Background and overview[1][2]
Glaucoma is one of the leading causes of blindness in developed countries around the world. The main pathological characteristic of glaucoma is increased intraocular pressure. Surgery and/or medications aimed at reducing intraocular pressure are the most common treatments for glaucoma. The main pharmacotherapies currently in use are the administration of miotics (e.g., pilocarpine, carbachol, and echothiophate), whose open trabecular meshwork increases the rate of fluid flow out of the eye; and the administration of beta-blockers (e.g., timolol, levobunolol, carteolol, and betaxolol), α2-adrenergic agonists (e.g., brimonidine), and carbonic anhydrase inhibitors (e.g., acetazole amines, methazolamide, and dorzolamide), which reduce the rate of fluid flow into the eye.
Inhibitors of carbonic anhydrase prevent the enzyme from catalyzing the combination of water and carbon dioxide to form bicarbonate ions. Inhibitors of carbonic anhydrase isoenzyme II acting in the ciliary body reduce intraocular pressure by reducing bicarbonate secretion, and thereby reducing aqueous fluid secretion from the ciliary epithelium into the posterior compartment. Orally administered carbonic anhydrase inhibitors include acetazolamide and methazolamide. Systemic inhibition of carbonic anhydrase is associated with significant side effects, including aplastic anemia, hypokalemia, nephrolithiasis, paresthesia of the hands and face, malaise, anorexia, and severe weight loss. Therefore, oral carbonic anhydrase inhibitors are usually used only in the acute management of increased intraocular pressure and as a last resort long-term when topical medications fail to control intraocular pressure.
Topical carbonic anhydrase inhibitors used in the treatment of open-angle glaucoma include dorzolamide and brinzolamide. Carbonic anhydrase inhibitors used clinically include acetazolamide, also known as acetazolamide, dichlorphenamide, also known as methanesulfonamide, and disulfofenamide, also known as methanesulfonamide. , the English name is disulfamide, ethozolamide, also known as ethoxzolamide, the English name is ethoxzolamide, methazolamide, also known as methazolamide, the English name is methazolamide.
Ethoxybenzamide is also known as etoxozamide and 6-ethoxy-2-benzothiazolesulfonamide, CAS number 452-35-7, chemical formula C9H 10N2O3S2. Molecular weight 258.31700, density 1.47g/cm3, melting point 190-193ºC (lit.), boiling point 464.9ºC at 760mmHg, flash point 235ºC, refractive index 1.644. Ethoxylin is a carbonic anhydrase inhibitor that was approved for marketing in 1966 but has now been withdrawn from the market.
Purpose[2]
Ethoxylin is used as a diuretic and glaucoma. In addition, studies have shown that carbonic anhydrase inhibitors such as ethoxylin have been clinically used for ten years as weak diuretics. They inhibit carbonic anhydrase in renal tubular epithelial cells in the human body, reducing the production of H+ and the exchange of H+ and Na+ ions. , increase the excretion of sodium, water and bicarbonate, resulting in a diuretic effect. It can also inhibit carbonic anhydrase in ciliary body epithelial cells and central nervous cells, reduce the production of aqueous humor and cerebrospinal fluid, and increase intraocular pressure. In addition, it can inhibit the secretion of gastric acid. Therefore, in addition to having a weak diuretic effect, carbonic anhydrase inhibitors such as ethoxylin are mainly used clinically to treat glaucoma, cerebral edema, epileptic seizures, and altitude deficiency. Oxygen causes edematous diseases and peptic ulcers.
Specifications[3]
Tablet 125mg
Usage and dosage[3]
Take it once a day or in divided doses. The daily dose is 62.5 to 250 mg. Intermittent administration is recommended.
Pharmacological effects[3]
Ethoxybenzamide is the same as acetazolamide. A powerful carbonic anhydrase inhibitor. The advantage of this drug is that it acts on the proximal convoluted tubule to reduce H+-Na+ exchange and become a diuretic without reducing uric acid excretion. However, due to its low diuretic effect and weak effect, it excretes a large amount of bicarbonate, causing metabolic acidosis. The reabsorption of ammonia also increases due to the urine becoming alkaline, so it is now rarely used. This product can reduce the secretion of aqueous humor and reduce intraocular pressure. It can combat metabolic alkalosis caused by hyperventilation at low partial pressure of oxygen, prevent and treat mountain sickness, and also treat certain functional insufficiencies of the central nervous system.
Adverse reactions[3]
1. Paralysis, hearing loss, loss of appetite, gastrointestinal confusion, drowsiness, etc.
2. Water and electrolyte balance imbalance: metabolic acidosis and hypokalemia.
3. Skin rash, hemoglobinuria, diabetes, liver insufficiency, photosensitive dermatitis and convulsions, etc.
Notes[3]
1. This product may cause severe sulfonamide hypersensitivity reaction, which may occasionally lead to death. Including Stevens-Johson syndrome, toxic liver necrosis, skin necrosis, agranulocytosis, aplastic anemia, etc., the drug must be discontinued.
2. A daily dose of more than 1g does not increase the diuretic effect, but increases the side effects of drowsiness
3. When climbing, it is best to increase the climbing height slowly. If you climb quickly, this product cannot eliminate the symptoms of severe mountain sickness, such as high altitude pulmonary edema and high altitude cerebral edema.
4. Regularly check blood routine and blood electrolytes.
Taboo[3]
1. Generally not used for pregnant and lactating women.
2. It is prohibited to be used in patients with hyponatremia and hypokalemia, liver and kidney dysfunction, and liver cirrhosis.
Main reference materials
[1] Paul Ashton; Guo Hong. Sustained release systems and methods for ocular delivery of carbonic anhydrase inhibitors. CN200480002830.2, application date 2004-01-23
[2] Li Xuejun; Yu Heming. Application of carbonic anhydrase inhibitor acetazolamide in the preparation of male contraceptives. CN00109104.2, application date 2000-06-08
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