Acetazolamide clinical pharmacology
| 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]
Clinical Pharmacology
DIAMOX is a potent carbonic anhydrase inhibitor, effective in the control of fluid secretion (e.g., some types of glaucoma), in the treatment of certain convulsive disorders (e.g., epilepsy), and in the promotion of diuresis in instances of abnormal fluid retention (e.g., cardiac edema).
DIAMOX is not a mercurial diuretic. Rather, it is a non-bacteriostatic sulfonamide possessing a chemical structure and pharmacological activity distinctly different from the bacteriostatic sulfonamides.
DIAMOX is an enzyme inhibitor that acts specifically on carbonic anhydrase, the enzyme that catalyzes the reversible reaction involving the hydration of carbon dioxide and the dehydration of carbonic acid. In the eye, this inhibitory action of acetazolamide decreases the secretion of aqueous humor and results in a drop in intraocular pressure, a reaction considered desirable in cases of glaucoma and even in certain non-glaucomatous conditions. Evidence seems to indicate that DIAMOX has utility as an adjuvant in treatment of certain dysfunctions of the central nervous system (e.g., epilepsy). Inhibition of carbonic anhydrase in this area appears to retard abnormal, paroxysmal, excessive discharge from central nervous system neurons. The diuretic effect of DIAMOX is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. The result is renal loss of HCO3 ion, which carries out sodium, water, and potassium. Alkalinization of the urine and promotion of diuresis are thus affected. Alteration in ammonia metabolism occurs due to increased reabsorption of ammonia by the renal tubules as a result of urinary alkalinization.
DIAMOX SEQUELS provide prolonged action to inhibit aqueous humor secretion for 18 to 24 hours after each dose, whereas tablets act for only eight to 12 hours. The prolonged continuous effect of SEQUELS permits a reduction in dosage frequency.
Plasma concentrations of acetazolamide peak from three to six hours after administration of DIAMOX SEQUELS, compared to one to four hours with tablets. Food does not affect bioavailability of DIAMOX SEQUELS.
Placebo-controlled clinical trials have shown that prophylactic administration of DIAMOX at a dose of 250 mg every eight to 12 hours (or a 500 mg controlled release capsule once daily) before and during rapid ascent to altitude results in fewer and/or less severe symptoms of acute mountain sickness (AMS) such as headache, nausea, shortness of breath, dizziness, drowsiness, and fatigue. Pulmonary function (e.g., minute ventilation, expired vital capacity, and peak flow) is greater in the DIAMOX treated group, both in subjects with AMS and asymptomatic subjects. The DIAMOX treated climbers also had less difficulty in sleeping.[1]
References
- ↑ "DIAMOX SEQUELS (ACETAZOLAMIDE) CAPSULE, EXTENDED RELEASE [DURAMED PHARMACEUTICALS, INC.]". Retrieved 25 February 2014.
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