Fosinopril, tablets 10 mg 30 pcs

Pharmgroup:

APP inhibitor.

Pharmic action:

The ACE inhibitor, has hypotensive, vasodilatory, diuretic and potassium-saving effects. Reduces the formation of angiotensin II from angiotensin I, which leads to a decrease in RPS and systemic BP.
Suppresses the synthesis of aldosterone, inhibits tissue ACE.

The hypotensive effect is also due to inhibition of bradykinin metabolism, which has a pronounced vasodilator effect. Decrease of AP is not accompanied by changes in CBC, cerebral and renal blood flow, blood supply of internal organs, skeletal muscles, skin, myocardial reflex activity.

In hypertension and LV hypertrophy, treatment leads to a decrease in its mass and septal wall thickness. Long-term treatment does not lead to metabolic disturbances.

After oral administration, the hypotensive effect develops within 1 h, reaches a maximum after 3-6 h and lasts for 24 h.

Pharmacokinetics:

Absorption – 36% (regardless of ingestion). In the gastrointestinal mucosa and the liver is hydrolyzed to form fosinoprilat. TCmax – 3 hours, T1/2 – 11.5 hours.

Cross-linkage to plasma proteins is 95%, it has relatively low volume of distribution and is poorly sorbed by cellular components.
It does not penetrate through the BBB. It is excreted with bile and urine.

Indications

Arterial hypertension, CHF.

Active ingredient

Composition

Fosinopril 10 mg.

How to take, the dosage

Overly, 10 mg/day, once daily; if necessary, the dose may be increased to 40 mg.

The dose should be adjusted according to the dynamics of BP.

Interaction

It increases hypoglycemic effect of sulfonylurea derivatives, insulin, risk of leukopenia when concomitant use with allopurinol, cytostatic drugs, immunosuppressants, procainamide.

In concomitant use with preparations of Li+ an increase in its concentration in blood is observed.

Hypotensive drugs, diuretics, narcotic analgesics, drugs for general anesthesia increase the hypotensive effect. NSAIDs and table salt weaken the effect.

K+ preparations, potassium-saving diuretics (amiloride, spironolactone, triamterene) increase the risk of hyperkalemia.
NSAIDs including selective COX-2 inhibitors and estrogens (fluid retention) may decrease the intensity of hypotensive effect.
Simultaneous use of ACE inhibitors and gold drugs (sodium aurothiomalate) described symptomcomplex including facial hyperemia, nausea, vomiting and BP decrease.

Insulin and oral hypoglycemic drugs – risk of hypokalemia.

Special Instructions

Patients with malignant arterial hypertension or concomitant decompensated CHF should start treatment in a hospital setting.
Before therapy with ACE inhibitors and during treatment, total leukocyte count and leukocyte formula determination are performed (once a month during the first 3-6 months of treatment and at periodic intervals up to 1 year in patients with increased risk of neutropenia: in renal function disorders, systemic connective tissue diseases, in those receiving high doses), as well as at first signs of infection.
Before and during the treatment it is necessary to control BP, renal function, plasma concentration of K+, Hb and creatinine, urea, electrolyte concentration and activity of “liver” enzymes in blood.

Based on the results of epidemiological studies, it is assumed that simultaneous use of ACE inhibitors and insulin, as well as oral hypoglycemic drugs may lead to the development of hypoglycemia. The highest risk of development is observed during the first weeks of combined therapy, as well as in patients with impaired renal function. In patients with diabetes mellitus careful glycemic control is required, especially during the first month of ACE inhibitor therapy.

Patients on a low-salt or no-salt diet should be treated with caution (increased risk of hypotension).

Safety and effectiveness in pediatric practice: In newborns who have had intrauterine exposure to ACE inhibitors, close monitoring is recommended to detect hypotension, oliguria, and hyperkalemia.

In newborns and infants, there is a risk of oliguria and neurologic impairment, possibly due to decreased renal and cerebral blood flow due to lower BP caused by ACE inhibitors; lower initial doses and close monitoring are recommended.
Caution should be exercised when driving motor vehicles or performing other work requiring increased attention because dizziness may occur, especially after the initial dose of ACE inhibitor in patients taking diuretic drugs.

Cautions should be taken when exercising or in hot weather because of the risk of dehydration and decrease in BP due to decreased fluid volume.

Before surgery (including dentistry), the surgeon/anesthesiologist should be warned about the use of ACE inhibitors.

The use of ACE inhibitors in the second to third trimesters of pregnancy can cause oligohydroamnion, fetal and neonatal hypotension, oliguria and fatal outcomes.

Contraindications

Hypersensitivity to fosinopril, pregnancy, lactation.

With caution. Angioneurotic edema in history of ACE inhibitor therapy, hereditary or idiopathic angioedema, aortic stenosis, cerebro- and cardiovascular diseases (including cerebrovascular insufficiency, CHD, coronary artery disease), severe autoimmune systemic connective tissue diseases (including SLE, scleroderma), suppression of medullary hematopoiesis, diabetes mellitus, hyperkalemia, bilateral stenosis of renal arteries, stenosis of artery of single kidney, conditions after kidney transplantation, liver insufficiency, Na+-restricted diet, conditions accompanied with OBC reduction (including diarrhea, vomiting), elderly age, age under 18 years old (safety and efficacy of administration have not been studied).

Side effects

System adverse reactions: decreased BP, orthostatic collapse, tachycardia, palpitations, arrhythmias, angina pectoris, myocardial infarction.

Urinary system disorders: development or worsening of CPN, proteinuria.

Nervous system disorders: stroke, cerebral ischemia, dizziness, headache, weakness; when used in high doses – insomnia, anxiety, depression, confusion, vestibular disorders, paresthesias.

Sensory organs: hearing and vision disorders, tinnitus.

Digestive system disorders: nausea, intestinal obstruction, pancreatitis, hepatitis, cholestatic jaundice, abdominal pain, vomiting, dyspepsia, constipation, decreased appetite, stomatitis, glossitis.

Respiratory system: dry cough, pulmonary infiltrates, bronchospasm, dyspnea, rhinorrhea, pharyngitis, dysphonia.

Allergic, toxic-allergic and immunopathological reactions, including angioedema of the small intestine (very rare).

Laboratory parameters: hypercreatininemia, increased concentration of urea, increased “hepatic” transaminase activity, hyperbilirubinemia, hyperkalemia, hyponatremia; decreased Hb and hematocrit, neutropenia, leukopenia, eosinophilia, increased sedimentation. Cases of hypoglycemia have been reported in patients with diabetes mellitus who were taking insulin and oral hypoglycemic agents.

Teratogenic, fetotoxic effects – impaired fetal renal development, decreased fetal and neonatal BP, impaired renal function, hyperkalemia, skull hypoplasia, oligohydramnion, limb contracture, skull deformity, lung hypoplasia.

Overdose

Symptoms: decreased BP, bradycardia, shock, water-electrolyte imbalance, acute renal failure, stupor.

Treatment: place patient in supine position with elevated legs.

In mild cases of overdose – gastric lavage, administration of adsorbents and sodium sulfate within 30 minutes after intake.
In case of BP decrease – intravenous administration of catecholamines, angiotensin II; in bradycardia – administration of pacing agent.
Not excreted during hemodialysis.

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