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.

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.

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

UNDESIRABLE DRUG COMBINATIONS

Lithium preparations:

with the simultaneous use of indapamide and lithium preparations, as well as when following a salt-free diet, an increase in the concentration of lithium in the blood plasma may be observed due to a decrease in its excretion, accompanied by the appearance of signs of lithium overdose. If necessary, diuretics can be used in combination with lithium preparations, and the dose of the drugs should be carefully selected, regularly monitoring the concentration of lithium in the blood plasma.

DRUG COMBINATIONS REQUIRING SPECIAL ATTENTION

Drugs that can cause polymorphic ventricular tachycardia of the “pirouette” type:

• class IA antiarrhythmic drugs (quinidine, hydroquinidine, disopyramide);
• class III antiarrhythmic drugs (amiodarone, sotalol, dofetilide, ibutilide);
• some neuroleptics: phenothiazines (chlorpromazine, cyamemazine, levomepromazine, thioridazine, trifluoroperazine), benzamides (amisulpride, sulpiride, sultopride, tiapride), butyrophenones (droperidol, haloperidol);
• others: bepridil, cisapride, difemanil, erythromycin (iv), halofantrine, mizolastine, pentamidine, sparfloxacin, moxifloxacin, astemizole, vincamine (iv).

Increased risk of ventricular arrhythmias, especially polymorphic ventricular tachycardia of the “pirouette” type (risk factor - hypokalemia).

The concentration of potassium in the blood plasma should be determined and, if necessary, adjusted before starting combination therapy with indapamide with the above drugs. It is necessary to monitor the patient’s clinical condition, monitor the content of blood plasma electrolytes, and ECG indicators.

In patients with hypokalemia, it is necessary to use drugs that do not cause polymorphic ventricular tachycardia of the “pirouette” type.

Nonsteroidal anti-inflammatory drugs (when administered systemically), including selective COX-2 inhibitors, high doses of acetylsalicylic acid (≥ 3 g/day):

the antihypertensive effect of indapamide may be reduced.

There is a risk of developing acute renal failure due to decreased glomerular filtration. Patients need to compensate for fluid loss and carefully monitor renal function at the beginning of treatment.

Angiotensin-converting enzyme (ACE) inhibitors:

Prescribing ACE inhibitors to patients with an initially reduced concentration of sodium ions in the blood (especially patients with renal artery stenosis) is accompanied by a risk of sudden arterial hypotension and/or acute renal failure.

Patients with arterial hypertension and possibly reduced sodium ion content in the blood plasma due to diuretics should:

• 3 days before starting treatment with an ACE inhibitor, stop taking diuretics. In the future, if necessary, taking a non-potassium-sparing diuretic can be resumed;
• or begin ACE inhibitor therapy with low doses, followed by a gradual increase in dose if necessary.

In chronic heart failure, treatment with ACE inhibitors should begin with the lowest doses, with a possible preliminary reduction in the doses of diuretics. In all cases, in the first weeks of taking ACE inhibitors in patients, it is necessary to monitor renal function (plasma creatinine content).

Other drugs that can cause hypokalemia: amphotericin B (iv), gluco- and mineralocorticosteroids (when administered systemically), tetracosactide, laxatives that stimulate intestinal motility:

increased risk of hypokalemia (additive effect).

Regular monitoring of potassium levels in the blood plasma is necessary and, if necessary, its correction. Particular attention should be paid to patients concomitantly receiving cardiac glycosides. It is recommended to use laxatives that do not stimulate intestinal motility.

Baclofen:

it is possible to enhance the antihypertensive effect.

Patients need to compensate for fluid loss and carefully monitor renal function at the beginning of treatment.

Cardiac glycosides:

hypokalemia enhances the toxic effect of cardiac glycosides.

With the simultaneous use of indapamide and cardiac glycosides, the content of potassium in the blood plasma, ECG parameters should be monitored, and, if necessary, therapy should be adjusted.

COMBINATION OF DRUGS REQUIRING ATTENTION

Potassium-sparing diuretics (amiloride, spironolactone, triamterene):

simultaneous administration of indapamide with potassium-sparing diuretics is advisable in some patients, however, the possibility of developing hypokalemia or hyperkalemia cannot be excluded (especially in patients with diabetes mellitus and renal failure).

It is necessary to monitor the concentration of potassium in the blood plasma, ECG indicators and, if necessary, adjust therapy.

Metformin

: functional renal failure, which can occur while taking diuretics, especially loop diuretics, with simultaneous administration of metformin increases the risk of developing lactic acidosis.

Metformin should not be used if the creatinine concentration exceeds 15 mg/L (135 µmol/L) in men and 12 mg/L (110 µmol/L) in women.

Iodinated contrast agents:

Dehydration of the body while taking diuretics increases the risk of developing acute renal failure, especially when using high doses of iodine-containing contrast agents.

Before using iodinated contrast agents, patients need to compensate for fluid loss.

Tricyclic antidepressants, antipsychotics (neuroleptics):

drugs of these classes enhance the antihypertensive effect of indapamide and increase the risk of orthostatic hypotension (additive effect).

Calcium salts:

with simultaneous administration, hypercalcemia may develop due to a decrease in the excretion of calcium ions by the kidneys.

Cyclosporine tacrolimus:

it is possible to increase the creatinine content in the blood plasma without changing the concentration of circulating cyclosporine, even with normal fluid and sodium ion levels.

Corticosteroids (mineral and glucocorticosteroids), tetracosactide (if administered systemically):

decreased antihypertensive effect (retention of fluid and sodium ions as a result of the action of corticosteroids).

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.

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

If you are taking any other medications, you should consult your doctor before starting treatment. Not recommended combinations When used simultaneously with lithium preparations, it is possible to increase the concentration of lithium ions in the blood plasma due to a decrease in its excretion from the body by the kidneys, accompanied by the appearance of signs of overdose (nephrotoxic effect), as well as when following a salt-free diet (decreased excretion of lithium ions by the kidneys). In case of simultaneous use with lithium preparations, careful monitoring of the concentration of lithium in the blood plasma and dosage adjustment are necessary. Combinations that require special attention Drugs that, when used simultaneously with them, increase the likelihood of ari (“torsades de pointes”): class IA antiarrhythmics (quinidine, hydroquinidine, disopyramide), class III antiarrhythmics (amiodarone, dofetilide, ibutilide, bretylium tosylate) , sotalol, some antipsychotics: phenothiazines (chlorpromazine, cyamemazine, levomepromazine, thioridazine, trifluoperazine), benzamides (amisulpride, sulpiride, sultopride, tiapride), butyrophenones (droperidol, haloperidol), others (bepridil, cisapride, difemanil, erythromycin (intravenous administration ( iv)), halofantrine, mizolastine, pentamidine, sparfloxacin, moxifloxacin, vincamine (iv), astemizole. Concomitant use with any of these drugs, especially against the background of hypokalemia, increases the risk of ventricular arrhythmias. Before starting combination therapy with indapamide and Using the above drugs, the potassium content in the blood plasma should be monitored and, if necessary, adjusted. It is recommended to monitor the patient’s clinical condition, as well as the content of electrolytes in the blood plasma and ECG. In patients with hypokalemia, it is necessary to use drugs that do not provoke the development of arrhythmias. With the simultaneous administration of nonsteroidal anti-inflammatory drugs (NSAIDs) (for systemic use), including selective cyclooxygenase-2 (COX-2) inhibitors, high doses of salicylic acid (3 g/day or more), it is possible: a decrease in the antihypertensive effect of indapamide, the development of acute renal failure in dehydrated patients (due to decreased glomerular filtration rate). At the beginning of indapamide therapy, it is necessary to restore water and electrolyte balance and monitor renal function. Angiotensin-converting enzyme (ACE) inhibitors, when used concomitantly with indapamide in patients with hyponatremia (especially in patients with renal artery stenosis), increase the risk of sudden arterial hypotension and/or acute renal failure. Patients with arterial hypertension and a reduced content of sodium ions in the blood plasma due to diuretics should stop taking diuretics 3 days before starting treatment with ACE inhibitors. In the future, if necessary, resume taking diuretics. Therapy with ACE inhibitors should be started with low doses, followed by a gradual increase in dose if necessary. In chronic heart failure, treatment should begin with low doses of ACE inhibitors, after first reducing the dose of diuretics. In all cases, in the first week of taking ACE inhibitors, it is necessary to monitor renal function (plasma creatinine content). Drugs that increase the risk of hypokalemia: amphotericin B (iv); gluco- and mineralocorticosteroids (if administered systemically), tetracosactide, laxatives that stimulate intestinal motility. When taken simultaneously with indapamide, the above drugs increase the risk of developing hypokalemia (additive effect). If necessary, the content of potassium ions in the blood plasma should be monitored and adjusted. Simultaneous therapy with baclofen enhances the antihypertensive effect of indapamide. Cardiac glycosides: hypokalemia increases the toxic effect of cardiac glycosides (glycoside intoxication). With the simultaneous use of indapamide and cardiac glycosides, the content of potassium ions in the blood plasma, ECG parameters should be monitored, and, if necessary, therapy should be adjusted. A combination with potassium-sparing diuretics (amiloride, spironolactone, triamterene) may be effective in some patients, however, the possibility of developing hypo- or hyperkalemia is not completely excluded, especially in patients with diabetes mellitus and renal failure. In such cases, the level of potassium in the blood plasma, ECG parameters should be monitored and, if necessary, therapy should be adjusted. With the simultaneous use of diuretics and metformin, the appearance of lactic acidosis is possible, which is apparently associated with the development of functional renal failure caused by the action of diuretics (mostly “loop”). It is not recommended to use metformin in combination with indapamide if the creatinine level is more than 15 mg/l (135 µmol/l) in men and 12 mg/l (110 µmol/l) in women. When using iodine-containing radiocontrast agents, it should be borne in mind that the diuretic effect of indapamide increases the risk of developing renal failure. This risk is especially high when using iodinated contrast agents in high doses. Before using iodine-containing radiocontrast agents, patients need to restore fluid loss. Tricyclic antidepressants and antipsychotics enhance the hypotensive effect and increase the risk of developing orthostatic hypotension (additive effect). Preparations containing calcium salts increase the risk of developing hypercalcemia due to decreased excretion of calcium ions by the kidneys. With the simultaneous use of cyclosporine and tacrolimus, an increase in the content of creatinine in the blood plasma is possible (without changing the concentration of circulating cyclosporine), which is observed even with normal levels of water and sodium ions. Glucocorticosteroid drugs, tetracosactide (when used systemically) reduce the hypotensive effect (sodium and fluid retention). 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 circulating blood volume 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.

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.