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PubMedDate not supplied

Acetazolamide toxicity and pharmacokinetics in patients receiving hemodialysis.

Acetazolamide-induced central nervous system toxicity occurred in two patients undergoing hemodialysis. Symptoms of toxicity included fatigue, lethargy, and confusion, which resolved several days after discontinuing acetazolamide. Pharmacokinetic studies showed markedly elevated serum concentrations of the drug during the period of toxicity, which decreased at a slower rate compared with that reported in patients with normal renal function. The effect of hemodialysis on acetazolamide clearance was quantified. The agent should be avoided in patients receiving dialysis unless the dosage is reduced and serum concentration monitoring can be performed in a timely manner. These patients should be monitored closely for central nervous system toxicity if acetazolamide is given.

Acetazolamide↗
PubMed1995

Vascular reserve in chronic cerebral ischemia measured by the acetazolamide challenge test: comparison with positron emission tomography.

PURPOSE: To determine the value of the acetazolamide challenge test with stable xenon-enhanced CT (Xe CT) for making therapeutic decisions in patients with chronic cerebrovascular disease. METHODS: We compared the Xe CT-measured acetazolamide response with various measures obtained by positron emission tomography. We performed both a positron emission tomographic scan and a Xe CT study in 11 patients with chronic cerebral ischemic diseases within a 1-week interval. An increase of cerebral blood flow after injection of acetazolamide was expressed as delta AT. Regional cerebral blood flow, cerebral oxygen metabolism, oxygen extraction fraction, and cerebral blood volume were measured with oxygen-15-labeled gases by positron emission tomography. RESULTS: In low-cerebral blood flow regions, decreased delta AT was accompanied by a significant elevation of oxygen extraction fraction and cerebral blood volume, compared with oxygen extraction fraction and cerebral blood volume in regions of normal delta AT. Plotting of regional data indicated that delta was significantly dependent on oxygen extraction fraction and cerebral blood volume. The area of decreased vascular reserve determined by the Xe CT image corresponded to the area of "misery perfusion" determined by positron emission tomography. CONCLUSION: The acetazolamide challenge test with Xe CT may offer an alternative to positron-emission tomography in detecting lesions with elevated oxygen extraction fraction and cerebral blood volume (misery perfusion) that result from chronic hemodynamic stress.

Acetazolamide↗
PubMed1994

Normal values of cerebrovascular reserve capacity after stimulation with acetazolamide measured by xenon 133 single-photon emission CT.

PURPOSE: To determine whether a standardized stimulation challenge with acetazolamide will be helpful for assessing the vasodilatory capacity in patients with obstructive cerebrovascular disease. METHODS: To establish normative data of the cerebrovascular reserve capacity, a group of 41 control patients was investigated. The regional cerebral blood flow was measured quantitatively before and after stimulation with acetazolamide using the xenon 133 inhalation method and dynamic single-photon emission CT. RESULTS: A significant increase of regional cerebral blood flow was found after administration of 1 g of acetazolamide. By doubling the dose no significant further increase was measured. We found no correlation of either baseline or stimulated flow values with age. However, a linear dependence between the stimulated flow values and their respective baseline values was observed. CONCLUSION: The standardized challenge with acetazolamide seems to be a reliable method to determine cerebrovascular reserve capacity quantitatively.

Acetazolamide↗
PubMed1993

Drug effects on cerebral blood flow in the baboon model--acetazolamide and nimodipine.

The sensitivity of the baboon model under anaesthesia for single photon emission computed tomography (SPECT) of the brain with 99mTc-HMPAO, as recently developed by us to study cerebral blood flow patterns, was investigated using drugs that are known to increase cerebral blood flow, e.g. acetazolamide, the carbonic anhydrase inhibitor and nimodipine, the calcium channel blocker. Increases in cerebral blood flow for both acetazolamide and nimodipine were observed that correspond well with other studies. Statistically significant regional specificity was noted for acetazolamide and nimodipine. Interestingly a combination of these drugs did not enhance cerebral blood flow but rather decreased it in comparison with the individual drug responses. The results were correlated with arterial blood pressure, heart rate, pCO2 and pO2. A blood pressure decrease was noted for both drugs, while acetazolamide had a marked influence on pO2. The results indicate that the baboon model is sensitive for evaluation of drug effects on cerebral blood flow.

Acetazolamide↗
PubMed1993

[Long-term prognosis and blood flow reactivity to acetazolamide in atherothrombotic brain ischemia].

We report the results of a prospective follow-up study which was designed to identify the sequential change of regional vasodilatory capacity and its relation to long-term prognosis in patients with atherothrombotic brain ischemia. We evaluated a total of 139 acetazolamide tests using 123I-IMP SPECT in 76 patients with occlusion or greater than 75% stenosis of the carotid or middle cerebral arteries. Reduced vasodilatory capacity was demonstrated in 34 patients (44.7%) at entry. Patients were divided into two groups on the basis of the initial acetazolamide test, i.e., impaired and non-impaired group. All patients were prospectively followed for 28.4 +/- 15.9 (Mean +/- S.D.) months and acetazolamide tests were repeated every 1-2 years. Follow-up acetazolamide tests demonstrated normalization of impaired vasodilatory capacity in 14 patients, including 12 without surgical revascularization. The survival analysis comparing the two groups for all strokes and all death, and for ipsilateral ischemic strokes and all death did not demonstrate the poor prognosis of imparied group. However, the recurrence of ischemic stroke was found in 4 out of 8 cases without improvement of vasodilatory capacity. The present data indicate that the sequential evaluation of vasodilatory capacity is of importance in the clinical management of patients with major cerebral artery occlusion or severe stenosis.

Acetazolamide↗
PubMed1993

The effects of acetazolamide on visual function in retinitis pigmentosa.

PURPOSE: To study the effects of acetazolamide on central and peripheral visual function in patients with retinitis pigmentosa (RP) who showed no evidence of macular edema. METHODS: Thirteen patients with retinitis pigmentosa participated in a preliminary study. Measures of central and peripheral visual function were obtained before and after an 8 wk period on acetazolamide. An additional 10 patients participated in a cross-over study. They were placed on a placebo for an 8 wk period, then on acetazolamide for a second 8 wk period. RESULTS: None of the patients in the preliminary study showed significant changes in visual acuity, color vision, foveal cone pathway sensitivities, focal electroretinogram (ERG) amplitudes, or in any ERG parameter. Three patients, however, showed significant changes in visual field area and in dark-adapted thresholds. None of the patients in the cross-over study showed significant increases in visual field area. CONCLUSIONS: Given the results and the reports of side-effects, it is difficult to justify using acetazolamide to improve retinal function in RP patients who show no evidence of cystoid macular edema.

Acetazolamide↗
PubMed1995

Adaptive changes of autoregulation in chronic cerebral hypotension with arteriovenous malformations: an acetazolamide-enhanced single-photon emission CT study.

PURPOSE: To evaluate the relationship among feeding arterial pressure, lesion size, and perfusion in cerebral cortex adjacent to cerebral arteriovenous malformations (AVMs). METHODS: Eleven patients with hemispheric AVMs underwent 99mTc hexamethyl-propyleneamine oxime single-photon emission CT before and after 1 g of acetazolamide was administered intravenously. AVM volume was estimated from MR dimensions and measured according to the method described by Pasqualin. Pressure measurements were obtained in arteries feeding the cortex adjacent to AVMs. Single-photon emission CT regions of interest were defined in cortex adjacent to the AVM and compared with contralateral regions using the Mountz method to estimate a baseline and dynamic (acetazolamide-challenged) perfusion defect volume. RESULTS: Eight of 11 patients had baseline perfusion defects, but these defects were unrelated to feeding artery pressures (y = -.06x + 9.92, r2 = .04) or the dynamic change in defect volume after acetazolamide administration (y = .01x + .02, r2 = .002). However, there was a correlation between AVM volume and the baseline defect volume (y = .75x - 1.9, r2 = .76). Five patients had increased defect volume after acetazolamide administration; 5 patients had either no change in or improvement of perfusion. Dynamic changes in defect volume were related to feeding artery pressures. CONCLUSION: Perilesional baseline perfusion defects appear to be related to lesion size and not to local arterial pressure. Cerebrovascular reserve generally was preserved, and perfusion defects appeared to be more pronounced with lower arterial pressures in feeding vessels. Although vasodilatory testing can unmask hemodynamic failure with severe local hypotension, baseline perfusion defects near the lesion and distant perfusion changes are more likely attributable to other causes such as mass-related or neurogenic changes.

Acetazolamide↗
PubMed1977

Effects and interactions of furosemide and acetazolamide on tubular function in rat kidney.

Furosemide and acetazolamide effects on tubular function in rat kidney have been studied by micropuncture. Furosemide produced a marked rise in fractional proximal fluid reabsorption when urine loss was not replaced, and sodium excretion rose significantly indicating a distal effect. If urinary losses were replaced proximal fractional reabsorption was depressed and fractional sodium excretion increased more than 60%. After replacing urinary losses, acetazolamide had a greater depressive effect on proximal tubular fluid reabsorption than furosemide but sodium excretion values were about 1/3 of those obtained with furosemide. Superimposition of one drug during the action of the other resulted in potentiation of proximal inhibition, suggesting a different mechanism of action. The changes observed in potassium excretion are of great interest. Separately, furosemide or acetazolamide produced kaliuresis. When furosemide was administered during acetazolamide diuresis, however, potassium excretion was reduced despite the sharp rise in sodium excretion.

Acetazolamide↗
PubMedDate not supplied

Assessment of whole-brain vasodilatory capacity with acetazolamide challenge at 1.5 T using dynamic contrast imaging with frequency-shifted burst.

PURPOSE: To determine whether whole-brain acetazolamide-induced changes in regional cerebral blood volume (rCBV) can be assessed on a conventional gradient 1.5-T MR system using 3-D dynamic susceptibility contrast-enhanced MR imaging. METHODS: A 3-D frequency-shifted (FS) burst technique was used to assess the intravascular first pass of contrast agent. Changes in rCBV were calculated in 40 volunteers before and after acetazolamide (n = 30) or saline (n = 10) injection using customized analysis software on an independent workstation. A single-section gradient-echo technique with better spatial resolution was used in one additional volunteer to examine the effect of partial volume averaging on calculation of absolute rCBV. RESULTS: A statistically significant increase in rCBV (gray matter = 23%, white master = 32.5%) was noted after acetazolamide compared with saline. Baseline fractional CBVs were 22% +/- 3% for gray matter and 12% +/- 2% for white matter. Partial volume averaging was probably responsible for a systematic but linear overestimation of absolute rCBV. CONCLUSION: Acetazolamide-induced changes in rCBV can be assessed using 3-D dynamic susceptibility contrast-enhanced MR imaging with FS-burst on a conventional gradient 1.5-T MR system. Values obtained with this technique overestimate absolute rCBV but are systematically biased and can be used for intersubject and intrasubject ratio comparisons.

Acetazolamide↗
PubMed1997

[Familial periodic ataxia with myokymia sensitive to acetazolamide: a family case].

INTRODUCTION: Acetazolamide responsive hereditary paroxysmal cerebellar ataxia with myokymia is a type of autosomal dominant cerebellar ataxia which locus was found to be linked to the short arm of chromosome 12 and the etiology is unknown. CLINICAL CASE: A 12 years-old man who suffered from childhood daily episodes of sudden attacks sport induced with giddiness, ataxia and dysarthria for minutes. The familial history shows the same clinical findings in three generations. Intercritical general neurologic evaluation is otherwise normal. The following tests were performed with normal results: Biochemistry, electroencephalogram, cerebral magnetic resonance imaging. The electromyography showed myokymic discharges. The patient's symptoms improve on treatment with acetazolamide immediately. CONCLUSIONS: Acetazolamide responsive hereditary paroxysmal cerebellar ataxia with myokymia needs to think on it to be diagnosed. No typical complementary test (electromyography exception) induces to base diagnosis in the clinical findings, the familial history and the fast clinical improvement after starting treatment with acetazolamide.

Acetazolamide↗
PubMed1999

Regional differences in cerebrovascular reactivity to acetazolamide in Alzheimer's disease.

The cerebral blood flow and cerebrovascular reactivity to acetazolamide were investigated in Alzheimer's disease using stable xenon computed tomography (CT). Ten patients with Alzheimer's disease and 10 healthy controls were studied. The regional cerebral blood flow was measured using the xenon delivery and analysis system (AZ-7000 model, Anzai Sogyo, Tokyo, Japan) and CT (PreSage, Yokogawa Medical Systems, Tokyo, Japan). The subjects inhaled room air followed by a mixture of 30% xenon and 50% oxygen for 3 min. Serial scanning was performed once before xenon inhalation, three times in the wash-in process and five times in the washout process of 5 min. The xenon concentration in the end-tidal expired gas was recorded continuously by the thermoconductivity method. The regional cerebral blood flow was measured before and 20 min after i.v. injection of 17 mg/kg acetazolamide. The blood flows in the frontal lobe, parietal lobe and temporal lobe were reduced but the blood flows in the caudate nucleus, putamen and thalamus were normal in the Alzheimer's disease group. The cerebrovascular reactivity to acetazolamide was reduced in the frontal, parietal and temporal cortex but was normal in the other areas. There is a regional difference in the cerebral blood flow and the cerebrovascular reactivity to acetazolamide in Alzheimer's disease Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗
PubMed1985

Topical acetazolamide and methazolamide delivered by contact lenses.

Topical acetazolamide has been previously found to be ineffective in lowering intraocular pressure (IOP). Using high-water-content soft contact lenses (Sauflon PW) soaked in acetazolamide, we observed a statistically significant ipsilateral decrease in IOP of 6.3 +/- 0.4 mm Hg in the treated eyes of albino rabbits. The duration of the effect was up to 7 1/2 hours. Methazolamide-soaked contact lenses produced a maximum unilateral reduction of similar magnitude but shorter duration. Both serum and aqueous humor analyses for pH, carbon dioxide pressure, bicarbonate, and base excess indicate that acetazolamide delivered by soft contact lenses is able to penetrate the cornea in sufficient concentration to lower IOP by a local mechanism in rabbits without significant systemic absorption.

Acetazolamide↗
PubMed1975

Assay for acetazolamide in plasma.

A method for the analysis of acetazolamide, 5-acetamido-1,3,4-thiadiazole-2-sulfonamide, sensitive to 25 ng/ml in plasma, was developed. After extraction of acetazolamide and its propionyl analog, 5-propionamido-1,3,4-thiadiazole-2-sulfonamide, the internal standard, from plasma with ethyl acetate and removal of lipids from the residue of the ethyl acetate extract with methylene chloride, the sulfonamides were chromatographed on an octadecyl trichlorosilane bonded phase using high-pressure liquid chromatography. The method was developed to study plasma level profiles of different dosage forms of acetazolamide.

Acetazolamide↗
PubMed1976

Effect of edetate disodium and reduced glutathione on absorption of acetazolamide from GI tract of rats.

The absorption of acetazolamide suspensions from in situ rat gastric and intestinal loop segments was studied. In 1 hr, 66.2 and 64.3% remained unabsorbed from the rat stomach and intestine, respectively. Although 1% (w/v) reduced glutathione and 1% (w/v) (24 mM) edetate disodium had no effect on gastric absorption, drug absorption from the rat intestine (1 hr) was increased 1.5 and 2 times, respectively. It was hypothesized that the relatively poor intestinal absorption was due primarily to the formation of a pH-dependent (pH 4.5-10), nonabsorbable complex between acetazolamide and carbonic anhydrase present in the gut and that reduced glutathione acted as an inhibitor to promote intestinal absorption. Equilibrium dialysis studies showed that reduced glutathion could reduce the fraction of drug bound to human carbonic anhydrase B by one-half when present in a molar ratio 10 times that of acetazolamide; edetate disodium had no effect on the in vitro binding. It was, therefore, assumed that edetate disodium promoted an increase in intestinal absorption by altering the permeability of intestinal epithelium. Based upon present experimentation, however, the alteration of intestinal epithelium by reduced glutathione cannot be ruled out.

Acetazolamide↗
PubMed1977

GLC analysis of acetazolamide in blood, plasma, and saliva following oral administration to normal subjects.

An electron-capture GLC assay for acetazolamide in biological fluids was developed. Extraction efficiency was 69-104%. The minimum detectable amount of acetazolamide was 10 ng/sample. Concentrations of acetazolamide were determined by GLC in blood, plasma, plasma water, and saliva after oral administration of a single 250-mg dose to five volunteers. Erythrocyte levels were calculated from whole blood and plasma data. Concentration of free drug in the plasma was measured in samples of plasma water obtained by microultrafiltration. Peak plasma levels of 10-18 microng/ml were reached 1-3 hr after the dose. At least 1 hr later, erythrocyte levels reached peak concentrations of 13-29 microng/ml. Over 31 hr, plasma levels declined more rapidly than erythrocyte levels. Saliva concentrations averaged 1% of those in plasma and decreased at a rate equal to that of plasma. Saliva levels were proportional to, but not equal to, water concentration. Saliva to plasma ratios were consistent for any given individual and, therefore, offer a means of monitoring drug dosage without resorting to frequent blood sampling.

Acetazolamide↗
PubMed1978

Bioavailability of acetazolamide tablets.

Plasma acetazolamide levels were measured by an enzymatic assay following single 250-mg oral tablet doses to 20 healthy volunteers; five different lots of acetazolamide tablets from a single manufacturer were used in a balanced incomplete block design. From the measured plasma levels, estimates of the bioavailability parameters (area under the plasma concentration versus time curve, time to peak plasma concentration, and peak plasm concentration) were obtained by least-squares digital computer fitting. No significant differences among the tablets were observed (alpha = 0.05) for the analysis of variance of the area under the curve or time to peak parameters. Two tablets, however, provided statistically higher peak plasma concentrations than the other three. Thus, lot-to-lot bioinequivalence of acetazolamide tablets was observed. Some in vitro tests employed showed general trends for correlation with the in vivo data. However, considerable refinement of these technique appears necessary for in vitro prediction of the observed lot-to-lot bioinequivalence.

Acetazolamide↗
PubMed1990

Development of oral liquid dosage forms of acetazolamide.

Two oral liquid dosage forms of acetazolamide have been developed. Using the solubility profiles, polyethylene glycol 400 (7%, v/v) was used as the solubilizing agent and propylene glycol (53%, v/v) as the cosolvent to keep acetazolamide in solution. Because of the bitter taste of acetazolamide, sweetening agents (simple syrup, sorbitol solution, and artificial sweeteners) and flavors (raspberry, sweet, and menthol) were added to the final formulations. A buffer (either phosphate or citrate) solution was used to maintain a pH value of 4 (pH of maximum stability as reported earlier) to minimize hydrolysis. The final dosage forms were stable for at least 90 days at 37 degrees C (loss of potency of 5%). According to FDA guidelines, a tentative expiry date of 2 years at 25 degrees C is justifiable.

Acetazolamide↗
PubMed1996

The electroencephalogram in acetazolamide-responsive periodic ataxia.

Acetazolamide-responsive periodic ataxia (ARPA) is a rare movement disorder, characterized by recurrent episodes of vertigo, cerebellar ataxia, and nystagmus, which has recently been characterized genetically. The pathophysiology is unknown, but it is probably not epileptic. By definition, acetazolamide produces an impressive symptomatic relief. Because of the paroxysmal nature of the disorder, EEG tracings were often obtained. We report four new cases (two familial and two sporadic) with typical ARPA (none of whom had metabolic abnormalities or continuous electrical muscle activity) and review the EEG findings associated with this disorder. EEG findings were reported in 18 kindreds and nine sporadic cases (including ours). EEG was described in 54 of the 140 affected cases and was abnormal in 52% (28/54). Most commonly seen was intermittent generalized slow activity, observed in 35% (19/54), frequently intermingled with spikes (10 cases). Other abnormalities included nonspecific mild generalized or focal slowing in seven (13%) and focal epileptic activity in two (4%) patients. The paroxysmal EEG activity frequently seen in ARPA should not establish a diagnosis of epilepsy. Although not specific, it may suggest the correct diagnosis and indicate treatment with acetazolamide.

Acetazolamide↗