Treatment of glaucoma: – chronic open-angle glaucoma; ‒ secondary glaucoma; – closed-angle glaucoma (for short-term preoperative therapy and before ophthalmological procedures, to reduce intraocular pressure). Treatment of edema: ‒ heart failure; – edema caused by the use of drugs. Treatment of epilepsy (in combination with other anticonvulsants): – petit mal (small attacks) in children; – grand mal (large seizures) in adults; – mixed form. Treatment of altitude sickness (the drug reduces the time of acclimatization, but its effect on the manifestations of this disease is insignificant).
active substance: acetazolamide;
1 tablet contains acetazolamide 250 mg;
Diuremid excipients: potato starch, talc, sodium starch glycolate (type A).
Diuremid Dosage form
Basic physical and chemical properties: flat-cylindrical tablets with beveled edges, white or almost white.
Antiglaucoma drugs and miotics. Carbonic anhydrase inhibitors. ATX code S01E C01.
Diuretic, antiglaucoma, antiepileptic agent. The mechanism of action is due to the selective inhibition of carbonic anhydrase, an enzyme that catalyzes the reversible hydration reaction of carbon dioxide and the subsequent dissociation of carbonic acid. The diuretic effect is due to inhibition of carbonic anhydrase activity in the kidneys (mainly in the proximal renal tubules), which leads to a decrease in the reabsorption of bicarbonate, sodium and potassium ions, increased diuresis, an increase in urine pH, and an increase in ammonia reabsorption. Does not affect the excretion of chlorine ions. As a result of inhibition of carbonic anhydrase of the ciliary body, it reduces the secretion of aqueous humor and reduces intraocular pressure. Inhibition of carbonic anhydrase in the brain leads to the accumulation of CO2 in the brain and inhibition of excessive paroxysmal discharges of neurons, which determines the antiepileptic activity of the drug. The use of the drug with increased intracranial pressure is associated with the suppression of carbonic anhydrase in the vascular plexuses of the ventricles of the brain and a decrease in the production of cerebrospinal fluid.
Acetazolamide is well absorbed from the digestive tract. The maximum concentration of Cmax in blood plasma is reached within 1-3 hours after application. Small concentrations of acetazolamide remain in the blood for 24 hours.
Distribution. Acetazolamide is distributed to many tissues. Due to its high affinity for carbonic anhydrase, it accumulates mainly in tissues containing this enzyme, in particular in erythrocytes, kidneys, muscles, tissues of the eyeball and the central nervous system.
The drug does not accumulate in tissues.
The fraction with proteins is 70-90% of the total acetazolamide content in the blood. The half-life is about 4-9 hours.
Acetazolamide crosses the placental barrier.
Acetazolamide passes into breast milk in small amounts.
Metabolism. Acetazolamide is not metabolized.
Excretion. The drug is excreted by the kidneys unchanged. After oral administration, about 90% of the dose taken is excreted in the urine within 24 hours.
chronic open-angle glaucoma;
angle-closure glaucoma (for short-term preoperative therapy and before ophthalmic procedures, to reduce intraocular pressure).
with heart failure;
edema caused by the use of drugs.
Treatment of epilepsy (in combination with other anticonvulsants):
petit mal (small seizures) in children;
grand mal (large seizures) in adults;
Treatment of altitude sickness (the drug shortens the acclimatization time, but its effect on the manifestations of this disease is insignificant).
Hypersensitivity to the drug components and sulfonamides, impaired liver and kidney function, acute renal failure, hepatic failure, urolithiasis (with hypercalciuria), hyperchloremic acidosis, hypokalemia, chronic decompensated angle-closure glaucoma (for long-term therapy), diabetes mellitus, uremia, insufficiency of the adrenal glands, Addison’s disease. Acetazolamide should not be used in patients with cirrhosis of the liver, as it may increase the risk of hepatic encephalopathy.