite perindoprilat crosses the human placenta. The molecular weights (about 368 for the free acid and 442 for the salt form) suggest that transfer to the foetus will occur (Briggs, 2011).

ACE inhibitors are contraindicated during the second and third trimesters of pregnancy as exposure during these trimesters is known to induce human foetal toxicity (renal dysfunction, oligohydramnios, pulmonary hypoplasia, patent ductus arteriosus, delay in skull ossification, neonatal toxicity and even death). Severe and sometimes fatal anuria in the foetus and in the newborn have been observed and is thought to be caused by the compromise of the foetal renal system. Foetal renal failure resulting from in utero exposure to ACE inhibitors has been reported where dialysis has been required shortly after birth. Evidence of a risk of teratogenicity after first trimester exposure is conflicting, however, the MHRA recommends that a risk cannot be excluded. Recent data published does associate first trimester ACE inhibitor exposure with congenital CNS and cardiovascular defects. Unless treatment with an ACE inhibitor is considered absolutely essential, women who are planning to become pregnant should be switched to an alternative drug with an established safety record. If exposure has occurred in the first trimester a detailed ultrasound diagnosis is advisable. Exposure to an ACE inhibitor during pregnancy is not an indication for either invasive diagnostic procedures or termination of pregnancy. In cases involving long term prenatal therapy in the second and/ or third trimesters, the foetus should be monitored for the potential development of oligohydramnios, and foetal growth should be assessed with detailed ultrasound scans (Schaefer, 2007).

Infants whose mothers have taken ACE inhibitors should be closely observed for hypotension.

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 ).

Known human teratogen? - Yes (other ACE inhibitors)

Effects on foetus - ACE inhibitors can cause renal dysfunction, oligohydramnios, pulmonary hypoplasia, patent ductus arteriosus, death, anuria, renal failure.

Lactation

Perindopril is contraindicated during breastfeeding.

The effect of perindopril treatment on nursing infants has not been determined, however, due to its molecular size it is likely that perindopril and the active metabolite perindoprilat are excreted in breast milk, lactating mothers are advised not to breast feed while taking perindopril.

The MHRA has stated that although ACE inhibitors are not generally recommended for use by breastfeeding mothers they are not absolutely contraindicated and may be prescribed if treatment is considered essential. The MHRA state that ACE inhibitors should not be used by breastfeeding mothers in the first few weeks after delivery because of possible profound neonatal hypotension particularly in preterm infants. If ACE inhibitor therapy is considered essential for the mother the use of captopril, enalapril or quinapril may be considered when the infant is older. The infant should be carefully followed up for signs of hypotension should ACE inhibitor treatment be deemed necessary.

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

Drug excreted in breast milk? - Unknown but expected, as molecular weights of pro-drug and active metabolite are low enough

Considered suitable or recommended by manufacturer? - No

Drug substance licensed in infants? - No

Side Effects

Abdominal pain
Abnormal vision
Acute renal failure
Agranulocytosis
Angina pectoris
Angioedema
Arrhythmias
Asthenia
Blood urea increased
Bronchospasm
Cardiac arrest
Cholestatic hepatitis
Confusion
Constipation
Cough
Cytolytic hepatitis
Decrease in haematocrit
Decrease in haemoglobin
Diarrhoea
Dizziness
Dry mouth
Dysgeusia
Dyspepsia
Dyspnoea
Electrolyte disturbances
Eosinophilic pneumonia
Erythema multiforme
Fever
Fulminant hepatic necrosis
Haemolytic anaemia
Headache
Hepatic failure
Hepatitis
Hyperkalaemia
Hypersensitivity reactions
Hypoglycaemia
Hypotension
Impotence
Inappropriate secretion of antidiuretic hormone
Increase in creatinine
Increases in hepatic enzymes
Jaundice
Leucopenia
Mood changes
Muscle cramps
Myocardial infarction
Nausea
Neutropenia
Pancreatitis
Pancytopenia
Paraesthesia
Pruritus
Rash
Renal impairment
Rhinitis
Serum bilirubin increased
Sleep disturbances
Sore throat
Stroke
Sweating
Thrombocytopenia
Tinnitus
Urticaria
Vasculitis
Vertigo
Vomiting

Presentation

Oral formulations of perindopril arginine.

Drugs List

Therapeutic Indications

Uses

Stable coronary artery disease: Reduce risk of cardiovascular events
Symptomatic cardiac failure: treatment
Treatment of essential hypertension

Dosage

Hypertension
Combinations with a diuretic
Symptomatic hypotension may occur when perindopril treatment is initiated in patients receiving diuretic treatment, in particular if diuretic treatment was begun only a short time before. It is therefore recommended to discontinue the diuretic 2 to 3 days before beginning treatment with perindopril. If diuretic therapy cannot be discontinued then perindopril should be initiated with 2.5 mg perindopril and serum potassium and renal function should be monitored. The subsequent dose should be adjusted according to blood pressure. The diuretic may be re-introduced at the lowest effective dose if required.

Potassium sparing diuretics should be avoided or used with extreme caution.

Adults

Elderly

Patients with Renal Impairment

Contraindications

Children under 18 years
Desensitisation therapy
Within 36 hours of discontinuing a sacubitril containing product
Breastfeeding
Galactosaemia
Haemodialysis with high flux membranes
Haemodynamic instability
Hereditary angioneurotic oedema
Idiopathic angioneurotic oedema
Pregnancy
Renal artery stenosis

Precautions and Warnings

Elderly
General anaesthesia
Immunosuppression
Aortic stenosis
Atherosclerosis
Cerebral ischaemia
Collagen vascular disease
Diabetes mellitus
Electrolyte depletion
Glucose-galactose malabsorption syndrome
Hepatic impairment
History of angioedema
Hyperkalaemia
Hypertrophic cardiomyopathy
Hyponatraemia
Hypotension
Hypovolaemia
Ischaemic heart disease
Lactose intolerance
Left ventricular outflow obstruction
Metabolic acidosis
Mitral stenosis
Peripheral vascular disease
Renal impairment
Renal impairment - creatinine clearance < 60ml/minute/1.73m sq
Renovascular disorder
Unstable cardiac disorder

Adjustment of hypoglycaemic therapy may be necessary in diabetes mellitus
Anaphylaxis possible with concomitant hyposensitisation to wasp/bee venom
Patients with primary aldosteronism may not benefit from this treatment
Advise ability to drive/operate machinery may be affected by side effects
Afro-Caribbean or black patients may show reduced response
Consider stopping diuretic 2-3 days prior to therapy if appropriate
Contains lactose
Place patient in supine position if severe hypotension occurs
Evaluate renal function before and during treatment
Monitor serum electrolytes before and during treatment
Consider monitoring white blood cell counts in collagen vascular disease
If unstable angina occurs during first month: re-evaluate therapy
Monitor blood pressure regularly
Monitor serum potassium regularly
Reduce dose/discontinue if serum creatinine or blood urea increases
Advise patients at risk of neutropenia to report any signs of infection
Higher incidence of angioedema in black patients
Increased risk of hyperkalaemia with K+ suppl. and K+ sparing diuretic
Discontinue treatment 24 hours prior to surgery
Withdraw before desensitisation
Withdraw for at least 24 hours before LDL apheresis
Discontinue at first signs of jaundice,cholestasis,hepatitis
Discontinue immediately if angioedema of the tongue/glottis/larynx occurs
Advise patient not to take NSAIDs unless advised by clinician
Advise on problems of salt substitutes/high intake of potassium-rich food
Female: Ensure adequate contraception during treatment

A marked water and sodium depletion (salt free diet and/or diuretic treatment) or stenosis of the renal arteries stimulate the renin-angiotensin system. Inhibition by an ACE inhibitor, especially during the first two weeks of treatment, may lead to an abrupt fall in blood pressure and/or to functional and possibly acute renal failure, although the latter is uncommon and the time interval variable. Discontinuation of perindopril or reduction of the diuretic may be required.

Elevated potassium levels may occur during ACE inhibitor therapy. Those especially at risk of hyperkalaemia include renal impairment, worsening of renal function, age (greater than 70 years), diabetes mellitus, inter-current events, in particular dehydration, acute cardiac decompensation and metabolic acidosis.
Concurrent use of potassium sparing diuretics, potassium supplements, or potassium-containing salt substitutes may lead to a significant increase in plasma potassium. Hyperkalaemia can cause serious, sometimes fatal arrhythmias. Where combination therapy is considered essential, it should be used with caution and with frequent monitoring of plasma potassium. Advise on problems of salt substitutes/high intake of potassium-rich food.

Use with extreme caution in patients with collagen vascular disease, treatment with allopurinol or procainamide and therapy with immunosuppressive agents, it may lead to increased risk of neutropenia. Monitor white blood cell counts.

Serious infections, unresponsive to antibiotic may develop. Periodic monitoring of white blood count is advised. Instruct patients to report signs of infection.

ACE inhibitors should be initiated under specialist supervision and with careful clinical monitoring in those with severe cardiac failure or in those receiving multiple or high-dose diuretic therapy (e.g. more than 80 mg of furosemide daily or its equivalent).

If renovascular hypertension is present there may be an increased risk of severe hypotension and renal impairment.

Consider stopping diuretic a few days before starting treatment to prevent symptomatic hypotension, if a diuretic is considered necessary the diuretic dose should be initiated at the lowest dose. Potassium
sparing diuretics should be avoided.
May cause first-dose hypotension and perindopril should subsequently be restarted cautiously titrating dose against blood pressure after correction of hypovolaemia and hypotension. In most instances symptoms are relieved by lying the patient down, but volume repletion with oral fluids or intravenous infusion with normal saline may be required.

Severe angioedema: angioedema of the extremities, face, lips, mucous membranes, tongue, glottis and/or larynx may occur during treatment with ACE inhibitors at any point during therapy. Treatment should be discontinued promptly and replaced by an agent belonging to another class of drugs. When confined to the face and lips, angioedema usually resolves without treatment. However antihistamines have been used. Angioedema involving the tongue, glottis or larynx may be fatal.

Appropriate emergency therapy should be given (e.g. adrenaline/maintenance of patent airway). The patient should be hospitalised and observed for at least 12 to 24 hours and should not be discharged until complete resolution of symptoms has occurred.
Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Intestinal angioedema can occur in patients treated with ACE inhibitors, and should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain.

Symptomatic hypotension is more likely to occur in patients who have been volume-depleted and salt-depleted e.g. by diuretic therapy, dietary salt restriction, dialysis, diarrhoea or vomiting, or who have severe renin-dependent hypertension. Patients at risk should be closely supervised during initiation of therapy and during dose adjustment. Similar considerations apply to patients with ischaemic heart or cerebrovascular disease in whom an excessive fall in blood pressure could result in a myocardial infarction or cerebrovascular accident.

An additional lowering of blood pressure is anticipated in patients with congestive heart failure and should not be the cause of discontinuation of perindopril therapy unless the hypotension becomes symptomatic.

A persistent, non-productive cough may occur which usually resolves itself after therapy is discontinued.

Pregnancy and Lactation

Pregnancy

Perindopril is contraindicated during the second and third trimesters of pregnancy and should be avoided during the first trimester. If a pregnancy is confirmed or planned, the switch to alternative medication should be made as soon as possible.

It is not known if perindopril or its metabolite perindoprilat crosses the human placenta. The molecular weights (about 368 for the free acid and 442 for the salt form) suggest that transfer to the foetus will occur (Briggs, 2011).

ACE inhibitors are contraindicated during the second and third trimesters of pregnancy as exposure during these trimesters is known to induce human foetal toxicity (renal dysfunction, oligohydramnios, pulmonary hypoplasia, patent ductus arteriosus, delay in skull ossification, neonatal toxicity and even death). Severe and sometimes fatal anuria in the foetus and in the newborn have been observed and is thought to be caused by the compromise of the foetal renal system. Foetal renal failure resulting from in utero exposure to ACE inhibitors has been reported where dialysis has been required shortly after birth. Evidence of a risk of teratogenicity after first trimester exposure is conflicting, however, the MHRA recommends that a risk cannot be excluded. Recent data published does associate first trimester ACE inhibitor exposure with congenital CNS and cardiovascular defects. Unless treatment with an ACE inhibitor is considered absolutely essential, women who are planning to become pregnant should be switched to an alternative drug with an established safety record. If exposure has occurred in the first trimester a detailed ultrasound diagnosis is advisable. Exposure to an ACE inhibitor during pregnancy is not an indication for either invasive diagnostic procedures or termination of pregnancy. In cases involving long term prenatal therapy in the second and/ or third trimesters, the foetus should be monitored for the potential development of oligohydramnios, and foetal growth should be assessed with detailed ultrasound scans (Schaefer, 2007).

Infants whose mothers have taken ACE inhibitors should be closely observed for hypotension.

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 ).

Known human teratogen? - Yes (other ACE inhibitors)

Effects on foetus - ACE inhibitors can cause renal dysfunction, oligohydramnios, pulmonary hypoplasia, patent ductus arteriosus, death, anuria, renal failure.

Lactation

Perindopril is contraindicated during breastfeeding.

The effect of perindopril treatment on nursing infants has not been determined, however, due to its molecular size it is likely that perindopril and the active metabolite perindoprilat are excreted in breast milk, lactating mothers are advised not to breast feed while taking perindopril.

The MHRA has stated that although ACE inhibitors are not generally recommended for use by breastfeeding mothers they are not absolutely contraindicated and may be prescribed if treatment is considered essential. The MHRA state that ACE inhibitors should not be used by breastfeeding mothers in the first few weeks after delivery because of possible profound neonatal hypotension particularly in preterm infants. If ACE inhibitor therapy is considered essential for the mother the use of captopril, enalapril or quinapril may be considered when the infant is older. The infant should be carefully followed up for signs of hypotension should ACE inhibitor treatment be deemed necessary.

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

Drug excreted in breast milk? - Unknown but expected, as molecular weights of pro-drug and active metabolite are low enough

Considered suitable or recommended by manufacturer? - No

Drug substance licensed in infants? - No

Side Effects

Abdominal pain
Abnormal vision
Acute renal failure
Agranulocytosis
Angina pectoris
Angioedema
Arrhythmias
Asthenia
Blood urea increased
Bronchospasm
Cardiac arrest
Cholestatic hepatitis
Confusion
Constipation
Cough
Cytolytic hepatitis
Decrease in haematocrit
Decrease in haemoglobin
Diarrhoea
Dizziness
Dry mouth
Dysgeusia
Dyspepsia
Dyspnoea
Electrolyte disturbances
Eosinophilic pneumonia
Erythema multiforme
Fever
Fulminant hepatic necrosis
Haemolytic anaemia
Headache
Hepatic failure
Hepatitis
Hyperkalaemia
Hypersensitivity reactions
Hypoglycaemia
Hypotension
Impotence
Inappropriate secretion of antidiuretic hormone
Increase in creatinine
Increases in hepatic enzymes
Jaundice
Leucopenia
Mood changes
Muscle cramps
Myocardial infarction
Nausea
Neutropenia
Pancreatitis
Pancytopenia
Paraesthesia
Pruritus
Rash
Renal impairment
Rhinitis
Serum bilirubin increased
Sleep disturbances
Sore throat
Stroke
Sweating
Thrombocytopenia
Tinnitus
Urticaria
Vasculitis
Vertigo
Vomiting

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

British National Formulary, 64th Edition (2012) Pharmaceutical Press, London.

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.

Summary of Product Characteristics: Coversyl Arginine. Servier Laboratories Ltd. Revised February 2018.

Summary of Product Characteristics: Perindopril tosilate 2.5 mg film-coated tablets. Teva UK Ltd. Revised December 2012.

Summary of Product Characteristics: Perindopril tosilate 5 mg film-coated tablets. Teva UK Ltd. Revised December 2012.

Summary of Product Characteristics: Perindopril tosilate 10 mg film-coated tablets. Teva UK Ltd. Revised December 2012.

MHRA Drug Safety Update: Volume 1, Issue 5, December 2007
https://www.mhra.gov.uk/Publications/Safetyguidance/DrugSafetyUpdate/CON2033216
Last accessed: February 18, 2013

MHRA Drug Safety Update: Volume 2, Issue 10, May 2009.
https://www.mhra.gov.uk/Publications/Safetyguidance/DrugSafetyUpdate/CON046451
Last accessed: February 18, 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
Perindopril. Last revised: March 1, 2012
Last accessed: February 18, 2013