Lisinopril is a peptidyl dipeptidase inhibitor. It inhibits ACE, which catalyzes the conversion of angiotensin I to the vasoconstrictor peptide, angiotensin II. Angiotensin II also stimulates the secretion of aldosterone by the adrenal cortex. Inhibition of ACE leads to a decrease in the concentration of angiotensin II, which leads to a decrease in vasoconstrictor activity and a decrease in aldosterone secretion. The latter decrease may lead to an increase in serum potassium.
Since the mechanism by which lisinopril lowers blood pressure is thought to be primarily through inhibition of the renin-angiotensin-aldosterone system (RAAS), lisinopril lowers blood pressure even in hypertensive patients with low-renin levels. ACE is identical to kininase II, the enzyme that degrades bradykinin. It remains uncertain whether elevated levels of bradykinin, a potent vasodilatory peptide, are important in the therapeutic effects of lisinopril.
In addition to lowering blood pressure, lisinopril reduces albuminuria by altering the histology and hemodynamics of the renal glomerular apparatus. Treatment with lisinopril does not affect glycemic control, as evidenced by the lack of a significant effect on glycosylated hemoglobin (HbA1c) levels.
Plays a positive role in restoring the function of damaged endothelium in patients with hyperglycemia.
It is known that in a clinical study involving 115 hypertensive children aged 6 to 16 years, patients weighing less than 50 kg received 0.625 mg, 2.5 mg, or 20 mg of lisinopril once daily, and patients weighing more than 50 kg received 1.25 mg, 5 mg, or 40 mg of lisinopril once daily. At the end of the second week of the study, lisinopril administered once daily reduced blood pressure in a dose-dependent manner, with consistent antihypertensive effects demonstrated at doses higher than 1.25 mg.
This effect was confirmed during the withdrawal phase, during which diastolic blood pressure was approximately 9 mm Hg higher in patients randomized to placebo than in patients randomized to medium and high doses of lisinopril. The dose-dependent antihypertensive effect of lisinopril was observed in several demographic subgroups: age, Tanner stage, gender, and race.
Pharmacokinetics
Lisinopril is an orally active, non-sulfhydryl ACE inhibitor.
Absorption.
With oral administration of lisinopril, maximum serum concentrations (Cmax) are reached after approximately 7 hours, although there is a tendency for a slight delay in the time required to reach peak serum concentrations in patients with acute myocardial infarction. Based on the amount excreted in the urine, the average absorption rate of lisinopril is approximately 25% for doses of 5–80 mg. Inter-patient variability can range from 6 to 60%. The absolute bioavailability of lisinopril is reduced to approximately 16% in patients with heart failure. Food intake does not affect the absorption of lisinopril.
Distribution.
Lisinopril does not bind to other serum proteins except circulating ACE. Animal studies show that lisinopril does not penetrate the blood-brain barrier well.
Breeding.
Lisinopril is not metabolized and is excreted exclusively by the kidneys unchanged. With multiple dosing, the effective half-life of accumulation is 12.6 hours. The clearance of lisinopril is approximately 50 ml/min in healthy volunteers. The decline in serum concentrations has a prolonged terminal phase, which does not contribute to drug accumulation. This terminal phase probably represents saturated binding to ACE and is not proportional to dose.
Liver dysfunction.
Impaired hepatic function in patients with cirrhosis resulted in reduced absorption of lisinopril (approximately 30% as determined by urinary recovery), but due to reduced clearance also resulted in increased exposure (approximately 50%) compared to healthy volunteers.
Renal impairment reduces the clearance of lisinopril, which is excreted by the kidneys. This reduction is clinically significant only when the glomerular filtration rate is less than 30 ml/min. In mild to moderate renal impairment (creatinine clearance 30-80 ml/min), the mean area under the curve (AUC) increases by only 13%. In severe renal impairment (creatinine clearance 5-30 ml/min), the mean AUC increases by 4.5 times compared to normal. Lisinopril can be removed by dialysis. During 4 hours of hemodialysis, plasma concentrations of lisinopril decreased by an average of 60% with a dialysis clearance of 40-55 ml/min.
Heart failure.
Patients with heart failure have a higher exposure to lisinopril compared to healthy subjects (an increase in AUC of 125% on average), but due to urinary excretion of lisinopril, have a reduced absorption of approximately 16% compared to healthy volunteers.
Children.
The pharmacokinetic profile of lisinopril was studied in 29 hypertensive patients aged 6 to 16 years with a glomerular filtration rate greater than 30 mL/min/1.73 m2. At doses of 0.1 to 0.2 mg/kg, steady-state plasma concentrations of lisinopril achieved within 6 hours and the extent of absorption based on urinary excretion were approximately 28%. These values were similar to those obtained in adult patients. The AUC and Cmax values in children in this study were consistent with those obtained in adults.
Elderly patients.
In elderly patients, lisinopril levels are higher; AUC is approximately 60% higher than in young patients.
Indication
Arterial hypertension. Heart failure (symptomatic treatment). Acute myocardial infarction (short-term treatment for 6 weeks in hemodynamically stable patients no later than 24 hours after acute myocardial infarction). Treatment of kidney disease in patients with arterial hypertension, type II diabetes mellitus and initial nephropathy.
Contraindication
Hypersensitivity to the active substance or excipients of the drug. Hypersensitivity to any other ACE inhibitor. History of angioedema associated with previous treatment with other ACE inhibitors. Hereditary or idiopathic angioedema. Pregnant women or women planning to become pregnant (see "Use during pregnancy or breastfeeding"). Breastfeeding. Simultaneous use of Diroton® with drugs containing aliskiren in patients with diabetes mellitus or renal insufficiency (glomerular filtration rate <60 ml/min/1.73 m2).
Interaction with other medicinal products and other types of interactions
Other antihypertensive agents
Taking other antihypertensive drugs (e.g. nitroglycerin and other nitrates or other vasodilators) may enhance the hypotensive effect of Diroton®.
Clinical trial data have shown that dual blockade of the RAAS through the combined use of ACE inhibitors, angiotensin II receptor blockers and aliskiren is associated with a higher incidence of adverse reactions such as hypotension, hyperkalemia and decreased renal function (including acute renal failure) compared with the use of a single RAAS-acting agent.
Diuretics
The addition of a diuretic to a patient taking lisinopril generally enhances the hypotensive effect.
Patients taking diuretics, especially those newly initiated on them, may experience excessive reduction in blood pressure after initiating therapy with lisinopril. The likelihood of symptomatic hypotension resulting from lisinopril may be reduced by discontinuing the diuretic prior to initiating therapy with lisinopril.
Potassium-sparing diuretics, potassium supplements, or salt substitutes containing potassium
Although serum potassium levels were generally within normal limits in clinical trials, hyperkalemia has been observed in some patients. Risk factors for the development of hyperkalemia include renal insufficiency, diabetes mellitus, and concomitant use of potassium-sparing diuretics (e.g., spironolactone, triamterene, or amiloride), potassium supplements, or potassium-containing salt substitutes. The use of potassium supplements, potassium-sparing diuretics, or potassium-containing salt substitutes, especially in patients with impaired renal function, may lead to significant increases in serum potassium. When lisinopril is used with potassium-losing diuretics, diuretic-induced hypokalemia may be attenuated.
With the simultaneous use of ACE inhibitors with NSAIDs (for example, acetylsalicylic acid as an anti-inflammatory drug, COX-2 inhibitors and non-selective NSAIDs), a weakening of the antihypertensive effect is possible. The simultaneous use of ACE inhibitors and NSAIDs may lead to deterioration of renal function, there is also a possibility of developing acute renal failure and an increase in serum potassium, especially in patients with a history of impaired renal function. Such effects are usually reversible. Such a combination should be prescribed with caution, especially in elderly patients. Patients should receive a sufficient volume of fluid, in addition, the need to monitor renal function should be considered immediately after the start of combination therapy and periodically thereafter.
Lisinopril can be used concomitantly with acetylsalicylic acid (in cardiological doses), thrombolytic drugs, beta-blockers and/or nitrates.
Lithium preparations
Reversible increases in serum lithium concentrations and toxic reactions have been reported with concomitant use of lithium and ACE inhibitors. Concomitant use of thiazide diuretics may increase the risk of lithium toxicity and may exacerbate existing toxicity with ACE inhibitors. The use of lisinopril with lithium is not recommended, but if the combination proves necessary, serum lithium levels should be monitored closely (see section 4.4).
Antidiabetic agents
Concomitant use of antidiabetic agents (insulin, oral hypoglycaemic agents) with ACE inhibitors may lead to an increased blood glucose lowering effect with a risk of hypoglycaemia. This phenomenon is generally more likely to occur during the first week of combined treatment and in patients with renal insufficiency.
Sympathomimetics
Sympathomimetics may reduce the antihypertensive effect of ACE inhibitors.
Concomitant administration of tricyclic antidepressants, neuroleptics or anesthetics may enhance the hypotensive effect of Diroton®.
Gold
Nitritoid reactions (symptoms of vasodilation including flushing, nausea, dizziness and hypotension, which may be severe) following gold injections (e.g. sodium aurothiomalate) are more common in patients receiving concomitant ACE inhibitors.
Tissue plasminogen activators
Concomitant use with tissue plasminogen activators may increase the risk of angioedema.
Application features
Symptomatic hypotension
Symptomatic hypotension is less common in patients with uncomplicated hypertension. In hypertensive patients receiving lisinopril, hypotension is more likely to occur in patients who have been volume-depleted by diuretic therapy or a salt-restricted diet, dialysis, diarrhoea or vomiting, and in patients with severe renin-dependent hypertension. Symptomatic hypotension has been reported in patients with symptomatic heart failure, with or without renal insufficiency. Symptomatic hypotension is more likely to occur in patients with more severe heart failure, high doses of loop diuretics, hyponatraemia or functional renal insufficiency. In patients at increased risk of symptomatic hypotension, initiation of therapy and dose adjustment should be carefully monitored. This also applies to patients with ischemic heart disease or cerebrovascular disease, in whom excessive reduction in blood pressure may lead to myocardial infarction or cerebrovascular accident.
If hypotension occurs, the patient should be placed in a horizontal position (as a mandatory measure), and intravenous fluid administration (saline solution) is recommended if necessary. Transient hypotension is usually not a contraindication to further use of the drug. Further treatment is usually without complications after normalization of blood pressure by increasing blood volume.
In the event of acute myocardial infarction, lisinopril should not be used if treatment with vasodilators could worsen the patient's hemodynamic status (e.g., if systolic blood pressure is 100 mm Hg or lower) or in the event of cardiogenic shock. If systolic blood pressure is 120 mm Hg or lower, low doses should be used for the first 3 days after the infarction. Maintenance doses should be reduced to 5 mg or temporarily to 2.5 mg if systolic blood pressure is 100 mm Hg or lower. If hypotension persists (systolic blood pressure less than 90 mm Hg for more than 1 hour), treatment with this drug should be discontinued.
Aortic and mitral valve stenosis/hypertrophic cardiomyopathy
As with all ACE inhibitors, lisinopril should be administered with caution to patients with mitral valve stenosis or left ventricular outflow obstruction such as aortic stenosis or hypertrophic cardiomyopathy.
Kidney dysfunction
In patients with renal impairment (creatinine clearance < 80 ml/min), the initial dose of lisinopril should be adjusted according to creatinine clearance (see Table 1 in the Dosage and Administration section) and the clinical response to treatment. Routine monitoring of serum potassium and creatinine is part of standard medical practice in these patients.
In patients with heart failure, hypotension occurring after initiation of therapy with ACE inhibitors may lead to deterioration of renal function. In such cases, acute renal failure may occur, which is usually reversible.
Some patients with bilateral renal artery stenosis or stenosis of the artery to a solitary kidney have developed increases in blood urea and serum creatinine during treatment with ACE inhibitors, which usually return to normal after discontinuation of treatment. This is particularly likely in patients with renal insufficiency. In the presence of renovascular hypertension, there is an increased risk of severe hypotension and renal insufficiency. Treatment of such patients should be initiated under close medical supervision with low doses and with careful titration of the dose. Since diuretic treatment is an additional risk factor, their use should be discontinued, and renal function should be monitored during the first weeks of treatment with lisinopril.
Some hypertensive patients without underlying renal vascular disease have developed increases in blood urea and serum creatinine, usually minor and transient, especially when lisinopril has been given concomitantly with diuretics. This may occur primarily in patients with pre-existing renal impairment. Dosage reduction and/or discontinuation of the diuretic and/or lisinopril may be necessary.
Treatment should not be initiated in the event of acute myocardial infarction, in patients with signs of renal impairment (serum creatinine level above 177 μmol/l and/or albuminuria above 500 mg/24 hours). In the event of renal impairment developing during treatment (serum creatinine level above 265 μmol/l or twice the initial level), the physician should consider discontinuing treatment.
Hypersensitivity, angioedema
Rare cases of angioedema of the face, extremities, lips, tongue, pharynx and/or larynx have been reported in patients treated with ACE inhibitors, including lisinopril. This may occur at any time during treatment. In such cases, the drug should be discontinued immediately, the patient should receive appropriate treatment and be kept under medical supervision until the symptoms have completely disappeared. In cases where the swelling is localized to the tongue, which does not cause respiratory distress, the patient may require prolonged observation, since treatment with antihistamines and corticosteroids may not be sufficient.
Very rarely, angioedema associated with laryngeal or tongue oedema can be fatal. If the oedema involves the tongue, glottis or larynx, respiratory distress may occur, particularly in patients who have previously undergone surgery on the respiratory tract. In such cases, emergency treatment should be initiated immediately. This may include the administration of adrenaline and/or the maintenance of a patent airway. The patient should be kept under close medical supervision until complete and sustained resolution of symptoms.
ACE inhibitors may cause more severe angioedema in patients of black race than in patients of other races.
Patients with a history of angioedema unrelated to ACE inhibitor use may be at increased risk of developing angioedema in response to this class of drugs (see section 4.3).
Hemodialysis
Anaphylactoid reactions have been reported in patients dialyzed with high-flux polyacrylonitrile membranes (e.g. AN 69) and concomitantly treated with ACE inhibitors. This combination should be avoided and consideration should be given to using a different type of dialysis membrane or a different class of antihypertensive agent.
Life-threatening anaphylactoid reactions (such as profound hypotension, respiratory distress, vomiting, allergic skin reactions) have rarely occurred in patients receiving ACE inhibitors during LDL apheresis with dextran sulfate. These reactions have been avoided by temporarily stopping ACE inhibitors before each apheresis.
Desensitization
Patients receiving ACE inhibitors during desensitization therapy (e.g., to hymenoptera venom) have developed persistent anaphylactoid reactions. These reactions have been avoided in such patients by temporarily stopping ACE inhibitors, but the reactions have recurred after inadvertent re-administration of the drug.
Neutropenia/agranulocytosis
Neutropenia/agranulocytosis, thrombocytopenia and anemia may develop during treatment with ACE inhibitors. Neutropenia has been rarely observed in patients with normal renal function and in the absence of other complications. Neutropenia and agranulocytosis resolved after discontinuation of ACE inhibitors. Diroton® should be used with particular caution in patients with collagen vascular disease (e.g., systemic lupus erythematosus or scleroderma), during concomitant immunosuppressive therapy (e.g., corticosteroids, cytotoxic agents, antimetabolites), allopurinol or procainamide, or a combination of these complicating factors, especially in the presence of impaired renal function. The use of ACE inhibitors in such patients may be accompanied by the development of particularly severe infections, which in some cases do not respond to intensive antibiotic treatment.
In such patients, the level of leukocytes in the blood should be checked periodically during treatment with Diroton®, and the patient should also be warned about the need to report the occurrence of any signs of infections.
Ethnic characteristics (race)
ACE inhibitors cause angioedema more frequently in black patients than in non-blacks. As with other ACE inhibitors, lisinopril may be less effective in lowering blood pressure in black patients than in non-blacks because of a higher proportion of blacks with low-renin hypertension.
Liver failure
Very rarely, ACE inhibitors have been associated with a syndrome that begins with cholestatic jaundice and progresses rapidly to fulminant necrosis and (sometimes) death. The underlying cause of this process is unknown.
If patients taking Diroton® develop jaundice or marked elevations in liver enzymes, the drug should be discontinued and appropriate medical care should be provided.
Dual blockade of RAAS
There is evidence that the concomitant use of ACE inhibitors, angiotensin II receptor blockers and aliskiren increases the risk of hypotension, hyperkalemia and decreased renal function (including acute renal failure). Therefore, dual blockade of the RAAS through the combined use of ACE inhibitors, angiotensin II receptor blockers and aliskiren is contraindicated.
If the use of dual blockade is considered absolutely necessary, it should only be done under specialist supervision and with frequent and careful monitoring of renal function, electrolytes and blood pressure. ACE inhibitors and angiotensin II receptor blockers should not be used concomitantly in patients with diabetic nephropathy.
Hyperkalemia
Treatment with ACE inhibitors, including lisinopril, may increase serum potassium levels. The risk of hyperkalemia is increased in the presence of the following factors: renal insufficiency, diabetes mellitus, concomitant use of potassium-sparing diuretics, potassium supplements or salt substitutes containing potassium, concomitant use of drugs that increase serum potassium levels (e.g. heparin).
If concomitant use of the above drugs is necessary, regular monitoring of serum potassium levels is recommended.
Cough
Cough has been reported during treatment with ACE inhibitors. The cough is usually dry, nonproductive, persistent and resolves after discontinuation of treatment. Cough caused by ACE inhibitors should be considered as part of the differential diagnosis of cough.
Surgery/anesthesia
In patients undergoing surgery and those receiving antihypertensive agents during anaesthesia, lisinopril may block the formation of angiotensin II due to compensatory renin release. If hypotension occurs, which is thought to be due to this mechanism, treatment may be by increasing the circulating blood volume.
Diabetes mellitus
More careful glucose monitoring is required during the first month of treatment with ACE inhibitors in addition to prior treatment with insulin or oral hypoglycemic agents.
Lithium preparations
In general, the combination of lithium and lisinopril is not recommended.
Ability to influence reaction speed when driving vehicles or other mechanisms
Therefore, you should refrain from driving or operating other mechanisms until you determine your individual reaction to the drug.
Use during pregnancy or breastfeeding
Pregnancy. The drug is contraindicated for use in pregnant women or women planning to become pregnant. If pregnancy is confirmed during treatment with this drug, its use should be discontinued immediately and, if necessary, replaced with another drug approved for use in pregnant women (see section "Contraindications").
Breastfeeding: Since there is no information on the use of lisinopril during breastfeeding, lisinopril is contraindicated during this period.
Method of administration and doses
Dosage should be individualized according to the patient's disease and blood pressure response. Take orally once daily, at the same time each day, regardless of food intake.
Arterial hypertension.
Diroton® can be used as monotherapy or in combination with other classes of antihypertensive agents.
Initial dose. The recommended initial dose is usually 10 mg. In patients with a very active RAAS (especially in renovascular hypertension, sodium and/or dehydration, cardiac decompensation or severe hypertension), an excessive decrease in blood pressure may occur after the first dose. Therefore, at the beginning of treatment, such patients should be under medical supervision, the recommended initial dose is 2.5-5 mg. Patients with renal insufficiency also need to reduce the initial dose (see Table 1 below).
Maintenance dose. The usual effective maintenance dose is 20 mg once daily. If the desired therapeutic effect is not achieved after 2-4 weeks of use of the prescribed dose, the dose may be increased. The maximum daily dose should not exceed 80 mg.
If possible, patients taking diuretics should discontinue these drugs 2-3 days before starting lisinopril therapy. If this is not possible, the initial dose of lisinopril should not exceed 5 mg/day. Renal function and serum potassium should be monitored. Subsequent doses of Diroton® should be adjusted according to blood pressure response. Diuretic therapy may be resumed if necessary.
Symptomatic hypotension may occur after initiation of treatment with lisinopril. This is more likely in patients receiving diuretics during treatment with lisinopril. Since dehydration and/or excess sodium excretion may occur in these patients, the drug should be used with caution.
Patients with renal failure.
Dosage for patients with renal impairment should be based on creatinine clearance as shown in Table 1 below.
Table 1.
Dosage selection for patients with renal insufficiency
Creatinine clearance (ml/min)
Starting dose (mg/day)
31-80
5-10
10-30
2.5-5
<10 (including dialysis patients)*
2.5*
*dosage and/or frequency of administration should be calculated based on blood pressure response.
The dose can be gradually increased until blood pressure normalizes, or until the maximum dose of 40 mg/day is reached.
Use in children with arterial hypertension aged 6 to 16 years.
The recommended starting dose is 2.5 mg/day for patients weighing 20 to 50 kg and 5 mg/day for patients weighing ≥ 50 kg. The dose should be adjusted individually to a maximum of 20 mg/day for patients weighing 20 to 50 kg and up to 40 mg/day for patients weighing ≥ 50 kg.
≥ 50 kg. Doses above 0.61 mg/kg (or exceeding 40 mg) have not been studied in children (see section 5.1).
Children with reduced renal function should be given a lower initial dose or the dosing interval should be increased.
Heart failure.
In patients with symptomatic heart failure, Diroton® may be used as an adjunct to diuretics and, if necessary, digitalis or beta-blockers. Treatment should be monitored to determine the initial effect on blood pressure. The initial daily dose of lisinopril, 2.5 mg, may be gradually increased to a maintenance dose.
The recommended dose increase rate after 2 weeks is no more than 10 mg.
The dose of Diroton® should be increased to the maximum daily dose tolerated by the patient - 35 mg/day.
Dosage selection should be based on the clinical response of each individual patient.
Patients at high risk of symptomatic hypotension, such as patients with salt depletion with or without hyponatremia, patients with hypovolemia, or patients who have undergone intensive diuretic therapy, should be rehydrated, if possible, before initiating therapy with Diroton®. Renal function and serum potassium should be monitored.
Acute myocardial infarction.
Initial dose (first 3 days after a heart attack).
Treatment with Diroton® can be started within 24 hours of the first symptoms. Treatment should not be started if the systolic blood pressure is less than 100 mm Hg. The initial dose of Diroton® is 5 mg orally, followed by 5 mg after 24 hours, 10 mg after 48 hours, and then 10 mg once daily.
With low systolic blood pressure (≤ 120 mm Hg) or during the first 3 days after a heart attack, a low dose (2.5 mg/day) is indicated.
In case of renal insufficiency (creatinine clearance <80 ml/min), the initial dose of Diroton® should be selected according to the patient's creatinine clearance (see Table 1).
Maintenance dose. The maintenance dose is 10 mg once a day. In case of arterial hypotension (systolic pressure ≤100 mm Hg), the maintenance daily dose is 5 mg per day; if necessary, this dose can be reduced to 2.5 mg. If prolonged arterial hypotension is observed after taking Diroton® (systolic pressure remains less than 90 mm Hg for more than 1 hour), therapy with the drug should be discontinued.
Therapy is recommended for 6 weeks, after which the patient's condition should be re-evaluated. Patients with symptoms of heart failure should continue treatment with Diroton®.
Diabetic nephropathy.
For patients with type 2 diabetes, hypertension and early nephropathy, the dose is 10 mg once daily, which, if necessary, can be increased to 20 mg once daily to achieve a stable diastolic blood pressure below 90 mm Hg.
In case of renal insufficiency (creatinine clearance <80 ml/min), the initial dose of Diroton® should be selected according to the patient's creatinine clearance (see Table 1).
Children
In children with hypertension aged > 6 years, the drug has limited efficacy and safety, but there are no data for other indications (see section "Pharmacological properties"). Lisinopril is not recommended for the treatment of children for indications other than arterial hypertension.
Lisinopril is not recommended for use in children under 6 years of age or in children with severe renal impairment (GFR <30 ml/min/1.73 m2) (see section 5.1).
Use in elderly patients.
Clinical trials have not shown any difference in the efficacy or safety of lisinopril treatment based on age. Since renal function is often impaired in the elderly, the initial dose of lisinopril should be adjusted according to the guidelines in Table 1. Thereafter, the dose should be adjusted according to response and blood pressure.
Use in kidney transplant patients.
There is no experience with the use of lisinopril in patients with a kidney transplant, therefore, treatment with Diroton® is not recommended in such patients.
Children
The drug Diroton® can only be used in children with arterial hypertension aged 6 years and older.
Overdose
Data on overdose of Diroton® in humans are limited. Symptoms associated with overdose of ACE inhibitors may include hypotension, circulatory shock, electrolyte imbalance, renal failure, hyperventilation, tachycardia, palpitations, bradycardia, dizziness, restlessness and cough.
In case of overdose, intravenous administration of saline solution is recommended. In cases of hypotension, the patient should be placed in a horizontal position. If possible, infusion of angiotensin II and/or intravenous administration of catecholamines can be used.
If the drug has been used recently, measures should be taken to remove lisinopril from the body (e.g., induce vomiting, gastric lavage, use absorbents and sodium sulfate). Lisinopril can be removed from the general circulation by hemodialysis. It is necessary to frequently check vital signs, electrolytes and serum creatinine. The use of a pacemaker is indicated in bradycardia resistant to therapy.
Adverse reactions
The following adverse reactions have been observed and reported during treatment with lisinopril and other ACE inhibitors with the following frequencies.
Table 2.
Organ system classes
Frequent
(≥1/100 to <1/10)
Infrequent
(≥1/1000 to <1/100)
Single
(≥1/10,000 to <1/1,000)
Rare
(<1/10000)
Frequency not known (cannot be estimated from the available data)
Blood and lymphatic system disorders
bone marrow suppression,
anemia,
thrombocytopenia,
leukopenia,
neutropenia,
Specifications
Characteristics
Active ingredient
Lisinopril
Adults
Can
ATC code
C MEDICINES AFFECTING THE CARDIOVASCULAR SYSTEM; C09 MEDICINES AFFECTING THE RENIN-ANGIOTENSIN SYSTEM; C09A ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS; C09A A ACE inhibitors, single-component; C09A A03 Lisinopril
Country of manufacture
Hungary
Diabetics
With caution
Dosage
5 мг
Drivers
Contraindicated until individual reaction is detected
For allergies
With caution
For children
It is impossible.
Form
Tablets
Method of application
Inside, solid
Nursing
It is impossible.
Pregnant
It is impossible.
Primary packaging
blister
Producer
Gideon Richter
Quantity per package
28 pcs
Trade name
Diroton
Vacation conditions
By prescription
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