Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACETAZOLAMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed2002

Mineral status of embryos of domestic fowl following exposure in vivo to the carbonic anhydrase inhibitor acetazolamide.

Eggs of domestic fowl were given daily injections of vehicle (DMSO) or vehicle plus acetazolamide, a potent inhibitor of the enzyme carbonic anhydrase, beginning on day 12 of incubation. Embryos were removed from eggs on days 16 and 18, and carcasses and yolks were analyzed for calcium, magnesium, and phosphorus. Treatment with acetazolamide did not affect the quantity of calcium or phosphorus in carcasses and the effect, if any, on magnesium in carcasses was small. However, calcium content of yolk was reduced substantially by acetazolamide both on day 16 and day 18. The reduction in calcium content of yolk led, in turn, to a reduction in the total quantity of calcium in eggs on days 16 and 18. Embryos exposed to acetazolamide seemingly mobilized less calcium from the eggshell than did control embryos. When faced with a shortfall in the availability of calcium from the eggshell, embryos defended carcass calcium, and the shortfall was reflected in a reduction in the quantity of calcium deposited in yolk. The results of this study support the concept that the enzyme carbonic anhydrase plays a role in solubilization of the eggshell and provision of calcium to embryos.

Acetazolamide↗
PubMed2006

CACNA1A mutation in a EA-2 patient responsive to acetazolamide and valproic acid.

BACKGROUND: Episodic ataxia type-2 (EA-2) is an autosomal dominant neurological disorder that has been shown to result from mutations in the CACNA1A gene encoding the P/Q-type calcium channel. Affected individuals experience episodes of cerebellar ataxia usually associated with migraine symptoms, interictal nystagmus, mild residual and in some cases a progressive cerebellar incoordination and respond to acetazolamide treatment. We identified a patient with a positive family history for episodic ataxia, who was originally diagnosed with epilepsy and treated with valproic acid. Subsequent examination revealed that the symptoms were consistent with a diagnosis of EA-2. The patient responded positively to a combination of acetazolamide and valproic acid. Molecular genetic analysis of the CACNA1A gene was performed in order to confirm a diagnosis of EA-2. METHODS: The CACNA1A gene was evaluated for mutations using single strand conformational polymorphism analysis and direct DNA sequencing. Allele specific oligo hybridization was used to confirm that the mutation was segregating with only affected family members and was not present in the control group. RESULTS: In this study we identified a new missense mutation in exon 12 of the CACNA1A gene from a patient with EA-2 whose symptoms could be controlled with a combination of acetazolamide and valproic acid. This G to A transition changes a highly conserved glutamic acid residue to a lysine residue in domain II S2 of the P/Q-type calcium channel alpha1A subunit. CONCLUSIONS: The use of valproic acid in treating patients with EA-2 is not well documented. Here we describe a patient with a novel mutation in the CACNA1A gene who responded positively to a combination of acetazolamide and valproic acid.

Acetazolamide↗
PubMed2001

Is acetazolamide effective in the treatment of diabetic macular edema? A pilot study.

AIM: To investigate whether acetazolamide, already found to be helpful in decreasing cystoid macular edema in patients with retinitis pigmentosa, was also effective in the treatment of diabetic macular edema in nonproliferative retinopathy. METHODS: Two randomized age- and sex-matched groups (cases and controls) of 12 diabetics (five Type 1 and seven Type 2) were selected for this pilot study and graded for retinopathy (Early Treatment of Diabetic Retinopathy Study-Airlie House Classification). Cases were treated with acetazolamide for three months according to a standard protocol. The Early Treatment of Diabetic Retinopathy Study chart was used for assessing far-best corrected visual-acuity, and fluorescein angiography was performed using the Heidelberg Retina Angiograph. The Amsler grid-test and computerized-perimetry (Octopus 2000R) were also performed. RESULTS: Fluorescein-angiographic findings and perimetric data improved significantly (p < 0.01) in the acetazolamide-treated cases compared to the controls while visual-acuity varied only slightly (p > 0.01). The Amsler grid-test resulted insignificant in our study (p > 0.05). No adverse effects or significant variations in laboratory tests were recorded. CONCLUSION: Further clinical investigations involving larger numbers of patients and a longer follow-up are required to confirm these preliminary results. However, the present study seems to suggest that acetazolamide could be effective in reducing fluorescein-angiographic findings and improving perimetric data in diabetics with macular edema, even though the mechanism of action remains obscure. Visual-acuity varied only slightly.

Acetazolamide↗
PubMed2001

Clinical trial of acetazolamide in SCA6, with assessment using the Ataxia Rating Scale and body stabilometry.

OBJECTIVE: To investigate the effect of acetazolamide on spinocerebellar ataxia type 6 (SCA6). METHODS: Acetazolamide (250-500 mg/day) was administered orally for 88 weeks to 6 patients with SCA6, and its effect was quantitatively monitored using the Ataxia Rating Scale (ARS) and body sway analysis by stabilometry. RESULTS: During administration of acetazolamide, the ARS score and the amplitude of body sway were significantly reduced compared with before administration. However, the response became weaker after 1 year of treatment. CONCLUSION: Although this was an open trial, the results suggested that acetazolamide can temporarily reduce the severity of symptoms during the progression of SCA6.

Acetazolamide↗
PubMed1993

The effect of acetazolamide on the retinal circulation.

The effect of the carbonic anhydrase inhibitor, acetazolamide, on the retinal circulation was studied in 10 healthy volunteers. Acetazolamide was administered intravenously at a dose of 500 mg. Retinal blood flow was determined from red cell velocity using laser Doppler velocimetry and vessel diameter measurement using computerised digital image analysis of monochromatic fundus photographs. There was a significant increase in retinal blood flow at 30 minutes and 60 minutes after acetazolamide injection (p = 0.002). Retinal vessels showed vasodilatation reaching significant levels 60 minutes after the injection (p < 0.03). An increase in red cell velocity was observed at 30 and 60 minutes (p < 0.002). A significant reduction in intraocular pressure occurred at 30 and 60 minutes after the injection (p < 0.001). The mechanisms responsible for the increase in retinal blood flow acted via significant increases in perfusion pressure (p < 0.05), red cell velocity (p < 0.002) and retinal vessel dilatation (p < 0.03). An increase in tissue PCO2 and a reduction in pH are thought to be responsible for the vascular dilatation. The increase in retinal blood flow with acetazolamide may serve to limit optic disc and retinal ischaemia in acute glaucoma and central retinal artery occlusion respectively.

Acetazolamide↗
PubMed1976

Effect of parathyroid hormone on phosphate reabsorption in the presence of acetazolamide.

The hypothesis that parathyroid hormone and carbonic anhydrase inhibitors have a common mechanism or site of action on phosphate reabsorption by the renal tubule was tested by administration of parathyroid hormone in the absence and presence of acetazolamide in thyroparathyroidectomized dogs. Re-collection micropuncture and electron probe microanalysis methodologies were utilized. In the absence of acetazolamide, parathyroid hormone increased fractional delivery of phosphate (and volume) from the proximal tubule from 25 +/- 2 to 38 +/- 3%, P less than 0.025, and increased fractional phosphate excretion from 3.8 +/- 1.2 to 19.9 +/- 3.7%, P less than 0.005 (eight dogs). In the presence of acetazolamide, parathyroid hormone increased fractional delivery of phosphate (but not volume) from the proximal tubule from 50 +/- 4 to 58 +/- 5%, P less than 0.025, and increased fractional excretion of phosphate from 8.7 +/- 2.2 to 31.0 +/- 4.3%, P less than 0.001 (12 dogs). Thus, the effects of parathyroid hormone were additive to the effects of maximal inhibition of carbonic anhydrase indicating that parathyroid hormone and carbonic anhydrase inhibitors have different mechanisms of action on phosphate reabsorption by the renal tubule. In addition, phosphate reabsorption beyond the point of micropuncture in the late proximal tubule was much more markedly inhibited by parathyroid hormone than by acetazolamide.

Acetazolamide↗
PubMed2002

Acetazolamide inhibits stimulated feline liver and gallbladder bicarbonate secretion.

Bile acidification is a key factor in preventing calcium carbonate precipitation and gallstone formation. Carbonic anhydrase II (CA II), that is inhibited by acetazolamide, plays a role in regulation of the acid-base balance in many tissues. This study examines the effect of acetazolamide on secretin- and vasoactive intestinal peptide (VIP)-stimulated gallbladder mucosal bicarbonate and acid secretion. Gallbladders in anaesthetized cats were perfused with a bicarbonate buffer bubbled with CO2 in air. In 20 experiments VIP (10 microg kg(-1) h(-1)) and in 10 experiments secretin (4 microg kg(-1) h(-1)) were infused continuously intravenous (i.v.). Hepatic bile and samples from the buffer before and after perfusion of the gallbladder were collected for calculation of ion and fluid transport. During basal conditions a continuous secretion of H+ by the gallbladder mucosa was seen. Intravenous infusion of vasoactive intestinal peptide (VIP) and secretin caused a secretion of bicarbonate from the gallbladder mucosa (P < 0.01). This secretion was reduced by intraluminal (i.l.) acetazolamide (P < 0.01). Bile flow was enhanced by infusion of VIP and secretin (P < 0.01) but this stimulated outflow was not affected by i.v. acetazolamide. The presence of CA II in the gallbladder was demonstrated by immunoblotting. Biliary CA activity has an important function in the regulation of VIP- and secretin-stimulated bicarbonate secretion across the gallbladder mucosa.

Acetazolamide↗
PubMed1999

Clinical efficacy and indication of acetazolamide treatment on sleep apnea syndrome.

The efficacy and indication of acetazolamide treatment on patients with sleep apnea syndrome (SAS) were discussed from assessing the changes of polysomnographic findings with the treatment in 75 SAS patients. For the patients as a whole, respiratory disorder variables improved significantly during the treatment. However, the number of acetazolamide treatment responders who showed a decrease of apnea hypopnea index (AHI) to 50% or less of the pretreatment value numbered only 34 (45.3%). The lower values of body mass index and AHI in the responder group indicated that monotherapy with acetazolamide is the treatment choice only for mild SAS cases without obesity. However, combined treatment with acetazolamide and uvulopalatopharyngoplasty was thought to be beneficial for severe cases.

Acetazolamide↗
PubMed1992

The influence of acetazolamide on cerebral low-flow regions in migraine--an interictal 99mTc-HMPAO SPECT study.

Acetazolamide, a carbonic anhydrase inhibitor, has proved to be useful in the assessment of "vasodilatory capacity" in cerebrovascular disease. To obtain further information on the nature of interictal low-flow regions in migraine, we reinvestigated 20 asymptomatic patients suffering from migraine with aura (n = 15) or without aura (n = 5) and who had either minor (n = 12) or marked (n = 8) regional hypoperfusion when examined in a previous 99mTc-HMPAO SPECT investigation. These patients received acetazolamide IV prior to tracer application. In 14/20 cases regional hypoperfusion resolved. Three patients with migraine with aura had less pronounced regional hypoperfusion compared to baseline. No change in baseline hypoperfusion was detectable in three older patients. No further decreases in flow were measured. In contrast to patients with cerebrovascular ischemia, in whom acetazolamide usually enhances low-flow regions, vasodilatory capacity appears intact in most migraine patients with interictal regional hypoperfusion. Thus, the "acetazolamide test" might be useful in the differential diagnosis of migraine with aura from transient cerebrovascular ischemia.

Acetazolamide↗
PubMed2001

The effect of acetazolamide on the kinetics of four newer beta-lactams in the aqueous humor.

OBJECTIVE: To evaluate whether the effect of acetazolamide on piperacillin's aqueous humor concentrations observed in animals exists also in humans for ceftazidime, cefotaxime, ceftriaxone and aztreonam. METHODS: One hundred and eighty-eight patients undergoing eye cataract surgery were randomly allocated to receive intravenous ceftazidime, cefotaxime, aztreonam or ceftriaxone with (subgroup A) or without (subgroup B) concomitant oral administration of acetazolamide. Antibiotic concentrations in serum and the aqueous humor, simultaneously sampled during the operation, were measured using an agar well diffusion technique, and the ratios of the concentrations of aqueous humor to serum were calculated and compared. Statistical analysis was performed by using the paired t-test. RESULTS: Mean aqueous humor ceftazidime concentrations at 2, 4 and 6 h were 24.65, 16.4 and 8.6 mg/L (subgroup A), and 4.26, 8.66 and 5.61 mg/L (subgroup B). Corresponding concentrations of cefotaxime were 1.75, 1.0 and 0.77 mg/L (subgroup A), and 1.11, 0.81 and 0.58 mg/L (subgroup B), and of aztreonam 6.9, 5.84 and 3.61 mg/L (subgroup A), and 3.38, 2.57 and 1.48 mg/L (subgroup B). Ceftriaxone concentrations at 2, 4, 6 and 12 h were 1.78, 1.49, 1.57 and 1.41 mg/L (subgroup A), and 1.35, 0.95, 1.08 and 0.85 mg/L (subgroup B). The differences in aqueous humor concentrations when acetazolamide was administered were statistically significant (P < 0.05), with the exception of ceftazidime 6 h, cefotaxime 6 h and ceftriaxone 2 h. CONCLUSIONS: Although acetazolamide resulted in statistically significant increases in the aqueous humor concentrations of all the antibiotics tested, this effect was most marked for ceftazidime.

Acetazolamide↗
PubMed2003

Transepithelial short circuit currents in human and porcine isolated ciliary bodies: effect of acetazolamide and epinephrine.

BACKGROUND: To investigate in human and porcine isolated ciliary bodies the effect of acetazolamide and epinephrine on ciliary transepithelial ionic currents (a parameter linked to aqueous humor production). MATERIAL AND METHODS: Isolated ciliary bodies were mounted in a Ussing-type chamber to measure transepithelial potential difference (PD) and short circuit current (Isc) before and after exposure to either 100 micro M acetazolamide or 10 micro M epinephrine. RESULTS: In humans (N = 27), baseline PD was 1184 +/- 100 micro V (negative on the non-pigmented epithelial [NPE] side) and Isc 19.9 +/- 1.5 micro A/cm 2. Acetazolamide (N = 7 - 8) decreased Isc (NPE side: 8.4 +/- 1.1 micro A/cm 2; pigmented epithelial [PE] side: 7.4 +/- 0.9 micro A/cm 2) while epinephrine (N = 6) increased Isc only on the NPE side (9.9 +/- 0.8 micro A/cm 2). In pigs, baseline PD was in some preparations negative (862 +/- 84 micro V, N = 18) and in others positive (814 +/- 81 micro V, N = 10) on the NPE side with Isc 15.6 +/- 1.6 micro A/cm 2 and 16.3 +/- 2.6 micro A/cm 2, respectively. In all preparations, acetazolamide (N = 6 - 7) decreased Isc (NPE side: 6.1 +/- 0.6 micro A/cm 2; PE side: 4.8 +/- 0.3 micro A/cm 2) while epinephrine (N = 8) increased it only on the NPE side (10.5 +/- 0.6 micro A/cm 2). CONCLUSIONS: To our knowledge, this is the first time that this methodology is applied to measure transepithelial ionic currents in isolated human and porcine ciliary bodies. This method could be used to test drugs modulating aqueous humor production.

Acetazolamide↗
PubMed1996

[Combination therapy of circumscribed choroid hemangioma in contralateral Sturge-Weber syndrome with acetazolamide and laser coagulation].

BACKGROUND: In Sturge-Weber syndrome choroidal hemangiomas occur in up to 55%. With a few exceptions it is a diffuse hemangioma and it always affects the eye ipsilateral to the naevus flammeus. To the best of our knowledge, a contralateral circumscribed choroidal hemangioma has not yet been described. HISTORY AND CLINICAL FINDINGS: We present a 34-year-old male caucasian with a left-sided naevus flammeus and a right-sided circumscribed choroidal hemangioma. Ipsilateral to the naevus, the left eye showed typical vascular anomalies of the conjunctiva and episclera as well as in the anterior chamber angle with anterior synechia formation and circumscribed iris atrophy without secondary glaucoma. Retinal and choroidal vasculature was normal. In the contralateral eye the anterior segment was normal, but there was a juxtafoveolar circumscribed choroidal hemangioma of about 7.5 x 4.5 mm along the superior temporal vascular arcade. The tumor was detected when vision dropped to 0.4 due to an exsudative retinal detachment over the tumor involving the fovea. THERAPY AND CLINICAL COURSE: Complete regression of the exsudative detachment occurred under oral Acetazolamide (1000 mg/d), but after dose reduction to 500 mg/d the exsudation recurred. Thereafter, the surface of the tumor was treated with argongreen grid lasercoagulation in 3 sessions under Acetazolamide cover. Following scar formation the retina has stayed completely attached even after discontinuation of oral Acetazolamide therapy with a follow-up of now 7 months. CONCLUSIONS: Visual prognosis after exsudative macula detachment is depended on rapid retinal reattachment. Therefore, early and effective treatment is mandatory. Systemic application of Acetazolamid (1000 mg/d orally) led to a rapid reattachment of the retina with an excellent visual result. However, dose-reduction was followed by an immediate recurrency. We therefore suggest to perform an Argongreen grid lasercoagulation of the tumor surface while the patient is still under systemic Aceazolamid. This strategy has proven successful in this case.

Acetazolamide↗
PubMed2004

A dose-response study of acetazolamide for acute mountain sickness prophylaxis in vacationing tourists at 12,000 feet (3630 m).

The study objective was to determine whether acetazolamide is effective in prophylaxis of acute mountain sickness (AMS) at moderate altitude in ambulatory travelers not undergoing vigorous exercise. Volunteers vacationing in La Paz, Bolivia (3630 m), immediately after arrival from sea level were studied. The design was a double-blind, randomized trial of two doses of acetazolamide (125 mg twice daily, 250 mg twice daily) versus placebo twice daily over a 24-h period. The main outcome measure was AMS score and score trend, using the Lake Louise consensus questionnaire. Nine of 32 subjects (28%) had symptom scoring diagnostic of AMS at 0 h. At 0 and 24 h (respectively), the mean Lake Louise scores were 1.73 and 1.09 for the 11 subjects receiving placebo, 1.45 and 1.36 for the 11 subjects receiving the 125-mg dose, and 2.7 and 0.6 for the 11 subjects receiving the 250-mg dose. The absolute change in these mean scores was not significant for placebo (p = 0.21) or the 125-mg dose (p = 0.88), but was significant for the 250-mg dose (p = 0.008). A comparison of a difference in decline in average AMS score over time showed a statistically significant decline for the 250-mg dosing group versus placebo (p = 0.002). The 250-mg dose of acetazolamide twice daily (but not 125 mg twice daily) was effective in inducing a significant decline in AMS symptoms over the 24-h period after arrival to 3630 m. These results suggest that the dosing of acetazolamide for AMS prevention in nonmountaineering tourists at altitudes below 3700 m should not be lowered below 250 mg twice daily.

Acetazolamide↗
PubMed1994

End-tidal partial pressure of carbon dioxide does not accurately reflect PaCO2 in rabbits treated with acetazolamide during anaesthesia.

Acetazolamide, a carbonic anhydrase inhibitor, may cause significant disturbances in carbon dioxide transport and elimination. In this study, end-tidal carbon dioxide monitoring has been used to study the correlation between arterial carbon dioxide (PaCO2) and end-tidal carbon dioxide partial pressure (PE'CO2) in rabbits treated with acetazolamide. A significant difference in (PaCO2-PE'CO2) developed immediately after administration of acetazolamide and persisted for more than 2 h. It is concluded that PE'CO2 did not reflect accurately PaCO2 and the ventilatory status of the rabbit which received acetazolamide within 2 h.

Acetazolamide↗
PubMed1992

Acetazolamide improves action myoclonus in Ramsay Hunt syndrome.

The myoclonus of two patients with Ramsay Hunt syndrome was only partially controlled under treatment with clonazepam, sodium valproate, primidone, and piracetam. Acetazolamide (200 mg daily) was added to these drugs, resulting in a dramatic improvement. Placebo substitution (one patient) and withdrawal of acetazolamide in the other patient resulted in marked aggravation of the myoclonus. The mechanism of action of acetazolamide in myoclonus is unknown. Acetazolamide may be an additional therapeutic possibility for patients with severe action myoclonus.

Acetazolamide↗
PubMedDate not supplied

Long-term effect of acetazolamide treatment of patients with uveitic chronic cystoid macular edema is limited by persisting inflammation.

PURPOSE: To assess the long-term effect of acetazolamide treatment on patients with cystoid macular edema (CME) in the course of intermediate or posterior chronic uveitis and to define those patients who may particularly benefit from the drug. METHODS: Fifty-two eyes (45 patients) with chronic uveitic CME were treated with acetazolamide at an initial dosage of 500 mg/d. The effect of treatment was assessed by fluorescein angiography, ophthalmoscopy, visual acuity, and Amsler testing. Therapy was withdrawn when CME did not improve at 3 weeks. In cases with CME improvement, the dosage was gradually tapered. RESULTS: The mean follow-up was 3.1 years (minimum, 1.5 years). Two subgroups were identified: group 1, quiescence of uveitis with acetazolamide as the single therapeutic agent (33 eyes); and group 2, chronically active uveitis requiring additional systemic antiinflammatory drugs (19 eyes). In both groups, visual acuity improvement was statistically significant (group 1, P = 0.012; group 2, P = 0.025). In 12 patients with a stable visual acuity gain, the medication dose could be tapered off completely without any recurrent edema shown by fluorescein angiography after a minimum follow-up of 1 year. Sixteen patients required a maintenance dosage, ranging from 125 to 500 mg daily. No major adverse effects of the medication were observed. CONCLUSIONS: During long-term follow-up, low-dose acetazolamide can be a useful therapeutic option for chronic CME in uveitis. The effect was better in patients with quiescence of uveitis than in those with chronically active uveitis. Permanent therapy is not imperative in every case.

Acetazolamide↗
PubMed1995

Pustular psoriasis precipitated by acetazolamide.

We report a case of pustular psoriasis precipitated by acetazolamide, a carbonic anhydrase inhibitor. A 28-year-old man suffering from 20 years-standing generalized pustular psoriasis developed psoriatic arthritis and glaucoma and experienced a precipitation of pustular lesions and widespread erythema after initiation of oral acetazolamide for glaucoma. The cutaneous lesions and systemic symptoms improved after restriction of acetazolamide and administration of oral etretinate. Readministration of acetazolamide confirmed that generalized pustules arose within 24 hours.

Acetazolamide↗
PubMed2004

Comparison of regional vasomotor responses to acetazolamide and CO2 in rabbit cerebrum and cerebellum, measured by a hydrogen clearance method.

AIM: Many investigators have proved the usefulness of acetazolamide provocation and the carbon dioxide test for assessment of the local cerebrovascular reactivity by measurement of the regional cerebral blood flow in patients with occlusive cerebrovascular disease. Data originating from a comparison of these two different vasomotor stimuli as concerns the differences in sensitivity to them in various parts of the central nervous system are scarce. Our aim was to compare the cerebral blood flow responses to hypercapnic and acetazolamide stimuli in different brain regions. METHODS: The cerebral blood flow was measured in the cerebrum (cortex and caudate nucleus) and cerebellum (cortex), as measured by a hydrogen clearance method in anaesthetized, artificially ventilated rabbits. RESULTS: In normocapnia, the cerebral blood flow values in the cerebrum and the cerebellum differed significantly. The cerebral blood flow responses to both vasodilatory stimuli were to be significantly higher in the cerebrum than in the cerebellum, but the relative increases, i.e. the mean relative reactivities, were similar in the different regions measured. CONCLUSION: The regional dissimilarity might explain to some extent the different sensitivities of the various brain areas to sudden blood pressure changes (infarction or haemorrhage). The results further suggest that heterogeneity in cerebrovascular reactivity should be considered in the assessment of vasoreactivity in patients with occlusive cerebrovascular disease. Since the comparison of the carbon dioxide and acetazolamide-induced cerebrovascular reactivities revealed a strong linear relationship, it was concluded that acetazolamide provocation is equivalent to the carbon dioxide test in the evaluation of cerebrovascular reactivity.

Acetazolamide↗