Indapamide MB Stada sustained release pills 1.5mg, 30pcs

Composition

1 tablet contains:

Active ingredient:  

Indapamide – 1.5 mg;

Auxiliary substances:  

Hypromellose (hypromellose 4000) — 42-78.4 mg;

Lactose monohydrate — 168.5-132.1 mg;

Colloidal silicon dioxide (aerosil) — 1 mg;

Magnesium stearate — 2 mg;

Shell:  

Hypromellose (hydroxypropylmethylcellulose) — 5.94 mg;

Macrogol (polyethylene glycol 4000) — 1.29 mg;

Talcum powder — 0.462 mg.

Titanium dioxide — 1.29 mg;

Dye tropeolin O-0,018 mg

Pharmacological action

Antihypertensive agent (diuretic, vasodilator)Pharmacological properties are similar to thiazide diuretics (it violates the reabsorption of sodium ions in the cortical segment of the Henle loop). Increases urinary excretion of sodium, chlorine and, to a lesser extent, potassium and magnesium ions, which is accompanied by increased diuresis. Having the ability to selectively block “slow” calcium channels, it increases the elasticity of arterial walls and reduces total peripheral vascular resistance. Helps to reduce hypertrophy of the left ventricle of the heart. It does not affect the content of lipids in blood plasma (triglycerides, low-density lipoproteins, high-density lipoproteins); it does not affect carbohydrate metabolism (including in patients with diabetes mellitus). Reduces the sensitivity of the vascular wall to norepinephrine and angiotensin II, stimulates the synthesis of prostaglandin E2 and prostacyclin PGI2, reduces the production of free and stable oxygen radicals. Indapamide has a hypotensive effect in doses that do not have a pronounced diuretic effect. The hypotensive effect develops by the end of the first week, persists for 24 hours against the background of a single dose. Pharmacokineticsafter oral use, it is rapidly and completely absorbed from the gastrointestinal tract; bioavailability is high (93%). Food intake slightly slows down the rate of absorption, but does not affect the amount of absorbed substance. The maximum concentration in blood plasma is reached 12 hours after ingestion. With repeated doses, fluctuations in the concentration of the drug in blood plasma in the interval between two doses are reduced. The equilibrium concentration is established after 7 days of regular use. The elimination half-life is 18 hours, and the binding to plasma proteins is about 79%. It also binds to the smooth muscle elastin of the vascular wall. It has a high volume of distribution, passes through histohematic barriers (including placental), and penetrates into breast milk. It is metabolized in the liver. 60-80% is excreted by the kidneys in the form of metabolites (about 5% is excreted unchanged), and 20% is excreted through the intestines. In patients with renal insufficiency, the pharmacokinetics do not change. It doesn’t accumulate.

Active ingredients

Indapamide

Indications

Arterial hypertension.

Individual component incompatibility.

Chronic heart failure.

Use during pregnancy and lactation

Indapamide MV is not recommended during pregnancy and lactation.

Contraindications

Hypersensitivity to indapamide and other sulfonamide derivatives, severe renal failure (anuria stage), severe hepatic insufficiency( including encephalopathy), hypokalemia; pregnancy, lactation; age up to 18 years (efficacy and safety have not been established); lactose intolerance, galactosemia, glucose/galactose malabsorption syndrome (the drug contains lactose). With caution: Impaired liver and/or kidney function, impaired water-electrolyte balance, hyperparathyroidism; prolongation of the QT interval or simultaneous use of drugs that prolong the QT interval(see “Interaction with other drugs”); diabetes mellitus in the decompensation stage, hyperuricemia (especially accompanied by gout and urate nephrolithiasis). If you have one of these diseases, be sure to consult your doctor before taking the drug.

Side effects

Determination of the frequency of adverse reactions: very often-10% or more; often-1% or more, less than 10%; infrequently-0.1% or more, less than 1%; rarely-0.01% or more, less than 0.1%; very rarely-less than 0.01%. From the cardiovascular system: very rarely — arrhythmia, orthostatic hypotension, palpitations, changes in the electrocardiogram (ECG) characteristic of hypokalemia. Hematopoietic disorders: very rare — thrombocytopenia, leukopenia, agranulocytosis, aplastic anemia, hemolytic anemia, bone marrow aplasia. From the central and peripheral nervous system: rarely-dizziness, headache, paresthesia, increased excitability, asthenia, drowsiness, vertigo, insomnia, depression, increased fatigue, malaise, spasm of the muscles of the extremities, tension, irritability, anxiety. Patients with hepatic insufficiency may develop hepatic encephalopathy. From the digestive system: infrequently-vomiting; rarely-nausea, constipation, dryness of the oral mucosa; very rarely-pancreatitis, anorexia, abdominal pain, diarrhea. From the genitourinary system: very rarely — renal failure, nocturia, infections, polyuria. From the respiratory system: cough, pharyngitis, sinusitis, rhinitis. Allergic reactions: often-macular-papular rash; infrequently-purpura, very rarely-angioedema and / or urticaria, hemorrhagic vasculitis, toxic epidermal necrolysis, Stevens-Johnson syndrome, pruritus. Other: some reports — exacerbation of systemic lupus erythematosus( SLE), photosensitivity reactions. Laboratory data: reduced potassium levels and the development of hypokalemia (especially pronounced in patients at risk). In clinical studies, hypokalemia (blood plasma potassium content less than 3.4 mmol/l) was observed in 10% of patients and 3.2 mmol/l in 4% of patients after 4-6 weeks of treatment. After 12 weeks of therapy, the potassium content in the blood plasma decreased by an average of 0.23 mmol/l. Very rarely — hypercalcemia; hyponatremia is possible, accompanied by hypovolemia and orthostatic hypotension. Simultaneous loss of chlorine ions can lead to compensatory metabolic alkalosis, but the frequency of development of metabolic alkalosis and its severity are insignificant; hyperuricemia and hyperglycemia (unspecified frequency), increased blood urea nitrogen concentration, hypercreatininemia, glucosuria. If any of the above side effects get worse or you notice any other side effects that are not listed in the instructions, tell your doctor.

Interaction

If you are taking any other medications, you should consult your doctor before starting treatment. Not recommended combinations When used concomitantly with lithium preparations, it is possible to increase the concentration of lithium ions in 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 with a salt-free diet (reduced excretion of lithium ions by the kidneys). In the 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 attentionpreparations that, when used simultaneously, increase the likelihood of arrhythmias of the “pirouette” type (“torsades de pointes”): Class IA antiarrhythmics (quinidine, hydroquinidine, disopyramide), class III antiarrhythmics (amiodarone, dofetilide, ibutilide, bretilia tosylate), sotalol, some neuroleptics: phenothiazines (chlorpromazine, cyamemazine, levomepromazine, thioridazine, trifluoperazine), benzamides (amisulpride, sulpiride, sultoprid, tiaprid), butyrophenones (droperidol, haloperidol), other (bepridil, cisaprid, difemanil, erythromycin (intravenous use (iv)), halofantrin, 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 of the “pirouette”type. Before starting combination therapy with indapamide and the above drugs, the potassium content in the blood plasma should be monitored and adjusted if necessary. It is recommended to monitor the patient’s clinical condition, as well as the content of blood plasma electrolytes and ECG. In patients with hypokalemia, it is necessary to use drugs that do not provoke the development of arrhythmia of the “pirouette”type. Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) (with systemic use), including selective cyclooxygenase-2 (COX-2) inhibitors, high doses of salicylic acid (3 g / day or more), may reduce the antihypertensive effect of indapamide, the development of acute renal failure in dehydrated patients (due to a decrease in glomerular filtration rate). At the beginning of indapamide therapy, it is necessary to restore the water-electrolyte balance and monitor kidney function. Angiotensin-converting enzyme (ACE) inhibitors used concomitantly with indapamide in patients with hyponatremia (especially in patients with renal artery stenosis) increase the risk of developing sudden arterial hypotension and/or acute renal failure. Patients with arterial hypertension and reduced levels 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, the use of diuretics should be resumed. ACE inhibitor therapy should be initiated at low doses, followed by a gradual increase in the dose if necessary. In patients with chronic heart failure, treatment should begin with low doses of ACE inhibitors, first reducing the dose of diuretics.In all cases, renal function (plasma creatinine) should be monitored during the first week of ACE inhibitor therapy. Drugs that increase the risk of hypokalemia: amphotericin B (IV); gluco-and mineralocorticosteroids (with systemic use), tetracosactide, laxatives that stimulate intestinal motility. Concomitant use of the above drugs with indapamide increases the risk of hypokalemia (additive effect). If necessary, the content of potassium ions in the blood plasma should be monitored and corrected. Concomitant therapy with baclofen enhances the antihypertensive effect of indapamide. Cardiac glycosides: hypokalemia increases the toxic effect of cardiac glycosides (glycoside intoxication). When using indapamide and cardiac glycosides simultaneously, the content of potassium ions in blood plasma, ECG indicators should be monitored, and, if necessary, therapy should be adjusted. Combination with potassium-sparing diuretics (amiloride, spironolactone, triamterene) may be effective in some patients, however, the possibility of hypo – or hyperkalemia is not completely excluded, especially in patients with diabetes mellitus and renal insufficiency. In such cases, the level of potassium in the blood plasma, ECG parameters should be monitored and, if necessary, therapy should be adjusted. Concomitant use of diuretics and metformin may cause lactic acidosis, which is probably associated with the development of functional renal failure due to the action of diuretics (mostly “loop”). It is not recommended to use metformin in combination with indapamide if the creatinine level exceeds 15 mg / l (135 mmol/l) in men and 12 mg/l (110 mmol/l) for women. When using iodine-containing radiopaque drugs, 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 iodine-containing radiopaque substances in high doses. Before using iodine-containing radiopaque substances, patients need to restore fluid loss. Tricyclic antidepressants and neuroleptics enhance the hypotensive effect and increase the risk of orthostatic hypotension (additive effect). Preparations containing calcium salts increase the risk of hypercalcemia due to a decrease in the excretion of calcium ions by the kidneys. Concomitant use of cyclosporine and tacrolimus may increase the level of creatinine in blood plasma (without changing the concentration of circulating cyclosporine), which is observed even with normal water and sodium ions. Glucorticosteroid drugs, tetracosactide (with systemic use) reduce the hypotensive effect (retention of sodium ions and fluid). Reduces the effect of indirect anticoagulants (coumarin or indandione derivatives) due to an increase in the concentration of clotting factors as a result of a decrease in the volume of circulating blood and an increase in their production by the liver (dose adjustment may be required). Increases the blockade of neuromuscular transmission, which develops under the influence of non-depolarizing muscle relaxants.

How to take, course of use and dosage

Tablets are taken orally at 1.5 mg 1 time a day (in the morning).

If the hypotensive effect is not sufficiently pronounced after 2 weeks of treatment, the dose is increased to 5-7.5 mg / day.

Maximum dose: 10 mg / day in 2 divided doses (in the morning).

Overdose

Symptoms:marked decrease in blood pressure, water and electrolyte disturbances (hyponatremia, hypokalemia), nausea, vomiting, convulsions, dizziness, drowsiness, lethargy, confusion, respiratory depression, polyuria or oliguria up to anuria (due to hypovolemia). Patients with cirrhosis of the liver may develop hepatic coma. Treatment:gastric lavage, correction of water-electrolyte balance, symptomatic therapy. There is no specific antidote.

Description

Round, biconvex tablets, film-coated in white or almost white color. On a cross-section, the core is white or almost white in color.

Complete set

Long-acting film-coated tablets,1.5 mg. 10 tablets in a contour cell package made of polyvinyl chloride film and aluminum foil printed varnished. 3 contour cell packages together with instructions for use in a cardboard pack.

Special instructions

In case of insufficient effectiveness, after 4-8 weeks it is advisable to add an antihypertensive drug with a different mechanism of action to the therapy. It is not recommended to increase the dose of the drug (in the absence of a significant increase in the hypotensive effect, the risk of side effects increases). In patients taking cardiac glycosides, laxatives, against the background of hyperaldosteronism, as well as in the elderly, regular monitoring of the content of potassium and creatinine ions is indicated. When taking indapamide, the concentration of potassium, sodium, and magnesium ions in the blood plasma should be systematically monitored (electrolyte disturbances may develop), pH, glucose, uric acid, and residual nitrogen concentrations. Determination of the sodium ion content in blood plasma is recommended before starting treatment. The first measurement of the concentration of potassium ions in the blood plasma should be carried out within the first week after the start of treatment. The most careful monitoring is indicated in patients with ischemic heart disease, heart failure, cirrhosis of the liver (especially with edema or ascites — the risk of developing metabolic alkalosis, increasing the manifestation of hepatic encephalopathy), weakened patients or receiving concomitant drug therapy. The high-risk group also includes patients with an extended QT interval on an electrocardiogram (congenital or developed against the background of some pathological process) and patients taking drugs that extend the QT interval, such as indapamide (see “Interaction with other drugs”). Thiazide diuretics may reduce urinary excretion of calcium ions, resulting in minor and temporary hypercalcemia. Severe hypercalcemia with indapamide may be a consequence of previously undiagnosed hyperparathyroidism. You should stop taking diuretic medications before examining the function of the parathyroid gland. When prescribing thiazide diuretics to patients with hepatic insufficiency, hepatic encephalopathy may develop. In such cases, the drug should be discontinued immediately. In patients with diabetes, it is extremely important to monitor blood glucose levels, especially in the presence of hypokalemia. Significant dehydration can lead to acute renal failure (decreased glomerular filtration rate). Patients need to compensate for water loss and carefully monitor kidney function at the beginning of treatment. Indapamide can give a positive result during doping control. In patients with high plasma uric acid levels, the incidence of gout attacks may increase with indapamide therapy. Sulfonamide derivatives can exacerbate the course of systemic lupus erythematosus (it is necessary to keep in mind when prescribing indapamide). Effects on the ability to drive vehicles and work with mechanisms: somnolence, dizziness, and other nervous system side effects may occur in some patients, mainly at the beginning of treatment or when another antihypertensive agent is added. If they occur, the patient should take special precautions when driving a vehicle and working with complex mechanisms.

Form of production

Long-acting film-coated tablets,1.5 mg. 10 tablets in a contour cell package made of polyvinyl chloride film and aluminum foil printed varnished. 3 contour cell packages together with instructions for use in a cardboard pack.

Storage conditions

Store in a dry place, protected from light, at a temperature not exceeding 25 ° C. Keep out of reach of children.

Shelf

life is 3 years. Do not use after the expiration date indicated on the package.

Active ingredient

Indapamide

Conditions of release from pharmacies

By prescription

Dosage form

long-acting tablets