Acetazolamide (extended-release capsule)

Acetazolamide
DIAMOX SEQUELS® FDA Package Insert
Indications and Usage
Dosage and Administration
Contraindications
Warnings and Precautions
Adverse Reactions
Drug Interactions
Use in Specific Populations
Overdosage
Description
Clinical Pharmacology
Nonclinical Toxicology
How Supplied/Storage and Handling
Labels and Packages
Clinical Trials on Acetazolamide
ClinicalTrials.gov

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sheng Shi, M.D. [2]

For patient information about Acetazolamide, click here. Synonyms / Brand Names: DIAMOX SEQUELS^®

Overview

Acetazolamide, sold under the trade name Diamox, is a carbonic anhydrase inhibitor that is used to treat glaucoma, epileptic seizures, benign intracranial hypertension, altitude sickness, cystinuria, and dural ectasia. Acetazolamide is available as a generic drug and is also used as a diuretic.

Category

Carbonic anhydrase inhibitors;Mountaineering and health;Anticonvulsants;Sulfonamides;World Health Organization essential medicines;Thiadiazoles;Amides;Cardiovascular Drugs

FDA Package Insert

DIAMOX SEQUELS (acetazolamide) capsule, extended release

Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages

Mechanism of Action

Acetazolamide is a carbonic anhydrase inhibitor. It can be used for the medical treatment of moderate to severe metabolic or respiratory alkalosis. Acetazolamide does this by interfering with bicarbonate (HCO₃^-) reabsorption in the kidneys, thereby reacidifying the blood – hence alkalyzing the urine.

Carbonic anhydrase (CA) catalyzes the first part of the following reversible reaction in which carbon dioxide (CO₂) and water (H₂O) are converted to carbonic acid (H₂CO₃) and vice-versa (the second half happens spontaneously, favouring production of H⁺ + HCO₃^-):

CO₂ + H₂O <--^CA--> H₂CO₃ <--> H⁺ + HCO₃^-

In the kidney tubules, locally secreted hydrogen ions normally combine with filtered bicarbonate (HCO₃^-) to form carbonic acid (H₂CO₃). Carbonic acid in turn is normally acted upon by carbonic anhydrase, leading to formation of CO₂. As CO₂ rapidly leaves the tubules by diffusing across cell membranes, the above reaction normally runs shifted strongly to the left (i.e. reversed), and more bicarbonate can be continuously reabsorbed from the preurine. However, in the presence of acetazolamide, carbonic anhydrase is inhibited and carbonic acid levels build up. The inhibition of carbonic anhydrase in turn leads to a slowing of the reverse reaction and a decrease in the body's ability to reabsorb serum bicarbonate, resulting in urinary bicarbonate wasting. This leads to a decreased ability to exchange Na⁺ for H⁺ in the presence of acetazolamide (in proximal convoluted tubules of kidney) resulting in a mild diuresis. By contrast, the H⁺ that is also present in the lumen is reabsorbed via an alternative pathway along with Cl^-; it then passes into the bloodstream, leading to hyperchloremic metabolic acidosis. This effect can also be used for therapeutic correction of alkalosis seen in altitude sickness or other forms of respiratory alkalosis.