$26.80
Manufacturer: Poland
The sensitivity to dorzolamidu and to any of the components of the drug was improved. Nirkov’s deficiency is severe (creatine clearance is less than 30 ml/XB). Hyperchloremic acidosis.
Description
Dorzoptik Combi COMPOSITION
active ingredients: dorzolamide, timolol
1 ml 20 mg dorzolamide (as dorzolamide hydrochloride) and 5 mg timolol (as timolol maleate)
Dorzoptik Combi excipients: mannitol (E 421) sodium hydroxyethyl cellulose sodium benzalkonium hydroxide chloride, 50% water for injection solution.
DOSAGE FORM
Eye drops, solution.
MAIN PHYSICAL AND CHEMICAL PROPERTIES:
light, transparent, somewhat astringent, colorless aqueous solution.
PHARMACOLOGICAL GROUP
Means used in ophthalmology. Antiglaucoma drugs and miotics. Beta-adrenergic blockers.
ATX code S01E D51.
PHARMACOLOGICAL PROPERTIES
Pharmacological. The preparation contains two active ingredients: dorzolamide hydrochloride and timolol maleate. Each of these components reduces increased intraocular pressure by decreasing the secretion of intraocular fluid, but the mechanism of action is different.
Dorzolamide hydrochloride is a potent type II carbonic anhydrase inhibitor. Inhibition of carbonic anhydrase of the miliary body reduces the secretion of intraocular fluid by slowing down the formation of bicarbonate ions, which, in turn, reduces the transport of sodium and fluid.
Timolol maleate is a non-selective beta-adrenergic receptor blocker. The exact mechanism of action of timolol, which is manifested in a decrease in intraocular pressure, is still not known. Fluorimetric and tonographic studies indicate that the effect of timolol is due to a decrease in the secretion of humoral fluid. In addition, timolol can increase moisture drainage.
The combined effect of the two components leads to a more pronounced decrease in intraocular pressure than with monotherapy with these drugs.
After topical application, Dorzoptic Combi reduces intraocular pressure, regardless of whether it is associated with an increase with glaucoma. Increased intraocular pressure plays a significant role in the pathogenesis of optic nerve damage and loss of visual fields in glaucoma.
Dorzoptic Combi reduces intraocular pressure without the development of side effects characteristic of miotic drugs, such as night blindness, accommodation spasm, pupil constriction.
Dorzoptik Combi Pharmacokinetics.
Dorzolamide hydrochloride. When applied topically, dorzolamide enters the systemic circulation. With prolonged use, dorzolamide accumulates in erythrocytes as a result of binding to type II carbonic anhydrase, maintaining very low plasma concentrations of the free drug. Due to metabolism, dorzolamide forms a single N-desethyl metabolite, which blocks type II carbonic anhydrases less pronounced than its original form, but incubates type I carbonic anhydrases less active isoenzymes. The metabolite also accumulates in erythrocytes, where it binds mainly to type I carbonic anhydrase. Approximately 33% of dorzolamide binds to blood plasma proteins. Dorzolamide is excreted in the urine unchanged and as a metabolite. After discontinuation of the drug, dorzolamide is excreted from erythrocytes nonlinearly, with an initial rapid decrease in concentration and a subsequent phase of slow excretion with a half-life of about 4 months.
Timolol maleate. After topical ophthalmic application, timolol is absorbed systemically. Systemic exposure of timolol was determined after topical application of an ophthalmic 0.5% solution 2 times a day. The maximum plasma concentration after the morning dose was 0.46 ng / ml, and after the evening dose was 0.35 ng / ml.
INDICATIONS
Increased intraocular pressure in patients with open-angle glaucoma or pseudoexfoliative glaucoma when topical use of beta-blockers alone is not sufficient.
CONTRAINDICATIONS
Hypersensitivity to one or both of the active ingredients or to any of the components of the drug
diseases of the respiratory tract, including bronchial asthma, and a history of bronchial asthma or severe chronic obstructive pulmonary disease,
sinus bradycardia, syndrome of weakness of the sinoatrial node, antrioventricular block II or III degree, not controlled by a pacemaker, severe heart failure, cardiogenic shock
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