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			{{Short description|Chemical compound}}
	{{distinguish|acetohexamide}}
			{{Distinguish|acetohexamide|methazolamide}}
	{{Drugbox| verifiedrevid = 417739236
			{{Use dmy dates|date=May 2024}}
	|
			{{cs1 config |name-list-style=vanc |display-authors=6}}
	|IUPAC_name = ''N''-(5-sulfamoyl-1,3,4-thiadiazol-2-yl)acetamide
			{{Drugbox
	| image = Acetazolamide skeletal.svg
			| Watchedfields = changed
	| image2 = Acetazolamide 3D.png
			| verifiedrevid = 477238754
			| image = Acetazolamide.svg
			| image_class = skin-invert-image
			| width = 200
			| alt = Skeletal formula of acetazolamide
			| image2 = Acetazolamide 3D ball.png
			| width2 = 180
			| alt2 = Ball-and-stick model of the acetazolamide molecule
			<!--Clinical data-->
			| tradename = Diamox, Diacarb, others
			| Drugs.com = {{drugs.com|monograph|acetazolamide}}
			| pregnancy_AU = B3
			| routes_of_administration = ], ]
			| class = ]
			| ATC_prefix = S01
			| ATC_suffix = EC01
			| legal_AU = S4
			| legal_CA = Rx-only
			| legal_UK = POM
			| legal_US = Rx-only
			<!--Pharmacokinetic data-->
			| bioavailability =
			| protein_bound = 70–90%<ref name = MSR/>
			| metabolism = None<ref name = MSR/>
			| elimination_half-life = 2–4 hours<ref name = MSR/>
			| excretion = Urine (90%)<ref name=MSR>{{cite web|title=Diamox Sequels (acetazolamide) dosing, indications, interactions, adverse effects, and more|work=Medscape Reference|publisher=WebMD|access-date=10 April 2014|url=http://reference.medscape.com/drug/diamox-acetazolamide-342809#showall|url-status=live|archive-url=https://web.archive.org/web/20140413145313/http://reference.medscape.com/drug/diamox-acetazolamide-342809#showall|archive-date=13 April 2014}}</ref>
			<!--Identifiers-->
			| IUPHAR_ligand = 6792
			| CAS_number_Ref = {{cascite|correct|CAS}}
			| CAS_number = 59-66-5
			| PubChem = 1986
			| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
			| DrugBank = DB00819
			| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID = 1909
	| UNII_Ref = {{fdacite|correct|FDA}}		| UNII_Ref = {{fdacite|correct|FDA}}
	| UNII = O3FX965V0I		| UNII = O3FX965V0I
			| KEGG_Ref = {{keggcite|correct|kegg}}
	| InChI = 1/C4H6N4O3S2/c1-2(9)6-3-7-8-4(12-3)13(5,10)11/h1H3,(H2,5,10,11)(H,6,7,9)
			| KEGG = D00218
	| InChIKey = BZKPWHYZMXOIDC-UHFFFAOYAA
			| ChEBI_Ref = {{ebicite|correct|EBI}}
			| ChEBI = 27690
	| ChEMBL_Ref = {{ebicite|correct|EBI}}		| ChEMBL_Ref = {{ebicite|correct|EBI}}
	| ChEMBL = 20		| ChEMBL = 20
			| PDB_ligand = AZM
			<!--Chemical data-->
			| IUPAC_name = ''N''-(5-Sulfamoyl-1,3,4-thiadiazol-2-yl)acetamide
			| C=4 | H=6 | N=4 | O=3 | S=2
			| smiles = NS(=O)(=O)c1nnc(s1)NC(=O)C
	| StdInChI_Ref = {{stdinchicite|correct|chemspider}}		| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
	| StdInChI = 1S/C4H6N4O3S2/c1-2(9)6-3-7-8-4(12-3)13(5,10)11/h1H3,(H2,5,10,11)(H,6,7,9)		| StdInChI = 1S/C4H6N4O3S2/c1-2(9)6-3-7-8-4(12-3)13(5,10)11/h1H3,(H2,5,10,11)(H,6,7,9)
	| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}		| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
	| StdInChIKey = BZKPWHYZMXOIDC-UHFFFAOYSA-N		| StdInChIKey = BZKPWHYZMXOIDC-UHFFFAOYSA-N
			| melting_point = 258
	| CAS_number=59-66-5
			| melting_high = 259
	| CASNo_Ref = {{cascite|correct|CAS}}
			| melting_notes =
	| ATC_prefix=S01
	| ATC_suffix=EC01
	| ATC_supplemental=
	| ChEBI = 27690
	| PubChem=1986
	| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
	| ChemSpiderID = 1909
	| DrugBank=APRD00119
	| KEGG_Ref = {{keggcite|correct|kegg}}
	| KEGG = D00218
	| C = 4 | H = 6 | N = 4 | O = 3 | S = 2
	| molecular_weight = 222.245 g/mol
	| smiles = O=S(=O)(c1nnc(s1)NC(=O)C)N
	| bioavailability=
	| metabolism = None
	| elimination_half-life = 3 to 9 hours
	| excretion = ]
	| pregnancy_AU = B3
	| pregnancy_US = C
	| legal_US = Rx-only
	| legal_UK = POM
	| routes_of_administration= Oral, ]
	}}		}}
			<!-- Definition and medical uses -->
	'''Acetazolamide''', sold under the trade name '''Diamox''', is a ] that is used to treat ], ]s, ] (pseudotumor cerebri), ], ], and ]. Acetazolamide is available as a ] and is also a ].
			'''Acetazolamide''', sold under the trade name '''Diamox''' among others, is a medication used to treat ], ], ], ], ] (raised brain pressure of unclear cause), ] and to alkalinize urine.<ref name=AHFS2016/><ref>{{cite journal | vauthors = Smith SV, Friedman DI | title = The Idiopathic Intracranial Hypertension Treatment Trial: A Review of the Outcomes | journal = Headache | volume = 57 | issue = 8 | pages = 1303–1310 | date = September 2017 | pmid = 28758206 | doi = 10.1111/head.13144 | s2cid = 13909867 }}</ref> It may be used long term for the treatment of ] and short term for ] until surgery can be carried out.<ref name=WHO2008/> It is taken ] or ].<ref name=AHFS2016/> Acetazolamide is a first generation ] inhibitor and it decreases the ocular fluid and ] in the eye to decrease intraocular pressure.<ref>{{cite book | vauthors = Scozzafava A, Supuran CT | title = Carbonic Anhydrase: Mechanism, Regulation, Links to Disease, and Industrial Applications | chapter = Glaucoma and the Applications of Carbonic Anhydrase Inhibitors | series = Subcellular Biochemistry | volume = 75 | pages = 349–359 | date = 2014 | publisher = Springer | pmid = 24146387 | doi = 10.1007/978-94-007-7359-2_17 | isbn = 978-94-007-7358-5 }}</ref><ref>{{cite web|url=https://www.openanesthesia.org/acetazolamide_mechanism_of_action/|title=Acetazolamide: mechanism of action|website=www.openanesthesia.org|language=en-US|access-date=10 May 2017}}</ref>
			<!-- Side effects and mechanisms -->
	== Mechanism of action ==
			Common side effects include numbness, ], loss of appetite, vomiting, and sleepiness.<ref name=AHFS2016/> It is not recommended in those with significant ], ], or who are ].<ref name=AHFS2016/><ref name=WHO2008>{{cite book | title = WHO Model Formulary 2008 | year = 2009 | isbn = 9789241547659 | vauthors = ((World Health Organization)) | veditors = Stuart MC, Kouimtzi M, Hill SR | hdl = 10665/44053 | author-link = World Health Organization | publisher = World Health Organization | hdl-access=free | page=439 }}</ref> Acetazolamide is in the ] and ] families of medication.<ref name=AHFS2016/> It works by decreasing the formation of ] and ] from carbon dioxide and water.<ref name=AHFS2016>{{cite web|title=Acetazolamide|url=https://www.drugs.com/monograph/acetazolamide.html|publisher=The American Society of Health-System Pharmacists|access-date=8 December 2016|url-status=live|archive-url=https://web.archive.org/web/20161228200154/https://www.drugs.com/monograph/acetazolamide.html|archive-date=28 December 2016}}</ref>
	Acetazolamide is a ]. Medically it may be used to treat conditions of moderate to severe metabolic or respiratory alkalosis. It does this by interfering with bicarbonate (HCO<sub>3</sub><sup>-</sup>) resorption in the kidneys, thereby re-acidifying the blood (and thus alkalinizing the urine).
			<!-- Society and culture -->
	] (CA) catalyzes the first part of the following ], in which carbon dioxide (CO<sub>2</sub>) and water (H<sub>2</sub>O) are converted to carbonic acid (H<sub>2</sub>CO<sub>3</sub>) and vice-versa:
			Acetazolamide came into medical use in 1952.<ref>{{cite book| vauthors = Sneader W |title=Drug Discovery: A History|date=2005|publisher=John Wiley & Sons|isbn=9780471899792|page=390|url=https://books.google.com/books?id=Cb6BOkj9fK4C&pg=PA390|language=en|url-status=live|archive-url=https://web.archive.org/web/20161228195543/https://books.google.ca/books?id=Cb6BOkj9fK4C&pg=PA390|archive-date=28 December 2016}}</ref> It is on the ].<ref name="WHO23rd">{{cite book | vauthors = ((World Health Organization)) | title = The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023) | year = 2023 | hdl = 10665/371090 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MHP/HPS/EML/2023.02 | hdl-access=free }}</ref> Acetazolamide is available as a ].<ref name=AHFS2016/>
			==Medical uses==
	CO<sub>2</sub> + H<sub>2</sub>O <--<sup>CA</sup>--> H<sub>2</sub>CO<sub>3</sub> <--> H<sup>+</sup> + HCO<sub>3</sub><sup>-</sup>
			It is used in the treatment of ], drug-induced ], heart failure-induced edema, ] and in reducing intraocular pressure after surgery.<ref name = AMH/><ref name = TGA/> It has also been used in the treatment of ],<ref>{{cite journal | vauthors = Low EV, Avery AJ, Gupta V, Schedlbauer A, Grocott MP | title = Identifying the lowest effective dose of acetazolamide for the prophylaxis of acute mountain sickness: systematic review and meta-analysis | journal = BMJ | volume = 345 | pages = e6779 | date = October 2012 | pmid = 23081689 | pmc = 3475644 | doi = 10.1136/bmj.e6779 }}</ref> ], ] and neuromuscular disorders.<ref name = MD/> Acetazolamide is also used in the critical care setting to stimulate respiratory drive in patients with ] as an ] indication.<ref>{{cite journal | vauthors = Heming N, Urien S, Faisy C | title = Acetazolamide: a second wind for a respiratory stimulant in the intensive care unit? | journal = Critical Care | volume = 16 | issue = 4 | pages = 318 | date = August 2012 | pmid = 22866939 | doi = 10.1186/cc11323 | pmc = 3580678 | doi-access = free }}</ref>
			In epilepsy, the main use of acetazolamide is in menstrual-related epilepsy and as an add on to other treatments in refractory epilepsy.<ref name = AMH/><ref>{{cite journal | vauthors = Reiss WG, Oles KS | title = Acetazolamide in the treatment of seizures | journal = The Annals of Pharmacotherapy | volume = 30 | issue = 5 | pages = 514–519 | date = May 1996 | pmid = 8740334 | doi = 10.1177/106002809603000515 | s2cid = 25763746 }}</ref> Though various websites on the internet report that acetazolamide can be used to treat ] in individuals with ], the only supporting evidence for this assertion exists from a small study of 14 patients which was not peer-reviewed or submitted for publication.<ref>{{cite web | vauthors = Ahn NU, Sponseller PD, Ahn UM, Nallamshetty L, Rose P, Buchowski J, Lemma M, Garrett E | date = July 2005 | work = SpineUniverse.com |title= Dural ectasia|url=http://www.spineuniverse.com/displayarticle.php/article922.html|archive-url=https://web.archive.org/web/20070926233505/http://www.spineuniverse.com/displayarticle.php/article922.html|archive-date=26 September 2007}}</ref><ref>{{cite book|date=2020| vauthors = Farzam K, Abdullah M | chapter = Acetazolamide | title = StatPearls | location = Treasure Island (FL) | publisher = StatPearls Publishing |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK532282/ | pmid = 30335315 }}</ref> Several published cases of intracranial hypotension related to Marfan syndrome would warrant caution in using acetazolamide in these patients unless there is a clear indication, as it could lower intracranial pressure further.<ref>{{cite journal | vauthors = Cheuret E, Edouard T, Mejdoubi M, Acar P, Pienkowski C, Cances C, Lebon S, Tauber M, Chaix Y | title = Intracranial hypotension in a girl with Marfan syndrome: case report and review of the literature | journal = Child's Nervous System | volume = 24 | issue = 4 | pages = 509–513 | date = April 2008 | pmid = 17906865 | doi = 10.1007/s00381-007-0506-3 | s2cid = 5734726 }}</ref> A 2012 review and meta-analysis found that there was "limited supporting evidence" but that acetazolamide "may be considered" for the treatment of central (as opposed to obstructive) ].<ref>{{cite journal | vauthors = Aurora RN, Chowdhuri S, Ramar K, Bista SR, Casey KR, Lamm CI, Kristo DA, Mallea JM, Rowley JA, Zak RS, Tracy SL | title = The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses | journal = Sleep | volume = 35 | issue = 1 | pages = 17–40 | date = January 2012 | pmid = 22215916 | pmc = 3242685 | doi = 10.5665/sleep.1580 }}</ref>
	In the kidney tubules, locally secreted hydrogen ions normally combine with ] bicarbonate (HCO<sub>3</sub><sup>-</sup>) to form carbonic acid (H<sub>2</sub>CO<sub>3</sub>). Carbonic acid in turn is normally acted upon by carbonic anhydrase, leading to formation of CO<sub>2</sub>. As CO<sub>2</sub> 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 serum. 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. By contrast, the H<sup>+</sup> that is also present in the lumen is reabsorbed via an alternative pathway along with Cl<sup>-</sup>; it then passes into the bloodstream, leading to hyperchloremic metabolic acidosis.<ref>Renal and Electrolyte Disorders Schrier 1976: page 89</ref> This effect can also be used for therapeutic correction of alkalosis seen in altitude sickness or other forms of ].
			It has also been used to prevent ]-induced kidney damage by alkalinizing the urine, hence speeding up methotrexate excretion by increasing its solubility in urine.<ref name = MD/><ref>{{cite journal | vauthors = Shamash J, Earl H, Souhami R | title = Acetazolamide for alkalinisation of urine in patients receiving high-dose methotrexate | journal = Cancer Chemotherapy and Pharmacology | volume = 28 | issue = 2 | pages = 150–151 | date = 1991 | pmid = 2060085 | doi = 10.1007/BF00689708 | s2cid = 375183 }}</ref> There is some evidence to support its use to prevent ].<ref>{{cite journal | vauthors = Russell MB, Ducros A | title = Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management | journal = The Lancet. Neurology | volume = 10 | issue = 5 | pages = 457–470 | date = May 2011 | pmid = 21458376 | doi = 10.1016/S1474-4422(11)70048-5 | s2cid = 25823747 }}</ref>
	==Uses==
	Acetazolamide is often used in the treatment of various diseases.
	===Glaucoma===		===High altitude sickness===
			Acetazolamide is also used for the treatment of acute mountain sickness. In the prevention or treatment of mountain sickness, acetazolamide inhibits the ability of the ]s to reabsorb ], the ] of ]. Increasing the amount of bicarbonate excreted in the urine leads to acidification of the blood.<ref name="MD" /> Because the body senses CO<sub>2</sub> concentration indirectly via blood pH (increase in CO<sub>2</sub> causes a decrease in pH), acidifying the blood through decreased renal reabsorption of bicarbonate is sensed as an increase in CO<sub>2</sub>. This, in turn, causes the body to increase minute ventilation (the amount of air breathed per minute) in order to "breathe off" CO<sub>2</sub>, which in turn increases the amount of oxygen in the blood.<ref name="altorg">{{cite web |title=Altitude.org |year=2004 |url=http://www.altitude.org |access-date=5 June 2009 |url-status=live |archive-url=https://web.archive.org/web/20090208180452/http://altitude.org/ |archive-date=8 February 2009 }}</ref><ref name="Leaf_2007" /> Acetazolamide is not an immediate cure for acute mountain sickness; rather, it speeds up (or, when taking before traveling, forces the body to early start) part of the ] process which in turn helps to relieve symptoms.<ref name="Acclimatization">{{cite journal | vauthors = Muza SR, Fulco CS, Cymerman A |title=Altitude Acclimatization Guide |journal=US Army Research Inst. Of Environmental Medicine Thermal and Mountain Medicine Division Technical Report |issue=USARIEM–TN–04–05 |year=2004 |url=http://archive.rubicon-foundation.org/7616 |url-status=usurped |archive-url=https://web.archive.org/web/20090423042451/http://archive.rubicon-foundation.org/7616 |archive-date=23 April 2009 |access-date=5 March 2009 }}</ref> Acetazolamide is still effective if started early in the course of mountain sickness. As prevention, it is started one day before travel to altitude and continued for the first two days at altitude.<ref>{{cite web |url=http://who.int/ith/ITH_EN_2012_WEB_1.2.pdf |author=World Health Organization|title=International Travel and Health 2012|access-date=27 January 2017 |url-status=live |archive-url=https://web.archive.org/web/20170319214120/http://who.int/ith/ITH_EN_2012_WEB_1.2.pdf |archive-date=19 March 2017 }}</ref>
	Acetazolamide has been used for the treatment of suffers of ].<ref name="pmid12429455">{{cite journal |author=Kaur IP, Smitha R, Aggarwal D, Kapil M |title=Acetazolamide: future perspective in topical glaucoma therapeutics |journal=Int J Pharm |volume=248 |issue=1–2 |pages=1–14 |year=2002 |month=November |pmid=12429455 |doi= 10.1016/S0378-5173(02)00438-6|url=http://linkinghub.elsevier.com/retrieve/pii/S0378517302004386}}</ref> Acetazolamide decreases the formation of aqueous humor in the ], resulting in lower intraocular pressure.
	===Neurologic===		===Pregnancy and lactation===
			Acetazolamide is pregnancy category B3 in Australia, which means that studies in rats, mice and rabbits in which acetazolamide was given intravenously or orally caused an increased risk of fetal malformations, including defects of the limbs.<ref name = TGA/> Despite this, there is insufficient evidence from studies in humans to either support or discount this evidence.<ref name = TGA/>
	In epilepsy, its main use is in ]s and ]s.<ref name="urlTreatment of Epilepsy | Comprehensive Epilepsy Center | NYU Medical Center, New York, NY">{{cite web |url=http://www.med.nyu.edu/cec/treatment/medications/side_effects/aceta.html |title=Treatment of Epilepsy &#124; Comprehensive Epilepsy Center &#124; NYU Medical Center, New York, NY |work= |accessdate=2008-12-19}}</ref> It can be used in both episodic ] types 1 and 2 (although the mechanisms are presumed to be different between the two).
			Limited data are available on the effects of nursing mothers taking acetazolamide. Therapeutic doses create low levels in breast milk and are not expected to cause problems in infants.<ref>{{cite web|url=http://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+lactmed:@term+@DOCNO+489|publisher=]|title=LactMed: Acetazolamide|access-date=10 October 2017|url-status=live|archive-url=https://web.archive.org/web/20171011072459/https://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+lactmed:@term+@DOCNO+489|archive-date=11 October 2017}}</ref>
	In catamential epilepsy, an increase in seizure frequency around menses, acetazolamide can be an adjunct to an anti-seizure medication regimen to aid in decreasing seizure frequency around menses.
			==Side effects==
	Acetazolamide is also used to decrease the production of ] in ]<ref name="pmid17922725">{{cite journal |author=Celebisoy N, Gökçay F, Sirin H, Akyürekli O |title=Treatment of idiopathic intracranial hypertension: topiramate vs acetazolamide, an open-label study |journal=Acta Neurol. Scand. |volume=116 |issue=5 |pages=322–7 |year=2007 |month=November |pmid=17922725 |doi=10.1111/j.1600-0404.2007.00905.x |url=http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0001-6314&date=2007&volume=116&issue=5&spage=322}}</ref> and has shown efficacy in some forms of ].<ref name="pmid8058156">{{cite journal |author=Ptáĉek LJ, Tawil R, Griggs RC, ''et al.'' |title=Sodium channel mutations in acetazolamide-responsive myotonia congenita, paramyotonia congenita, and hyperkalemic periodic paralysis |journal=Neurology |volume=44 |issue=8 |pages=1500–3 |year=1994 |month=August |pmid=8058156 |doi= |url=}}</ref>
			Common adverse effects of acetazolamide include the following: ], fatigue, drowsiness, depression, decreased libido, bitter or metallic taste, nausea, vomiting, abdominal cramps, diarrhea, black stool, ], ], ] and electrolyte changes (], ]).<ref name="AMH">{{cite book | veditors = Rossi S | isbn = 978-0-9805790-9-3 | title = Australian Medicines Handbook | place = Adelaide | publisher = The Australian Medicines Handbook Unit Trust | year = 2013 | edition = 2013 }}</ref> Whereas less common adverse effects include ], ] and ].<ref name = AMH/>
	===Marfan's syndrome===		===Contraindications===
			Contraindications include:<ref name=TGA>{{cite web|title=Product Information Diamox Acetazolamide Tablets|date=25 February 2005|access-date=10 April 2014|url=https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2009-PI-00910-3|format=PDF|work=TGA eBusiness Services|publisher=Aspen Pharma Pty Ltd|url-status=live|archive-url=https://web.archive.org/web/20161104143431/https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2009-PI-00910-3|archive-date=4 November 2016}}</ref>
	It's been demonstrated in drug trials to relieve symptoms associated with ] in individuals with ].<ref>{{cite web |author=Scoliosis Research Society |title=Dural Ectasia in the Marfan Spine: Symptoms and Treatment.also it's been used in high-altitude mountain sickness |url=http://www.spineuniverse.com/displayarticle.php/article922.html |date=2006-11-27 |publisher=SpineUniverse |accessdate=2007-11-15}}</ref>
			* Hyperchloremic acidosis
			* ] (low blood potassium)
			* ] (low blood sodium)
			* ]
			* Impaired kidney function
			* Hypersensitivity to acetazolamide or other sulphonamides.
			* Marked liver disease or impairment of liver function, including cirrhosis because of the risk of development of hepatic encephalopathy. Acetazolamide decreases ammonia clearance.
			==Interactions ==
	===Central sleep apnea===
			It is possible that it might interact with:<ref name = TGA/>
	Off-label uses include acetazolamide as a conjunction drug to merely assist patients with ''central'' ] by lowering blood pH and encourage respiration.<ref name="pmid6812522">{{cite journal |author=White DP, Zwillich CW, Pickett CK, Douglas NJ, Findley LJ, Weil JV |title=Central sleep apnea. Improvement with acetazolamide therapy |journal=Arch. Intern. Med. |volume=142 |issue=10 |pages=1816–9 |year=1982 |month=October |pmid=6812522 |doi= 10.1001/archinte.142.10.1816|url=}}</ref>
			* ]s, because it increases the pH of the renal tubular urine, hence reducing the clearance of amphetamines.
			* Other carbonic anhydrase inhibitors—potential for additive inhibitory effects on carbonic anhydrase and hence potential for toxicity.
			* ], may increase plasma levels of ciclosporin.
			* ]s such as ], ], ] and ].
			* ]s, acetazolamide can both increase or decrease blood glucose levels.
			* ], increases excretion, hence reducing therapeutic effect.
			* ] compounds, reduces the urinary excretion of methenamines.
			* ], reduces phenytoin excretion, hence increasing the potential for toxicity.
			* ], reduces plasma levels of primidone. Hence reducing anticonvulsant effect.
			* ], reduces urinary excretion of quinidine, hence increasing the potential for toxicity.
			* ], potential for severe toxicity.
			* ], potential for kidney stone formation.
			* ], ], may have their effects potentiated by acetazolamide.
	===Acute mountain sickness ===		== Mechanism of action ==
			]) complex with a sulfonamide inhibitor (])]] ]
	To reduce the incidence of ] acetazolamide is sometimes taken ], anywhere between 125 milligrams (mg) to 1000&nbsp;mg per day,<ref name=MedicalProblems>{{cite journal |author=Cymerman, A; Rock, PB |title=Medical Problems in High Mountain Environments. A Handbook for Medical Officers |publisher=US Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report |volume=USARIEM-TN94-2 |url=http://archive.rubicon-foundation.org/7976 |accessdate=2010-09-06}}</ref><ref name=FDAinfo>{{cite web |url=http://dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?archiveid=11119 |title=FDA drug information, acetazolamide capsule, extended release | author= | publisher=Barr Laboratories, Inc. |accessdate=2010-09-06 |format= |work=}}</ref> starting a few days before going to higher altitudes. Such use is recommended for those ascending from sea level to 3000 meters (9800&nbsp;feet) in one day, or for those ascending more than 600 meters (2000&nbsp;feet) per day once above an altitude of 2500 meters (8200&nbsp;feet).<ref>{{cite journal |author=Hackett, P.H. & Roach, R.C. |title=High-altitude illness |journal=The New England Journal of Medicine |volume=345 |issue=2 |pages=107–114 |year=2001 |doi=10.1056/NEJM200107123450206 |pmid=11450659}}</ref><ref name=ADA398545>{{cite journal |title=Effect of Acetazolamide on Isolated Quadriceps Muscle Endurance Performance at Sea Level and During Acute Altitude Exposure |year=2002 |author=Fulco, CS; Ditzler, D; Soares, R; Lammi, E; Muza, SR; Degroot, DW |journal=US Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report |issue=USARIEM–TR–T02/9 |url=http://archive.rubicon-foundation.org/7602 |accessdate=2008-09-30 }}</ref> Also, prophylactic use is recommended for those with a significant history of acute mountain sickness.
			Acetazolamide is a ], hence causing the accumulation of ].<ref name = MD>{{cite web|title=Acetazolamide|work=Martindale: The Complete Drug Reference|publisher=Pharmaceutical Press|date=7 January 2014|access-date=10 April 2014|url=http://www.medicinescomplete.com/mc/martindale/current/ms-2301-x.htm| veditors = Brayfield A }}</ref> Carbonic anhydrase is an enzyme found in ] and many other tissues that catalyses the following reaction:<ref>{{cite web|title=January 2004: Carbonic Anhydrase|work=RCSB PDB Protein Data Bank|date=January 2004|access-date=10 April 2014|url=http://www.rcsb.org/pdb/education_discussion/molecule_of_the_month/download/CarbonicAnhydrase.pdf| vauthors = Dutta S, Goodsell D |url-status=live|archive-url= https://web.archive.org/web/20130514071456/http://rcsb.org/pdb/education_discussion/molecule_of_the_month/download/CarbonicAnhydrase.pdf |archive-date=14 May 2013}}</ref>
			:H<sub>2</sub>CO<sub>3</sub> ⇌ H<sub>2</sub>O + CO<sub>2</sub>
	] forces the ]s to excrete ], the ] of ]. By increasing the amount of bicarbonate excreted in the urine, the blood becomes more acidic.<ref name=ADA398545/> Acidifying the blood stimulates ventilation, which increases the amount of oxygen in the blood.<ref name=altorg>{{cite web |title=Altitude.org |year=2004 |url=http://www.altitude.org |accessdate=2009-06-05}}</ref><ref>{{cite journal |author=Leaf DE, Goldfarb DS |title=Mechanisms of action of acetazolamide in the prophylaxis and treatment of acute mountain sickness |journal=J. Appl. Physiol. |volume=102 |issue=4 |pages=1313–22 |year=2007 |month=April |pmid=17023566 |doi=10.1152/japplphysiol.01572.2005 |url=}}</ref> At high altitudes, climbers hyperventilate in response to lower oxygen levels. The hyperventilation results in reduced carbon dioxide (an acid) and a ]. The normal physiologic response to a respiratory alkalosis is for the kidneys to increase excretion of bicarbonate (a base) to compensate for the loss of carbon dioxide. This kidney response takes a few days, however acetazolamide in a sense accelerates this process by leading to a more rapid renal bicarbonate loss (]).
			hence lowering blood pH, by means of the following reaction that carbonic acid undergoes:<ref name = chem/>
	Note that acetazolamide is not an immediate fix for acute mountain sickness; it speeds up part of the ] process which in turn helps to relieve symptoms.<ref name=MedicalProblems/><ref name=Acclimatization>{{cite journal |author=Muza, SR; Fulco, CS; Cymerman, A |title=Altitude Acclimatization Guide |journal=US Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report |issue=USARIEM–TN–04–05 |year=2004 |url=http://archive.rubicon-foundation.org/7616 |accessdate=2009-03-05 }}</ref> This may take up to a day or two, and requires waiting without any further rapid ascent. It is often advisable to descend if even mild acute mountain sickness is experienced. If serious sickness is encountered, descent to a lower elevation is considered to be mandatory unless other circumstances present greater danger.
			:H<sub>2</sub>CO<sub>3</sub> ⇌ HCO<sub>3</sub><sup>−</sup> + H<sup>+</sup>
	===Congestive Heart Failure===
	For diuresis in congestive heart failure, the starting dose is usually 250 to 375 mg once daily in the morning (five mg per kg). If, after an initial response, the patient fails to continue to lose edema fluid, do not increase the dose but allow for kidney recovery by skipping medication for a day.
			which has a ] of 6.3.<ref name = chem>{{cite web|title=Carbonic Anhydrase 2|work=UC Davis Chemwiki|publisher=University of California| vauthors = Larsen D |access-date=10 April 2014|url=http://chemwiki.ucdavis.edu/@api/deki/pages/2479/pdf?stylesheet=default&deep=false&showtoc=false}}</ref>
	Acetazolamide yields best diuretic results when given on alternate days, or for two days alternating with a day of rest.
			The mechanism of diuresis involves the proximal tubule of the kidney. The enzyme carbonic anhydrase is found here, allowing the reabsorption of bicarbonate, sodium, and chloride. By inhibiting this enzyme, these ions are excreted, along with excess water, lowering blood pressure, intracranial pressure, and intraocular pressure. A general side effect of carbonic anhydrase inhibitors is loss of potassium due to this function. By excreting bicarbonate, the blood becomes acidic, causing compensatory hyperventilation with deep respiration (Kussmaul breathing), increasing levels of oxygen and decreasing levels of carbon dioxide in the blood.<ref name="Leaf_2007">{{cite journal | vauthors = Leaf DE, Goldfarb DS | title = Mechanisms of action of acetazolamide in the prophylaxis and treatment of acute mountain sickness | journal = Journal of Applied Physiology | location = Bethesda, Md. | volume = 102 | issue = 4 | pages = 1313–1322 | date = April 2007 | pmid = 17023566 | doi = 10.1152/japplphysiol.01572.2005 | s2cid = 5873210 | url = https://www.life.illinois.edu/ib/426/handouts/Diamox%20mechanism_review_2007.pdf | access-date = 8 December 2014 | url-status = live | archive-url = https://web.archive.org/web/20141213211909/http://www.life.illinois.edu/ib/426/handouts/Diamox%20mechanism_review_2007.pdf | archive-date = 13 December 2014 }}</ref>
	Failures in therapy may be due to overdosage or too frequent dosage. The use of Acetazolamide does not eliminate the need for other therapy such as digitalis, bed rest, and salt restriction.
			In the eye this results in a reduction in ].<ref name="TGA" />
	===Drug-Induced Edema===
	Recommended dosage is 250 to 375 mg of Acetazolamide once a day for one or two days, alternating with a day of rest.
			Bicarbonate (HCO<sub>3</sub><sup>−</sup>) has a pK<sub>a</sub> of 10.3 with carbonate (CO<sub>3</sub><sup>2−</sup>), far further from physiologic pH (7.35–7.45), and so it is more likely to accept a proton than to donate one, but it is also far less likely for it to do either, thus bicarbonate will be the major species at physiological pH.
	Note: The dosage recommendations for glaucoma and epilepsy differ considerably from those for congestive heart failure, since the first two conditions are not dependent upon carbonic anhydrase inhibition in the kidney which requires intermittent dosage if it is to recover from inhibitory effect of the therapeutic agent.
			Under normal conditions in the proximal convoluted tubule of the kidney, most of the carbonic acid (H<sub>2</sub>CO<sub>3</sub>) produced intracellularly by the action of carbonic anhydrase quickly dissociates in the cell to ] (HCO<sub>3</sub><sup>−</sup>) and an H<sup>+</sup> ion (a ]), as previously mentioned. The bicarbonate (HCO<sub>3</sub><sup>−</sup>) exits at the basal portion of the cell via sodium (Na<sup>+</sup>) symport and chloride (Cl<sup>−</sup>) antiport and re-enters circulation, where it may accept a proton if blood pH decreases, thus acting as a weak, basic buffer. The remaining H<sup>+</sup> left over from the intracellular production of carbonic acid (H<sub>2</sub>CO<sub>3</sub>) exits the apical (urinary lumen) portion of the cell by Na<sup>+</sup> antiport, acidifying the urine. There, it may join with another bicarbonate (HCO<sub>3</sub><sup>−</sup>) that dissociated from its H<sup>+</sup> in the lumen of the urinary space only after exiting the proximal convoluted kidney cells/glomerulus as carbonic acid (H<sub>2</sub>CO<sub>3</sub>) because bicarbonate (HCO<sub>3</sub><sup>−</sup>) itself can not diffuse across the cell membrane in its polar state. This will replenish carbonic acid (H<sub>2</sub>CO<sub>3</sub>) so that it then may be reabsorbed into the cell as itself or CO<sub>2</sub> and H<sub>2</sub>O (produced via a luminal carbonic anhydrase). As a result of this whole process, there is a greater net balance of H<sup>+</sup> in the urinary lumen than bicarbonate (HCO<sub>3</sub><sup>−</sup>), and so this space is more acidic than physiologic pH. Thus, there is an increased likelihood that any bicarbonate (HCO<sub>3</sub><sup>−</sup>) that was left over in the lumen diffuses back into the cell as carbonic acid, CO<sub>2</sub>, or H<sub>2</sub>O.
	Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
			In short, under normal conditions, the net effect of carbonic anhydrase in the urinary lumen and cells of the proximal convoluted tubule is to acidify the urine and transport bicarbonate (HCO<sub>3</sub><sup>−</sup>) into the body. Another effect is excretion of Cl<sup>−</sup> as it is needed to maintain electroneutrality in the lumen, as well as the reabsorption of Na<sup>+</sup> into the body.
	==Side-effects==
	Common ] of using this drug include ] in the fingers and toes, and ] alterations (]), especially for carbonated drinks. Some may also experience blurred ] but this usually disappears shortly after stopping the medication. Acetazolamide also increases the risk of developing ] and calcium phosphate kidney stones. Everyone will experience more frequent ] as a result of using acetazolamide. One should drink more fluids than usual to prevent ] and ]s. Acetazolamide prolongs the effects of ] and related drugs. Acetazolamide also causes ].
			Thus, by disrupting this process with acetazolamide, urinary Na<sup>+</sup> and bicarbonate (HCO<sub>3</sub><sup>−</sup>) are increased, and urinary H<sup>+</sup> and Cl<sup>−</sup> are decreased. Inversely, serum Na<sup>+</sup> and bicarbonate (HCO<sub>3</sub><sup>−</sup>) are decreased, and serum H<sup>+</sup> and Cl<sup>−</sup> are increased. H<sub>2</sub>O generally follows sodium, and so this is how the clinical diuretic effect is achieved, which reduces blood volume and thus preload on the heart to improve contractility and reduce blood pressure, or achieve other desired clinical effects of reduced blood volume such as reducing edema or intracranial pressure.<ref name="pmid19948674">{{cite journal | vauthors = Koeppen BM | title = The kidney and acid-base regulation | journal = Advances in Physiology Education | volume = 33 | issue = 4 | pages = 275–281 | date = December 2009 | pmid = 19948674 | doi = 10.1152/advan.00054.2009 | url = http://d3qpq7e7yxjovl.cloudfront.net/content/ajpadvan/33/4/275 | url-status = dead | archive-url = https://web.archive.org/web/20160420042900/http://d3qpq7e7yxjovl.cloudfront.net/content/ajpadvan/33/4/275 | archive-date = 20 April 2016 }}</ref>
	==Contraindications==
	Acetazolamide should not be taken by individuals if:
	* They have ]
	* They are ] to ] medications
	* They are allergic to any carbonic anhydrase inhibitor
	* They have ] or ] disease
	* They have ] failure (i.e. ])
	* They are pregnant or are nursing mothers
	==Chemistry==		==History==
			An early description of this compound (as 2-acetylamino-1,3,4-thiadiazole-5-sulfonamide) and its synthesis has been patented.<ref>{{cite patent|title=Heterocyclic sulfonamides and metyhods of preparation thereof|country=US|number=2554816|pubdate=1951-05-29|assign1=]| inventor = Clapp Jr JW, Roblin RO }}</ref>
	]
			== Research ==
	{{Cite journal|doi=10.1021/ja01167a011|year=1950|last1=Roblin|first1=Richard O.|last2=Clapp|first2=James W.|journal=Journal of the American Chemical Society|volume=72|pages=4890|issue=11}}
			Smaller clinical trials have also shown promising results in the treatment of ] (NPH).<ref>{{cite journal | vauthors = Alperin N, Oliu CJ, Bagci AM, Lee SH, Kovanlikaya I, Adams D, Katzen H, Ivkovic M, Heier L, Relkin N | title = Low-dose acetazolamide reverses periventricular white matter hyperintensities in iNPH | journal = Neurology | volume = 82 | issue = 15 | pages = 1347–1351 | date = April 2014 | pmid = 24634454 | doi = 10.1212/WNL.0000000000000313 | pmc = 4001191 }}</ref><ref>{{cite journal | vauthors = Ivkovic M, Reiss-Zimmermann M, Katzen H, Preuss M, Kovanlikaya I, Heier L, Alperin N, Hoffmann KT, Relkin N | title = MRI assessment of the effects of acetazolamide and external lumbar drainage in idiopathic normal pressure hydrocephalus | journal = Fluids and Barriers of the CNS | volume = 12 | issue = 1 | pages = 9 | date = April 2015 | pmid = 25928394 | pmc = 4432506 | doi = 10.1186/s12987-015-0004-z | doi-access = free }}</ref><ref>{{cite journal |url=https://n.neurology.org/content/acetazolamide-treatment-normal-pressure-hydrocephalus |title=Acetazolamide in the treatment of Normal Pressure Hydrocephalus | journal = Neurology | vauthors = Gilbert GJ |date=18 May 2022|volume=82 |issue=15 |pages=1347–1351 |doi=10.1212/WNL.0000000000000313 |pmid=24634454 |pmc=4001191 |via=n.neurology.org}}</ref><ref>{{cite journal | vauthors = Aimard G, Vighetto A, Gabet JY, Bret P, Henry E | title = | journal = Revue Neurologique | volume = 146 | issue = 6–7 | pages = 437–439 | date = 21 May 1990 | pmid = 2399408 | url = https://pubmed.ncbi.nlm.nih.gov/2399408/ }}</ref><ref>{{ClinicalTrialsGov|NCT03779594|Acetazolamide for Treating NPH in Shunt-candidates Patients: an Open Label Feasibility Trial}}</ref>
	==References==		== References ==
	{{reflist|2}}		{{reflist}}
	{{Anticonvulsants}}		{{Anticonvulsants}}
	{{Antiglaucoma preparations and miotics}}		{{Antiglaucoma preparations and miotics}}
	{{Diuretics}}		{{Diuretics}}
			{{Portal bar | Medicine}}
			{{Authority control}}
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