Equamer - instructions for use, doses, side effects, contraindications, price, where to buy

Ekvamer®

If you are admitted to a hospital, tell your doctor that you are taking Equamer®.

When using the drug Equamer®, you should take into account the recommendations for the use of individual components of the drug, described in detail below.

Amlodipine

It is necessary to maintain dental hygiene and follow-up with a dentist (to prevent pain, bleeding and gum hyperplasia).

In elderly patients, T1/2 may increase and amlodipine clearance may decrease. Dose changes are not required, but more careful monitoring of patients in this category is necessary.

The effectiveness and safety of amlodipine in hypertensive crisis have not been established.

Despite the absence of BMCC syndrome “Interaction with other drugs”, “Side effects”). In patients with CHF, with or without renal failure, symptomatic arterial hypotension may develop. It develops more often in patients with severe heart failure, which is associated with the use of high doses of diuretics, hyponatremia or impaired renal function. Such patients require careful medical monitoring (with careful selection of doses of lisinopril and diuretics). The same recommendations apply to patients with coronary heart disease and cerebrovascular insufficiency, when a rapid decrease in blood pressure can lead to the development of myocardial infarction or stroke.

Patients with a pronounced decrease in blood pressure should be placed in a horizontal position; if necessary, an infusion of 0.9% sodium chloride solution is performed. Transient hypotension is not a contraindication to the next dose of lisinopril.

In patients with CHF with normal or low blood pressure, the use of lisinopril may lead to a decrease in blood pressure; as a rule, this does not require discontinuation of treatment. If arterial hypotension is accompanied by clinical manifestations, indications for dose reduction or discontinuation of lisinopril should be assessed.

In patients at risk of developing symptomatic arterial hypotension (patients on a salt-free or low-salt diet) with or without hyponatremia, as well as in patients receiving high doses of diuretics, it is necessary to compensate for these deviations (loss of water and salts) before starting treatment.

It is necessary to monitor the effect of the starting dose of lisinopril on blood pressure.

Acute myocardial infarction

Standard treatment is recommended (thrombolytics, acetylsalicylic acid, beta-blockers).

It is possible to use lisinopril simultaneously with intravenous nitroglycerin or the use of a transdermal form of nitroglycerin.

In patients with acute myocardial infarction and the risk of further hemodynamic disturbances, deterioration after the administration of vasodilators, lisinopril therapy should not be started. These patients include those with systolic blood pressure ≤100 mm Hg. Art. or cardiogenic shock. In patients with systolic blood pressure ≤120 mm Hg. Art. it is necessary to reduce the dose during the first 3 days after myocardial infarction. 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 mmHg for 1 hour or longer), lisinopril should be discontinued.

Renal dysfunction

In patients with CHF, a significant decrease in blood pressure that occurs after starting therapy with 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 solitary kidney, cases of increased serum urea and creatinine concentrations associated with the use of ACE inhibitors have been reported; as a rule, these disorders were transient, ceased after discontinuation of lisinopril and occurred more often in patients with renal failure.

Lisinopril should not be prescribed to patients with acute myocardial infarction and significant renal impairment (serum creatinine concentration >177 µmol/L and/or proteinuria >500 mg/day). If renal dysfunction develops during treatment with lisinopril (serum creatinine clearance >265 µmol/l or its increase doubles compared to the initial value), the possibility of discontinuing lisinopril should be considered.

Hypersensitivity, angioedema

In patients receiving ACE inhibitors, including lisinopril, rare cases of angioedema of the face, extremities, lips, tongue, epiglottis and/or larynx have been reported, which could occur during any period of treatment. In such cases, it is necessary to immediately discontinue lisinopril; Patients should be monitored until symptoms disappear completely. Typically, cases of angioedema of the face and lips are temporary and do not require any treatment; it is possible to prescribe antihistamines.

Angioedema of the larynx can lead to death. Angioedema of the tongue, epiglottis or larynx can lead to secondary airway obstruction, so it is necessary to immediately begin appropriate therapy (0.3-0.5 ml of epinephrine solution (adrenaline) in a concentration of 1:1,000 subcutaneously) and/or take measures to 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. Diagnosis was made using abdominal computed tomography, ultrasound, or at the time of 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 use of ACE inhibitors may be associated with a higher risk of developing angioedema (see "Contraindications").

Anaphylactic reactions associated with desensitization by hymenoptera venom

There are reports of very rare cases of life-threatening anaphylactic reactions that developed in patients taking ACE inhibitors during desensitization with hymenoptera venom. To prevent such cases, ACE inhibitors should be temporarily discontinued before desensitization.

Hemodialysis

Anaphylactic reactions have also been reported in patients undergoing hemodialysis using high-permeability membranes (eg, AN69) who were concomitantly prescribed ACE inhibitors. In this group of patients, the use of other dialysis membranes or other antihypertensive drugs should be considered.

Cough

The use of ACE inhibitors may be associated with cough. A dry cough that continues for a long time usually disappears after discontinuation of the ACE inhibitor. When carrying out differential diagnosis, the possibility of cough associated with the use of ACE inhibitors should be taken into account.

Surgery/general anesthesia

The use of blood pressure-lowering drugs during major surgery or general anesthesia may suppress the formation of angiotensin II in response to compensatory renin secretion. A significant decrease in blood pressure, which is considered as a result of this effect, can be controlled by reducing the volume of blood volume.

Patients taking ACE inhibitors should inform their surgeon/anesthetist before undergoing surgery (including dental procedures).

Serum potassium content

Cases of hyperkalemia have been reported.

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

If simultaneous use of lisinopril and the above drugs is necessary, caution should be exercised and serum potassium levels should be regularly monitored.

Double blockade of the RAAS

It has been proven that the simultaneous use of ACE inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of arterial hypotension, hyperkalemia and renal dysfunction (including acute renal failure). Therefore, the use 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. Neutropenia and agranulocytosis are usually reversible after discontinuation of ACE inhibitors.

Equamer 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 Equamer® 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

In very rare cases, the use of ACE inhibitors was accompanied by a syndrome that began with cholestatic jaundice or hepatitis, progressed to fulminant hepatic necrosis and (sometimes) led to death. The mechanism of development of this syndrome is unclear. Patients receiving lisinopril who develop jaundice or significantly increase the activity of liver enzymes should discontinue Equamer® and monitor the patient's condition.

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.

Rosuvastatin

Proteinuria may be detected in patients receiving rosuvastatin. Changes in the amount of protein in the urine (from none or trace amounts to ++ or more) are observed in less than 1% of patients receiving 10-20 mg rosuvastatin and in approximately 3% of patients receiving 40 mg rosuvastatin. A slight change in the amount of protein in the urine was noted when taking a dose of 20 mg. In most cases, proteinuria decreases or disappears during therapy and does not indicate the onset of acute or progression of existing kidney disease.

From the musculoskeletal system

When using rosuvastatin in all dosages, and especially when taking doses exceeding 20 mg, the following undesirable side effects were reported: myalgia, myopathy, and in rare cases, rhabdomyolysis.

Determination of creatine phosphokinase activity

Determination of CPK activity should not be carried out after intense physical activity or in the presence of other possible reasons for increased CPK activity, which may lead to incorrect interpretation of the results obtained. If initially CPK activity is significantly increased (5 times higher than the upper limit of normal), a repeat measurement should be taken after 5-7 days. Therapy should not be started if a repeat test confirms initial CPK activity (more than 5 times the upper limit of normal).

Before starting therapy

When prescribing rosuvastatin, as when prescribing other HMG-CoA reductase inhibitors, caution should be exercised in patients with existing risk factors for the development of myopathy/rhabdomyolysis (see section “With caution”). It is necessary to consider the risk/benefit ratio of therapy and conduct clinical monitoring.

During therapy

The patient should be informed to immediately report to the doctor the unexpected onset of muscle pain, muscle weakness or spasms, especially in combination with malaise and fever. In such patients, CPK activity should be determined. Therapy should be discontinued if CPK activity is significantly increased (more than 5 times the upper limit of normal) or if muscle symptoms are severe and cause daily discomfort (even if CPK activity is less than 5 times the upper limit of normal). upper limit of normal). If symptoms disappear and CPK activity returns to normal, re-prescribing rosuvastatin or other HMG-CoA reductase inhibitors in lower doses should be considered with careful monitoring of the patient.

Routine monitoring of CPK activity in the absence of symptoms is impractical.

Very rare cases of immune-mediated necrotizing myopathy (IMN) have been reported during or after treatment with statins, including rosuvastatin. IONK is characterized by proximal muscle weakness and increased plasma CPK activity, which persist despite cessation of statin treatment.

There were no signs of increased effects on skeletal muscles when taking rosuvastatin and concomitant therapy. However, an increase in the number of cases of myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors (statins) in combination with fibric acid derivatives (including gemfibrozil), as well as cyclosporine, nicotinic acid in lipid-lowering doses (more than 1 g / day) , azole antifungals, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when combined with certain HMG-CoA reductase inhibitors. Therefore, concomitant use of rosuvastatin and gemfibrozil is not recommended. The risk/benefit ratio should be carefully weighed when using rosuvastatin and fibrates or nicotinic acid in lipid-lowering doses (more than 1 g/day). Taking rosuvastatin at a dose of 40 mg together with fibrates is contraindicated (see section “Interaction with other drugs”).

2-4 weeks after starting treatment and/or increasing the dose of rosuvastatin, monitoring of lipid metabolism parameters is necessary (if necessary, adjust the dose of rosuvastatin).

Rosuvastatin should not be used in conjunction with systemic fusidic acid drugs and within 7 days after stopping treatment with such drugs. In those patients who require treatment with systemic fusidic acid, statins should be discontinued throughout fusidic acid treatment. Patients should be advised to consult a physician immediately if symptoms of muscle weakness, muscle pain, or muscle tenderness occur. Statin treatment can be resumed 7 days after the last dose of fusidic acid.

In exceptional cases, when long-term systemic use of fusidic acid is necessary, for example, in severe infections, the need for its combined use with rosuvastatin should be considered by a doctor on a case-by-case basis and carried out under close medical supervision.

Rosuvastatin should not be used in patients with an acute, severe condition suggesting the presence of myopathy or the possibility of renal failure secondary to rhabdomyolysis (eg, sepsis, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disturbances, or uncontrolled seizures). .

Monitoring liver function

It is recommended to determine liver function indicators before starting therapy and 3 months after starting therapy. Rosuvastatin should be discontinued or its dose reduced if the activity of hepatic transaminases in the blood serum is 3 times higher than the upper limit of normal.

In patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome, treatment of underlying diseases should be carried out before starting treatment with rosuvastatin.

Race

During the study of pharmacokinetic parameters in patients belonging to the Mongoloid race, an increase in the systemic concentration of rosuvastatin was noted compared with that of Caucasian patients (see sections “Dosage and Administration” and “Pharmacokinetics”).

HIV protease inhibitors

The combined use of rosuvastatin with HIV protease inhibitors is not recommended (see section “Interaction with other drugs”).

Interstitial lung disease

Isolated cases of interstitial lung disease have been reported with the use of certain HMG-CoA reductase inhibitors (statins), especially over long periods of time. Manifestations of the disease may include shortness of breath, nonproductive cough and deterioration in general health (weakness, weight loss and fever). If interstitial lung disease is suspected, statin therapy should be discontinued.

Diabetes mellitus type 2

In patients with fasting glucose concentrations between 5.6 and 6.9 mmol/L, rosuvastatin therapy was associated with an increased risk of developing type 2 diabetes mellitus.

Excipients

Lactose

The drug Equamer® in a dosage of 5 mg + 10 mg + 10 mg and in a dosage of 10 mg + 20 mg + 10 mg contains 48.10 mg of lactose monohydrate in each capsule. The drug Equamer® in a dosage of 5 mg + 10 mg + 20 mg and in a dosage of 10 mg + 20 mg + 20 mg contains 96.20 mg of lactose monohydrate in each capsule.

Patients with rare hereditary diseases such as lactose intolerance, Lapp lactase deficiency or glucose-galactose malabsorption should not take Equamer®.

Azorubine dye

Equamer® contains the food coloring azorubine.

Azorubine may cause allergic reactions.

Sunset yellow dye

The drug Equamer® in a dosage of 5 mg + 10 mg + 10 mg and 10 mg + 20 mg + 20 mg contains sunset yellow food coloring.

Sunset yellow food coloring can cause allergic reactions.

Instructions for use EKVAMER®

In case of hospitalization, the patient should inform the doctor about taking Equamer®.

If you miss taking a capsule of Equamer®, you must take the next capsule at the usual time. Do not take a double dose to make up for a missed dose.

When using the drug Equamer®, you should take into account the recommendations for the use of individual components of the drug, described in detail below.

Amlodipine

The safety and effectiveness of amlodipine in hypertensive crisis has not been established.

Patients with heart failure

Patients with heart failure should be treated with amlodipine with caution. In long-term, placebo-controlled clinical studies involving patients with severe heart failure (NYHA functional class III-IV), it was found that in the group receiving amlodipine, compared with the placebo group, the number of cases of pulmonary edema increased. Slow calcium channel blockers, including amlodipine, should be used with caution in the treatment of patients with congestive heart failure. they may increase the risk of cardiovascular complications and mortality in this group of patients.

Patients with liver dysfunction

In patients with impaired liver function, amlodipine T1/2 and AUC values increase; recommended doses for such patients have not been established. Treatment with amlodipine should be started with minimal doses. Caution should be exercised when starting treatment and when increasing the dose. In patients with severe hepatic impairment, dose titration should be carried out slowly and under close medical supervision.

Patients with impaired renal function

In this group of patients, amlodipine can be used in normal doses. Changes in plasma concentrations of amlodipine do not correlate with the degree of renal failure. Amlodipine is not eliminated by hemodialysis.

Elderly patients

Increasing the dose in elderly patients should be done with caution.

Lisinopril

Symptomatic hypotension

Most often, a pronounced decrease in blood pressure occurs with a decrease in blood volume caused by diuretic therapy, a decrease in sodium chloride in food, dialysis, diarrhea and vomiting, or in patients with severe renin-dependent hypertension. In patients with CHF, both with and without concomitant renal failure, symptomatic arterial hypotension may develop. It was more often detected in patients with severe heart failure as a consequence of the use of large doses of loop diuretics, hyponatremia or impaired renal function. In such patients, therapy should be started under the strict supervision of a physician (with caution in selecting the dose of lisinopril and diuretics). Similar rules must be followed when prescribing lisinopril to patients with coronary heart disease, cerebrovascular insufficiency, in whom a sharp decrease in blood pressure can lead to myocardial infarction or stroke.

In case of a pronounced decrease in blood pressure, the patient should be laid down and, if necessary, fluid loss should be replaced (iv infusion of 0.9% sodium chloride solution). A transient hypotensive reaction is not a contraindication for taking the next dose of lisinopril; further treatment usually proceeds without complications after restoration of blood pressure as a result of correction of hypovolemia.

When using lisinopril, some patients with CHF, but with normal or reduced blood pressure, may experience a decrease in blood pressure, which is usually not a reason to discontinue therapy. If arterial hypotension becomes symptomatic, it is necessary to reduce the dose or discontinue therapy with lisinopril.

Aortic and mitral valve stenosis/hypertrophic obstructive cardiomyopathy

As with other ACE inhibitors, lisinopril should be administered with caution to patients with mitral valve stenosis and left ventricular outflow tract obstruction (aortic stenosis or hypertrophic obstructive cardiomyopathy).

Acute myocardial infarction

Lisinopril therapy should not be initiated in patients with acute myocardial infarction who are at risk of further serious hemodynamic deterioration after use of vasodilators (patients with systolic blood pressure 100 mmHg or lower, patients with cardiogenic shock). During the first 3 days after myocardial infarction, the dose of lisinopril should be reduced if systolic blood pressure is 120 mmHg. Art. or lower. Maintenance doses of lisinopril should be reduced to 5 mg or temporarily to 2.5 mg if systolic blood pressure is 100 mmHg. Art. or lower. If arterial hypotension persists (systolic blood pressure less than 90 mm Hg for more than 1 hour), lisinopril should not be continued.

Renal dysfunction

In case of impaired renal function (creatinine clearance <80 ml/min), the initial dose of lisinopril should be adjusted depending on the level of creatinine clearance and then on the patient's clinical response to therapy. Routine monitoring of serum potassium and creatinine concentrations is part of standard medical practice in treating these patients.

In patients with CHF, a pronounced decrease in blood pressure after initiation of treatment with ACE inhibitors may lead to further deterioration of renal function. Cases of acute renal failure, usually reversible, have been reported.

In patients with bilateral renal artery stenosis or solitary renal artery stenosis treated with ACE inhibitors, there was an increase in serum urea and creatinine concentrations, usually reversible after discontinuation of treatment and more common in patients with renal failure. In the presence of concomitant renovascular hypertension, the risk of severe arterial hypotension and renal failure increases. In such patients, treatment should be initiated under close medical supervision, using low doses and carefully titrating the dose. Because Diuretics may aggravate this condition and should be discontinued and renal function monitored during the first weeks of lisinopril therapy.

Lisinopril is not used for acute myocardial infarction in patients with severely impaired renal function, established by changes in serum creatinine concentration exceeding 177 µmol/l and/or proteinuria exceeding 500 mg/day. If renal dysfunction develops during lisinopril therapy (serum creatinine concentration exceeding 265 µmol/l, or doubling the value compared to the value before treatment), discontinuation of lisinopril should be considered.

Hypersensitivity/angioedema

Angioedema of the face, extremities, lips, tongue, epiglottis and/or larynx, which may occur during any period of therapy, has been reported rarely in patients treated with an ACE inhibitor, including lisinopril. In this case, it is necessary to immediately discontinue lisinopril, the patient should receive appropriate treatment and be under medical supervision until complete regression of symptoms. Even if swelling occurs only in the tongue area, without concomitant respiratory impairment, the patient may require long-term observation, since treatment with antihistamines and corticosteroids may not be sufficient.

Angioedema, with swelling of the larynx or tongue, can be fatal. Swelling of the tongue, epiglottis or larynx may cause airway obstruction, especially if there is a history of airway surgery, so appropriate therapy should be administered immediately (0.3-0.5 ml 1:

1000 solution of epinephrine (adrenaline) subcutaneously) and/or take measures to ensure airway patency. The patient should be under strict medical supervision until complete and sustained resolution of symptoms.

It was noted that in patients of the Negroid race taking ACE inhibitors, angioedema developed more often than in patients of other races.

Patients who have a history of angioedema not related to previous treatment with ACE inhibitors may be at increased risk of developing it during treatment with an ACE inhibitor.

Anaphylactoid reactions during LDL apheresis

In rare cases, life-threatening anaphylactoid reactions may develop in patients receiving ACE inhibitors during LDL apheresis using dextran sulfate. Such reactions were avoided if the ACE inhibitor was temporarily stopped before each apheresis procedure.

Anaphylactic reactions during desensitization procedures

Patients receiving ACE inhibitors during a course of desensitization (for example, hymenoptera venom) may develop life-threatening anaphylactic reactions. Such reactions can be avoided by temporarily stopping the ACE inhibitor before each desensitization procedure, but such reactions have reappeared with accidental use of these drugs.

Liver dysfunction

In very rare cases, therapy with ACE inhibitors can lead to the development of cholestatic jaundice with progression to fulminant liver necrosis and (sometimes) death. Therefore, it is necessary to stop taking lisinopril if the activity of liver transaminases increases and symptoms of cholestasis appear, the patient should be under appropriate medical supervision.

Patients on hemodialysis

Anaphylactic reactions have also been observed in patients undergoing hemodialysis using high-flow membranes (for example, AN69®) and concomitantly taking ACE inhibitors. If hemodialysis is necessary, a different type of membrane or a different antihypertensive drug must be used.

Neutropenia/agranulocytosis

Neutropenia/agranulocytosis, thrombocytopenia and anemia have been reported in patients receiving ACE inhibitors. In patients with normal renal function without other aggravating factors, neutropenia rarely develops. Neutropenia and agranulocytosis disappeared after cessation of treatment with ACE inhibitors. Lisinopril should be used with extreme caution in patients with collagen diseases, as well as in patients receiving immunosuppressive therapy, allopurinol or procainamide, or a combination of these complicating factors, especially if there is impaired renal function. Some patients developed serious infections, which in some cases did not respond to intensive antibiotic therapy. If lisinopril is used in such patients, periodic monitoring of the white blood cell count is recommended; in addition, patients should be advised to report any signs of infection.

Double blockade of the RAAS

Evidence has been obtained that the concomitant use of ACE inhibitors, angiotensin II receptor antagonists or aliskiren increases the risk of arterial hypotension, hyperkalemia and decreased renal function (including acute renal failure). Double blockade of the RAAS due to the combined use of ACE inhibitors, angiotensin II receptor antagonists or aliskiren is not recommended for this reason.

If double blockade of the RAAS is absolutely necessary, then treatment should be carried out under medical supervision with frequent careful monitoring of renal function, electrolytes and blood pressure levels. In patients with diabetic nephropathy, combination therapy with ACE inhibitors and angiotensin II receptor antagonists should not be used.

Race

In black patients, ACE inhibitors are more likely to cause angioedema than in patients of other races.

As with other ACE inhibitors, lisinopril may be less effective in lowering blood pressure in black patients than in patients of other races, which is likely due to a higher incidence of hyporenin hypertension.

Cough

When using an ACE inhibitor, a dry, prolonged cough was observed, which disappeared after stopping treatment with the ACE inhibitor. In the differential diagnosis of cough, cough caused by the use of an ACE inhibitor must also be taken into account.

Surgery/General anesthesia

In patients whose condition requires major surgery or general anesthesia with drugs that cause hypotension, lisinopril may block the formation of angiotensin II with compensatory renin release.

A pronounced decrease in blood pressure, which is considered a consequence of this mechanism, can be eliminated by increasing the volume of blood volume.

Before surgery (including dental surgery), the surgeon/anesthetist should be informed about the use of an ACE inhibitor.

Hyperkalemia

Cases of hyperkalemia have been reported.

Risk factors for the development of hyperkalemia include renal failure, diabetes mellitus, and concomitant use of potassium-sparing diuretics (spironolactone, eplerenone (a spironolactone derivative), triamterene, and amiloride), potassium supplements or salt substitutes containing potassium, and patients taking drugs that may increase potassium levels. in blood serum (for example, heparin).

If simultaneous use of lisinopril and these drugs is necessary, it is recommended to take precautions and regularly monitor potassium levels in the blood serum.

Patients with diabetes mellitus

In patients with diabetes mellitus taking oral hypoglycemic agents or receiving insulin, plasma glucose concentrations should be carefully monitored during the first month of treatment with an ACE inhibitor.

Lithium preparations

As a rule, simultaneous use of lithium and lisinopril is not recommended.

Rosuvastatin

In patients receiving rosuvastatin in high doses, especially at a dose of 40 mg, proteinuria was observed, predominantly of tubular origin, usually transient or short-term, detected using immunochromatographic test strips. Proteinuria was not a predictor of acute or progressive kidney disease. The incidence of post-marketing reports of serious renal adverse reactions was higher with the 40 mg dose. The assessment of renal function should be taken into account during the routine examination of patients receiving rosuvastatin at a dose of 40 mg/day.

From the musculoskeletal system

The following undesirable side effects have been reported with rosuvastatin at all dosages, and particularly at doses greater than 20 mg:

myalgia, myopathy, in rare cases, rhabdomyolysis.

Very rarely, cases of rhabdomyolysis have been observed when ezetimibe is used in combination with HMG-CoA reductase inhibitors. A pharmacodynamic interaction cannot be excluded and caution should be exercised when using these drugs concomitantly. As with other HMG-CoA reductase inhibitors, the incidence of rhabdomyolysis associated with rosuvastatin treatment in the post-marketing period was higher when used at a dose of 40 mg.

Determination of CPK activity

Determination of CPK activity should not be carried out after intense physical activity or in the presence of other possible reasons for increased CPK activity, which may lead to incorrect interpretation of the results obtained. If initially CPK activity is significantly increased (5 times higher than ULN), a repeat measurement should be taken after 5-7 days. Therapy should not be started if a repeat test confirms initial CPK activity (more than 5 times the ULN).

Before starting therapy

When prescribing rosuvastatin, as well as when prescribing other HMG-CoA reductase inhibitors, caution should be exercised in patients with existing risk factors for the development of myopathy/rhabdomyolysis.

Predisposing factors are:

renal failure;
hypothyroidism;
personal or family history of hereditary muscle diseases;
history of muscle toxicity when using another HMG-CoA reductase inhibitor or fibrates;
alcohol abuse;
age over 70 years;
situations where the concentration of rosuvastatin in the blood plasma may increase;
simultaneous use of fibrates.

It is necessary to consider the risk/benefit ratio of therapy and conduct clinical monitoring.

During therapy

The patient should be informed to immediately report to the doctor the unexpected onset of muscle pain, muscle weakness or cramps, especially in combination with malaise and fever. In such patients, CPK activity should be determined. Therapy should be discontinued if CPK activity is significantly increased (more than 5 times the ULN) or if muscle symptoms are severe and cause daily discomfort (even if CPK activity is 5 times less than the ULN). If symptoms disappear and CPK activity returns to normal, re-prescribing rosuvastatin or other HMG-CoA reductase inhibitors in lower doses should be considered with careful monitoring of the patient.

Routine monitoring of CPK activity in the absence of symptoms is impractical.

Very rare cases of immune-mediated necrotizing myopathy have been reported, clinically manifested by proximal muscle weakness and increased serum CPK activity during treatment or after discontinuation of treatment with statins, including rosuvastatin. This condition persists despite discontinuation of statin treatment.

There were no signs of increased effects on skeletal muscles when taking rosuvastatin and concomitant therapy. However, an increase in the number of cases of myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors (statins) in combination with fibric acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid in lipid-lowering doses (more than 1 g/day), azole antifungals agents, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when combined with certain HMG-CoA reductase inhibitors. Therefore, concomitant use of rosuvastatin and gemfibrozil is not recommended. The risk/benefit ratio should be carefully weighed when using rosuvastatin and fibrates or nicotinic acid in lipid-lowering doses (more than 1 g/day). Taking rosuvastatin at a dose of 40 mg together with fibrates is contraindicated.

Rosuvastatin should not be used in combination with systemic fusidic acid preparations or within 7 days after discontinuation of fusidic acid treatment.

In patients in whom the use of systemic fusidic acid preparations is considered necessary, statin treatment should be suspended during the entire period of fusidic acid treatment. There have been reports of rhabdomyolysis (including some deaths) in patients using fusidic acid and statins concomitantly. The patient should be advised to consult a physician immediately if muscle weakness, pain, or muscle sensitivity occurs.

Statin therapy can be restarted 7 days after the last dose of fusidic acid.

In exceptional cases, when long-term use of systemic fusidic acid preparations is necessary, for example, for the treatment of severe infections, the possibility of combined use of rosuvastatin with fusidic acid should be considered individually and under strict medical supervision.

Rosuvastatin should not be used to treat patients with acute, serious conditions suggesting the development of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis, hypotension, major surgery, trauma, serious metabolic, endocrine or balance disorders electrolytes; or uncontrolled seizures).

Monitoring liver function

As with other HMG-CoA reductase inhibitors, caution should be exercised when prescribing rosuvastatin to patients who abuse alcohol and/or patients with a history of liver disease.

In the post-marketing period, the incidence of serious liver complications (mainly including increased liver transaminases) was higher in patients receiving a dose of rosuvastatin 40 mg.

In patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome, treatment of underlying diseases should be carried out before starting treatment with rosuvastatin.

Race

HIV protease inhibitors

With simultaneous use of rosuvastatin and a combination of various HIV protease inhibitors with ritonavir, an increase in the systemic exposure of rosuvastatin is observed. The benefit of reducing blood lipid concentrations while taking rosuvastatin should be carefully assessed, and the possible increase in rosuvastatin plasma concentrations should be taken into account at the beginning of treatment and when the dose of rosuvastatin is increased in patients with HIV infection taking HIV protease inhibitors.

Concomitant use of rosuvastatin with HIV protease inhibitors without dose adjustment of rosuvastatin is not recommended.

Interstitial lung disease

Diabetes

There is evidence that statins cause an increase in blood glucose concentrations in some patients at high risk of developing diabetes mellitus and can provoke a level of hyperglycemia at which standard diabetes treatment is indicated. However, the reduction in the risk of developing vascular complications during treatment with statins exceeds the risk of developing hyperglycemia, and should not be a reason to discontinue statins. Clinical and biochemical parameters should be monitored in patients at risk of hyperglycemia (fasting glucose concentration from 5.6 to 6.9 mmol/l, BMI > 30 kg/m2, elevated triglyceride concentrations, arterial hypertension), in accordance with national recommendations.

Excipients

Lactose.

The drug Equamer® with a dosage of 10 mg/5 mg/10 mg and a dosage of 20 mg/10 mg/10 mg contains 48.10 mg of lactose monohydrate in each capsule. The drug Equamer® with a dosage of 10 mg/5 mg/20 mg and a dosage of 20 mg/10 mg/20 mg contains 96.20 mg of lactose monohydrate in each capsule. Patients with rare hereditary diseases such as lactose intolerance, lapp lactase deficiency or glucose-galactose malabsorption should not take Equamer®.

Azorubine dye.

Equamer® contains the food coloring azorubine. Azorubine dye can cause allergic reactions.

Sunset yellow dye.

The drug Equamer® in dosages of 10 mg/5 mg/10 mg and 20 mg/10 mg/20 mg contains sunset yellow food coloring. Sunset yellow dye may cause allergic reactions.

Impact on the ability to drive vehicles and operate machinery

There are no data on the effect of the drug on the ability to drive vehicles and machines. Due to the possible excessive decrease in blood pressure, the occurrence of dizziness, drowsiness and similar side effects, caution should be exercised when performing potentially hazardous activities that require special attention and quick reactions (including driving a car and other vehicles, working with moving mechanisms, work of the dispatcher and operator).

Equamer capsules 5 mg + 10 mg + 20 mg 30 pcs. in Vladimir

Hypersensitivity to amlodipine or other dihydropyridine derivatives.
Hypersensitivity to lisinopril or other ACE inhibitors.
Hypersensitivity to rosuvastatin.
Hypersensitivity to any of the excipients of the drug.
History of angioedema, including from the use of ACE inhibitors.
Hereditary or idiopathic angioedema.
Severe arterial hypotension (systolic blood pressure less than 90 mm Hg).
Left ventricular outflow tract obstruction (including severe aortic stenosis).
Hemodynamically unstable heart failure after acute myocardial infarction.
Concomitant use of Equamer® with aliskiren-containing drugs in patients with diabetes mellitus or renal failure (GFR less than 60 ml/min/1.73 m2).
Active liver disease, including a persistent increase in serum transaminase activity, as well as any increase in transaminase activity (more than 3 times the upper limit of normal).
Severe renal dysfunction (creatinine clearance less than 30 ml/min).
Myopathy.
Concomitant use of cyclosporine.
Predisposition to the development of myotoxic complications.
In women: pregnancy, breastfeeding, lack of adequate contraceptive methods.
Children under 18 years of age (efficacy and safety have not been established).
Lactose intolerance, lactase deficiency or glucose-galactose malabsorption.
Patients with liver failure
There is no experience with the use of rosuvastatin in patients with a score above 9 on the Child-Pugh scale (see section “Pharmacokinetics”).

With caution:
Aortic stenosis, mitral stenosis, hypertrophic obstructive cardiomyopathy, arterial hypotension, cerebrovascular diseases (including cerebrovascular insufficiency), coronary heart disease, coronary insufficiency, CHF of non-ischemic etiology of III-IV functional class according to the NYHA classification, acute myocardial infarction (and within 1 month after), unstable angina, sick sinus syndrome (severe tachycardia or bradycardia), severe autoimmune systemic connective tissue diseases (including systemic lupus erythematosus, scleroderma), suppression of bone marrow hematopoiesis, diabetes mellitus, hyperkalemia, bilateral renal artery stenosis, stenosis of the artery of a single kidney, condition after kidney transplantation, mild to moderate renal failure (creatinine clearance 30-80 ml/min), azotemia, primary aldosteronism, salt-restricted diet, conditions accompanied by volume reduction circulating blood (incl. vomiting, diarrhea), advanced age, mild (Child-Pugh score 5–6) and moderate liver failure (Child-Pugh score 7–9), hypothyroidism, personal or family history of hereditary muscle diseases and previous history of muscle toxicity when using other HMG-CoA reductase inhibitors or fibrates, alcohol abuse, conditions in which increased plasma concentrations of rosuvastatin were noted, race (Mongoloid race), concomitant use of fibrates, history of liver disease, sepsis, extensive surgery , trauma, severe metabolic, endocrine or electrolyte disturbances or uncontrolled seizures.