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PubMed1984

Oral acetazolamide in Menière's disease.

The therapeutic efficacy of oral acetazolamide has been evaluated in a small pilot study of 14 patients with Menière's disease (23 hydropic ears). Symptomatic improvement was found in 4 cases. In 2 of these patients the improvement was not sustained, whilst another had to stop the drug due to the development of bilateral renal calculi. A deterioration in symptoms was seen in 3 cases. Significant adverse side-effects were encountered in 6 of the 13 patients (46.2 per cent) who complied with drug dosage instructions. It is suggested that this high incidence of side-effects may be consistent with a general metabolic difference between Menière's patients and normal subjects. We conclude that oral acetazolamide has no place in the medical treatment of Menière's disease.

Acetazolamide↗
PubMed1997

The polymorphic drug substances of the European pharmacopoeia. Part 9. Physicochemical properties and crystal structure of acetazolamide crystal forms.

The crystal structure of acetazolamide modification I (mod. I) was determined, and its differences compared with the already known crystal structure of the triclinic modification II (mod. II) are discussed. The monoclinic mod. I crystallizes in space group P2(1)/n with four molecules in the unit cell: a = 4.7674, b = 21.956, and c = 8.186 A, beta = 104.23 degrees. In both modifications, the molecules form hydrogen-bonded centrosymmetric dimers. The two modifications differ distinctly in the spatial arrangement of these pairs and in the hydrogen bonds formed between them. The thermodynamic relationship between the two modifications is demonstrated by a semischematic energy/temperature diagram, based on the results of thermal analysis and solubility experiments. Mod. II is the thermodynamically stable modification at 20 degrees C and enantiotropically related to mod. I. The thermodynamic transition point lies between 120 and 148 degrees C. The solid-state properties of acetazolamide are mainly directed by the strong intermolecular hydrogen bond forces. Thus, the metastable mod. I exhibits a higher density than mod. II and a very high kinetic stability at 20 degrees C. Both modifications can be crystallized from water and the solubility differences are very small, so, in addition to mod. II, the metastable but extremely resistant mod. I is suggested to be suitable for use in solid pharmaceutical formulations.

Acetazolamide↗
PubMed1999

Effects of interactions between drugs on the renal excretion of trientine in rats--acetazolamide and furosemide increase trientine excretion.

PURPOSE: To elucidate the effects of drug interactions on the urinary excretion of trientine in rats. METHOD: Trientine and various other drugs were intravenously administered to rats and the urinary excretion of trientine was investigated. To clarify the mechanisms of drug-drug interactions, we also investigated the effects of various drugs on spermine uptake by rat renal brushborder membrane vesicles. RESULTS: Cimetidine, a substrate of the H+/organic cation antiporter, and aminoglycoside antibiotics did not affect trientine excretion, while acetazolamide and furosemide, which increase the concentration of sodium ions in renal proximal tubules, increased the excretion of trientine. However, trichlormethiazide, which acts in renal distal tubules, did not affect trientine excretion. Acetazolamide and furosemide did not directly affect the Na+/spermine transporter because these diuretics had no effect on the uptake of spermine into the rat renal brush-border membrane vesicles. CONCLUSIONS: There is no interaction between trientine and the substrate of the H+/organic cation antiporter or aminoglycoside antibiotics. However, drugs that change the concentration of sodium ions in renal proximal tubules, such as diuretics, can increase the trientine excretion since the increase in the luminal concentration of sodium ion accelerates the Na+/spermine antiporter.

Acetazolamide↗
PubMed1980

Effects of disease and acetazolamide on procaine hydrolysis by red blood cell enzymes.

Procaine hydrolysis in vitro has been studied in whole blood, plasma, and washed erythrocytes. Esterase activity was higher in whole blood than in either diluted plasma or resuspended erythrocytes. Eserine and echothiophate specifically inhibited plasma procaine esterase activity, while acetazolamide blocked hydrolysis of procaine by washed erythrocytes. Kinetic studies in whole blood also identified 2 different enzymes. Procaine esterase activity associated with red blood cells was not impaired in patients with renal failure or hepatic cirrhosis, but procaine half-life (t 1/2) in whole blood of normal subjects was longer after 250 mg acetazolamide.

Acetazolamide↗
PubMed1985

Net tubular secretion of bicarbonate by the alligator kidney. Antimammalian response to acetazolamide.

Net tubular secretion of bicarbonate by the alligator kidney was demonstrated during acute clearance experiments where the animals were infused with an isosmotic solution of one-half 5% mannitol and one-half 0.9% NaCl. Tubular secretion of bicarbonate averaged 3.38 mumoles/min in animals with a mean wt of 1.0 kg. During these experiments, mean tubular secretion of urate was 0.51 mumole/min and urinary ammonia excretion was 4.3 mumoles/min. Urinary pNH3 was high and ranged from 22,231 to 41,223 mm Hg X 10(-6). The administration of acetazolamide 25 mg/kg resulted in abolition of bicarbonate secretion, which was replaced by bicarbonate reabsorption. At the same time, the tubular secretion of urate fell by 70% and the excretion of ammonia fell by 77%. This is the first time that net tubular secretion of bicarbonate is demonstrated in a living animal. Acetazolamide has an antimammalian effect. It is proposed that the alligator that lives with a low plasma bicarbonate concentration (10 mM) possesses a kidney in which the renal tubular cells secrete bicarbonate in the tubular lumen and hydrogen at the peritubular site, in contrast to that which takes place in mammalia and other animal species.

Absorption↗
PubMed1998

Acetazolamide-induced severe pancytopenia mimicking myelodysplasia relapse following allogeneic bone marrow transplantation.

Pancytopenia with severe bone marrow dysplasia following allogeneic bone marrow transplantation for acute myeloid leukemia (M6) may pose a diagnostic problem. We report a case of M6 acute myeloid leukemia in which progressive macrocytosis, pancytopenia and severe bone marrow dysplasia induced by acetazolamide therapy developed after successful engraftment of a donor marrow. We discuss the diagnostic problems and the usefulness of conventional cytogenetics and interphase fluorescence in situ hybridisation in excluding recipient myelodysplasia relapse. We also suggest that acetazolamide should be used with caution, especially following bone marrow transplantation.

Acetazolamide↗
PubMed2001

Acetazolamide poisoning in a toddler.

Acetazolamide ingestion and its sequelae have not been previously reported in children. A 12-month-old girl, weighing 10 kg, developed metabolic acidosis following ingestion of between 500 and 1250 mg of acetazolamide. The maximum base deficit recorded was 11.6. She was treated with sodium bicarbonate and recovered completely. Accidental poisoning should be included in the differential diagnosis of a child presenting with metabolic acidosis.

Acetazolamide↗
PubMed2003

Acetazolamide acts on neuromuscular transmission abnormalities found in some migraineurs.

Mild subclinical impairment of neuromuscular transmission can be detected with single-fibre electromyography (SFEMG) in subgroups of patients suffering from migraine and could be due to dysfunctioning Ca2+-channels on motor axons controlling stimulation-induced acetylcholine release. Acetazolamide, which is thought to ameliorate ion channel function, was shown effective in familial hemiplegic migraine and episodic ataxia type 2, both of which are associated with mutations of the neuronal Ca2+-channel gene CACNA1A, as well as in aura status. We treated therefore in an open pilot study five non-hemiplegic migraineurs showing mild SFEMG abnormalities with acetazolamide for several weeks. This was followed by a normalization of SFEMG recordings in all patients and by clinical improvement in four. These results support the assumption that the subclinical impairment of neuromuscular transmission found in certain migraineurs might be due to dysfunctioning Ca2+-channels.

Acetazolamide↗
PubMedDate not supplied

Acetazolamide testing of cerebral vasodilator capacity provokes "vascular" but not tension headaches.

Cerebrovascular capacitance was tested by measuring local cerebral blood flow (LCBF) by xenon-contrasted CT scanning before and after the oral administration of 14.3 mg/kg of acetazolamide among 45 subjects including 15 age-matched controls without history of headache, 20 migraineurs with and without aura, 3 patients with cluster headache, and 7 patients with tension-type headache. Percentage increases of LCBF were measured in 10 regions located throughout both hemispheres. Laterality indices for asymmetric LCBF increases were calculated. Local cerebral blood flow in cortical gray matter increased 5.9% in controls, 9.9% in patients with tension headaches, but 18.6% in both migraine and cluster headache patients; significantly greater LCBF increases than among controls or among patients with tension headaches (P < 0.05). Increases in LCBF were significantly asymmetric among migraine and cluster patients and provoked typical unilateral vascular headaches which responded to sumatriptan. Maximal asymmetric LCBF increases also corresponded to the reported side of the induced headaches confirming their vascular pathogenesis. Patients with tension headaches and controls without history of headache did not develop head pain after acetazolamide.

Acetazolamide↗
PubMed1991

[Effects of acetazolamide (Diamox, Glaupax) on tear production].

In view of personal clinical observations, it appeared possible that a therapy with the carboanhydrase inhibitor acetazolamide leads to a reduction of tear production and induces a dry eye syndrome. Tear secretion was therefore measured by Schirmer tests in a control group of 66 patients after cataract surgery and in a test group of 20 patients who were treated with acetazolamide (Diamox, Glaupax) on the day after the cataract operation. The results were subjected to a statistical analysis with 3-factor anova. The cataract operation induced a significant increase of tear flow. Independent of this effect, administration of the carboanhydrase inhibitor caused a significant decrease of tear production, both in the operated eyes and the untouched fellow eyes.

Acetazolamide↗
PubMed1989

[Acetazolamide stimulation test in the preoperative assessment of cerebrovascular reserve capacity in unilateral carotid obstruction].

Using the 16-detector 133Xe-NaCl technique (Novo Cerebrograph) quantitative measurements of regional cerebral blood flow (rCBF) were performed in 13 patients with unilateral carotid obstruction before and after stimulation with 1 g acetazolamide. In all patients resting studies showed no significant difference in hemispheric perfusion and a 47% flow increase after acetazolamide on the side with normal carotid artery. On the obstructed side in 8 patients the hemispheric flow increased equally indicating a sufficient and adequate intracerebral collateral circulation and capacity. In 5 patients a significant redistribution of brain flow occurred with diminished increase on the occluded side. This flow pattern indicates an inadequate vasodilator response and insufficient collateral capacity. The rCBF stimulation test identifies patients with a restricted collateral capacity and these patients could benefit from a surgical treatment.

Acetazolamide↗
PubMed1980

[Effect of timolol and acetazolamide on intraocular hypertension after intracapsular lens extraction with alpha-chymotrypsin (author's transl)].

After intracapsular lens extraction with alpha-chymotrypsin three groups of 14 patients were formed. The first group was given Timolol 0.25% 2 x 1 drops, the second acetazolamide in sustained release form 1 x 500 mg and the third served as control. In all three groups the postoperatively elevated pressure diminished significantly in the first five postoperative days. The pressure diminution on the fourth and fifth postoperative day was accelerated by Timolol but not by acetazolamide.

Acetazolamide↗
PubMed1980

Responses to hydrochlorothiazide and acetazolamide in patients with calcium stones. Evidence suggesting a defect in renal tubular function.

Urinary excretion of sodium, calcium, and magnesium has been measured after single oral doses of hydrochlorothiazide (100 mg) and acetazolamide (500 mg) in unselected patients with calcareous renal stone formation and in normal control subjects. With hydrochlorothiazide, 36 stone formers had significantly greater increments in sodium (P less than 0.01), calcium (P less than 0.05), and magnesium (P less than 0.05) excretion than 20 normal subjects. With acetazolamide, 13 stone formers had a smaller increment in sodium excretion (P less than 0.05) than 10 normal subjects. The abnormal responses to both diuretics were most marked in the patients with hypercalciuria during fasting. These data suggest that the tubular handling of sodium, magnesium, and calcium may be abnormal in patients with calcareous renal stones and are consistent with the presence of a defect in proximal-tubular reabsorption of fluid and electrolytes that may be partly offset by increased reabsorption in the distal nephron.

Acetazolamide↗
PubMed1992

Acetazolamide stimulation test in patients with unilateral internal carotid artery obstructions using transcranial Doppler and 99mTc-HM-PAO-Spect.

Fifteen patients with symptoms of cerebral ischaemia and angiographically confirmed unilateral stenoses or occlusions of the extracranial internal carotid artery (ICA) and 20 controls were studied by a 2 MHz transcranial Doppler (TCD) at rest and after stimulation with 1 g acetazolamide i.v., a cerebral vasodilator. In addition, the patients underwent 99mTc-HM-PAO-Spect measurement of regional cerebral blood flow (rCBF) at rest and after stimulation with 1 g acetazolamide. In 10 patients with ICA stenoses greater than 80% or occlusions, time-mean velocity (Vmean) increase and pulsatility index (PI) decrease in the postobstructive middle cerebral artery (MCA) as well as the increase of the ipsilateral rCBF were reduced in comparison with the contralateral side. The remaining 5 patients showed a normal Vmean increase and PI decrease in TCD.

Acetazolamide↗
PubMed2002

A randomized, double-blind, placebo-controlled trial of acetazolamide for the treatment of elevated intracranial pressure in cryptococcal meningitis.

We conducted a trial of oral acetazolamide for the treatment of cryptococcal meningitis in 22 Thai adults with headache and an opening cerebrospinal fluid pressure of >/=200 mm H(2)0. The trial was terminated prematurely because patients who received acetazolamide developed significantly lower venous bicarbonate levels and higher chloride levels and had more-frequent serious adverse events than did subjects who received placebo.

Acetazolamide↗
PubMed2006

Acetazolamide improves cerebral oxygenation during exercise at high altitude.

Vuyk, Jaap, Jan Van Den Bos, Kees Terhell, Rene De Bos, Ad Vletter, Pierre Valk, Martie Van Beuzekom, Jack Van Kleef, and Albert Dahan. Acetazolamide improves cerebral oxygenation during exercise at high altitude. High Alt. Med. Biol. 7:290-301, 2006.--Acute mountain sickness is thought to be triggered by cerebral hypoxemia and be prevented by acetazolamide (Actz). The effect of Actz on cerebral oxygenation at altitude remains unknown. In 16 members of the 2005 Dutch Cho Oyu (8201 m, Tibet) expedition, the influence of Actz and exercise (750 mg PO daily) on heart rate, peripheral and regional cerebral oxygen saturation (Sa(O(2) ) and rS(O(2) )), the Lake Louise score (LLS), and psychomotor function were studied at 0 m 14 days prior to the expedition, after arrival at 3700 m on day 3, after arrival at 5700 m on day 29, and again at 5700 m before the end of the expedition on day 51. After arrival at 3700 m, the LLS of the climbers taking Actz (n = 8) was significantly lower compared to those who did not take Actz (n = 8): 0.75 +/- 1.0 versus 2.9 +/- 2.0, p < 0.05 (ANOVA). High LLSs were associated with low rS(O(2) ) values in rest and exercise (p < 0.01 and p < 0.001). With altitude, resting Sa(O(2) ) and resting rS(O(2) ) decreased significantly (p < 0.001), irrespective of Actz use. Exercise at 3700 m and 5700 m reduced Sa(O(2) ) and rS(O(2) ) even further compared to rest (p < 0.001), although at 3700 m the rS(O(2) ) was preserved better in those who took Actz (55.3 +/- 4.3% versus 47.9 +/- 5.7%, p < 0.05). Irrespective of Actz use, with altitude, the percentage of omissions in the vigilance and tracking test increased while the climbers' scores on vigor decreased (p < 0.05). In conclusion, at altitude, exercise-induced reduction in cerebral oxygenation is less in climbers on Actz compared to climbers not taking Actz. This effect is nullified after several weeks at altitude due to acclimatization in climbers not taking Actz.

Acetazolamide↗
PubMed1996

Stability of acetazolamide, allopurinol, azathioprine, clonazepam, and flucytosine in extemporaneously compounded oral liquids.

The stability of drugs commonly prescribed for use in oral liquid dosage forms but not commercially available as such was studied. Acetazolamide 25 mg/mL, allopurinol 20 mg/mL, azathioprine 50 mg/mL, clonazepam 0.1 mg/mL, and flucytosine 10 mg/mL were prepared in 1:1 mixture of Ora-Sweet and Ora-Plus (Paddock Laboratories), a 1:1 mixture of Ora-Sweet SF and Ora-Plus (Paddock Laboratories), and cherry syrup and placed in polyethylene terephthalate bottles. The sources of the drugs were capsules and tablets. Six bottles were prepared per liquid; three were stored at 5 degrees C and three at 25 degrees C, all in the dark. A sample was removed from each bottle initially and at intervals up to 60 days and analyzed for drug concentration by stability-indicating high-performance liquid chromatography. At least 94% of the initial drug concentration was retained in all the oral liquids for up to 60 days. There were no substantial changes in the appearance or odor of the liquids, or in the pH. Acetazolamide 25 mg/mL, allopurinol 20 mg/mL, azathioprine 50 mg/mL, clonazepam 0.1 mg/mL, and flucytosine 10 mg/mL were stable for up to 60 days at 5 and 25 degrees C in three extemporaneously compounded oral liquids.

Acetazolamide↗
PubMed1997

Acetazolamide-responsive episodic ataxia in an Italian family refines gene mapping on chromosome 19p13.

Episodic ataxia type 2 is an autosomal dominant disorder with attacks of vertigo and ataxia which respond to acetazolamide treatment. The gene, distinct from the KCNA1 responsible for episodic ataxia type 1, has been mapped on chromosome 19p13 in a 11-12 cM region. A large Italian kindred affected with acetazolamide-responsive episodic ataxia is reported, with onset in adulthood, a strong vestibular component during attacks and a high frequency of cerebellar vermis degeneration. The genetic analysis (i) showed strong linkage between the disease and the 19p13 microsatellite markers in a region which widely overlaps that previously reported and (ii) set a new distal boundary of the gene-containing region. Combining present and previous mapping data, the gene of episodic etaxia type 2 is most probably located in an interval approximately 1.5 Mb between markers D19S221 and D19S226.

Acetazolamide↗