Captopril tablets 25 mg No. 20

Instructions for Captopril tablets 25 mg No. 20

Composition

active ingredient: captopril;

1 tablet contains captopril* 25 mg;

Excipients: microcrystalline cellulose; lactose monohydrate; potato starch; magnesium stearate.

* Calculated on 100% substance.

Dosage form

Pills.

Main physicochemical properties: white tablets with a specific odor, flat-cylindrical in shape with beveled edges and a score.

Pharmacotherapeutic group

Agents acting on the renin-angiotensin system. Angiotensin-converting enzyme (ACE) inhibitors, monocomponent. ATC code C09A A01.

Pharmacological properties

Pharmacodynamics.

Captopril is the first synthetic angiotensin-converting enzyme (ACE) inhibitor to be used in medical practice. By blocking the conversion of angiotensin I to angiotensin II, captopril has a vasodilating effect, due to which it reduces total peripheral vascular resistance (afterload), pulmonary capillary wedge pressure (preload) and pulmonary vascular resistance; increases cardiac output and exercise tolerance. With prolonged use, captopril reduces the severity of left ventricular myocardial hypertrophy, prevents the progression of heart failure and slows the development of left ventricular dilatation. It reduces the tone of the efferent arterioles of the renal glomeruli, thereby improving intraglomerular hemodynamics and preventing the development of diabetic nephropathy.

The beneficial effects of ACE inhibitors are mainly due to inhibition of the plasma renin-angiotensin-aldosterone system (RAAS). Renin is an endogenous enzyme synthesized by the kidneys and released into the systemic circulation, where it converts angiotensinogen to angiotensin-I, a relatively inactive decapeptide. Angiotensin-I is then converted by ACE, a peptidyl dipeptidase, to angiotensin-II. Angiotensin-II is a potent vasoconstrictor responsible for constricting arterial vessels and increasing blood pressure, as well as stimulating the adrenal glands to produce aldosterone. Inhibition of ACE results in a decrease in plasma angiotensin-II levels, which reduces vasopressor activity and aldosterone production. Although the decrease in the latter is small, a slight increase in serum potassium concentrations may occur, paralleling sodium and fluid loss. Blocking the negative feedback of angiotensin-II on renin production leads to an increase in renin activity in blood plasma.

Another function of the converting enzyme is the degradation of the potent vasodepressant kinin peptide bradykinin to inactive metabolites. Therefore, inhibition of ACE leads to increased activity of the kallikrein-kinin system, which is involved in peripheral vasodilation through activation of the prostaglandin system; this mechanism may be involved in the hypotensive effect of ACE inhibitors and responsible for some of the adverse reactions.

The blood pressure lowering effect usually occurs within 60-90 minutes after oral administration of an individual dose of captopril. The duration of the effect is dose-dependent. The blood pressure lowering effect may be progressive, and several weeks of therapy may be required to achieve the maximum therapeutic effect. The blood pressure lowering effects of captopril and thiazide diuretics are additive.

Pharmacokinetics.

When administered orally, the drug is rapidly and almost completely (not less than 75%) absorbed from the digestive tract. In the presence of food, bioavailability decreases by 30-40%. The maximum concentration in blood plasma is reached after 30-90 minutes. Protein binding, mainly albumin, is 25-30%. Captopril passes through histohematological barriers, with the exception of the blood-brain barrier, penetrates the placenta. It is metabolized in the liver. The half-life is less than 3 hours and increases in renal failure.

Excreted mainly by the kidneys both in the form of metabolites and in unchanged form (up to 50%). Within 24 hours, 95% of the absorbed drug is excreted. The maximum decrease in blood pressure after oral administration is observed after 60-90 minutes. The duration of the hypotensive effect is dose-dependent and reaches optimal values within several weeks.

The disulfide metabolites of captopril are excreted by the kidneys more slowly than captopril. Since the disulfide metabolites are converted back to captopril in the body, accumulation of captopril can be expected in patients with renal insufficiency. The accumulation of captopril metabolites in patients with renal insufficiency leads to a stronger pharmacodynamic effect and a prolonged effect. Therefore, the dose of captopril should be adjusted according to renal function in such patients.

In patients with impaired liver function (RAAS) functions normally. Since captopril is a drug, not a prodrug, its effect is comparable to that observed in patients with arterial hypertension without impaired liver function.

In patients with heart failure, the elimination of captopril is slowed. Therefore, patients with heart failure should be treated with a lower initial dose of captopril, and the dose should be adjusted according to the achieved therapeutic effect.

The pharmacokinetics of captopril in healthy elderly volunteers are the same as in healthy younger volunteers. Therefore, elderly patients with arterial hypertension and normal renal function can be administered the usual daily doses of captopril.

Indication

Arterial hypertension.

Heart failure. Captopril is indicated for the treatment of chronic heart failure with decreased ventricular systolic function, as well as in combination with diuretics and, if necessary, digitalis and β-blockers.

Myocardial infarction:

For short-term (4 weeks) treatment, captopril may be prescribed within 24 hours after myocardial infarction in patients with a stable condition;

For long-term prevention of symptomatic heart failure, the drug is indicated in clinically stable patients with asymptomatic left ventricular dysfunction (ejection fraction ≤ 40%).

Diabetic nephropathy in patients with type I diabetes mellitus, manifested by macroproteinuria.

Contraindication

Hypersensitivity to captopril or to any of the excipients of the drug, as well as to other ACE inhibitors;

Quincke's edema (including history, after use of ACE inhibitors, hereditary/idiopathic);

narrowing of the aortic orifice or mitral stenosis, the presence of other obstacles to the outflow of blood from the left ventricle of the heart;

hypertrophic cardiomyopathy with low cardiac output;

primary hyperaldosteronism;

hyperkalemia;

severe renal dysfunction; bilateral renal artery stenosis or stenosis of the artery to a single kidney; condition after kidney transplantation;

congenital (idiopathic) angioedema;

porphyria;

galactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome;

pregnancy; also contraindicated in women planning to become pregnant (see section "Use during pregnancy or breastfeeding");

breastfeeding period (see section "Use during pregnancy or breastfeeding");

simultaneous use of captopril with drugs containing aliskiren in patients with diabetes mellitus or patients with renal insufficiency (glomerular filtration rate < 60 ml/min/1.73 m2).

Interaction with other medicinal products and other types of interactions

Potassium-sparing diuretics or potassium supplements. ACE inhibitors reduce potassium loss caused by diuretics. Potassium-sparing diuretics (e.g. spironolactone, triamterene or amiloride), potassium supplements or salt substitutes containing potassium may lead to hyperkalaemia. They should be used with great caution and with frequent monitoring of serum potassium when co-administered because of pre-existing hypokalaemia.

Diuretics (thiazide or loop diuretics). Previous treatment with high doses of diuretics may result in volume depletion and an increased risk of significant hypotension (see section 4.4). The hypotensive effect can be reduced by discontinuing the diuretic, increasing salt and fluid intake, or initiating therapy with a low dose of captopril. However, no clinically significant interaction has been observed with hydrochlorothiazide or furosemide.

Other antihypertensive drugs: Concomitant use of captopril with other antihypertensive drugs (e.g., β-blockers and long-acting calcium channel blockers) is safe, and concomitant use of such drugs may enhance the hypotensive effect of captopril. Caution should be exercised when treating with nitroglycerin, other nitrates, or other drugs.

Clinical trial data have shown that dual blockade of the RAAS through the combined use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is associated with a higher incidence of adverse reactions, such as hypotension, hyperkalemia and decreased renal function (including acute renal failure), compared with the separate use of drugs acting on the RAAS.

Lithium. Concomitant use of ACE inhibitors and lithium may lead to a transient increase in serum lithium levels and lithium toxicity. Concomitant use of ACE inhibitors and thiazide diuretics may further increase serum lithium levels and increase the risk of lithium toxicity. Therefore, concomitant use of captopril and lithium is not recommended. If this combination proves necessary, careful monitoring of serum lithium levels should be performed.

Tricyclic antidepressants/neuroleptics: Concomitant use of certain tricyclic antidepressants and neuroleptics with ACE inhibitors may lead to an additional decrease in blood pressure (see section 4.4). Postural hypotension may occur.

Allopurinol, procainamide, cytostatic or immunosuppressive drugs. Their simultaneous use with ACE inhibitors increases the risk of leukopenia, especially when the latter are used in doses exceeding the recommended ones.

Nonsteroidal anti-inflammatory drugs (NSAIDs). ACE inhibitors and NSAIDs have an additive effect on serum potassium, which may lead to renal impairment. This effect is usually reversible. Acute renal failure may occur rarely, especially in patients with compromised renal function, such as the elderly or dehydrated. Prolonged use of NSAIDs may reduce the antihypertensive effect of ACE inhibitors.

Sympathomimetics: May reduce the antihypertensive effect of ACE inhibitors, so the patient's blood pressure should be carefully monitored.

Antidiabetic agents: ACE inhibitors, including captopril, may enhance the antiglycaemic effect of insulin and other oral antidiabetic agents (sulfonylureas) in patients with diabetes mellitus. This effect is very rare, but if it occurs, it may be necessary to reduce the dose of the antidiabetic agent during concomitant treatment with ACE inhibitors.

mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus): Patients taking concomitant mTOR inhibitors may be at increased risk of developing angioedema (see section 4.4).

Application features

Dual blockade of the RAAS. The combined use of ACE inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of hypotension, hyperkalemia and decreased renal function (including acute renal failure). Therefore, dual blockade of the RAAS through the combined use of ACE inhibitors, angiotensin II receptor blockers or aliskiren is not recommended.

If dual blockade therapy is absolutely necessary, it should be carried out under medical supervision with frequent monitoring of renal function, electrolyte levels and blood pressure.

ACE inhibitors and angiotensin-II receptor blockers should not be used simultaneously in patients with diabetic nephropathy.

Hypotension. Hypotension may occur rarely in hypertensive patients who are volume and/or sodium depleted by diuretic therapy, dietary salt restriction, diarrhea, vomiting, or hemodialysis. Before prescribing ACE inhibitors, volume expansion should be corrected and the lowest effective dose should be considered.

Patients with heart failure are also at risk of symptomatic hypotension when taking ACE inhibitors. Therefore, a lower initial dose of captopril is recommended in such patients. Increasing the dose of ACE inhibitors and diuretics should be done under close medical supervision.

Excessive decrease in blood pressure in patients with cerebrovascular and ischemic heart disease increases the risk of myocardial infarction and stroke. In case of hypotension, the patient should be placed in a horizontal position (on his back), and if necessary, increase the BCC by administering 0.9% sodium chloride solution.

Renovascular hypertension. There is an increased risk of hypotension and renal failure when patients with bilateral renal artery stenosis or stenosis of the artery to a solitary kidney are treated with ACE inhibitors. In such cases, renal function may decline with little change in serum creatinine, and it is recommended that these patients be started on low doses of captopril under close medical supervision, and that the dose be titrated and renal function monitored.

Angioedema. Rarely, during treatment with ACE inhibitors, especially during the first weeks of treatment, angioedema of the extremities, face, lips, mucous membranes, tongue, larynx and/or glottis may develop. However, extremely rarely, angioedema may develop as a result of prolonged treatment with ACE inhibitors. In such cases, treatment should be discontinued immediately. Angioedema of the tongue, glottis and/or larynx can be fatal, therefore such reactions should be stopped immediately, the patient should be hospitalized and observed for at least 12-24 hours until the symptoms disappear completely.

Cough: Cough has been reported during treatment with ACE inhibitors. The cough has been described as persistent, dry, non-productive and resolved after discontinuation of therapy.

Hepatic failure. ACE inhibitors have been associated in rare cases with a syndrome that begins with cholestatic jaundice, progresses to sudden necrotizing hepatitis, and is sometimes fatal. The mechanism of this syndrome remains unclear. Therefore, if jaundice or elevations in liver enzymes occur during treatment with ACE inhibitors, treatment should be discontinued immediately and the patient should be closely monitored.

Hyperkalemia. During treatment with ACE inhibitors, including captopril, some patients may develop increased serum potassium levels. The risk of hyperkalemia is increased in patients with renal insufficiency, diabetes mellitus, or those taking concomitant potassium-sparing diuretics, potassium supplements or salt substitutes containing potassium, or other drugs that may cause hyperkalemia (e.g. heparin). If concomitant use of the above drugs is considered necessary, regular monitoring of serum potassium is recommended.

Aortic or mitral valve stenosis/hypertrophic cardiomyopathy. ACE inhibitors should be used with caution in patients with aortic or mitral valve stenosis and left ventricular outflow tract obstruction. Captopril should be avoided in patients with cardiogenic shock and significant hemodynamic compromise.

Lithium: The combination of lithium and captopril is not recommended (see section 4.5).

Neutropenia/agranulocytosis: Neutropenia/agranulocytosis, thrombocytopenia and anemia have been reported in patients receiving ACE inhibitors. Neutropenia is rare in patients with normal renal function and no other complicating factors.

Captopril should be used with caution in patients with vascular disease in collagen diseases (e.g. systemic lupus erythematosus, scleroderma), in case of concomitant treatment with antidepressants, allopurinol or procainamide, especially if there is impaired renal function. Some of these patients may develop serious infections, which sometimes do not respond to intensive antibiotic therapy.

If captopril is used in such patients, it is recommended to monitor the white blood cell count and complete blood count before starting treatment, every 2 weeks during the first 3 months of treatment and periodically thereafter. Patients should be instructed to report any signs of infection (e.g. sore throat, fever) to their physician immediately and to have a complete blood count. Captopril and any concomitant medication (see section 4.5) should be discontinued immediately if neutropenia (neutrophils < 1000/mm3) is detected or suspected.

In most patients, the neutrophil count quickly returns to normal after stopping captopril.

Proteinuria: Proteinuria may occur in patients with impaired renal function or when taking high doses of ACE inhibitors.

Total protein in the urine of more than 1 g per day was observed in approximately 0.7% of patients taking captopril. Most of these patients had kidney disease or were taking relatively high doses of captopril (more than 150 mg per day), or both. Nephrotic syndrome occurs in 1/5 of patients with proteinuria. In most cases, proteinuria decreases or disappears within 6 months regardless of taking captopril. In patients with proteinuria, parameters of renal function such as serum urea and creatinine rarely change.

In patients with a history of kidney disease, urine protein levels should be determined (dipstick analysis of first morning urine) before starting treatment and periodically thereafter.

Anaphylactoid reactions have been reported in patients undergoing dialysis with high-flux membranes/LDL apheresis with dextrin sulfate. A decision should be made to use a different type of dialysis, membrane, or drug class for these patients.

Hypersensitivity/angioedema: Patients taking concomitant mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) may be at increased risk of developing angioedema (e.g. swelling of the airways or tongue with or without respiratory distress) (see section 4.5).

Surgery/anesthesia: In the case of major surgery, patients may experience hypotension during anesthesia. If blood pressure decreases, volume replacement is recommended.

Diabetes mellitus: In diabetic patients taking oral antidiabetic agents or insulin, blood glucose levels should be closely monitored during the first month of concomitant use of ACE inhibitors.

Ethnic characteristics: Like other ACE inhibitors, captopril is a less effective antihypertensive drug in patients of the black race, possibly due to a higher prevalence of low-renin essential hypertension.

Use during pregnancy or breastfeeding

Pregnancy.

The drug is contraindicated for use in pregnant women or women planning to become pregnant. If pregnancy is confirmed during treatment with this drug, its use should be immediately discontinued and replaced with another drug approved for use in pregnant women.

Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy is inconclusive. Some increased risk cannot be excluded. Patients planning pregnancy should be changed to alternative antihypertensive treatments which have an established safety profile for use in pregnancy.

It is known that the use of ACE inhibitors during the 2nd and 3rd trimesters of pregnancy can cause fetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalemia).

Should exposure to an ACE inhibitor occur 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 (see also sections "Contraindications" and "Special Instructions").

Breastfeeding period.

Captopril is contraindicated during breastfeeding.

Ability to influence reaction speed when driving vehicles or other mechanisms

Caution is required when driving vehicles or performing other work that requires increased attention, as a decrease in reaction speed is possible, especially at the beginning of treatment or when changing the dosage of the drug, as well as with simultaneous use of alcohol-containing substances. Such effects manifest themselves individually and depend on the characteristics of the patient's body.

Method of administration and doses

The dosage should be adjusted depending on the nature of the patient's disease.

Captopril is taken orally before, during or after meals. The drug should be taken regularly, at the same time each day. If a tablet is missed, it should be taken as soon as possible; however, if it is several hours before the next dose, it is recommended to take the next dose as scheduled and not take the missed dose. You should not take 2 doses of captopril at the same time.

If it is necessary to prescribe captopril at a dose of 6.25 mg, the drug should be used in the appropriate dosage or in another dosage form.

Arterial hypertension.

The recommended initial dose is 25-50 mg/day in 2 divided doses daily. After 2-4 weeks of treatment, the dose can be titrated depending on the achieved blood pressure to 100-150 mg/day in 2 divided doses. Captopril can be used alone or with other antihypertensive drugs, especially thiazide diuretics. A once-daily dosing regimen can be used when a concomitant antihypertensive drug such as a thiazide diuretic is added.

In patients with increased RAAS activity (hypovolemia, renovascular hypertension, decompensated heart failure), it is advisable to start therapy with a single dose of 6.25 mg or 12.5 mg. The beginning of such treatment should be carried out under careful medical supervision with subsequent use of the drug 2 times a day. The dose can be gradually increased to 50 mg or 100 mg per day in 1 or 2 doses.

Heart failure.

The initial dose is 6.25-12.5 mg 2 or 3 times a day. Titration to a maintenance dose (75-150 mg per day) should be based on the patient's response to treatment (objective examination data and tolerability of the drug). The dose should be increased gradually, at intervals of at least 2 weeks in order to assess the patient's response to treatment. The maximum daily dose is 150 mg in 2 doses.

Short-term treatment. The drug should be used in the first 24 hours after myocardial infarction according to the following scheme: initial dose - 6.25 mg, after 2 hours - 12.5 mg and after 12 hours - another 25 mg of captopril. From the next day, for 4 weeks, captopril should be taken at a dose of 100 mg per day, divided into 2 doses. At the end of the 4-week treatment, the patient's condition should be re-evaluated to make a decision on treatment at the stage after myocardial infarction.

Long-term treatment. If captopril is not started within the first 24 hours of the acute myocardial infarction, it is recommended to start treatment between the third and sixteenth days after the infarction, once the necessary treatment conditions (stable haemodynamics and treatment of any residual ischaemia) have been established. Treatment should be initiated in hospital under close monitoring (particularly of blood pressure) until a dose of 75 mg/day is reached. The initial dose should be low (see section 4.4), particularly if the patient has normal or low blood pressure at the start of therapy. Treatment should be initiated with a dose of 6.25 mg, then increased to 12.5 mg 3 times a day for 2 days, then to 25 mg 3 times a day in the absence of adverse haemodynamic reactions. The recommended dose for effective cardioprotection during long-term treatment is 75-150 mg daily in 2 or 3 divided doses. In the case of symptomatic hypotension, as in heart failure, the dose of diuretics and/or other vasodilators can be reduced to achieve a stable dose of captopril. If necessary, the dose of captopril can be adjusted depending on the clinical response of the patient. Captopril can be used in combination with other treatments for myocardial infarction, such as thrombolytic agents, β-blockers and acetylsalicylic acid.

Diabetic nephropathy in patients with type 1 diabetes.

Captopril should be used at a dose of 75-100 mg per day in 2 divided doses, if necessary, combined with other antihypertensive drugs.

Kidney dysfunction.

Since captopril is mainly excreted by the kidneys, in case of impaired renal function, the dose of the drug should be reduced or the interval between its administration should be increased. If concomitant diuretic therapy is required, loop diuretics (furosemide) should be preferred over thiazides.

The following captopril dosage regimen is recommended for patients with impaired renal function to prevent its accumulation in the body.

Children.

The efficacy and safety of Captopril in children have not been sufficiently studied. The use of Captopril in children should be initiated under close medical supervision. The initial dose of Captopril is 0.3 mg/kg body weight. For special groups of patients (children with renal insufficiency and in case of immaturity of the urinary system) the initial dose should be 0.15 mg/kg body weight. Usually Captopril is prescribed to children 3 times a day, but the interval between administrations should be selected individually, depending on the patient's response to the administration of the drug.

Elderly patients.

As with other antihypertensive drugs, captopril therapy should be initiated at a dose of 6.25 mg twice daily, since elderly patients may be more likely to have impaired renal function and other organ and system function. The dose should be titrated according to the blood pressure response to the drug, with the lowest dose required to adequately control blood pressure.

Children.

The efficacy and safety of captopril in children have not been sufficiently studied.

Captopril should be used in children only when absolutely necessary, as prescribed and under the close supervision of a doctor.

Overdose

Symptoms: severe hypotension, possible development of shock, stupor, bradycardia, electrolyte imbalance and renal failure.

Treatment: To prevent the absorption of a large dose of captopril, it is necessary to wash the stomach as soon as possible, use sorbents and sodium sulfate within 30 minutes after taking captopril. In case of symptoms of arterial hypotension, the patient should be placed in a horizontal position and immediately correct the plasma volume and salt balance.

In case of severe symptoms of overdose, the patient should be urgently hospitalized for intensive detoxification measures, including hemodialysis, and measures aimed at increasing the volume of circulating blood, normalizing the functions of the cardiovascular, respiratory and nervous systems, and restoring kidney function. It is necessary to avoid hemodialysis through high-performance membranes made of polyacrylonitrile metallosulfate (AN69), hemofiltration due to the possibility of developing anaphylactoid reactions. Peritoneal dialysis is ineffective.

Angiotensin II may be used. Bradycardia or excessive general reactions should be treated with atropine. Pacemaker use should be considered. Effective hemodialysis.

Side effects

Cardiovascular system: tachycardia, tachyarrhythmia, angina pectoris, hypotension, Raynaud's syndrome, hot flashes, facial pallor, cardiac arrest, cardiogenic shock, orthostatic hypotension, palpitations.

Respiratory system: dry, irritating (non-productive) cough and shortness of breath. Dry cough usually resolves within a few weeks after discontinuation of captopril treatment. Bronchospasm, rhinitis, allergic alveolitis/eosinophilic pneumonia may also occur.

On the part of the digestive tract: nausea, vomiting, stomach irritation, abdominal pain, diarrhea, constipation, dry mouth, stomatitis/apthous ulcers, glossitis, peptic ulcer, pancreatitis.

Hepatobiliary disorders: liver dysfunction, cholestasis, including jaundice, hepatitis, including necrotizing hepatitis, increased liver enzymes and bilirubin. Liver dysfunction usually resolves after discontinuation of captopril.

Nervous system: dizziness, headache, fatigue, asthenia, taste disturbance, drowsiness, paresthesia, cerebrovascular manifestations; ataxia, including stroke and loss of consciousness.

On the part of the blood system: neutropenia, in patients with autoimmune diseases - agranulocytosis, leukopenia, pancytopenia (especially in patients with impaired renal function), anemia (including aplastic and hemolytic), thrombocytopenia, lymphadenopathy, eosinophilia.

Immune system: autoimmune diseases and/or positive test for antinuclear antibodies.

Metabolic disorders: anorexia, acidosis, hypoglycemia.

Psychiatric: sleep disturbances, confusion, depression.

On the part of the organs of vision: blurred vision.

Skin changes: itching, rash, alopecia, angioedema (see section "Special warnings and precautions for use"), urticaria, Stevens-Johnson syndrome, erythema multiforme, photosensitivity, erythroderma, pemphigoid reactions and exfoliative dermatitis.

Musculoskeletal system: myalgia, arthralgia.

From the urinary system: renal dysfunction, including renal failure, polyuria, oliguria and frequent urination, nephrotic syndrome.

From the reproductive system: impotence, gynecomastia.

General disorders: chest pain, fatigue, weakness, fever.

Laboratory indicators: proteinuria, hyperkalemia, hyponatremia (most often observed when following a salt-free diet with simultaneous use of diuretics), increased levels of urea, creatinine and bilirubin in the blood serum, as well as a decrease in hemoglobin, hematocrit and an increase in the erythrocyte sedimentation rate, leukopenia, thrombocytopenia, eosinophilia, increased titer of antinuclear antibodies. Captopril may cause a false-positive result of urine analysis for acetone.

Angioedema of the face, eyelids, tongue, and peripheral edema occurred in approximately one in 1,000 patients.

Interstitial angioedema has been observed in patients treated with ACE inhibitors.

Expiration date

3 years.

Storage conditions

Store in the original packaging at a temperature not exceeding 25 ºС.

Keep out of reach of children.

Packaging

10 tablets in a blister; 2 or 6 blisters in a box.

Vacation category

According to the recipe.

Producer

"ASTRAPHARM" LLC.

Address

Ukraine, 08132, Kyiv region, Kyiv-Svyatoshynskyi district, Vyshneve, Kyivska st., 6.