Fosinap, tablets 20 mg 28 pcs

Pharmacodynamics

ACE inhibitor. It has hypotensive, vasodilatory, diuretic and potassium-saving effects. Fosinopril prevents conversion of angiotensin I into vasoconstrictor angiotensin II; as a result, vasopressor activity and aldosterone secretion decrease, which can lead to a slight increase in serum potassium ions with simultaneous loss of sodium ions and fluid. As a result, total peripheral vascular resistance and systemic arterial pressure (BP) decrease. Suppresses aldosterone synthesis and inhibits tissue ACE.

Fosinopril inhibits metabolic degradation of bradykinin, which has a potent vasopressor effect; this may increase the antihypertensive effect of the drug.

The decrease of BP is not accompanied with changes in the volume of circulating blood, cerebral and renal blood flow, blood supply of internal organs, skeletal muscles, skin, myocardial reflex activity. In arterial hypertension and left ventricular hypertrophy, treatment leads to a decrease in the mass of the left ventricle and a decrease in the thickness of the interventricular septum. Prolonged therapy does not result in metabolic disturbances. After oral administration, the hypotensive effect develops within 1 hour, reaches a maximum after 3 to 6 hours and persists for 24 hours.

In chronic heart failure, positive effects of fosinopril are achieved mainly through inhibition of renin-aldosterone system activity. ACE inhibition leads to reduction of both preload and postload on myocardium.

Fosinopril helps to increase exercise tolerance and reduce the severity of the course of chronic heart failure.

Pharmacokinetics

After oral administration, absorption from the gastrointestinal tract is about 30-40%. The degree of absorption is independent of food intake, but the rate of absorption may be delayed.

The metabolism of fosinopril by enzymes to form fosinoprilate occurs mainly in the liver and in the mucosa of the gastrointestinal tract.

The time of reaching the maximum plasma concentration of fosinoprilat is 3 hours and does not depend on the dose taken.

The binding to plasma proteins is more than 95%. Fosinoprilat has relatively low volume of distribution and is insignificantly bound to the cellular components of the blood. It does not penetrate the blood-brain barrier.

Fosinopril is excreted from the body equally by the kidneys and through the liver. In patients with arterial hypertension with normal renal and hepatic function, the elimination half-life of fosinoprilat is about 11.5 h. In chronic heart failure, the elimination half-life is 14 h.

Indications

Active ingredient

Composition

1 tablet contains:

acting substance:

fosinopril sodium 20.00 mg

excipients:

colloidal silica (aerosil) 1.0 mg;

croscarmellose sodium (primellose) 5.7 mg;

Lactose (milk sugar) 97.3 mg;

Macrogol (polyethylene glycol 4000) 1.0 mg;

sodium stearyl fumarate 1.5 mg;,

povidone (collidone 30) 10.5 mg;

microcrystalline cellulose 73.0 mg.

How to take, the dosage

The drug is prescribed orally, regardless of meals. Take without chewing, with a small amount of liquid. The dose is set individually.

In case of arterial hypertension, the recommended starting dose is 10 mg once daily. The dose should be adjusted depending on the dynamics of BP decrease. Doses range from 10 to 40 mg once daily. The maximum daily dose is 40 mg.

In chronic heart failure, the recommended starting dose is 5 mg (1/2 tablet of 10 mg) once or twice daily. The maximum daily dose is 40 mg/day.

Patients with impaired renal and/or hepatic function and elderly patients do not require dosage adjustment.

Interaction

Concomitant use of antacids (including aluminum hydroxide, magnesium hydroxide) may decrease absorption of fosinopril (fosinopril and these agents should be taken at least 2 hours apart).

Patients receiving fosinopril concomitantly with lithium preparations may have increased plasma lithium concentrations and risk of lithium intoxication (plasma lithium concentrations should be monitored).

When prescribing fosinopril, it should be considered that indomethacin and other nonsteroidal anti-inflammatory drugs (including acetylsalicylic acid in dose greater than 3 g and cyclooxygenase-2 inhibitors) may decrease the antihypertensive effect of ACE inhibitors, especially in patients with low-grade hypertension.

When fosinopril is coadministered with diuretics or in combination with a strict diet restricting sodium intake or with hemodialysis, severe arterial hypotension may develop, especially in the first hour after the initial dose of fosinopril.

When fosinopril is coadministered with potassium preparations, potassium-saving diuretics (including amiloride, spironolactone, triamterene), with food supplements containing potassium, the risk of hyperkalemia increases. In patients with chronic heart failure, diabetes, simultaneously taking potassium-saving diuretics, potassium-containing salt substitutes, or other agents that cause hyperkalemia (e.g., heparin), ACE inhibitors increase the risk of hyperkalemia.

Fosinopril increases the hypoglycemic effect of sulfonylurea derivatives, insulin.

Concomitant use with allopurinol, cytostatics, immunosuppressants, procainamide increases the risk of leukopenia.

Estrogens weaken the hypotensive effect of fosinopril because of its ability to retain fluid.

Antihypertensives, opioid analgesics, and general anesthesia drugs increase the hypotensive effect of fosinopril.

The bioavailability of fosinopril with chlorthalidone, nifedipine, propranololol, hydrochlorothiazide, cimetidine, metoclopramide, propantelin bromide, digoxin, acetylsalicylic acid and warfarin does not change.

Special Instructions

Prior to treatment initiation, a review of previous antihypertensive therapy, degree of BP elevation, salt and/or fluid restriction of the diet, and other clinical situations is required.

If possible, prior antihypertensive treatment should be discontinued several days before starting Fosinap.

To reduce the likelihood of arterial hypotension, diuretics should be stopped 2-3 days before starting treatment with Fosinap.

Before and during treatment with Fosinap, BP, renal function, potassium ions, creatinine, urea, electrolyte concentrations and hepatic transaminase activity in blood should be monitored.

The development of angioedema has been reported in patients taking fosinopril. If swelling of the tongue, pharynx or larynx spreads, airway obstruction may develop with possible lethal outcome. If these reactions develop, the drug should be discontinued and emergency therapy measures should be taken, including subcutaneous administration of epinephrine (adrenaline) solution (1:1000).

In rare cases, intestinal mucosal edema has been observed while taking ACE inhibitors. Intestinal mucosal edema should be considered in the differential diagnosis in patients with complaints of abdominal pain during treatment with ACE inhibitors. Symptoms disappeared after discontinuation of ACE inhibitors.

Anaphylactic reactions may develop during hemodialysis through high-flow membranes and during low-density lipoprotein plasmapheresis with adsorption on dextran sulfate during therapy with ACE inhibitors. In such cases, another type of dialysis membrane or other drug treatment should be considered.

The development of agranulocytosis and suppression of bone marrow function during treatment with ACE inhibitors is possible. These cases occur more frequently in patients with impaired renal function, especially in the presence of systemic connective tissue diseases (including systemic lupus erythematosus or scleroderma). The total leukocyte count and leukocytic formula should be controlled before and during therapy with ACE inhibitors (once a month during the first 3-6 months of therapy and during the first year of therapy in patients with increased risk of neutropenia).

Symptomatic arterial hypotension when using ACE inhibitors most often develops in patients after intensive treatment with diuretics, diet that limits salt intake, or during renal dialysis. Transient arterial hypotension is not a contraindication for further use of the drug.

In patients with arterial hypertension with bilateral renal artery stenosis or artery stenosis of the single kidney, as well as with concomitant use of diuretics in patients with unchanged renal function, serum urea nitrogen and creatinine concentrations may increase during treatment with ACE inhibitors. If these effects do not go away after stopping treatment, doses of Fosinap and/or a diuretic should be reduced.

In some cases in patients with severe chronic heart failure, treatment with ACE inhibitors may cause a more pronounced antihypertensive effect, which may lead to oliguria or azotemia with fatal outcome. Therefore, patient monitoring is necessary when treating chronic heart failure with Fosinap, especially during the first 2 weeks of treatment and with any increase in the dose of Fosinap or a diuretic.

In the event of marked jaundice and marked elevation of hepatic transaminase activity, therapy with Fosinap should be discontinued and appropriate treatment administered.

ACE inhibitors may increase the hypotensive effect of agents used for general anesthesia. The anesthesiologist should be advised of the use of ACE inhibitors before surgical procedures (including dentistry).

Cautions should be taken when exercising or in hot weather because of the risk of dehydration and arterial hypotension due to decreased circulating blood volume.

Impact on driving and operating machinery

Perhaps caution should be exercised when driving vehicles or performing other work requiring increased attention because dizziness may develop, especially after the initial dose of Fosinap.

Contraindications

Side effects

Cardiovascular system: marked BP decrease, orthostatic hypotension, collapse, tachycardia, palpitations, arrhythmias, angina pectoris, myocardial infarction, blood flushes to the face, fainting, cardiac arrest.

Urinary system disorders: development or worsening of symptoms of chronic renal failure, proteinuria.

Central and peripheral nervous system disorders: stroke, cerebral vascular ischemia, dizziness, headache, weakness, memory impairment; when used in high doses – insomnia, anxiety, depression, confusion, somnolence, paresthesias.

Sensory organs: hearing and vision disorders, tinnitus.

Digestive system disorders: nausea, diarrhea, intestinal obstruction, pancreatitis, hepatitis, cholestatic jaundice, abdominal pain, vomiting, constipation, anorexia, stomatitis, glossitis, dysphagia, flatulence, appetite disorders, weight changes, dry mouth; intestinal edema (very rare).

Respiratory system: “dry” cough, pulmonary infiltrates, bronchospasm, dyspnea, rhinorrhea, pharyngitis, dysphonia, nasal bleeding.

Hematopoietic organs: lymphadenitis.

Muscular system disorders: arthritis.

Metabolism: gout.

Allergic reactions: skin rash, itching, angioedema.

Laboratory disorders: hypercreatininemia, increased concentration of urea, increased activity of “hepatic” transaminases, hyperbilirubinemia, hyperkalemia, hyponatremia; decrease of hemoglobin concentration and hematocrit, increased erythrocyte sedimentation rate, leukopenia, neutropenia, eosinophilia.

Fetal effects: impaired fetal renal development, decreased fetal and neonatal BP, impaired renal function, hyperkalemia, skull bone hypoplasia, oligohydramnios, limb contractures, lung hypoplasia.

Overdose

Symptoms: marked BP decrease, bradycardia, shock, impaired water-electrolyte state, acute renal failure, stupor.

Treatment: the drug should be stopped, gastric lavage, sorbents (e.g. activated charcoal), vasopressor drugs, infusion of 0.9% sodium chloride solution and further symptomatic and supportive treatment are indicated. The use of hemodialysis is ineffective.

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