Nhà máy Stada
Stada
stada
stada
Cardiovascular Agents

Captopril STADA® 25 mg

 

Pack size:

Box of 10 blisters x 10 tablets.

 

Composition:

Each tablet contains captopril 25 mg.

 

Shelf-life:

36 months from the date of manufacturing.

Store in a well-closed container, in a dry place. Do not store above 30oC.

 

  • Indications and Dosage & Administration
  • Contraindications
  • Adverse reactions
  • Precautions

  • Hypertension
    The management of mild to moderate hypertension. In severe hypertension it should be used where standard therapy is ineffective or inappropriate.
    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 6.25 mg or 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
    The drug should be used together with diuretics and, when appropriate, digitalis and beta-blockers.
    In patients on doses of over 100 mg daily plus or minus a diuretic, in those with severe renal impairment or those with severe congestive heart failure use of captopril should be under specialist supervision.
    Captopril therapy must be started under close medical supervision. The usual starting dose is 6.25 mg - 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 (4 weeks) treatment: Captopril is indicated in any clinically stable patient within the first 24 hours of an infarction.
    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. 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.
    Long-term prevention of symptomatic heart failure: Captopril is indicated in clinically stable patients with asymptomatic left ventricular dysfunction (ejection fraction ≤ 40%) following myocardial infarction to improve survival, delay the onset of symptomatic heart failure, reduce hospitalisations for heart failure and reduce recurrent myocardial infarction and coronary revascularisation procedures.
    Before starting therapy, cardiac function should be determined by radionuclide ventriculography or echocardiography.
    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. The recommended dose for effective cardio protection 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
    Captopril is indicated in insulin dependent diabetics for the treatment of macroproteinuric diabetic nephropathy (microalbuminuria greater than 30 mg/day). Captopril may prevent the progression of the renal disease and reduce associated clinical events e.g. dialysis, renal transplantation and death.
    Captopril can be used alone or 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.
    The recommended dose is 75 – 100 mg daily in divided doses. 
  • 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:

     
  • Elderly
    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.
    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. The use of captopril in children and adolescents should be initiated under close medical supervision.
    Children > 20 kg: The initial starting dose should be 0.3 mg per kg body weight. Generally, captopril is administered to children 3 times a day, but dose and interval of dose should be adapted individually according to patient's response.

    Captopril STADA® 25 mg is administered orally, may be taken before, during and after meals. Dose should be individualised according to patient's profile and blood pressure response. The recommended maximum daily dose is 150 mg.


Or as prescribed by physicians.
 

  • Hypersensitivity to captopril and other ACE inhibitors, or to any of the excipients.
  • History of angioedema associated with previous ACE inhibitor therapy.
  • Hereditary or idiopathic angioneurotic oedema.
  • Post-myocardial infarction (hemodynamic instability patients).
  • Bilateral renal artery stenosis, unilateral renal artery stenosis in a solitary kidney.
  • Pre-existing hypotension, aortic stenosis and severe obstructive cardiomyopathy.
  • Pregnancy and lactation.
  • Concomitant therapy with aliskiren-containing products in patients with diabetes mellitus or moderate and severe renal failure (GFR < 60 ml/min 1.73 m2).

     

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.
  • Hyperkalaemia and hypoglycaemia.
  • Confusion, depression.
  • Cerebrovascular incidents, including stroke and syncope.
  • Blurred vision.
  • Cardiac arrest, cardiogenic shock.
  • Bronchospasms, rhinitis, allergic alveolitis/ eosinophilic pneumonia.
  • Glossitis, peptic ulcer, and pancreatitis.
  • Elevation of liver enzymes and bilirubin, impaired hepatic function and cholestasis (including jaundice), hepatitis including necrosis.
  • Urticaria, Stevens Johnson syndrome, erythema multiforme, photosensitivity, erythroderma, pemphigoid reactions and exfoliative dermatitis.
  • Myalgia, arthralgia.
  • Nephrotic syndrome.
  • Impotence, gynaecomastia.
  • Fever.
  • Proteinuria, eosinophilia, increase of serum potassium, decrease of serum sodium, elevation of BUN, serum creatinine and serum bilirubin, decreases in haemoglobin, haematocrit, leucocytes, thrombocytes, positive ANA-titre, elevated ESR.

Rare:

  • Anorexia.
  • Paraesthesia, headache and drowsiness.
  • Weight loss and loss of appetite, stomatitis, resembling aphthous ulcers, mouth ulcers.
  • Renal function disorders including renal failure, polyuria, oliguria, increased urine frequency.

Common:

  • Sleep disorders.
  • Reversible and self-limiting taste impairment and dizziness.
  • Dry, irritating (non-productive) cough and dyspnoea.
  • Nausea, vomiting, loss of taste (usually reversible on stopping treatment), abdominal pain, dry mouth, diarrhoea or constipation and gastric irritations.
  • Pruritus with or without a rash, rash, and alopecia.

Uncommon:

  • Tachycardia or tachyarrhythmia, angina pectoris, palpitations.
  • Hypotension, Raynaud syndrome, flush, pallor.
  • Angioedema.
  • Chest pain, fatigue, malaise.

 

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. 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.
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 particularly during the first weeks of treatment. However, in rare cases, severe angioedema may develop after long-term treatment with an ACE inhibitor. Treatment should be discontinued promptly. Angioedema involving the tongue, glottis or larynx may be fatal. Emergency therapy should be instituted. 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.
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.
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:
Captopril STADA® 25 mg contains lactose, therefore patients with rare hereditary problems of galactose intolerance, the Lapp 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.
The use of captopril or other angiotensin converting enzyme inhibitors during the second and third trimesters of pregnancy has been associated with fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure and death. Oligohydramnios has also been reported presumably resulting from decreased fetal renal function. Prematurity, intrauterine growth retardation, and patent ductus arteriosus have also been reported, therefore captopril should never be used in pregnancy.
Lactation:
Captopril is excreted into breast milk. Because of the potential for serious adverse reactions in nursing infants from captopril, captopril or other ACE-inhibitors are not used in breast feeding.
Effect on ability to drive and use machines:
As with other antihypertensive, the ability to drive and use machines may be reduced, namely at the start of the treatment, or when posology is modified, and also when used in combination with alcohol, but these effects depend on the individual's susceptibility.

 

Contact us

FACTORY 1: K63/1 Nguyen Thi Soc St., Xuan Thoi Dong, Hoc Mon, HCMC
Tel: +84 28 3718 2141 - Fax: +84 28 3718 2140

FACTORY 2: 40 Tu Do Avenue, VietNam-Singapore Industrial Park, Binh Duong
Tel: +84 274 376 7470 - Fax: +84 274 376 7469
Email : stada@stada.com.vn
Website: www.stada.com.vn



Visitors Counter

Online
18
Total