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Torsemide 10 mg; Excipients: lactose monohydrate - 150 mg; corn starch - 35 mg; sodium carboxymethyl starch (sodium starch glycolate, type A) - 2 mg; colloidal silicon dioxide - 1.5 mg; magnesium stearate - 1.5 mg

Pharmacological effect

Torsemide is a “loopback” diuretic. The main mechanism of action of the drug is due to the reversible binding of Torsemide to the kontransiorger of sodium / chlorine / potassium ions located in the apical membrane of the thick segment of the ascending loop of Gale, as a result of which the reabsorption of sodium ions decreases or the osmotic pressure of the intracellular fluid and water reabsorption are reduced. Thorassmide blocks aldosteropic myocardial receptors, reduces fibrosis and improves the diastolic function of the myocardium .; Due to the anti-aldistronic action, Torsemide to a lesser extent than furosemide causes hypokalemia, while it is more active and its action lasts longer; The diuretic effect develops about an hour after ingestion, reaching a maximum after 2-3 hours, and lasts up to 18 hours, which facilitates tolerability of therapy due to the lack of very frequent urination in the first hours after taking the drug inside, which limits the activity of patients .; Thorassmid reduces systolic and diastolic blood pressure in the "lying" and "standing" .; The use of thorassmid is the most reasonable choice for long-term therapy.


Suction. After ingestion, Torsemide is rapidly and almost completely absorbed in the gastrointestinal tract. Eating does not have a significant impact on the absorption of the drug. Cmax of Torsemide in plasma is noted 1–2 hours after ingestion. Bioavailability is 80–90% with minor individual variations .; Distribution. Communication with plasma proteins - more than 99%. Vd in healthy volunteers and patients with mild to moderate renal failure or CHF is between 12 and 16 liters. In patients with liver cirrhosis, Vd is doubled .; Metabolism. Metabolized in the liver using cytochrome P450 isoenzymes.As a result of successive reactions of oxidation, hydroxylation or ring hydroxylation, three metabolites are formed (M1, M3 and M5), which bind to plasma proteins at 86, 95 and 97%, respectively; Inference. T1 / 2 of Torsemide and its metabolites in healthy volunteers is 3-4 hours. The total clearance of Torsemide is 40 ml / min, the renal clearance is 10 ml / min. On average, about 83% of the accepted dose is excreted by the kidneys: unchanged (24%) and predominantly inactive metabolites (M1 - 12%, M3 - 3%, M5 - 41%) .; Pharmacokinetics in special patient groups; In renal insufficiency, the T1 / 2 of Torsemide does not change, the metabolites M3 and M5 increase. Torsemide and its metabolites are slightly excreted by hemodialysis and hemofiltration .; In liver failure, the concentration of Torsemide in the blood plasma increases due to a decrease in the metabolic rate of the drug in the liver .; In patients with heart or liver failure, T1 / 2 of Torsemide and M5 metabolite are slightly increased, drug accumulation is unlikely.; The pharmacokinetic profile of Torsemide in elderly patients is similar to that in young patients, with the exception that there is a decrease in the renal clearance of the drug due to a characteristic age-related impairment of renal function in elderly patients. The total clearance and T1 / 2 do not change.


Edematous syndrome of various genesis, incl. in chronic heart failure, liver, lung and kidney diseases; ;arterial hypertension.


- hypersensitivity to Torsemide or to any of the components of the drug; Allergy to sulfonamides (sulfanilamide antimicrobial agents or sulfonylmoxvip drugs); - renal failure with anuria; -hepatic coma and precoma; - refractory hypocalism; - refractory hyponatremia; - hypovolemia (with or without hypotension) or dehydration; - severely expressed violations of the outflow of urine of any etiology (including unilateral damage to the urinary tract); - glycosidic intoxication: - acute glomerulonephritis; -Sinoatrial and atrioventricular block II-1II degree; -decompensated aortic and mitral stenosis; Hypertrophic obstructive cardiomyopathy; - increase in central venous pressure (over 10 mm Hg.Art.); -arrhythmia; - chronic renal failure with increasing azotemia; Hyperuricmia; - age up to 18 years (safety and efficacy not established); -pregnancy; - breastfeeding period; - simultaneous use of aminoglycosides and tsfalosnorinov; - lactose intolerance, deficiency of lactase or glucose-galactose malabsorption unit .; Carefully; -arterial hypotension; -stenosary atherosclerosis of cerebral arteries; - hypothyroidism; - disorders of urine outflow (benign prostatic hyperplasia, narrowing of the urethra or hydronephrosis); -ventricular arrhythmia in history; - acute myocardial infarction (increased risk of cardiogenic shock); -diarrhea; Pancreatitis Hypokalemia; - hyponatremia; - impaired liver function, liver cirrhosis, renal failure, hepatorenal syndrome; - diabetes mellitus (decrease in glucose tolerance); Gout, predisposition to hyperuricemia; -anemia; simultaneous use of cardiac glycosides, corticosteroids and adrenocorticotropic hormone (AKT1 ').

Use during pregnancy and lactation

Torsemide does not have a teratogenic effect and fetotoxicity, penetrates the placental barrier, causing impaired water-electrolyte metabolism and thrombocytopenia in the fetus .; Controlled studies on the use of Torsemide in pregnant women have not been conducted, the drug is contraindicated during pregnancy .; There is no data on the release of Torsemide into breast milk, so if you need to use Torsemide during lactation, you should stop breastfeeding.

Dosage and administration

Inside, once a day, ns chewed, squeezed enough water. Tablets can be taken at any convenient constant time, regardless of the meal. Edematous syndrome in chronic heart failure. The usual initial dose is 10-20 mg once a day. If necessary, the dose can be doubled to obtain the desired effect. Edematous syndrome in case of kidney disease. Edematous syndrome in case of liver disease. The usual initial dose is 5-10 mg once a day. If necessary, the dose can be doubled to obtain the desired effect.The maximum single dose is 40 mg, ss is recommended to exceed ns (no experience with the application). The drug is used for a long period or until the disappearance of edema. Arterial hypertension. The initial dose is 2.5 mg (1/2 pills of 5 mg) once a day. In the absence of a therapeutic effect within 4 weeks, the dose is increased to 5 mg once a day. In the absence of an adequate reduction in blood pressure, with a dose of 5 mg once a day for 4-6 weeks, the dose is increased to 10 mg once a day. If the dose of K) mg ps gives the desired effect, the antihypertensive drug of another group should be added to the treatment regimen. Elderly patients dose adjustment is not required. The usual starting dose is 20 mg once a day. If necessary, the dose can be doubled to obtain the desired effect.

Side effects

On the part of the nervous system: often - headache, dizziness, drowsiness; infrequently - muscle cramps of the lower limbs; frequency is unknown - unconsciousness, fainting, paresthesias in the limbs (feeling of numbness, crawling and tingling); From the senses -; frequency is unknown - impaired vision, hearing loss, tinnitus and hearing loss (wears, as a rule, reversible) usually in patients with renal insufficiency or hypoprothism (nephrotic syndrome) .; From the side of the cardiovascular system: infrequently - oxycystole, arrhythmia, tachycardia; frequency is unknown - excessive reduction in blood pressure, orthostatic hypotension, collapse, deep vein thrombosis, thromboembolism, decrease in circulating blood volume; On the part of the respiratory system: rarely - nosebleeds; On the part of the digestive system: often - diarrhea; infrequently - abdominal pain, flatulence, polydipsia; frequency is unknown - dry mouth, nausea, vomiting, loss of appetite, pancreatitis, dyspeptic disorders, intrahepatic cholestasis. photosensitization. From the musculoskeletal system: the frequency is unknown - muscle weakness.; From the urinary system: often - an increase in frequency of urination, noliuria, nocturia; infrequently - increased urge to urinate; frequency is unknown - oliguria, urinary retention (in patients with urinary tract obstruction), interstitial nephritis,hematuria.; On the part of the reproductive system: frequency is unknown - decrease in potency.; On the part of metabolism: frequency is unknown - hypokalasmia. hyponatremia, hypomagnemia, hypocalcemia, hypochloremia, metabolic alkalosis, hypovolemia, dehydration (more often in elderly patients); From the laboratory point of view: rarely - hypercholesterolemia, hypertriglyceridemide; frequency unknown - giirurukemia, a slight increase in plasma alkaline phosphatase activity, an increase in plasma creatinine and urea concentrations, an increase in the activity of certain “liver” enzymes in the blood plasma (eg, gamma-glutamyltransferase), thrombocytopsia, leukopenia, agranulocytosis, hyperglycemia, glucose tolerance (latent diabetes mellitus is possible to manifest).


Symptoms: enhanced diuresis, accompanied by a decrease in BCC and impaired water-electrolyte balance in the blood, followed by a pronounced decrease in blood pressure, drowsiness and confusion, collapse. Gastrointestinal disturbances may occur .; Treatment: induction of vomiting, gastric lavage, the appointment of activated carbon. Treatment is symptomatic, dose reduction or drug withdrawal and at the same time replenishment of the BCC and correction of water-electrolyte balance and acid-base status under the control of electrolyte content in blood plasma and hematocrit. Hemodialysis is ineffective because excretion of Torsemide and its metabolites is not accelerated. There is no specific antidote.

Interaction with other drugs

With simultaneous use of Torsemide with minsralo- and glucocorticosteroids, amphotsricin B increases the risk of hypokalemia; with cardiac glycosides, the risk of development of glycoside intoxication due to hypokalemia (for high-and low-polar cardiac glycosides) and lengthening the half-life (for low-polar cardiac glycosides) will increase .; Taking Torsemide increases the concentration and risk of the development of the NSF and ototoxic effect of cephalosporins, amipoglycosides, chloramphenicol, ethacrynic acid, antibiotics, salicylates, cisplatin, platinum preparations, amphotsricin B (due to competitive renal elimination) .; Consistent or simultaneous use of Torsemide with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists can lead to a sharp decrease in blood pressure.This can be avoided by reducing the initial dose of an ACE inhibitor or by lowering the dose of Torsemide (or temporarily canceling it) .; Pesteroidal anti-inflammatory drugs, sucralfate reduce the diuretic effect of Torsemide due to inhibition of prostaglandin synthesis, impaired plasma renin activity and removal of aldostron .; Torsemide enhances the aitihypertensive effect of antihypertensive drugs, the neuromuscular blockade of depolarizing muscle relaxants (suxamstonias) and weakens the effect of non-depolarizing muscle relaxants (tubocurarine) .; Thorassmid reduces the renal clearance of lithium preparations and increases the likelihood of intoxication .; Gorasemid increases the effectiveness of diazoxide and theophylline, reduces the effectiveness of hypoglycemic agents, allopurinol .; I [spring amines and thorassmide mutually reduce the effectiveness of each other. Drugs that block tubular secretion, increase the concentration of Torsemide in the blood plasma .; 11At simultaneous use of cyclosporine and Torsemide, the risk of developing gouty arthritis is increased due to the fact that cyclosporine can cause a violation of urate excretion of the urate by the kidneys, and the toramismide, a hyperuriumia .; The simultaneous use of irobenecid or methotrexate can reduce the effectiveness of Torsemide (the same secretion route). On the other hand, thorassmide can lead to a reduction in the renal elimination of these drugs. It was reported that patients with a high risk of nephropathy, taking goremide inside, with the introduction of X-ray contrast agents, renal dysfunction was observed more often than patients with a high risk of developing nephropathy who underwent intravenous hydration before X-ray contrast agents. Bioavailability and, as a result, the effectiveness of Torsemide can be reduced with co-therapy with co-stystyramine.

special instructions

Patients receiving high doses of Torsemide for a long period, in order to avoid the development of hyponatremia, hypokalemia and metabolic alkalosis, a diet with an adequate content of salt and the use of potassium preparations is recommended .; The risk of hypokalemia is greatest in patients with liver cirrhosis, enhanced diuresis, with insufficient consumption of electrolytes from food, as well as the simultaneous use of corticosteroids or ACT .; An increased risk of developing disorders of water and electrolyte balance is observed in patients with renal insufficiency.During the course of treatment with Gorasemid VERTEX, it is necessary to periodically monitor the electrolyte content in the blood plasma (including sodium, calcium, potassium, magnesium), the acid-base state, the concentration of residual nitrogen, creatinine, uric acid and, if necessary, carry out appropriate corrective therapy (with greater frequency in patients with frequent vomiting and on the background of parenterally injected fluids) .; In patients with advanced water electrolyte disturbances, hypovolemia, or nrenalny azotemia, laboratory test data may include: hyper or hyponatrism, hyper or hypochlormia, hyper or hypokalemia, acid-base balance disturbances, and elevated plasma urea levels. If these disorders occur, it is necessary to stop taking Gorasemid VERTEX until normal values ​​are restored, and then resume treatment with Thorassmide VERTEX at a lower dose .; With the onset or increase of azotemia and oliguria in patients with severe progressive kidney disease, it is recommended to suspend treatment with the drug 'Gorasemid VERTEX .; The selection of a dosing regimen for patients with ascites on the background of cirrhosis should be carried out in stationary conditions (violations of water and electrolyte balance may lead to the development of hepatic coma). This category of patients is shown regular monitoring of plasma electrolytes .; The use of Torsemide may cause aggravation of gout .; Patients with diabetes mellitus or with reduced glucose tolerance require periodic monitoring of the concentration of glucose in the blood and urine .; The Nazis in an unconscious state, with benign prostatic hyperplasia, narrowing of the ureters, need to control diuresis due to the possibility of acute urinary retention .; In patients with diseases of the cardiovascular system, especially those receiving cardiac glycosides, hypokalmia caused by diuretics can cause the development of arrhythmias .; Influence on ability to drive vehicles and mechanisms; During the period of treatment, patients should refrain from driving and engaging in other potentially hazardous activities that require increased concentration and psychomotor speed (the risk of dizziness and dizziness).