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Pronunciation
(a set a ZOLE a mide)
Generic Available (U.S.)
Yes
Brand Names: U.S.
Brand Names: Canada
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Treatment of glaucoma (chronic simple open-angle, secondary glaucoma, preoperatively in acute angle-closure); drug-induced edema or edema due to congestive heart failure (adjunctive therapy; I.V. and immediate release dosage forms); centrencephalic epilepsies (I.V. and immediate release dosage forms); prevention or amelioration of symptoms associated with acute mountain sickness (immediate and extended release dosage forms)
Use: Unlabeled
Metabolic alkalosis; respiratory stimulant in stable hypercapnic COPD
Pregnancy Risk Factor
C
Pregnancy Considerations
Teratogenic effects have been observed in animal reproduction studies.
Lactation
Enters breast milk/not recommended (AAP rates “compatible”; AAP 2001 update pending)
Breast-Feeding Considerations
In a case report, low concentrations of acetazolamide were detected in the breast milk and the infant serum following a maternal dose of acetazolamide 500 mg twice daily. Acetazolamide concentrations in the breast milk were 1.3-2.1 mcg/mL, 1-9 hours after the dose. Acetazolamide concentrations in the infant serum were 0.2-0.6 mcg/mL, 2-12 hours after nursing. Maternal plasma concentrations were 5.2-6.4 mcg/mL, 1-7 hours after the dose. All levels were obtained on days 4-5 of therapy, 10 days after delivery. Due to the potential for adverse events in a nursing infant, breast-feeding is not recommended by the manufacturer.
Contraindications
Hypersensitivity to acetazolamide, sulfonamides, or any component of the formulation; hepatic disease or insufficiency; decreased sodium and/or potassium levels; adrenocortical insufficiency, cirrhosis; hyperchloremic acidosis, severe renal disease or dysfunction; long-term use in noncongestive angle-closure glaucoma
Warnings/Precautions
Concerns related to adverse effects:
• CNS effects: Impairment of mental alertness and/or physical coordination may occur.
• Sulfa allergy: Chemical similarities are present among sulfonamides, sulfonylureas, carbonic anhydrase inhibitors, thiazides, and loop diuretics (except ethacrynic acid). Use in patients with sulfonylurea allergy is specifically contraindicated in product labeling, however, a risk of cross-reaction exists in patients with allergy to any of these compounds; avoid use when previous reaction has been severe. Discontinue if signs of hypersensitivity are noted.
Disease-related concerns:
• Diabetes: Use with caution in patients with prediabetes or diabetes mellitus; may see a change in glucose control.
• Hepatic impairment: Use with caution in patients with hepatic dysfunction; in cirrhosis, avoid electrolyte and acid/base imbalances that might lead to hepatic encephalopathy.
• Respiratory acidosis: Use with caution in patients with respiratory acidosis; may worsen acidosis.
Concurrent drug therapy issues:
• Aspirin (high dose): Use with caution or avoid in patients taking high-dose aspirin concurrently; may lead to severe adverse effects including tachypnea, anorexia, lethargy, coma, and death.
Special populations:
• Elderly: Use with caution in the elderly; may be more sensitive to side effects.
Other warnings/precautions:
• Appropriate use: Increasing the dose does not increase diuresis and may increase the incidence of drowsiness and/or paresthesia; often results in a reduction of diuresis.
• I.M. administration: Painful because of the alkaline pH of the drug; use by this route is not recommended.
Adverse Reactions
Frequency not defined.
Cardiovascular: Flushing
Central nervous system: Ataxia, confusion, convulsions, depression, dizziness, drowsiness, excitement, fatigue, fever, headache, malaise
Dermatologic: Allergic skin reactions, photosensitivity, Stevens-Johnson syndrome, toxic epidermal necrolysis, urticaria
Endocrine & metabolic: Electrolyte imbalance, growth retardation (children), hyperglycemia, hypoglycemia, hypokalemia, hyponatremia, metabolic acidosis
Gastrointestinal: Appetite decreased, diarrhea, melena, nausea, taste alteration, vomiting
Genitourinary: Crystalluria, glycosuria, hematuria, polyuria, renal failure
Hematologic: Agranulocytosis, aplastic anemia, leukopenia, thrombocytopenia, thrombocytopenic purpura
Hepatic: Cholestatic jaundice, fulminant hepatic necrosis, hepatic insufficiency, liver function tests abnormal
Local: Pain at injection site
Neuromuscular & skeletal: Flaccid paralysis, paresthesia
Ocular: Myopia
Otic: Hearing disturbance, tinnitus
Miscellaneous: Anaphylaxis
Metabolism/Transport Effects
Inhibits CYP3A4 (weak)
Drug Interactions
Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Risk C: Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy
Alpha-/Beta-Agonists: Carbonic Anhydrase Inhibitors may decrease the excretion of Alpha-/Beta-Agonists. Exceptions: Dipivefrin. Risk C: Monitor therapy
Amifostine: Antihypertensives may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, antihypertensive medications should be withheld for 24 hours prior to amifostine administration. If antihypertensive therapy can not be withheld, amifostine should not be administered. Risk D: Consider therapy modification
Amphetamines: Carbonic Anhydrase Inhibitors may decrease the excretion of Amphetamines. Risk C: Monitor therapy
Anticonvulsants (Barbiturate): Carbonic Anhydrase Inhibitors may enhance the adverse/toxic effect of Anticonvulsants (Barbiturate). Specifically, osteomalacia and rickets. Risk C: Monitor therapy
Anticonvulsants (Hydantoin): Carbonic Anhydrase Inhibitors may enhance the adverse/toxic effect of Anticonvulsants (Hydantoin). Specifically, osteomalacia and rickets. Risk C: Monitor therapy
Antihypertensives: May enhance the hypotensive effect of other Antihypertensives. Risk C: Monitor therapy
ARIPiprazole: CYP3A4 Inhibitors (Weak) may increase the serum concentration of ARIPiprazole. Management: Monitor for increased aripiprazole systemic exposure/affects with concomitant use of a weak CYP3A4 inhibitor. Decrease aripiprazole dose to 25% of the usual dose in patients receiving both a CYP3A4 and a CYP2D6 inhibitor (regardless of potencies). Risk C: Monitor therapy
CarBAMazepine: Carbonic Anhydrase Inhibitors may increase the serum concentration of CarBAMazepine. Risk C: Monitor therapy
Carbonic Anhydrase Inhibitors: May enhance the adverse/toxic effect of other Carbonic Anhydrase Inhibitors. The development of acid-base disorders with concurrent use of ophthalmic and oral carbonic anhydrase inhibitors has been reported. Management: Avoid concurrent use of different carbonic anhydrase inhibitors if possible. Monitor patients closely for the occurrence of kidney stones and with regards to severity of metabolic acidosis. Risk X: Avoid combination
CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Exceptions: Levocabastine (Nasal). Risk C: Monitor therapy
CycloSPORINE: AcetaZOLAMIDE may increase the serum concentration of CycloSPORINE. Risk C: Monitor therapy
CycloSPORINE (Systemic): AcetaZOLAMIDE may increase the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
Diazoxide: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy
Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Risk D: Consider therapy modification
Flecainide: Carbonic Anhydrase Inhibitors may increase the serum concentration of Flecainide. Risk C: Monitor therapy
Herbs (Hypertensive Properties): May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy
Herbs (Hypotensive Properties): May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy
HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Risk C: Monitor therapy
Hypotensive Agents: May enhance the adverse/toxic effect of other Hypotensive Agents. Risk C: Monitor therapy
Ketorolac: May diminish the therapeutic effect of Anticonvulsants. Risk C: Monitor therapy
Ketorolac (Nasal): May diminish the therapeutic effect of Anticonvulsants. Risk C: Monitor therapy
Ketorolac (Systemic): May diminish the therapeutic effect of Anticonvulsants. Risk C: Monitor therapy
Lithium: Carbonic Anhydrase Inhibitors may decrease the serum concentration of Lithium. Risk C: Monitor therapy
MAO Inhibitors: May enhance the orthostatic hypotensive effect of Orthostatic Hypotension Producing Agents. Risk C: Monitor therapy
Mefloquine: May diminish the therapeutic effect of Anticonvulsants. Mefloquine may decrease the serum concentration of Anticonvulsants. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of convulsions. Monitor anticonvulsant concentrations and treatment response closely with concurrent use. Risk D: Consider therapy modification
Memantine: Carbonic Anhydrase Inhibitors may decrease the excretion of Memantine. Risk C: Monitor therapy
MetFORMIN: Carbonic Anhydrase Inhibitors may enhance the adverse/toxic effect of MetFORMIN. Specifically, the risk of developing lactic acidosis may be increased. Risk C: Monitor therapy
Methenamine: Carbonic Anhydrase Inhibitors may diminish the therapeutic effect of Methenamine. Management: Consider avoiding this combination. Monitor for decreased therapeutic effects of methenamine if used concomitant with a carbonic anhydrase inhibitor. Risk D: Consider therapy modification
Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Risk D: Consider therapy modification
Methylphenidate: May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy
Pentoxifylline: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy
Pimozide: CYP3A4 Inhibitors (Weak) may increase the serum concentration of Pimozide. Risk X: Avoid combination
Primidone: Carbonic Anhydrase Inhibitors may enhance the adverse/toxic effect of Primidone. Specifically, osteomalacia and rickets. Carbonic Anhydrase Inhibitors may decrease the serum concentration of Primidone. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the hypotensive effect of Antihypertensives. Risk C: Monitor therapy
QuiNIDine: Carbonic Anhydrase Inhibitors may decrease the excretion of QuiNIDine. Risk C: Monitor therapy
RiTUXimab: Antihypertensives may enhance the hypotensive effect of RiTUXimab. Risk D: Consider therapy modification
Salicylates: May enhance the adverse/toxic effect of Carbonic Anhydrase Inhibitors. Salicylate toxicity might be enhanced by this same combination. Risk D: Consider therapy modification
Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Risk C: Monitor therapy
Sodium Bicarbonate: AcetaZOLAMIDE may enhance the adverse/toxic effect of Sodium Bicarbonate. Specifically, the risk of renal calculus formation may be increased. Risk C: Monitor therapy
Sodium Phosphates: Diuretics may enhance the nephrotoxic effect of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with diuretics, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, hydrate adequately and monitor fluid and renal status. Risk D: Consider therapy modification
Trientine: Carbonic Anhydrase Inhibitor Diuretics may decrease the serum concentration of Trientine. Risk C: Monitor therapy
Yohimbine: May diminish the antihypertensive effect of Antihypertensives. Risk C: Monitor therapy
Storage
Capsules, tablets: Store at controlled room temperature.
Injection: Store vial for injection (prior to reconstitution) at controlled room temperature. Reconstituted solution may be refrigerated (2°C to 8°C) for 1 week, however, use within 12 hours is recommended. Stability of IVPB solutions in D5W or NS is 5 days at room temperature (25°C) and 44 days under refrigeration (5°C).
Reconstitution
Injection: Reconstitute with at least 5 mL sterile water to provide a solution containing not more than 100 mg/mL. Further dilute in D5W or NS for I.V. infusion.
Compatibility
Stable in D5LR, D5NS, D51/2NS, D51/4NS, D5R, D5W, D10W, LR, NS, 1/2NS, R, SL.
Y-site administration:
Compatible: Pantoprazole. Incompatible: TrophAmine®. Variable (consult detailed reference): Diltiazem.
Compatibility in syringe: Compatible: Pantoprazole
Mechanism of Action
Reversible inhibition of the enzyme carbonic anhydrase resulting in reduction of hydrogen ion secretion at renal tubule and an increased renal excretion of sodium, potassium, bicarbonate, and water. Decreases production of aqueous humor and inhibits carbonic anhydrase in central nervous system to retard abnormal and excessive discharge from CNS neurons.
Pharmacodynamics/Kinetics
Onset of action: Capsule (extended release), tablet (immediate release): 2 hours; I.V.: 5-10 minutes
Peak effect: Capsule (extended release): 8-18 hours; I.V.: 15 minutes; Tablet: 2-4 hours
Duration: Inhibition of aqueous humor secretion: Capsule (extended release): 18-24 hours; I.V.: 4-5 hours; Tablet: 8-12 hours
Distribution: Erythrocytes, kidneys; blood-brain barrier
Time to peak, plasma: Capsule (extended release): 3-6 hours; Tablet: 1-4 hours
Excretion: Urine (70% to 100% as unchanged drug)
Dosage
Note: I.M. administration is not recommended because of pain secondary to the alkaline pH
Children:
Altitude illness:
Prevention: Oral: 2.5 mg/kg/dose every 12 hours started either the day before (preferred) or on the day of ascent and may be discontinued after staying at the same elevation for 2-3 days or if descent initiated; maximum dose: 125 mg/dose (Luks, 2010). Note: The International Society for Mountain Medicine does not recommend prophylaxis in children except in the rare circumstance of unavoidable rapid ascent or in children with known previous susceptibility to acute mountain sickness (Pollard, 2001).
Treatment: Oral: 2.5 mg/kg/dose every 8-12 hours; maximum dose: 250 mg/dose. Note: With high altitude cerebral edema, dexamethasone is the primary treatment; however, acetazolamide may be used adjunctively with the same treatment dose (Luks, 2010; Pollard, 2001).
Epilepsy: Oral: 8-30 mg/kg/day in divided doses. A lower dosing range of 4-16 mg/kg/day in 1-4 divided doses has also been recommended; maximum dose: 30 mg/kg/day or 1 g/day (Oles, 1989; Reiss, 1996). Note: Minimal additional benefit with doses >16 mg/kg/day. Extended release capsule is not recommended for treatment of epilepsy.
Adults:
Altitude illness: Oral: Manufacturer's labeling: 500-1000 mg/day in divided doses every 8-12 hours (immediate release tablets) or divided every 12-24 hours (extended release capsules). These doses are associated with more frequent and/or increased side effects. Alternative dosing has been recommended:
Prevention: 125 mg twice daily; beginning either the day before (preferred) or on the day of ascent; may be discontinued after staying at the same elevation for 2-3 days or if descent initiated (Basnyat, 2006; Luks, 2010). Note: In situations of rapid ascent (such as rescue or military operations), 1000 mg/day is recommended by the manufacturer. The Wilderness Medical Society recommends consideration of using dexamethasone in addition to acetazolamide in these situations (Luks, 2010).
Treatment: 250 mg twice daily. Note: With high altitude cerebral edema, dexamethasone is the primary treatment; however, acetazolamide may be used adjunctively with the same treatment dose (Luks, 2010).
Edema: Oral, I.V.: 250-375 mg once daily
Epilepsy: Oral: 8-30 mg/kg/day in divided doses. A lower dosing range of 4-16 mg/kg/day in 1-4 divided doses has also been recommended; maximum dose: 30 mg/kg/day or 1 g/day (Oles, 1989; Reiss, 1996). Note: Minimal additional benefit with doses >16 mg/kg/day. Extended release capsule is not recommended for treatment of epilepsy.
Glaucoma:
Chronic simple (open-angle): Oral, I.V.: 250 mg 1-4 times/day or 500 mg extended release capsule twice daily
Secondary or acute (closed-angle): Oral, I.V.: Initial: 250-500 mg; maintenance: 125-250 mg every 4 hours (250 mg every 12 hours has been effective in short-term treatment of some patients)
Metabolic alkalosis (unlabeled use): I.V.: 500 mg as a single dose; reassess need based upon acid-base status (Marik, 1991; Mazur, 1999)
Respiratory stimulant in stable hypercapnic COPD (unlabeled use): Oral: 250 mg twice daily (Wagenaar, 2003)
Elderly: Oral: Initial doses should begin at the low end of the dosage range.
Dosing adjustment in renal impairment: Note: Use is contraindicated in marked renal impairment; creatinine clearance cutoff not specified in manufacturer's labeling.
Clcr 10-50 mL/minute: Administer every 12 hours
Clcr <10 mL/minute: Avoid use
Hemodialysis: Moderately dialyzable (20% to 50%)
Peritoneal dialysis: Supplemental dose is not necessary (Schwenk, 1994)
Administration: Oral
May be administered with food. May cause an alteration in taste, especially carbonated beverages. Short-acting tablets may be crushed and suspended in cherry or chocolate syrup to disguise the bitter taste of the drug; do not use fruit juices. Alternatively, submerge tablet in 10 mL of hot water and add 10 mL honey or syrup.
Administration: I.M.
I.M. administration is painful because of the alkaline pH of the drug; use by this route is not recommended.
Administration: I.V.
I.V.: No specific guidance given by manufacturer, but I.V. push at a rate of up to 500 mg over 3 minutes has been reported in a clinical trial (Mazur, 1999); a study to assess cerebrovascular reserve has used rapid I.V. push of up to 1 g over ≤1 minute (Piepgras, 1990)
Administration: I.V. Detail
pH: 9.2
Monitoring Parameters
Intraocular pressure; serum electrolytes, periodic CBC with differential; monitor growth in pediatric patients
Test Interactions
May cause false-positive results for urinary protein with Albustix®, Labstix®, Albutest®, Bumintest®; interferes with HPLC theophylline assay and serum uric acid levels
Dietary Considerations
May be taken with food to decrease GI upset. May have additive effects with other folic acid antagonists. Some products may contain sodium.
Patient Education
Do not chew or crush long-acting capsule (contents may be sprinkled on soft food). May be administered with food to decrease GI upset. If taking for glaucoma, you will need periodic ophthalmic examinations while taking this medication. Monitor serum glucose closely (may cause altered blood glucose in some patients with diabetes or unusual response to some forms of glucose testing). You may experience increased sensitivity to sunlight, nausea, loss of appetite, or altered taste. Notify your doctor of unusual and persistent nausea, vomiting, diarrhea, sudden change in eyesight, eye pain or irritation, or if seizures are worse or change after starting this medication.
Geriatric Considerations
Oral carbonic anhydrase inhibitors are useful for patients who have difficulty administering ophthalmic drugs, who do not achieve sufficient lowering of intraocular pressure, or who cannot tolerate other agents. Malaise and complaints of tiredness and myalgia are signs of excessive dosing and acidosis in older adults. Orthostatic hypotension may occur; assess blood pressure. Note renal impairment recommendations; many elderly have Clcr <50 mL/minute.
Dental Health: Effects on Dental Treatment
Key adverse event(s) related to dental treatment: Metallic taste (resolves upon discontinuation)
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
Drowsiness is common, may produce depression less commonly
Mental Health: Effects on Psychiatric Treatment
Can rarely cause bone marrow suppression, therefore, use cautiously with clozapine and carbamazepine; may increase the excretion of lithium
Nursing: Physical Assessment/Monitoring
Assess allergy history prior to beginning therapy. Monitor for signs of excessive dosing and acidosis (especially in elderly). If for glaucoma, measure intraocular pressure at the beginning of therapy and periodically throughout. Monitor growth in pediatric patients. Monitor blood glucose levels closely if patients have diabetes.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, extended release, oral: 500 mg
Capsule, sustained release, oral:
Diamox® Sequels®: 500 mg
Injection, powder for reconstitution: 500 mg
Tablet, oral: 125 mg, 250 mg
Pricing: U.S. (www.drugstore.com)
Capsule, 12-hour (AcetaZOLAMIDE)
500 mg (100): $349.00
Capsule, 12-hour (Diamox Sequels)
500 mg (60): $359.90
Tablets (AcetaZOLAMIDE)
125 mg (90): $45.99
250 mg (60): $37.99
Extemporaneously Prepared
A 25 mg/mL oral suspension may be made with tablets and either a 1:1 mixture of Ora-Sweet® and Ora-Plus® or a 1:1 mixture of Ora-Sweet® SF and Ora-Plus®. Crush twelve 250 mg tablets in a mortar and reduce to a fine powder. Add small portions of chosen vehicle and mix to a uniform paste; mix while adding the vehicle in incremental proportions to almost 120 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 120 mL. Label “shake well” and “refrigerate”. Stable for 60 days (Allen, 1996). When diluted in 120 mL solution of cherry syrup concentrate diluted 1:4 with simple syrup, NF, it is stable 60 days refrigerated (preferred) or at room temperature (Nahata, 2004).
Allen LV Jr and Erickson MA 3rd, "Stability of Acetazolamide, Allopurinol, Azathioprine, Clonazepam, and Flucytosine in Extemporaneously Compounded Oral Liquids," Am J Health Syst Pharm, 1996, 53(16):1944-9.
Nahata MC, Pai VB, and Hipple TF, Pediatric Drug Formulations, 5th ed, Cincinnati, OH: Harvey Whitney Books Co, 2004.
References
American Academy of Pediatrics Committee on Drugs, "Transfer of Drugs and Other Chemicals Into Human Milk," Pediatrics, 2001, 108(3):776-89.
Aronoff GR, Bennett WM, Berns JS, et al, Drug Prescribing in Renal Failure: Dosing Guidelines for Adults and Children, 5th ed. Philadelphia, PA: American College of Physicians; 2007, p 97.
Basnyat B, Gertsch JH,. Holck PS, et al, “Acetazolamide 125 mg BD is Not Significantly Different from 375 mg BD in the Prevention of Acute Mountain Sickness: The Prophylactic Acetazolamide Dosage Comparison for Efficacy (PACE) Trial,” High Alt Med Biol, 2006, 7(1):17-27.
Chapron DJ, Gomolin IH, and Sweeney KR, “Acetazolamide Blood Concentrations Are Excessive in the Elderly: Propensity for Acidosis and Relationship to Renal Function,” J Clin Pharmacol, 1989, 29(4):348-53.
Chapron DJ, Sweeney KR, Feig PU, et al, “Influence of Advanced Age on the Disposition of Acetazolamide,” Br J Clin Pharmacol, 1985, 19:363-71.
Corbett JT, “Acetazolamide and Purpura,” Br Med J, 1985, 1:1122-3.
Hackett PH, Roach RC, "High-Altitude Illness," N Engl J Med, 2001, 345(2):107-14.
Heller I, Halevy J, Cohen S, et al, “Significant Metabolic Acidosis Induced by Acetazolamide,” Arch Intern Med, 1985, 145(10):1815-7.
Luks AM, McIntosh SE, Grissom CK, et al, “Wilderness Medical Society Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness,” Wilderness Environ Med, 2010, 21(2):146-55.
Marik PE, Kussman BD, Lipman J, et al, "Acetazolamide in the Treatment of Metabolic Alkalosis in Critically Ill Patients," Heart Lung, 1991, 20(5 Pt 1):455-9.
Mazur JE, Devlin JW, Peters MJ, et al, "Single Versus Multiple Doses of Acetazolamide for Metabolic Alkalosis in Critically Ill Medical Patients: A Randomized, Double-Blind Trial," Crit Care Med, 1999, 27(7):1257-61.
Moviat M, Pickkers P, van der Voort PH, et al, “Acetazolamide-Mediated Decrease in Strong Ion Difference Accounts for the Correction of Metabolic Alkalosis in Critically Ill Patients,” Critical Care, 2006, 10(1):R14.
Oles KS, Penry JK, Cole DLW, et al, “Use of Acetazolamide as an Adjunct to Carbamazepine in Refractory Partial Seizures,” Epilepsia, 1989, 30(1):74-8.
Parikh JR, Nolan RL, Bannerjee A, et al, “Acetazolamide-Associated Nephrocalcinosis in a Transplant Kidney,” Transplantation, 1995, 59(12):1742-3.
Piepgras A, Schmiedek P, Leinsinger G, et al, “A Simple Test to Assess Cerebrovascular Reserve Capacity Using Transcranial Doppler Sonography and Acetazolamide,” Stroke, 1990, 21(9):1306-11.
Pollard AJ, Niermeyer S, Barry P, et al, “Children at High Altitude: An International Consensus Statement by an Ad Hoc Committee of the International Society for Mountain Medicine, March 12, 2001,” High Alt Med Biol, 2001, 2(3):389-403.
Reiss WG and Oles KS, “Acetazolamide in the Treatment of Seizures,” Ann Pharmacother, 1996, 30(5):514-9.
Rousseau P and Fuentevilla-Clifton A, “Acetazolamide and Salicylate Interaction in the Elderly: A Case Report,” J Am Geriatr Soc, 1993, 41(8):868-9.
Schwenk MH, St. Peter WL, Meese MG, et al, “Acetazolamide Toxicity and Pharmacokinetics in Patients Receiving Hemodialysis,” Pharmacotherapy, 1995, 15(4):522-7.
Shinnar S, Gammon K, Bergman EW Jr, et al, “Management of Hydrocephalus in Infancy: Use of Acetazolamide and Furosemide to Avoid Cerebrospinal Fluid Shunts,” J Pediatr, 1985, 107(1):31-7.
Söderman P, Hartvig P, and Fagerlund C, "Acetazolamide Excretion Into Human Breast Milk," Br J Clin Pharmacol, 1984, 17(5):599-600.
Vaziri ND, Saiki J, Barton CH, et al, “Hemodialyzability of Acetazolamide,” South Med J, 1980, 73(4):422-3.
Wagenaar M, Vos P, Heijdra Y, et al, “Comparison of Acetazolamide and Medroxyprogesterone as Respiratory Stimulants in Hypercapnic Patients With COPD,” Chest, 2003, 123(5):1450-9.
Wandstrat TL and Phillips J, “Pseudotumor Cerebri Responsive to Acetazolamide,” Ann Pharmacother, 1995, 29(3):318.
Weiss IS, “Hirsutism After Chronic Administration of Acetazolamide,” Am J Ophthalmol, 1974, 78(2):327-8.
International Brand Names
Lexi-Comp.com
Last full review/revision March 2012
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