Indap, capsules 2.5mg 30 pcs

Indapamide is diuretic, antihypertensive, vasodilator.

Pharmacodynamics

Indapamide belongs to the group of non thiazide sulfonamides, with pharmacological properties similar to thiazide-like diuretics. It reduces the tone of arterial smooth muscle and decreases the RPS. It has moderate saluretic and diuretic effects which are associated with blockade of reabsorption of sodium, chloride, hydrogen and, to a lesser extent, potassium ions in proximal tubules and cortical segment of distal renal tubules. Having the ability to selectively block slow calcium channels, increases the elasticity of arterial walls and reduces ROS. Helps reduce left ventricular hypertrophy. It does not affect plasma lipid content (triglycerides, LDL, HDL), does not affect carbohydrate metabolism (including in patients with concomitant diabetes mellitus). The reduction of OPPS is also caused by decrease of sensitivity of vascular wall adrenoreceptors to noradrenaline and angiotensin II, increase of TG synthesis, which has vasodilator activity (PGE₂ and prostacyclin – PGI₂). Reduces the production of free and stable oxygen radicals.

When administered in high doses, it does not affect the degree of BP reduction, despite an increase in diuresis. Antihypertensive effect appears by the end of the 1st week, lasts for 24 hours after single use, and achieves its maximum after 8-12 weeks after the beginning of the drug.

Pharmacokinetics

Indapamide is quickly and completely absorbed from the gastrointestinal tract after oral administration; bioavailability is high (93%). Food intake slightly slows down the rate, but does not affect the completeness of absorption. After oral administration at a dose of 2.5 mg, T_max is 1-2 hours. Binding to plasma proteins is about 75%. It also binds with elastin of smooth muscles of the vascular wall. It has high V_d, passes through histohematic barriers (including placental), penetrates into breast milk.

Metabolized in the liver. T_1/2 averages 14-18 h. It is excreted mainly through the kidneys – 60-80% (in most cases – as metabolites, 5% – unchanged), through the intestines – 20-23%. Pharmacokinetics does not change in patients with renal insufficiency. It does not cumulate.

Indications

Arterial hypertension; sodium and water retention in chronic heart failure.

Active ingredient

Composition

1 capsule contains:

Active ingredient:

Indapamide 2.5 mg;

Associates:

MCC granulated;

lactose monohydrate;

corn starch;

magnesium stearate;

colloidal silicon dioxide;

titanium dioxide;

gelatin;

Indigo carmine dye

How to take, the dosage

Overly, in the morning, regardless of meals, swallow capsule without chewing, with water. The dose is 2.5 mg/day (1 capsule).

The drug may be used as monotherapy or in combination with other antihypertensive agents (β-adrenoblockers, BKK, ACE inhibitors). If the desired therapeutic effect is not achieved after 4 to 8 weeks of treatment, it is not recommended to increase the drug dose (the risk of side effects increases without increasing the antihypertensive effect). Instead, it is reasonable to add another antihypertensive drug, which is not a diuretic, to the treatment regimen. In cases where treatment must be initiated with 2 drugs, the dose of Indap® remains 2.5 mg/day in the morning.

Interaction

Indapamide and lithium preparations should not be used concomitantly (because of the possibility of development of toxic effects of lithium due to decrease of its renal clearance).

Co-administration of indapamide with astemizole, erythromycin (IV), sultopride, terfenadine, vincamine, Class Ia (quinidine, disopyramide) and Class III antiarrhythmic agents (amiodarone, sotalol) may weaken the hypotensive effect of indapamide and lead to “pirouette” arrhythmia due to synergistic effect (prolongation) on QT interval length.

NSAIDs, GCS, adrenostimulants decrease the hypotensive effect, baclofen increases it.

Saluretics (loop, thiazide), cardiac glycosides, gluco- and mineralocorticosteroids, laxatives, amphotericin B (IV) increase the risk of hypokalemia.

Concomitant administration with cardiac glycosides increases the likelihood of digitalis intoxication; with calcium preparations – hypercalcemia; with metformin – possible aggravation of lactic acidosis.

The combination with potassium-saving diuretics may be effective in some patients; however, the possibility of hypo- or hyperkalemia cannot be completely excluded, especially in patients with diabetes and renal insufficiency.

The ACE inhibitors increase the risk of arterial hypotension and/or acute renal failure (especially if there is renal artery stenosis).

Indapamide increases the risk of renal failure when using iodine-containing contrast agents in high doses with dehydration. Patients should restore fluid loss before using iodine-containing contrast agents.

Tricyclic antidepressants and antipsychotics may increase the antihypertensive effect of the drug and increase the risk of orthostatic hypotension.

Concomitant use with cyclosporine may increase plasma creatinine levels.

Decreases the effect of indirect anticoagulants (coumarin or indandion derivatives) due to the increased concentration of clotting factors as a result of decrease of the RBC and their increased production by the liver (dose adjustment may be required).

It increases the blockade of neuromuscular transmission that develops under the influence of nondepolarizing myorelaxants.

Special Instructions

When the drug is prescribed to patients taking cardiac glycosides, laxatives against a background of hyperaldosteronism, as well as the elderly, regular monitoring of potassium ions and creatinine levels is indicated.

The plasma concentrations of potassium ions, sodium ions, magnesium ions should be monitored regularly while taking indapamide (electrolyte disturbances may develop), pH, concentration of glucose, uric acid, and residual nitrogen.

The most careful control is indicated in patients with cirrhosis (especially with edema or ascites because of the risk of metabolic alkalosis, which worsens manifestations of hepatic encephalopathy), as well as in CHD, heart failure and the elderly. Patients with prolonged QT interval on ECG (congenital or developed against a background of some pathological process) are also at high risk. The first determination of potassium ion concentration in blood should be made during the first week of using the drug.

Hypercalcemia with indapamide may be due to previously undiagnosed hyperparathyroidism.

In diabetic patients it is extremely important to monitor blood glucose levels, especially if hypokalemia is present.

Significant dehydration can lead to acute renal failure (decreased glomerular filtration). Patients should compensate for water loss and carefully monitor renal function at the beginning of treatment.

Indapamide may give a positive result in doping control.

Patients with arterial hypertension and hyponatremia (due to diuretics) should discontinue diuretics 3 days before starting ACE inhibitors (diuretics may be resumed somewhat later if necessary), or ACE inhibitors are prescribed at low initial doses.

When prescribing indapamide, it should be borne in mind that sulfonamide derivatives may aggravate systemic lupus erythematosus.

Contraindications

Side effects

Digestive system disorders: nausea, discomfort or pain in the epigastrium may occur.

CNS disorders: weakness, fatigue, dizziness, nervousness are possible.

Cardiovascular system disorders: orthostatic hypotension is possible.

Metabolism: hypokalemia, hyperuricemia, hyperglycemia, hyponatremia, hypochloremia are possible.

Allergic reactions: skin manifestations are possible.

Overdose

Symptoms: nausea, vomiting, weakness, GI dysfunction, abnormal water-electrolyte balance, in some cases – excessive decrease of BP, respiratory depression. Patients with liver cirrhosis may develop hepatic coma.

Treatment: gastric lavage, correction of water-electrolyte balance; symptomatic therapy if necessary. There is no specific antidote.

Similarities