Diroton Plus, 10 mg+1.5 mg, modified-release capsules, 28 pcs.: instructions for use, reviews and analogues, prices in pharmacies. Buy and deliver to the nearest pharmacy or home in Moscow. Etc

Diroton Plus, 10 mg+1.5 mg, modified release capsules, 28 pcs.

Indapamide

When thiazide and thiazide-like diuretics are prescribed to patients with impaired liver function, hepatic encephalopathy may develop, especially in the presence of electrolyte imbalance. In this case, it is necessary to stop using diuretics.

Cases of photosensitivity have been reported with the use of thiazide and thiazide-like diuretics. If photosensitivity develops during therapy, discontinuation of these drugs is indicated. If it is necessary to continue treatment, it is recommended to protect the skin from sunlight or artificial UV radiation.

The sodium content in blood plasma must be determined before starting treatment. Regular monitoring of this parameter is indicated throughout the entire period of therapy. All diuretics can cause hyponatremia, which can sometimes have very serious consequences. Constant monitoring of sodium content in blood plasma is necessary, because at the beginning of therapy, such a decrease may not be accompanied by the appearance of pathological symptoms. Sodium monitoring should be carried out particularly carefully in patients with cirrhosis and in elderly patients.

It has been reported that thiazide and thiazide-like diuretics reduce the excretion of calcium by the kidneys, leading to a non-significant temporary increase in plasma calcium. Clinical hypercalcemia may result from previously undiagnosed hyperparathyroidism. In this case, it is necessary to discontinue diuretics before examining the function of the parathyroid glands.

Monitoring glucose concentrations is indicated in patients with diabetes mellitus, especially in the presence of hypokalemia.

Patients suffering from gout may experience an increase in the frequency of attacks or an exacerbation of gout.

Thiazide and thiazide-like diuretics are most effective in patients with normal or slightly reduced renal function (plasma creatinine in adults

At the beginning of treatment, patients experience a decrease in GFR due to hypovolemia, which may be associated with loss of water and sodium ions due to the action of diuretics. In this regard, an increase in the concentration of uric acid and creatinine in the blood plasma is possible. In the absence of renal dysfunction, such transient functional renal failure usually resolves without complications, but the general condition of patients may worsen in the presence of renal failure.

It is possible for athletes to test positive for doping tests.

The drug contains lactose, so it should not be taken by patients with rare hereditary galactose intolerance, lactase deficiency or glucose-galactose malabsorption syndrome.

Lisinopril

Most often, a significant decrease in blood pressure is associated with hypovolemia caused by the use of diuretics, reducing the amount of salt in food, dialysis, diarrhea or vomiting. In patients with chronic heart failure, regardless of whether it is associated with renal failure, arterial hypotension may develop. It has been found that in patients with severe heart failure, this condition occurs more often due to the administration of high doses of diuretics, hyponatremia or impaired renal function. In such patients, careful medical supervision is required (careful selection of doses of lisinopril and diuretics is indicated). The same instructions apply to patients with coronary artery disease and cerebrovascular insufficiency, in whom a sharp decrease in blood pressure can lead to myocardial infarction or stroke.

If there is a significant decrease in blood pressure, the patient must take a horizontal position; it is possible to administer a 0.9% sodium chloride solution intravenously. Transient hypotensive reactions are not a contraindication to the next dose of lisinopril.

In patients with chronic heart failure with normal or reduced blood pressure, the use of lisinopril may lead to a decrease in blood pressure; this usually does not serve as a reason to discontinue the drug. If arterial hypotension is accompanied by clinical manifestations, dose reduction or discontinuation of lisinopril should be considered.

In patients at risk of developing symptomatic arterial hypotension (on a low-salt or salt-free diet), regardless of the presence of hyponatremia, as well as in patients receiving high doses of diuretics, it is necessary to achieve compensation for these conditions (hypovolemia or sodium deficiency) before starting treatment.

Monitoring of the effect of the initial dose of lisinopril on blood pressure is indicated.

For acute myocardial infarction, standard treatment is recommended (thrombolytics, acetylsalicylic acid, beta-blockers). Lisinopril can be used in combination with intravenous nitroglycerin or transdermal nitroglycerin. In patients with acute myocardial infarction and the risk of further deterioration of hemodynamics, worsening of symptoms after the prescription of vasodilators, lisinopril therapy should not be started. These patients include patients with systolic blood pressure

In patients with chronic heart failure, a significant decrease in blood pressure during the administration of ACE inhibitors can lead to worsening renal dysfunction. Cases of acute renal failure have been reported.

In patients with bilateral renal artery stenosis or renal artery stenosis of a single kidney, an increase in serum urea and creatinine concentrations was observed during the use of ACE inhibitors; Usually such disturbances were temporary and ceased after discontinuation of therapy. They occurred more often in patients with renal failure.

In patients with acute myocardial infarction and severe renal impairment (serum creatinine concentration >177 µmol/l and/or proteinuria >500 mg/day), lisinopril is contraindicated. If renal dysfunction develops during treatment (serum creatinine concentration >265 µmol/l or doubling compared to the initial value), discontinuation of lisinopril is indicated.

In rare cases, during the use of ACE inhibitors, including lisinopril, the development of angioedema of the face, extremities, lips, tongue, epiglottis and/or larynx has been reported. In such cases, immediate discontinuation of lisinopril is required; Monitoring the condition of patients until symptoms are completely resolved is indicated. Typically, angioedema of the face and lips is temporary and does not require treatment; however, antihistamines may be prescribed. Angioedema of the larynx can cause death. Swelling of the tongue, epiglottis, or larynx can lead to secondary airway obstruction. In this case, it is necessary to immediately administer 0.3-0.5 ml of a 1:1000 solution of adrenaline subcutaneously, and also ensure patency of the airways. It was reported that angioedema occurred more often in black patients receiving ACE inhibitors than in patients of other ethnic groups. In patients with a history of angioedema not associated with taking ACE inhibitors, the risk of developing angioedema when using ACE inhibitors is higher.

In very rare cases, patients taking ACE inhibitors may develop life-threatening anaphylactic reactions during desensitization with hymenoptera venom, so it is necessary to temporarily discontinue ACE inhibitors before desensitization.

Anaphylactic reactions have also occurred in patients undergoing hemodialysis using high-flux dialysis membranes (eg, AN69) with concomitant use of ACE inhibitors. In such patients, the use of other dialysis membranes or other antihypertensive drugs is indicated.

Therapy with ACE inhibitors may cause cough, which should be taken into account when carrying out differential diagnosis. A prolonged dry cough usually stops after stopping ACE inhibitors.

The use of antihypertensive drugs during major surgery or during general anesthesia can lead to inhibition of the formation of angiotensin II due to compensatory secretion of renin. The significant decrease in blood pressure associated with this effect can be prevented by increasing blood volume. Patients taking ACE inhibitors should inform the surgeon/anesthesiologist before undergoing surgery (including dental procedures).

Cases of hyperkalemia have been reported. Risk factors for hyperkalemia include renal failure, diabetes mellitus, therapy with potassium-sparing diuretics (spironolactone, triamterene and amiloride), use of potassium supplements and potassium-based salt substitutes, especially in patients with impaired renal function. If combined use of lisinopril and these drugs is necessary, regular monitoring of potassium levels in the blood plasma is indicated.

It has been proven that the simultaneous administration of ACE inhibitors, angiotensin II receptor antagonists or aliskiren increases the risk of arterial hypotension, hyperkalemia and renal dysfunction (including acute renal failure). Therefore, it is not recommended to prescribe ACE inhibitors, angiotensin II receptor antagonists, or aliskiren for dual blockade of the RAAS. If there are absolute indications for double blockade of the RAAS, it should be carried out under the careful supervision of a specialist with frequent monitoring of blood pressure, renal function and electrolyte levels. ACE inhibitors and angiotensin II receptor antagonists should not be used concomitantly in patients with diabetic nephropathy.

Impact on the ability to drive vehicles and operate machinery

There is no data on the effect of lisinopril on the ability to drive vehicles and operate machinery. However, the possibility of dizziness should be taken into account. In this regard, care must be taken when driving vehicles and operating machinery. Indapamide does not cause impairment of psychomotor functions, however, in some patients, with a decrease in blood pressure, various individual reactions may develop, especially at the beginning of therapy or when an additional antihypertensive drug is prescribed to the main treatment regimen. In this case, the ability to drive vehicles and operate machinery may be reduced.

Diroton® Plus (Diroton® Plus)

If you are hospitalized, tell your doctor that you are taking Diroton® Plus.

When using the drug Diroton® Plus, special instructions regarding the individual components of the drug must be taken into account.

Indapamide related

Liver dysfunction

Photosensitivity

When using thiazide and thiazide-like diuretics, cases of photosensitivity have been reported (see section "Side effects"). If photosensitivity develops during therapy, discontinuation of these drugs is indicated. If it is necessary to continue treatment, it is recommended to protect the skin from sunlight or artificial UV radiation.

Water and electrolyte balance

Sodium content in blood plasma

The sodium content in blood plasma must be determined before starting treatment. Regular monitoring of this parameter is indicated throughout the entire period of therapy. Constant monitoring of sodium content in the blood plasma is necessary, since at the beginning of therapy such a decrease may not be accompanied by the appearance of pathological symptoms. Monitoring of sodium levels should be carried out especially carefully in patients with cirrhosis and in 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.

Potassium content in blood plasma

During therapy with thiazide and thiazide-like diuretics, a sharp decrease in the potassium content in the blood plasma, as well as the development of hypokalemia, is possible. It is necessary to prevent the risk of developing hypokalemia (<3.4 mmol/l) in the following groups of patients: elderly patients, debilitated patients, patients receiving concomitant drug therapy, patients with liver cirrhosis, peripheral edema and ascites, coronary heart disease, heart failure. In such patients, hypokalemia enhances the toxic effects of cardiac glycosides and increases the risk of developing arrhythmias. In addition, patients with a prolonged QT interval, both congenital and drug-induced, are considered a high-risk group.

Hypokalemia, like bradycardia, is a condition that contributes to the development of severe arrhythmias and, especially, torsades de pointes, which can be fatal. Regular monitoring of potassium levels in the blood plasma is indicated in these groups of patients, starting from the first week of treatment. If hypokalemia is detected, appropriate therapy is indicated.

Calcium content in blood plasma

Thiazide and thiazide-like diuretics reduce the excretion of calcium by the kidneys, which leads to an insignificant temporary increase in calcium levels in the blood plasma. Clinical hypercalcemia may result from previously undiagnosed hyperparathyroidism. In this case, it is necessary to discontinue diuretics before examining the function of the parathyroid glands.

Blood plasma glucose

Monitoring glucose concentrations is indicated in patients with diabetes mellitus, especially in the presence of hypokalemia.

Uric acid

In patients with gout, an increase in the frequency of attacks or an exacerbation of gout may occur.

Diuretics and kidney function

Thiazide and thiazide-like diuretics are most effective in patients with normal or slightly reduced renal function (plasma creatinine in adults <25 mg/l or 220 µmol/l). Plasma creatinine concentrations in elderly patients are assessed depending on age, body weight and gender.

At the beginning of treatment, patients experience a decrease in glomerular filtration rate due to hypovolemia, which may be associated with loss of water and sodium ions due to the action of diuretics. In this regard, an increase in the concentration of uric acid and creatinine in the blood plasma is possible. In the absence of renal dysfunction, such transient functional renal failure usually resolves without complications, but the general condition of patients may worsen in the presence of renal failure.

Choroidal effusion, acute myopia and secondary angle-closure glaucoma

Sulfonamides or sulfonamide derivatives can cause idiosyncratic reactions leading to the development of choroidal effusion with visual field defect, acute short-term myopia and acute angle-closure glaucoma. Symptoms include loss of visual acuity or eye pain, which usually occurs within hours to weeks after starting the drug. If left untreated, acute angle-closure glaucoma can lead to irreversible vision loss. If symptoms appear, you should stop taking the drug as soon as possible. If intraocular pressure remains uncontrolled, emergency medical treatment or surgery may be required. Risk factors for the development of acute angle-closure glaucoma may include a history of allergic reactions to sulfonamides or penicillin.

Athletes

Indapamide may cause a positive doping test result in athletes.

Lactose

The drug contains lactose, so it should not be taken by patients with rare hereditary galactose intolerance, lactase deficiency or glucose-galactose malabsorption syndrome.

Related to lisinopril

Symptomatic hypotension

Most often, a significant decrease in blood pressure is associated with hypovolemia caused by the use of diuretics, a decrease in the amount of salt in food, dialysis, diarrhea or vomiting (see “Interaction with other drugs”, “Side effects”).

In patients with CHF, regardless of whether it is associated with renal failure, arterial hypotension may develop. It has been found that in patients with severe heart failure, this condition occurs more often due to the administration of high doses of diuretics, hyponatremia or impaired renal function. In such patients, careful medical supervision is required (careful selection of doses of lisinopril and diuretics is indicated).

The same instructions apply to patients with coronary heart disease and cerebrovascular insufficiency, in whom a sharp decrease in blood pressure can lead to myocardial infarction or stroke.

If there is a significant decrease in blood pressure, the patient must take a horizontal position; intravenous administration of 0.9% sodium chloride solution is possible.

Transient hypotensive reactions are not a contraindication to the next dose of lisinopril.

In patients with CHF with normal or reduced blood pressure, the use of lisinopril may lead to a decrease in blood pressure; this usually does not serve as a reason to discontinue the drug. If arterial hypotension is accompanied by clinical manifestations, dose reduction or discontinuation of lisinopril should be considered.

In patients at risk of developing symptomatic arterial hypotension (on a low-salt or salt-free diet), regardless of the presence of hyponatremia, as well as in patients receiving high-dose diuretics, it is necessary to compensate for hypovolemia or sodium deficiency before starting treatment.

It is necessary to monitor blood pressure when taking the first dose of lisinopril.

Acute myocardial infarction

Standard treatment is recommended (thrombolytics, acetylsalicylic acid, beta-blockers). Lisinopril can be used in combination with intravenous nitroglycerin or with the use of a transdermal form of nitroglycerin.

In patients with acute myocardial infarction and the risk of further deterioration of hemodynamics, worsening of symptoms after the prescription of vasodilators, lisinopril therapy should not be started. These patients include those with systolic blood pressure ≤100 mm Hg. Art. and patients with cardiogenic shock. In patients with systolic blood pressure ≤120 mm Hg. Art. During the first three days after myocardial infarction, a dose reduction is indicated. In patients with systolic blood pressure ≤100 mm Hg. Art. the maintenance dose should be reduced to 5 mg (or temporarily to 2.5 mg). In patients with persistent arterial hypotension (systolic blood pressure <90 mm Hg for 1 hour or more), discontinuation of lisinopril is indicated.

Renal dysfunction

In patients with CHF, a significant decrease in blood pressure during the administration of ACE inhibitors can lead to worsening renal dysfunction. Cases of acute renal failure have been reported.

Hypersensitivity, angioedema

In rare cases, during the use of ACE inhibitors, including lisinopril, the development of angioedema of the face, extremities, lips, tongue, epiglottis and/or larynx has been observed. In such cases, immediate discontinuation of lisinopril is required; Monitoring the condition of patients until symptoms are completely resolved is indicated. Typically, angioedema of the face and lips is temporary and does not require treatment; however, antihistamines may be prescribed.

Angioedema of the larynx can cause death. Swelling of the tongue, epiglottis, or larynx can lead to secondary airway obstruction. In this case, it is necessary to immediately administer 0.3-0.5 ml of a 1:1000 solution of adrenaline subcutaneously, and also ensure airway patency.

In rare cases, angioedema of the intestine has developed during therapy with ACE inhibitors. In this case, patients experienced abdominal pain as an isolated symptom or in combination with nausea or vomiting, in some cases without previous angioedema of the face and with normal levels of C1-esterase. The diagnosis was made using computed tomography of the abdominal organs, ultrasound, or during surgery. Symptoms disappeared after stopping the ACE inhibitors. Therefore, in patients with abdominal pain receiving ACE inhibitors, when carrying out differential diagnosis, it is necessary to take into account the possibility of developing angioedema of the intestine.

In patients with a history of angioedema not associated with taking ACE inhibitors, the risk of its development when using ACE inhibitors is higher (see “Contraindications”).

Anaphylactic reactions associated with desensitization by hymenoptera venom

Patients on hemodialysis

Cough

Therapy with ACE inhibitors may cause cough, which should be taken into account when carrying out differential diagnosis. A prolonged dry cough usually stops after stopping ACE inhibitors.

Surgical interventions / general anesthesia

The use of antihypertensive drugs during major surgery or during general anesthesia can lead to inhibition of angiotensin II formation due to compensatory secretion of renin. The significant decrease in blood pressure associated with this effect can be prevented by increasing circulating blood volume.

Patients taking ACE inhibitors. must inform the surgeon/anesthetist prior to surgery (including dental procedures).

Blood plasma potassium

Cases of hyperkalemia have been reported.

Risk factors for hyperkalemia include renal failure, diabetes mellitus, therapy with potassium-sparing diuretics (spironolactone, triamterene and amiloride), use of potassium supplements and potassium-based salt substitutes, especially in patients with impaired renal function.

If combined use of lisinopril and these drugs is necessary, regular monitoring of potassium levels in the blood plasma is indicated.

Double blockade of the RAAS

It has been proven that the simultaneous administration of ACE inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of arterial hypotension, hyperkalemia and renal dysfunction (including acute renal failure). Thus, the combined administration of ACE inhibitors, angiotensin II receptor blockers or aliskiren for dual blockade of the RAAS is not recommended.

If there are absolute indications for double blockade of the RAAS, then it should be carried out under the careful supervision of a specialist with frequent monitoring of blood pressure, renal function and electrolyte levels.

The simultaneous use of ACE inhibitors with drugs containing aliskiren is contraindicated in patients with diabetes mellitus and/or with moderate or severe renal impairment (GFR less than 60 ml/min/1.73 m2 body surface area) and is not recommended in other patients.

Concomitant use of ACE inhibitors with angiotensin II receptor antagonists is contraindicated in patients with diabetic nephropathy and is not recommended in other patients.

Neutropenia / agranulocytosis / thrombocytopenia / anemia

While taking ACE inhibitors, neutropenia, agranulocytosis, thrombocytopenia and anemia may occur. In patients with normal renal function and in the absence of other aggravating factors, neutropenia rarely develops. Diroton® Plus should be prescribed with extreme caution to patients with systemic connective tissue diseases, while taking immunosuppressants, allopurinol or procainamide, or a combination of these risk factors, especially patients with impaired renal function. Some patients developed severe infections, in some cases resistant to intensive antibiotic therapy. When prescribing Diroton® Plus to such patients, it is recommended to periodically monitor the number of leukocytes in the blood plasma. Patients should report any signs of infectious diseases (eg, sore throat, fever) to their doctor.

Mitral stenosis/aortic stenosis/hypertrophic cardiomyopathy

ACE inhibitors should be prescribed with caution to patients with mitral stenosis, as well as to patients with left ventricular outflow tract obstruction (aortic stenosis, hypertrophic cardiomyopathy).

Liver failure

Very rarely, cholestatic jaundice occurs while taking ACE inhibitors. As this syndrome progresses, fulminant liver necrosis develops, sometimes with death. The mechanism of development of this syndrome is unclear. If jaundice or a significant increase in the activity of liver enzymes occurs while taking ACE inhibitors, the drug Diroton® Plus should be discontinued and the patient should be carefully monitored.

Ethnic differences

In patients of the Negroid race, angioedema develops more often than in representatives of other races while taking ACE inhibitors. ACE inhibitors may have a less pronounced antihypertensive effect in patients of the Black race compared to representatives of other races. This difference may be due to the fact that black patients with arterial hypertension are more likely to have low renin activity.