Indapamide MV Stada, 30 pcs., 1.5 mg, extended-release film-coated tablets

Compound

Indapamide

Indapamide MV Stada

pharmachologic effect

Pharmacological action - hypotensive, diuretic.

Reduces the sensitivity of the vascular wall to norepinephrine and angiotensin II, promotes an increase in the synthesis of vasodilating PGs, reduces the influx of calcium ions into the smooth muscle cells of the vascular walls, inhibits the reabsorption of sodium, chlorine and water ions in the cortical segment of the nephron loop. Causes a decrease in the tone of the smooth muscles of the arteries, peripheral vascular resistance. In therapeutic doses, it has virtually no effect on lipid and carbohydrate metabolism. The hypotensive effect occurs only when blood pressure is initially elevated.

Interaction

When used simultaneously with potassium-sparing diuretics, hypokalemia or hyperkalemia may develop (especially in patients with diabetes mellitus and renal failure), with ACE inhibitors - the risk of developing hyponatremia increases, with iodine-containing radiocontrast agents - the risk of developing renal failure, with lithium preparations - the concentration of lithium in the blood increases. plasma, with cyclosporine - the content of creatinine in plasma increases.

NSAIDs, glucocorticoids, tetracosactide can reduce the hypotensive effect of indapamide, baclofen, tricyclic antidepressants such as imipramine - increase; amphotericin B (iv), corticosteroids (when used systemically), tetracosactide, laxatives that stimulate peristalsis may increase the risk of hypokalemia.

Astemizole, bepridil, erythromycin (iv), pentamidine, sultopride, terfenadine, vincamine, antiarrhythmic drugs (including quinidine, amiodarone, bretylium tosylate, etc.) may increase the risk of developing torsade de pointes.

Indapamide MV Stada tablet prolong release p o film 1.5 mg x30 (300482) Makis-Pharma

Trade name: Indapamide MR International name: Indapamide

Release form: modified-release film-coated tablets 1.5 mg (polyethylene bags, blister packs)

Composition: indapamide 1.5 mg

Pharmacological group: diuretic

Pharmacological group according to ATK: C03BA11 (Indapamide)

Pharmacological action: BMCC selective, vasodilating, hypotensive, diuretic,

Indications: Arterial hypertension.

Dosage regimen: Inside, preferably in the morning. For arterial hypertension, the initial dose is 1.25-2.5 mg (non-extended form) once a day or 1.5 mg (retard tablet) in the morning. If the effectiveness is insufficient, after 4-8 weeks it is advisable to add drugs with a different mechanism of action to therapy (increasing the dose is not advisable - in the absence of a significant increase in effect, an increase in side effects is observed).

Contraindications: Hypersensitivity, severe hepatic (including encephalopathy) and/or renal failure (anuria), hypokalemia. Acute cerebrovascular accident, decompensated diabetes mellitus with ketoacidosis - for high doses required for the treatment of edema syndrome. Lactose intolerance, galactosemia, glucose/galactose malabsorption syndrome - for dosage forms containing lactose.

Side effects: The incidence of side effects is dose-dependent. From the digestive system: when used at a dose of 1.25 mg: more than 5% - constipation or diarrhea, dyspepsia, nausea, abdominal pain. At a dose of 2.5-5 mg (additionally): more than 5% - vomiting, gastralgia, loss of appetite, dry mouth. From the nervous system: when used at a dose of 1.25 mg: more than 5% - asthenia, nervousness, less than 5% - headache, dizziness. At a dose of 2.5-5 mg (additionally): more than 5% - mild dizziness, drowsiness, vertigo, insomnia, depression, less than 5% of cases - increased fatigue, asthenia, lethargy, lethargy, malaise, muscle spasms, nervousness, tension, anxiety, irritability, agitation. From the senses: when used at a dose of 1.25 mg: more than 5% - conjunctivitis. At a dose of 2.5-5 mg (additionally): more than 5% - visual impairment. Other: when used at a dose of 1.25 mg: more than 5% - flu-like syndrome, chest pain, less than 5% - infections, back pain. At a dose of 2.5-5 mg (additionally): more than 5% - decreased potency and/or libido, rhinorrhea, increased sweating, loss of body weight, paresthesia in the extremities. From the respiratory system: when used at a dose of 1.25 mg: less than 5% - cough, pharyngitis, sinusitis, more than 5% - rhinitis. From the cardiovascular system: more than 5% - orthostatic hypotension, ECG changes (hypokalemia), arrhythmia, palpitations. From the urinary system: more than 5% - frequent infections, nocturia, polyuria. Allergic reactions: more than 5% - rash, urticaria, itching, vasculitis. Laboratory indicators: more than 5% - hyperuricemia, hyperglycemia, hyponatremia, hypochloremia, increased plasma urea nitrogen, hypercreatininemia, glucosuria, hypercalcemia. Overdose. Symptoms: nausea, vomiting, weakness, dysfunction of the gastrointestinal tract, water and electrolyte disturbances, in some cases - excessive decrease in blood pressure, respiratory depression. Patients with liver cirrhosis may develop hepatic coma. Treatment: gastric lavage, correction of water and electrolyte balance, symptomatic therapy. There is no specific antidote.

Pharmacodynamics: Antihypertensive agent (diuretic, vasodilator). Its pharmacological properties are similar to thiazide diuretics (impaired Na+ reabsorption in the cortical segment of the loop of Henle). Increases urinary excretion of Na+, Cl- and, to a lesser extent, K+ and Mg2+. Having the ability to selectively block “slow” calcium channels, it increases the elasticity of arterial walls and reduces peripheral vascular resistance. Helps reduce LV hypertrophy of the heart. Does not affect the content of lipids in plasma (TG, LDL, HDL), does not affect carbohydrate metabolism (including in patients with concomitant diabetes mellitus). Reduces the sensitivity of the vascular wall to norepinephrine and angiotensin II, stimulates the synthesis of PgE2 and prostacyclin PgI2, reduces the production of free and stable oxygen radicals. When prescribed in high doses, it does not affect the degree of reduction in blood pressure, despite an increase in diuresis. After multiple doses, the therapeutic effect is observed after 1-2 weeks, reaches a maximum at 8-12 weeks and lasts up to 8 weeks; after taking a single dose, the maximum effect is observed after 24 hours.

Pharmacokinetics: Rapidly and completely absorbed from the gastrointestinal tract, bioavailability is high. Eating slightly slows down the rate of absorption, but does not affect the final amount of the drug absorbed. TCmax - 1-2 hours after taking the usual dosage form and 12 hours after taking retard tablets. Cmax after oral administration at a dose of 5 mg is 260 ng/ml. With repeated doses, fluctuations in plasma concentrations of the drug in the interval between 2 doses decrease. Css is established after 7 days of regular use. Bonding with plasma proteins is 71-79%. It also binds to elastin of smooth muscles of the vascular wall. It has a high volume of distribution and passes through histohematic barriers (including placental). Metabolized in the liver. T1/2 - 14 hours, final T1/2 - 26 hours. 60-70% is excreted by the kidneys in the form of metabolites (about 5-7% is excreted unchanged), through the intestines - 20-23%. In patients with renal failure, pharmacokinetics do not change. Does not accumulate.

Special instructions: In patients taking cardiac glycosides, laxatives, against the background of hyperaldosteronism, as well as in the elderly, careful monitoring of K+ and creatinine levels is indicated. While taking indapamide, the concentration of K+, Na+, Mg2+ in plasma (electrolyte disturbances may develop), pH, concentration of glucose, uric acid and residual nitrogen should be systematically monitored. The most careful monitoring is indicated in patients with liver cirrhosis (especially with edema or ascites - the risk of developing metabolic alkalosis, which increases the manifestations of hepatic encephalopathy), ischemic heart disease, heart failure, as well as in the elderly. The high-risk group also includes patients with an increased QT interval on the ECG (congenital or developed against the background of any pathological process). The first measurement of K+ concentration in the blood should be performed within 1 week of treatment. Hypercalcemia while taking indapamide may be a consequence of previously undiagnosed hyperparathyroidism. In patients with diabetes mellitus, it is extremely important to control blood glucose levels, especially in the presence of hypokalemia. Significant dehydration can lead to the development of acute renal failure (decreased glomerular filtration rate). Patients need to compensate for water loss and carefully monitor renal function at the beginning of treatment. Indapamide may give a positive result during a doping test. Patients with arterial hypertension and hyponatremia (due to taking diuretics) need to stop taking diuretics 3 days before starting ACE inhibitors (if necessary, diuretics can be resumed a little later) or they are prescribed initial low doses of ACE inhibitors. May aggravate the course of SLE. Efficacy and safety in children have not been established. Carefully. Hyponatremia and other disorders of water-electrolyte metabolism, moderate liver and/or renal failure, ascites, ischemic heart disease, heart failure, prolongation of the QT interval, hyperuricemia (especially manifested by gout or urate nephrolithiasis), hyperparathyroidism, pregnancy, lactation, old age and age before 18 years old (lack of sufficient experience). Acute cerebrovascular accident, decompensated diabetes mellitus with ketoacidosis - for low doses required for the treatment of arterial hypertension. Category of action on the fetus. B

Interaction: Increases the concentration of Li+ in plasma (decreased urinary excretion), lithium has a nephrotoxic effect. Increases the risk of developing renal dysfunction when using iodine-containing contrast drugs in high doses (dehydration). Before using iodine-containing contrast drugs, patients need to restore fluid loss. Reduces the effect of indirect anticoagulants (coumarin or indanedione derivatives) due to an increase in the concentration of coagulation factors as a result of a decrease in BCC and an increase in their production by the liver (dose adjustment may be required). Strengthens the blockade of neuromuscular transmission that develops under the influence of non-depolarizing muscle relaxants. Saluretics (loop, thiazide), cardiac glycosides, GCS and MCS, tetracosactide, amphotericin B (iv), laxatives increase the risk of hypokalemia. When taken simultaneously with cardiac glycosides, the likelihood of developing digitalis intoxication increases, with Ca2+ drugs - hypercalcemia, and with metformin, lactic acidosis may worsen. Astemizole, intravenous erythromycin, pentamidine, sultopride, terfenadine, vincamine, class Ia (quinidine, disopyramide) and class III antiarrhythmic drugs (amiodarone, bretylium tosylate, sotalol) can lead to the development of arrhythmias due to the synergistic effect (extension) on the duration of the interval QT. NSAIDs, corticosteroids, tetracosactide, adrenergic stimulants reduce the hypotensive effect, baclofen enhances it. A combination with potassium-sparing diuretics may be effective in some categories of patients, however, the possibility of developing hypo- or hyperkalemia is not completely excluded, especially in patients with diabetes mellitus and renal failure. ACE inhibitors increase the risk of developing arterial hypotension and/or acute renal failure (especially with existing renal artery stenosis). Imipramine (tricyclic) antidepressants and antipsychotic drugs (neuroleptics) enhance the hypotensive effect and increase the risk of developing orthostatic hypotension. Cyclosporine increases the risk of developing hypercreatininemia.

Drug registration number: LS-000610

Date of registration (re-registration) of the drug: 05.08.2005

Directions for use and doses

Indapamide

Orally, once, in the morning, without chewing, with a sufficient amount of liquid. Daily dose - 1 tablet. (2.5 mg). If after 4–8 weeks of treatment the desired therapeutic effect is not achieved, it is not recommended to increase the dose of the drug (increasing the risk of side effects without enhancing the antihypertensive effect). Instead, it is recommended to include another antihypertensive drug that is not a diuretic in the drug treatment regimen.

In cases where treatment must be started with 2 drugs, the dose of Indapamide remains equal to 1 table. in the morning once a day.

Indapamide MV Stada

Orally, preferably in the morning, without chewing, with a sufficient amount of liquid. The daily dose of the drug is 1 table. (1.5 mg) once daily. Increasing the dose of the drug does not increase the hypotensive effect.

Instructions for use INDAPAMIDE PHARMLAND

In patients with hepatic impairment, thiazide-like diuretics may accelerate the development of hepatic encephalopathy. If symptoms of hepatic encephalopathy occur, indapamide should be discontinued immediately.

Water and electrolyte balance

Plasma sodium level:

Before starting treatment with the drug, and then regularly it is necessary to monitor the concentration of sodium in the serum. Any diuretic treatment can lead to low sodium levels with very serious consequences. A decrease in plasma sodium may initially be asymptomatic, so regular monitoring of sodium levels is required. In elderly people or in patients with cirrhosis of the liver, these studies should be performed more often.

Plasma potassium content:

Serum potassium should be monitored regularly during treatment. A decrease in potassium levels with possible subsequent hypokalemia is the main risk of taking thiazide and other diuretics based on it. Prevention of the risk of hypokalemia (<3.4 mmol/L) should be carried out in certain high-risk populations, for example, the elderly, people who are malnourished and/or taking multiple medications at the same time, cirrhotic patients with edema and ascites, patients with coronary vascular disease and hearts. In this situation, hypokalemia increases the cardiac toxicity of digitalis drugs and the risk of arrhythmias. Patients with a prolonged QT interval are also at risk, regardless of whether it is congenital or iatrogenic. Hypokalemia, as well as bradycardia, are a predisposing factor for the occurrence of severe arrhythmias, in particular the potentially fatal atrial flutter-fibrillation. In all of the above situations, more frequent monitoring of plasma potassium levels is necessary. The first measurement of plasma potassium should be performed in the first week of starting treatment. In case of hypokalemia, potassium deficiency should be compensated.

Plasma calcium content:

Thiazide and thiazide-like diuretics may reduce urinary calcium excretion, causing mild transient hypercalcemia. Severe hypercalcemia may result from unrecognized hyperparathyroidism. In this case, it is necessary to interrupt treatment and examine the patient for the function of the parathyroid glands.

Blood sugar level

In patients with diabetes mellitus, especially those with concomitant hypokalemia, it is necessary to monitor blood glucose levels.

Uric acid

Patients with hyperuricemia tend to have an increased frequency of gout attacks. If uric acid levels increase, dose adjustment is necessary.

Kidney function and diuretics

Thiazides and thiazide-like diuretic drugs are fully effective only in the case of normal renal function or only mild impairment (creatinine content below 25 mg/l, i.e. 220 mmol/l). Hypovolemia associated with fluid loss, which may occur at the beginning of diuretic treatment, leads to a decrease in glomerular filtration, which in turn causes an increase in serum urea and creatinine concentrations. Such transient functional renal failure passes without consequences in patients with normal renal function, but at the same time it can aggravate existing renal failure.

Athletes

The drug may cause false-positive anti-doping test results in athletes.

Impact on the ability to drive vehicles and machinery

While taking Indapamide Pharmland, especially at the beginning of treatment or when prescribing another antihypertensive drug for combination treatment, symptoms associated with a drop in blood pressure may occur. In such a situation, the ability to drive vehicles and maintain machinery may be impaired.

special instructions

If hepatic encephalopathy develops (in patients with liver failure), the drug should be stopped immediately.

Before starting a study of parathyroid function, diuretics should be discontinued.

Against the background of indapamide, a positive result of doping control in athletes is possible.

When blood pressure decreases (especially with combined antihypertensive therapy), psychomotor reactions may decrease in some patients, which may affect the ability to drive vehicles and machines.

Indapamide MV (tablets)

Liver dysfunction

When prescribing thiazide and thiazide-like diuretics in patients with impaired liver function, hepatic encephalopathy may develop, especially in the case of electrolyte imbalance. In this case, diuretics should be stopped immediately.

Photosensitivity

While taking thiazide and thiazide-like diuretics, cases of photosensitivity reactions have been reported (see section “Side effects”). If photosensitivity reactions develop while taking the drug, treatment should be discontinued. If it is necessary to continue diuretic therapy, it is recommended to protect the skin from exposure to sunlight or artificial ultraviolet rays.

Water and electrolyte balance

Content of sodium ions in blood plasma

Before starting treatment, it is necessary to determine the content of sodium ions in the blood plasma.

While taking the drug, this indicator should be regularly monitored. Constant monitoring of the content of sodium ions is necessary, since initially a decrease in sodium concentration in the blood plasma may not be accompanied by the appearance of pathological symptoms. The most careful monitoring of sodium levels is necessary for patients with liver cirrhosis and elderly patients (see sections “Side effects” and “Overdose”).

All diuretic drugs can cause hyponatremia, sometimes leading to extremely serious consequences. Hyponatremia and hypovolemia can lead to dehydration and orthostatic hypotension. A concomitant decrease in chloride ions can lead to secondary compensatory metabolic alkalosis: the frequency and severity of this effect are insignificant.

Content of potassium ions in blood plasma

When treating with thiazide and thiazide-like diuretics, the main risk is a decrease in the concentration of potassium in the blood plasma and the development of hypokalemia. It is necessary to prevent the risk of developing hypokalemia (potassium content less than 3.4 mmol/l) in patients at high risk in the following categories: elderly, debilitated and/or receiving concomitant drug therapy, patients with liver cirrhosis, peripheral edema and ascites, coronary heart disease, heart failure. Hypokalemia in patients of these groups increases the toxic effect of cardiac glycosides and increases the risk of developing arrhythmias.

In addition, patients with an increased QT interval, both congenital and drug-induced, are at increased risk.

Hypokalemia, as well as bradycardia, is a condition that contributes to the development of severe arrhythmias and, especially, polymorphic ventricular tachycardia of the “pirouette” type, which can be fatal. In all the cases described above, it is necessary to regularly monitor the concentration of potassium in the blood plasma. The first measurement of the concentration of potassium ions in the blood must be carried out within the first week from the start of treatment. If hypokalemia occurs, appropriate treatment should be prescribed.

Calcium content in blood plasma

It should be borne in mind that thiazide and thiazide-like diuretics can reduce the excretion of calcium ions by the kidneys, leading to a slight and temporary increase in the concentration of calcium in the blood plasma. Severe hypercalcemia may be a consequence of previously undiagnosed hyperparathyroidism.

Diuretics should be discontinued before testing parathyroid function.

Plasma glucose levels

It is necessary to monitor blood glucose concentrations in patients with diabetes mellitus, especially in the presence of hypokalemia.

Uric acid

In patients with gout, the frequency of attacks may increase or the course of gout may worsen.

Diuretics and kidney function

Thiazide and thiazide-like diuretics are fully effective only in patients with normal or slightly impaired renal function (plasma creatinine concentration in adult patients below 25 mg/l or 220 µmol/l). In elderly patients, the concentration of creatinine in blood plasma is calculated taking into account age, body weight and gender.

It should be taken into account that at the beginning of treatment, patients may experience a decrease in glomerular filtration rate due to hypovolemia, which, in turn, is caused by the loss of fluid and sodium ions while taking diuretic drugs. As a result, the concentration of urea and creatinine in the blood plasma may increase.

If renal function is not impaired, such temporary functional renal failure, as a rule, passes without consequences, however, with existing renal failure, the patient's condition may worsen.

Athletes

Indapamide may give a positive result during doping control in athletes.