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  • Aceril
    / Dexcel

    Active Ingredient
    Captopril 12.5, 25, 50 mg

    Status in Israel

    Presentation and Status in Health Basket

    Presentation Basket Yarpa Pharmasoft


    90 x 12.5 mg

    full basket chart 33614 1426


    90 x 25 mg

    full basket chart 33615 1437


    90 x 50 mg

    full basket chart 33616 1438

    Related information


    Hypertension: Treatment with captopril should be at the lowest effective dose which should be titrated according to the needs of the patient.
    The recommended starting dose is 25-50 mg daily in two divided doses. The dose may be increased incrementally, with intervals of at least 2 weeks, to 100-150 mg/day in two divided doses as needed to reach target blood pressure. Captopril can be used alone or with other antihypertensive agents. A once-daily dosing regimen may be appropriate when concomitant antihypertensive medication such as thiazide diuretics is added.
    In patients with a strongly active renin-angiotensin-aldosterone system (hypovolaemia, renovascular hypertension, cardiac decompensation) it is preferable to commence with a single dose of 12.5 mg. The inauguration of this treatment should preferably take place under close medical supervision. These doses will then be administered at a rate of two per day. The dosage can be gradually increased to 50 mg per day in one or two doses and if necessary to 100 mg per day in one or two doses.
    Congestive heart failure: Captopril therapy must be started under close medical supervision. The usual starting dose is 12.5 mg BID or TID. Titration to the maintenance dose (75-150 mg per day) should be carried out based on patient’s response, clinical status and tolerability, up to a maximum of 150 mg per day in divided doses. The dose should be increased incrementally, with intervals of at least 2 weeks to evaluate patient’s response.
    Myocardial infarction:
    Short-Term Treatment: Captopril treatment should begin in hospital as soon as possible following the appearance of the signs and/or symptoms in patients with stable haemodynamics. A 6.25 mg test dose should be administered, with a 12.5 mg dose being administered 2 hours afterwards and a 25 mg dose 12 hours later (If 6.25 mg dose is not available, consider to start with a 12.5 mg dose or alternative therapy). From the following day, captopril should be administered in a 100 mg/day dose, in two daily administrations, for 4 weeks, if warranted by the absence of adverse haemodynamic reactions. At the end of the 4 weeks of treatment, the patient’s state should be reassessed before a decision is taken concerning treatment for the post-myocardial infarction stage.
    Chronic Treatment: if captopril treatment has not begun during the first 24 hours of the acute myocardial infarction stage, it is suggested that treatment be instigated between the 3rd and 16th day post-infarction once the necessary treatment conditions have been attained (stable haemodynamics and management of any residual ischaemia). Treatment should be started in hospital under strict surveillance (particularly of blood pressure) until the 75 mg dose is reached. The initial dose must be low, particularly if the patient exhibits normal or low blood pressure at the initiation of therapy. Treatment should be initiated with a dose of 6.25 mg followed by 12.5 mg 3 times daily for 2 days and then 25 mg 3 times daily if warranted by the absence of adverse haemodynamic reactions (If 6.25 mg dose is not available, consider to start with a 12.5 mg dose or alternative therapy). The recommended dose for effective cardioprotection during long-term treatment is 75 to 150 mg daily in two or three doses. In cases of symptomatic hypotension, as in heart failure, the dosage of diuretics and/or other concomitant vasodilators may be reduced in order to attain the steady state dose of captopril. Where necessary, the dose of captopril should be adjusted in accordance with the patient’s clinical reactions. Captopril may be used in combination with other treatments for myocardial infarction such as thrombolytic agents, beta-blockers and acetylsalicylic acid.
    Type I Diabetic nephropathy: The recommended dose is 75-100 mg daily in divided doses. Captopril may be used in combination with other antihypertensive agents, i.e. diuretics, beta blockers, centrally acting agents or vasodilators if the reduction in blood pressure is inadequate with captopril alone.
    Patients with renal impairment
    Since captopril is excreted primarily via the kidneys, dosage should be reduced or the dosage interval should be increased in patients with impaired renal function. When concomitant diuretic therapy is required, a loop diuretic (e.g. furosemide), rather than a thiazide diuretic, is preferred in patients with severe renal impairment.
    In patients with impaired renal function, the following daily dose may be recommended to avoid accumulation of captopril.
    Creatinine clearance > 40 ml/min/1.73 m2:
    Daily starting dose: 25-50 mg, Daily maximum dose: 150 mg.
    Creatinine clearance 21-40 ml/min/1.73 m2:
    Daily starting dose: 25 mg, Daily maximum dose: 100 mg.
    Creatinine clearance 10-20 ml/min/1.73 m2:
    Daily starting dose: 12.5 mg, Daily maximum dose: 75 mg.
    Creatinine clearance *<10 ml/min/1.73 m2:
    Daily starting dose: 6.25 mg, Daily maximum dose: 37.5 mg.
    *If 6.25 mg dose is not available, consider alternative therapy.
    As with other antihypertensive agents, consideration should be given to initiating therapy with a lower starting dose (6.25 mg BID) in elderly patients who may have reduced renal function and other organ dysfunctions (see above ‘renal impairment’). If 6.25 mg dose is not available, consider to start with a 12.5 mg dose or alternative therapy.
    Dosage should be titrated against blood pressure response and kept as low as possible to achieve adequate control.
    Children and adolescents
    The efficacy and safety of captopril have not been fully established


    Hypertension, congestive heart failure, insulin dependent diabetic nephropathy in hypertensive and non-hypertensive patients in cases where the serum creatinine level <2.5 mg/dl. Left ventricular dysfunction after myocardial infraction. Captopril is indicated to improve survival following myocardial infraction in clinically stable patients with left ventricular dysfunction manifested as an ejection fraction < or equal to 40% and to reduce the incidence of overt heart failure and subsequent hospitalization for congestive heart failure in this patients.


    Hypersensitivity to the active substance and other ACE inhibitors, or to any of the excipients.
    History of angioedema associated with previous ACE inhibitor therapy.
    Hereditary or Idiopathic angioneurotic oedema.
    Second and third trimesters of pregnancy.
    The concomitant use of Aceril with aliskiren-containing products is contraindicated in patients with diabetes mellitus or renal impairment (GFR < 60 ml/min/1.73 m2).


    Special Precautions

    Hypotension: rarely hypotension is observed in uncomplicated hypertensive patients. Symptomatic hypotension is more likely to occur in hypertensive patients who are volume and/or sodium depleted by vigorous diuretic therapy, dietary salt restriction, diarrhoea, vomiting or haemodialysis. Volume and/or sodium depletion should be corrected before the administration of an ACE inhibitor and a lower starting dose should be considered.
    Patients with heart failure are at higher risk of hypotension and a lower starting dose is recommended when initiating therapy with an ACE inhibitor. The magnitude of the decrease is greatest early in the course of treatment; this effect stabilises within a week or two, and generally returns to pre-treatment levels, without a decrease in therapeutic efficacy, within two months. Caution should be used whenever the dose of captopril or diuretic is increased in patients with heart failure.
    As with any antihypertensive agent, excessive blood pressure lowering in patients with ischaemic cardiovascular or cerebrovascular disease may increase the risk of myocardial infarction or stroke. If hypotension develops, the patient should be placed in a supine position. Volume repletion with intravenous normal saline may be required.
    Infants, especially new-borns, may be more susceptible to the adverse haemodynamic effects of captopril. Excessive, prolonged and unpredictable decreases in blood pressure and associated complications, including oliguria and seizures have been reported.
    Renovascular hypertension: there is an increased risk of hypotension and renal insufficiency when patients with bilateral renal artery stenosis or stenosis of the artery to a single functioning kidney are treated with ACE inhibitors. Loss of renal function may occur with only mild changes in serum creatinine. In these patients, therapy should be initiated under close medical supervision with low doses, careful titration and monitoring of renal function.
    Renal impairment: The incidence of adverse reactions to captopril is principally associated with renal function since the drug is excreted primarily by the kidney. In cases of renal impairment (creatinine clearance ≤ 40 ml/min), the initial dosage of captopril must be adjusted according to the patient’s creatinine clearance, and then as a function of the patient’s response to treatment. The dose should not exceed that necessary for adequate control and should be reduced in patients with impaired renal function.

    Evaluation of the patient should include assessment of renal function (monitoring of potassium and creatinine) prior to initiation of therapy and at appropriate intervals thereafter. Patients with renal impairment should not normally be treated with captopril.
    Aortic and mitral valve stenosis/ Obstructive hypertropic cardiomyopathy: Captopril should be used with caution in patients with left ventricular valvular and outflow tract obstruction. As limited experience has been obtained in the treatment of acute hypertensive crises, the use of captopril should be avoided in cases of cardiogenic shock and haemodynamically significant obstruction.
    Angioedema: angioedema of the extremities, face, lips, mucous membranes, tongue, glottis or larynx may occur in patients treated with ACE inhibitors including Captopril. This may occur anytime during treatment. However, in rare cases, severe angioedema may develop after long-term treatment with an ACE inhibitor. In such cases, Captopril should be discontinued promptly and appropriate monitoring should be instituted to ensure complete resolution of symptoms prior to dismissing the patient. In those instances where swelling has been confined to the face and lips the condition generally resolved without treatment, although antihistamines have been useful in relieving symptoms. Angioedema involving the tongue, glottis or larynx may be fatal. Where there is involvement of the tongue, glottis or larynx, likely to cause airway obstruction, appropriate therapy, which may include subcutaneous epinephrine solution 1:1000 (0.3 ml to 0.5 ml) and/or measures to ensure a patent airway, should be administered promptly. 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.
    Black patients receiving ACE inhibitors have been reported to have a higher incidence of angioedema compared to non-blacks.
    Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor.
    Intestinal angioedema has also been reported rarely in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases, there was no prior facial angioedema and C-1 esterase levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan, or ultrasound or at surgery and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain.
    Cough: cough has been reported with the use of ACE inhibitors. Characteristically, the cough is non-productive, persistent and resolves after discontinuation of therapy.
    Dual blockade of the renin-angiotensin-aldosterone system (RAAS)
    There is evidence that the concomitant use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of hypotension, hyperkalaemia and decreased renal function (including acute renal failure). Dual blockade of RAAS through the combined use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren is therefore not recommended.
    If dual blockade therapy is considered absolutely necessary, this should only occur under specialist supervision and subject to frequent close monitoring of renal function, electrolytes and blood pressure.
    ACE-inhibitors and angiotensin II receptor blockers should not be used concomitantly in patients with diabetic nephropathy.
    Hepatic failure: rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
    Hyperkalaemia: Elevations in serum potassium have been observed in some patients treated with ACE inhibitors, including captopril. Patients at risk for the development of hyperkalaemia include those with renal insufficiency, diabetes mellitus, or those using concomitant potassium-sparing diuretics, potassium supplements or potassium-containing salt substitutes; or those patients taking other drugs associated with increases in serum potassium (e.g. heparin). If concomitant use of the above mentioned agents is deemed appropriate, regular monitoring of serum potassium is recommended.
    Lithium: the combination of lithium and captopril is not recommended.
    Proteinuria: Proteinuria may occur particularly in patients with existing renal function impairment or on relatively high doses of ACE inhibitors.
    Total urinary proteins greater than 1 g per day were seen in about 0.7% of patients receiving captopril. The majority of patients had evidence of prior renal disease or had received relatively high doses of captopril (in excess of 150 mg/day), or both. Nephrotic syndrome occurred in about one-fifth of proteinuric patients. In most cases, proteinuria subsided or cleared within six months whether or not captopril was continued. Parameters of renal function, such as BUN and creatinine, were seldom altered in the patients with proteinuria.
    In patients with evidence of prior renal disease should have urinary protein estimations (dip stick on first morning urine) prior to treatment, and periodically thereafter.
    Although membranous glomerulopathy was found in biopsies taken from some proteinuric patients, a causal relationship to captopril has not been established.
    Anaphylactoid reactions during desensitisation: There have been rare reports of sustained life-threatening anaphylactoid reactions in patients undergoing desensitisation treatment with hymenoptera venom while receiving another ACE inhibitors. In the same patients, these reactions were avoided when the ACE inhibitor was temporarily withheld, but they reappeared upon inadvertent rechallenge. Therefore caution should be used in patients treated with ACE inhibitors undergoing such desensitisation procedures.
    Anaphylactoid reactions during high-flux dialysis / lipoprotein apheresis membrane exposure: Recent clinical observations have shown a high incidence of anaphylactoid-like reactions during haemodialysis with high-flux dialysis membranes (e.g. AW 69) or undergoing low-density lipoprotein apheresis with dextran sulphate absorption in patients receiving ACE inhibitors. Therefore, this combination should be avoided. In these patients, consideration should be given to use a different type of dialysis, membrane or a different class of medication.
    Diabetic patients: the glycaemia levels should be closely monitored in diabetic patients previously treated with oral antidiabetic drugs or insulin, namely during the first month of treatment with an ACE inhibitor.
    Renal function in patients with Heart failure: Some patients may develop stable elevations of BUN and serum creatinine >20% above normal or baseline upon long-term treatment with captopril. A few patients, generally those with severe pre-existing renal disease, required discontinuation of treatment due to progressively increasing creatinine.
    Neutropenia/Agranulocytosis: neutropenia/agranulocytosis, thrombocytopenia and anaemia have been reported in patients receiving ACE inhibitors, including captopril. In patients with normal renal function and no other complicating factors, neutropenia occurs rarely.
    Captopril should be used with extreme caution in patients with pre-existing impaired renal function, collagen vascular disease, immunosuppressant therapy, treatment with allopurinol or procainamide, or a combination of these complicating factors. Some of these patients developed serious infections which in a few instances did not respond to intensive antibiotic therapy.

    If captopril is used in such patients, it is advised that white blood cell count and differential counts should be performed prior to therapy, every two weeks during the first three months of captopril therapy, and periodically thereafter.

    During treatment all patients should be instructed to report any sign of infection (e.g. sore throat, fever), when a differential white blood cell count should be performed. Captopril and other concomitant medication should be withdrawn if neutropenia (neutrophils less than 1000/mm3) is detected or suspected.
    In most patients neutrophil counts rapidly returned to normal upon discontinuing captopril.
    Surgery/Anaesthesia: In patients undergoing major surgery, or during anaesthesia with agents which produce hypotension, captopril will block angiotensin II formation secondary to compensatory renin release. This may lead to hypotension which can be corrected by volume expansion.
    Lactose: Aceril contains lactose. Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.
    Ethnic differences: As with other angiotensin converting enzyme inhibitors, captopril is apparently less effective in lowering blood pressure in black people than in non-blacks, possibly because of a higher prevalence of low-renin states in the black hypertensive population.
    Pregnancy: ACE inhibitors should not be initiated during pregnancy. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative antihypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started.

    Side Effects

    Frequency is defined using the following convention:
    Common (> 1/100, < 1/10)
    Uncommon (> 1/1,000, < 1/100)
    Rare (> 1/10,000, < 1/1,000) and
    Very rare (< 1/10,000).
    Undesirable effects reported for captopril and/or ACE inhibitor therapy include:
    Blood and lymphatic disorders:
    Very rare: neutropenia/agranulocytosis, pancytopenia particularly in patients with renal dysfunction, anaemia (including aplastic and haemolytic), thrombocytopenia, lymphadenopathy, eosinophilia, auto-immune diseases and/or positive ANA-titres.
    Metabolic and nutritional disorder:
    Rare: Anorexia
    Very rare: hyperkalaemia, hyponatremia and hypoglycaemia
    Psychiatric disorders:
    Common: sleep disorders
    Very rare: confusion, depression.
    Nervous system disorders:
    Common: reversible and self-limiting taste impairment and dizziness.
    Uncommon: paraesthesia, headache.
    Rare: Somnolence
    Very rare: cerebrovascular incidents, including stroke and syncope.
    Eye disorders:
    Very rare: blurred vision.
    Cardiac disorders:
    Uncommon: tachycardia or tachyarrhythmia, angina pectoris, palpitations.
    Very rare: cardiac arrest, cardiogenic shock
    Vascular disorders:
    Uncommon: hypotension , Raynaud syndrome, flush, pallor
    Respiratory, thoracic and mediastinal disorders:
    Common: dry, irritating (non-productive) cough and dyspnoea
    Vary rare: bronchospasms, rhinitis, allergic alveolitis/ eosinophilic pneumonia.
    Gastrointestinal disorders:
    Common: nausea, vomiting, epigastric discomfort, abdominal pain, diarrhoea, constipation, dry mouth, peptic ulcer, dyspepsia.Rare: stomatitis/aphthous stomatitis, small bowel angioedema
    Very rare: glossitis, pancreatitis.
    Hepato-biliary disorders:
    Very rare: hepatic function abnormal, cholestasis, jaundice, hepatitis, hepatic necrosis, hepatic enzyme increased, blood bilirubin increased, transaminase increased, blood alkaline phosphatase increased.
    Skin and subcutaneous tissue disorders:
    Common: pruritus with or without a rash, rash, and alopecia
    Uncommon: angioedema
    Very rare: urticaria, Stevens Johnson syndrome, erythema multiforme, photosensitivity, erythroderma, pemphigoid reactions and exfoliative dermatitis.
    Musculoskeletal, connective tissue and bone disorders:
    Very rare: myalgia, arthralgia.
    Renal and Urinary Disorders:
    Rare: renal impairment, renal failure, polyuria, oliguria, pollakiuria.
    Very rare: nephrotic syndrome.
    Reproductive system and breast disorders:
    Very rare: erectile dysfunction, gynaecomastia.
    General disorders and administration site conditions:
    Uncommon: chest pain, fatigue, malaise, asthenia
    Very rare: pyrexia
    Very rare: proteinuria, eosinophilia, blood potassium increased, blood sodium decreased, blood urea increased, blood creatinine increased, blood bilirubin increased, hemoglobin decreased, haematocrit decreased, white blood cell count decreased, platelet count decreased, antinuclear antibody positive, red blood cell sedimentation rate increased.

    Drug interactions

    Diuretics: (thiazide or loop diuretics): Prior treatment with high dose diuretics may result in volume depletion and a risk of hypotension when initiating therapy with captopril. The hypotensive effects can be reduced by discontinuation of the diuretic, by increasing volume or salt intake or by initiating therapy with a low dose of captopril. However, no clinically significant drug interactions have been found in specific studies with hydrochlorothiazide or furosemide.
    Potassium sparing diuretics or potassium supplements: ACE inhibitors attenuate diuretic induced potassium loss. Potassium-sparing diuretics (triamterene, amiloride and spironolactone), potassium-containing salt substitutes or potassium supplements may cause significant increase in serum potassium. If concomitant use is indicated because of demonstrated hypokalaemia they should be used with caution and with frequent monitoring of serum potassium.
    Other antihypertensive agents: Captopril has been safely co-administered with other commonly used anti-hypertensive agents (e.g. beta-blockers and long-acting calcium channel blockers). Concomitant use of these agents may increase the hypotensive effects of captopril. Treatment with nitroglycerine and other nitrates, or other vasodilators (such as minoxidil), should be used with caution.
    Alpha blocking agents: concomitant use of alpha blocking agents may increase the antihypertensive effects of captopril and increase the risk of orthostatic hypotension.
    Treatments of acute myocardial infarction: Captopril may be used concomitantly with acetylsalicylic acid (at cardiologic doses), thrombolytics, beta-blockers and/or nitrates in patients with myocardial infarction.
    Lithium: Reversible increases in serum lithium concentrations and toxicity have been reported during concomitant administration of lithium with ACE inhibitors. Concomitant use of thiazide diuretics may increase the risk of lithium toxicity and enhance the already increased risk of lithium toxicity with ACE inhibitors. Use of captopril with lithium is not recommended, but if the combination proves necessary, careful monitoring of serum lithium levels should be performed.
    Non-steroidal anti-inflammatory medicinal products: It has been described that non-steroidal anti-inflammatory medicinal products (NSAIDs) (such as Indomethacin, Ibuprofen) and ACE inhibitors exert an additive effect on the increase in serum potassium whereas renal function may decrease. These effects are, in principle, reversible. Rarely, acute renal failure may occur, particularly in patients with compromised renal function such as the elderly or dehydrated. Chronic administration of NSAIDs may reduce the antihypertensive effect of an ACE inhibitor.
    Clonidine: It has been suggested that the anti-hypertensive effect of captopril can be delayed when patients treated with clonidine are changed to captopril.
    Allopurinol, procainamide, cytostatic or immunosuppressive agents: concomitant administration with ACE inhibitors may lead to an increased risk for leucopenia especially when the latter are used at higher than currently recommended doses.
    Probenecid: The renal clearance of captopril is reduced in the presence of probenecid.
    Tricyclic antidepressants/Antipsychotics: ACE inhibitors may enhance the hypotensive effects of certain tricyclic antidepressants and antipsychotics. Postural hypotension may occur.
    Sympathomimetics: may reduce the antihypertensive effects of ACE inhibitors; patients should be carefully monitored.
    Antidiabetics: pharmacological studies have shown that ACE inhibitors, including captopril, can potentiate the blood glucose-reducing effects of insulin and oral antidiabetics such as sulphonylurea in diabetics. Should this very rare interaction occur, it may be necessary to reduce the dose of the antidiabetic during simultaneous treatment with ACE inhibitors.


    Pregnancy and Lactation

    The use of ACE inhibitors is not recommended during the first trimester of pregnancy.
    The use of ACE inhibitors is contra-indicated during the 2nd and 3rd trimester of pregnancy.
    Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy has not been conclusive; however a small increase in risk cannot be excluded. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started. Exposure to ACE inhibitor therapy during the second and third trimesters is known to induce human fetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalaemia). Should exposure to ACE inhibitor have occurred from the second trimester of pregnancy, ultrasound check of renal function and skull is recommended. Infants whose mothers have taken ACE inhibitors should be closely observed for hypotension.
    Limited pharmacokinetic data demonstrate very low concentrations in breast milk , Although these concentrations seem to be clinically irrelevant, the use of Aceril in breast feeding is not recommended for pre-term infants and for the first few weeks after delivery, because of the hypothetical risk of cardiovascular and renal effects and because there is not enough clinical experience, In the case of an older infant, the use of Aceril in a breast-feeding mother may be considered if this treatment is necessary for the mother and the child is observed for any adverse effect.


    Overdose: Symptoms of overdose are severe hypotension, shock, stupor, bradycardia, electrolyte disturbances and renal failure.
    Measures to prevent absorption (e.g. gastric lavage, administration of adsorbents and sodium sulphate within 30 minutes after intake) and hasten elimination should be applied if ingestion is recent. If hypotension occurs, the patient should be placed in the shock position and salt and volume supplementations should be given rapidly. Treatment with angiotensin-II should be considered. Bradycardia or extensive vagal reactions should be treated by administering atropine. The use of a pacemaker may be considered.
    Captopril may be removed from adult circulation by haemodialysis. Captopril is not adequately cleared by peritoneal dialysis.

    Important notes

    Laboratory tests:
    Captopril may cause a false-positive urine test for acetone.
    Clinical trial data has shown that dual blockade of the renin-angiotensin-aldosterone-system (RAAS) through the combined use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren is associated with a higher frequency of adverse events such as hypotension, hyperkalaemia and decreased renal function (including acute renal failure) compared to the use of a single RAAS-acting agent.


    Dexcel Ltd.
    Licence holder