Indications
- edematous syndrome of various origins, including in chronic heart failure, liver, lung and kidney diseases;
- arterial hypertension.
$35.00
Active ingredient: | |
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Dosage form: | |
Indications for use: |
With caution
Active substance:
torasamide-5.00 mg;
Excipients:
lactose monohydrate-75.00 mg;
corn starch-17.50 mg;
sodium carboxymethyl starch (sodium starch glycolate, type A) – 1.00 mg;
colloidal silicon dioxide-0.75 mg;
magnesium stearate-0.75 mg.
Active ingredient:
torasamide – 5.00 mg;
Auxiliary substances:
lactose monohydrate-75.00 mg;
corn starch-17.50 mg;
sodium carboxymethyl starch (sodium starch glycolate, type A) – 1.00 mg;
colloidal silicon dioxide-0.75 mg;
magnesium stearate-0.75 mg
Lotonel is a diuretic. Active ingredient-torasemide is a “loop” diuretic.
The main mechanism of action of the drug is due to the reversible binding of torasemide to the sodium / chlorine / potassium ion countertransmitter located in the apical membrane of the thick segment of the ascending Gale loop, which reduces or completely inhibits the reabsorption of sodium ions and reduces the osmotic pressure of intracellular fluid and water reabsorption.
Torasamide blocks myocardial aldosterope receptors, reduces fibrosis, and improves myocardial diastolic function. Due to the antialdosteron effect, torasemide causes hypokalemia to a lesser extent than furosemide, while it is more active and its effect is longer.
The diuretic effect develops approximately one hour after oral use, reaching a maximum in 2-3 hours, and persists for up to 18 hours, which facilitates the tolerability of therapy due to the lack of very frequent urination in the first hours after oral use, which limits the activity of patients. Torasamide reduces systolic and diastolic blood pressure in the “lying” and “standing” positions.
The use of torasamide is the most reasonable choice for long-term therapy.
With caution
Nervous system disorders: often-headache, dizziness, drowsiness; infrequently – muscle cramps of the lower extremities;frequency unknown-confusion, fainting, paresthesia in the extremities (numbness, “crawling” and tingling).
Sensory disorders-frequency unknown-visual impairment, hearing impairment, tinnitus and hearing loss (usually reversible), usually in patients with renal insufficiency or hypoprotxinsmis (nephrotic syndrome).
From the cardiovascular system: infrequently-oxrasystole, arrhythmia, tachycardia; frequency unknown-excessive decrease in blood pressure, orthostatic hypotension, collapse, deep vein thrombosis, thromboembolism, decreased blood volume.
From the respiratory system: infrequently-nosebleeds.
From the digestive system: often-diarrhea; infrequently-abdominal pain, flatulence, polydipsia; frequency unknown-dry mouth, nausea, vomiting, loss of appetite, pancreatitis, dyspeptic disorders, intrahepatic cholestasis.
From the side of knives and foot fabrics: frequency unknown – pruritus, rash, urticaria, erythema multiforme, exfoliative dermatitis, purpura, vasculitis, photosensitization.
Musculoskeletal disorders: frequency unknown-muscle weakness.
From the urinary system: frequently-increased urination rate, noliuria, nocturia; infrequently-frequent urge to urinate; frequency unknown-oliguria, urinary retention (in patients with urinary tract obstruction), interstitial nephritis, hematuria.
Reproductive system disorders: frequency unknown-decreased potency.
From the side of metabolism: frequency unknown-hypokalismia. hyponatremia, hypomagnesemia, hypocalcemia, hypochloremia, metabolic alkalosis, hypovolemia, dehydration (more often in elderly patients).
From the laboratory side, it is indicative: infrequently – hypercholesterolemia, hypertriglyceridemia;frequency unknown-giisruricemia, a slight increase in the activity of alkaline phosphatase in blood plasma, an increase in the concentration of creatinine and urea in blood plasma, an increase in the activity of certain “liver” enzymes in blood plasma (for example, gamma-glutamyltransferase), thrombocytopenia, leukopenia, agranulocytosis, hyperglycemia, a decrease in glucose tolerance (possible manifestation of latent diabetes mellitus).
Concomitant use of torasemide with minsralo – and glucocorticosteroids, amphotericin B increases the risk of hypokalemia; with cardiac glycosides, the risk of developing glycoside intoxication due to hypokalemia (for high – and low-polar cardiac glycosides) and prolongation of the half-life (for low-polar cardiac glycosides) increases. Taking torasemide increases the concentration and risk of developing nsfro – and ototoxic effects of cephalosporins, amipoglycosides, chloramphenicol, ethacric acid, antimicrobials, salicylates, cisplatin, platinum preparations, and amphotericin B (due to competitive renal elimination). Consistent or concomitant use of torasemide 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 reducing the dose of torasemide (or temporarily discontinuing it). Nonsteroidal anti-inflammatory drugs, sucralfate reduce the diuretic effect of torasemide due to inhibition of prostaglandin synthesis, impaired plasma renin activity and elimination of aldosterone. Torasemide enhances the antihypertensive effect of antihypertensive agents, neuromuscular blockade of depolarizing muscle relaxants (suxamstonium) and weakens the effect of non-depolarizing muscle relaxants (tubocurarin). Torasamide reduces the renal clearance of lithium preparations and increases the likelihood of intoxication. Horasemide increases the effectiveness of diazoxide and theophylline, reduces the effectiveness of hypoglycemic agents, allopurinol. I [spring amines and thorassimide mutually reduce the effectiveness of each other. Drugs that block tubular secretion increase the concentration of torasemide in blood plasma. 11. concomitant use of cyclosporine and torasemide increases the risk of gouty arthritis due to the fact that cyclosporine can cause impaired urate excretion by the kidneys, and torasemide can cause hyperuricemia. Concomitant use of irobenecid or methotrexate may reduce the effectiveness of torasemide (same secretion pathway). On the other hand, torasamide may lead to a decrease in the renal elimination of these drugs. It has been reported that patients with a high risk of developing nephropathy taking oral horasemide, when X-ray contrast agents were administered, renal function disorders were observed more often than in patients with a high risk of developing nephropathy, who underwent intravenous hydration before the introduction of X-ray contrast agents. The bioavailability and, consequently, efficacy of torasemide may be reduced when co-administered with colstiramine.
Inside, once a day, without chewing, with a sufficient amount of water. Tablets can be taken at any convenient constant time, regardless of food intake. Edematous syndrome in chronic heart failure
The usual starting dose is 10-20 mg once a day. If necessary, the dose can be doubled until the desired effect is obtained. Edematous syndrome in kidney disease Edematous syndrome in liver disease The usual starting dose is 5-10 mg once a day. If necessary, the dose can be doubled until the desired effect is obtained.
The maximum single dose is 40 mg, ss is not recommended to exceed ns (no experience of use). The drug is used for a long period or until the edema disappears. Arterial hypertension The initial dose is 2.5 mg (1/2 tablet of 5 mg) once a day.
In the absence of a therapeutic effect for 4 weeks, the dose is increased to 5 mg once a day. 11 if there is no adequate reduction in blood pressure when taking a dose of 5 mg once a day for 4-6 weeks, the dose is increased to 10 mg once a day.
If a dose of K) mg ps gives the desired effect, a hypotensive drug of another group should be added to the treatment regimen. Elderly patients do not need to adjust the dose. The usual starting dose is 20 mg once daily. If necessary, the dose can be doubled until the desired effect is obtained.
Patients receiving high doses of torasemide for a long period of time, in order to avoid the development of hyponatremia, hypokalemia and metabolic alkalosis, a diet with sufficient table salt and the use of potassium preparations is recommended. The risk of hypokalemia is greatest in patients with cirrhosis of the liver, increased diuresis, with insufficient intake of electrolytes with food, as well as with simultaneous use of corticosteroids or ACTE. An increased risk of developing water-electrolyte balance disorders is noted in patients with renal insufficiency. During the course of treatment with Gorasemide VERTEX, it is necessary to periodically monitor the content of electrolytes in the blood plasma (including sodium, calcium, potassium, magnesium), acid-base state, concentration of residual nitrogen, creatinine, uric acid and, if necessary, conduct appropriate correction therapy (with greater frequency in patients with frequent vomiting and against the background of parenterally administered fluids). In patients with advanced water-electrolyte disorders, hypovolemia, or non-renal azotemia, laboratory test data may include: hyper-or hyponatremia, hyper-or hypochlorism, hyper – or hypokalemia, acid-base balance disorders, and increased plasma urea concentrations. If these disorders occur, it is necessary to stop taking Gorasemide VERTEX until normal values are restored, and then resume treatment with Torasemide VERTEX at a lower dose. If azotemia and oliguria appear or increase in patients with severe progressive kidney diseases, it is recommended to suspend treatment with Gorasemide VERTEX. Selection of the dosage regimen for patients with ascites on the background of cirrhosis of the liver should be carried out in a hospital setting (violations of the water-electrolyte balance can lead to the development of hepatic coma). Regular monitoring of blood plasma electrolytes is indicated for this category of patients. The use of torasemide may cause an exacerbation of gout. In patients with diabetes mellitus or with reduced glucose tolerance, periodic monitoring of blood and urine glucose concentrations is required. In the case of unconscious Nazis with benign prostatic hyperplasia and narrowing of the ureters, diuresis control is necessary due to the possibility of acute urinary retention. In patients with cardiovascular diseases, especially those taking cardiac glycosides, diuretic-induced hypokalismia can lead to the development of arrhythmias. Influence on the ability to drive vehicles and mechanisms During treatment, patients should refrain from driving vehicles and engaging in other potentially dangerous activities that require increased concentration of attention and speed of psychomotor reactions (risk of dizziness and drowsiness).
Torasemide
By prescription
Tablets
For adults as directed by your doctor
Heart Failure, Hypertension, Liver Damage
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