Tolvamac 30mg is an aquaretic drug which functions as a selective, competitivevasopressin receptor 2 (V2) antagonist will prevent hyponatremia (low blood sodium levels) along with congestive heart failure, cirrhosis, and the syndrome of inappropriate antidiuretic hormone (SIADH) Tolvamac 30mg decrease the level of a hormone whichmanage the balance of water and salt (sodium) in the body. High levels of this hormone can cause an imbalance that causes low sodium levels and fluid retention.
Tolvamac 30mg is used for the treatment of clinically important hypervolemic and euvolemic hyponatremia contains patients with heart failure and Syndrome of Inappropriate Antidiuretic Hormone (SIADH).
Mechanism of action of Tolvamac 30mg
Tolvaptan is a type of selective and competitive arginine vasopressin receptor 2 antagonist. Vasopressin show action on the V2 receptors found in the walls of the vasculature and luminal membranes of renal collecting ducts. By stopping V2 receptors in the renal collecting ducts, aquaporins do not enter themselves into the walls henceinhibiting water absorption.
This activitybasically results in arise in urine volume, reduce urine osmolality, and increase electrolyte-free water clearance to decrease intravascular volume and ahigher serum sodium levels. Tolvaptan is specificallyrequired for heart failure patients as they have higher serum levels of vasopressin.
Time to peak plasma concentration of Tolvamac is 2-4 hours and the absolute bioavailability is unknown. Food will not affect the bioavailability of Tolvamac.
The plasma protein bounding of Tolvamac is 99% and Volume of distribution in healthy subjects is 3L/kg.
Tolvamac is metabolism occurs by CYP3A4 enzyme in the liver.
< 1% is excreted in the urine (unchanged form) and through fecal is very small amount of renal elimination. In oral dose, half-life of Tolvamac is 12 hours
Dosage and administration of Tolvamac 30mg
The recommended starting dose for Tolvamac is 15 mg administered once daily without food. The dose is increased to 30 mg once daily, after at least 24 hours, to a maximum of 60 mg once daily, as required to achieve the desired level of serum sodium.
Do not administer Tolvamac for more than 30 days to minimize the risk of liver injury.
Following discontinuation from Tolvamac, advised the patients to resume fluid restriction and should be observed for changes in serum sodium and volume status. Administration of Tolvamac should be without food Grape juice should be avoided during therapy with Tolvamac
Administrating monotherapy oral doses up to 480 mg and multiple doses up to 300 mg once in a day for 5 days have been well accepted in studies in healthy subjects. There is no essentialantitoxin for Tolvamac intoxication.
The signs and symptoms of an acute overdose can be expected to be those of extra pharmacologic effect: aincrease in serum sodium concentration, polyuria, thirst, and dehydration/hypovolemia.
The conditions like Hypernatremia, hypovolemia, and/or dehydration; provoke patient to drink whenever thirsty
Risk of potassium level increased
Tolvamac 30mg produce Osmotic demyelination syndrome is a harmalong with too-fast correction of hyponatremia
Tolvamac 30mg can develops serious and likely fatal liver injury; acute liver failure needed liver transplantation reported; discontinue if laboratory abnormalities or signs or symptoms of liver injury are apparent.
Drug-drug interaction of Tolvamac 30mg
- Tolvamac 30mg interaction with strong CYP3A4 inhibitors like ketoconazole will have highest labelled dose would be normal to cause an even heavy increase in exposure.
- Tolvamac co administration with moderate CYP3A4 inhibitors willincrease in exposure of Tolvamac 30mg
- When concomitant use treated with P-gp inhibitors will have reductions in the dose of Tolvamac 30mg
- Combination of rifampin and Tolvamac 30mg decrease exposure to tolvaptan by 85%.
- Concomitant use of lovastatin, digoxin, furosemide, and hydrochlorothiazide has no clinically relevant impact on the exposure to Tolvamac 30mg
Tolvamac 30mg is contraindicated with following condition as
Patients with autosomal dominant polycystic kidney disease because the drug causes severe and possible fatal liver injury.
Required in acutely raised serum sodium, Patients inability to sense, Hypovolemic / hyponatremia