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PubMed1998

International randomised controlled trial of acetazolamide and furosemide in posthaemorrhagic ventricular dilatation in infancy. International PHVD Drug Trial Group.

BACKGROUND: Furosemide and acetazolamide are widely used in the treatment of posthaemorrhagic ventricular dilatation (PHVD) in the hope of avoiding the need for surgical management, but this approach has not been evaluated in a controlled trial. This multicentre randomised controlled trial tested the hypothesis that these drugs would reduce the rate of shunt placement and increase disability-free survival at 1 year of age. METHODS: Between 1992 and 1996, 177 infants aged less than 3 months past term, and with ventricular width more than 4 mm above 97th centile after intraventricular haemorrhage, were randomly assigned standard therapy alone or standard therapy plus treatment with acetazolamide (100 mg/kg daily) and furosemide (1 mg/kg daily). A minimisation algorithm ensured balance between groups with respect to both referral centre and the presence of a cerebral parenchymal lesion on cerebral ultrasonography at enrolment. The trial was stopped in September, 1996, because the data showed a clear advantage with standard therapy. FINDINGS: We report outcomes for 151 infants whose expected date of delivery was before the end of 1995, with complete information at 1 year for 129 infants. The median gestational age was 28 weeks, mean birthweight 1299 g, and mean postnatal age at enrolment 25 days. 44% had a parenchymal lesion at randomisation. Death or shunt placement occurred in 49 of 75 infants allocated drugs plus standard therapy, compared with 35 of 76 allocated to standard therapy alone. The relative risk was 1.42 (95% CI 1.06-1.90; p=0.026), which is equivalent to one extra death or shunt placement for every five infants allocated drug therapy. 84% (52/62) of infants assigned drug therapy had died or were disabled or impaired at 1 year, compared with 60% (40/67) of those assigned standard therapy (relative risk 1.40 [1.12-1.76]; p=0.012). INTERPRETATION: These preliminary results suggest that the use of acetazolamide and furosemide in preterm infants with PHVD is associated with a higher rate of shunt placement and increased neurological morbidity, and so cannot be recommended.

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PubMed1998

A comparison of the effectiveness of dorzolamide and acetazolamide in preventing post-operative intraocular pressure rise following phacoemulsification surgery.

The aim of this study was to evaluate the effectiveness of topical dorzolamide versus systemic acetazolamide in preventing the intraocular pressure (IOP) spike, following routine phacoemulsification surgery. In this prospective study, 59 eyes (59 patients), undergoing routine phacoemulsification surgery with posterior intraocular implant, were divided into three groups. Group 1 received acetazolamide 250 mg SR orally, immediately post-operatively. Group 2 received one drop of dorzolamide immediately after surgery. Group 3 or control, received neither. The IOP, was checked 4 h, 24 h and 2 weeks post-operatively. When compared with mean baseline pre-operative IOP, the 4 h mean post-operative IOP was slightly higher in the dorzolamide group by a mean of +2.49 mmHg (P = 0.2502). It was significantly higher in the acetazolamide group by a mean of +6.13 mmHg (P = 0.0034) and in the control group by a mean of +11.81 mmHg (P = 0.000). At 24 h the mean IOP in the control group remained significantly elevated by a mean of +5.87 mmHg (P = 0.003). Topical dorzolamide is effective in reducing the early IOP rise during the first 24 h following routine uncomplicated phacoemulsification surgery.

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PubMed1976

The effect of acetazolamide on the movement of sodium into the posterior chamber of the dog eye.

The rate of appearance (entry) of 22Na into the posterior chamber of the eye was determined in eight dogs under control conditions and again after pretreatment with acetazolamide, 50 mg/kg i.v. In comparison with the paired controls, pretreatment with acetazolamide decreased the average rate of entry of 22Na by 29% during the first 3 minutes after the intravenous administration of a tracer dose of the isotope. In separate experiments, the volumes of the chambers of the dog eye and the rate of aqueous humor formation were determined for the purpose of calculating nascent fluid ion concentrations. Comparisons of sodium data with the previously reported anion data are made. Results support the suggestion that reduction of intraocular pressure caused by acetazolamide is partially, if not wholly, the result of the action of the drug to reduce the secretion of aqueous humor.

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PubMed1963

EFFECT OF ACETAZOLAMIDE AND TRIPLE SULFONAMIDE ON CITRATE AND CALCIUM EXCRETION.

The administration of acetazolamide was shown to increase the excretion of calcium in both normal persons and in stone formers, while at the same time the urinary excretion of citrate was reduced. Urinary citrate is potentially of importance in chelating calcium and preventing it from precipitating. In view of the chemical similarity between acetazolamide and the sulfonamides it was considered that the latter might produce a similar effect, with potential hazard if administered to a stone former. This was shown not to be the case.

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PubMed1975

Acetazolamide treatment of hypokalemic periodic paralysis. Probable mechanism of action.

Following administration of glucose and insulin to three patients with hypokalemic periodic paralysis, serum K+ fell 1.9 mM. After administration of acetazolamide, 250 mg four times daily, serum K+ fell 0.9 mM, a substantial difference. In normal persons glucose and insulin lowered serum K+ 0.5 mM, and this was not changed substantially by acetazolamide. The metabolic acidosis induced by the drug appears to be responsible for the change in decrement of serum K+ and for the amelioration of symptoms in the patients. The findings agree with earlier reports that metabolic acidosis lowers the rate of entry of K+ into muscle, thus opposing the heightened or pathological entry of K+ into muscle cells during attacks of the disease.

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PubMed1977

Acetazolamide-induced interference with primidone absorption. Case reports and metabolic studies.

Effects of acetazolamide on primidone plasma levels were studied in three patients. Apparent interaction occurred in two patients. Primidone was not detected in the plasma when given orally with acetazolamide in one patient. In another, peak serum concentration was delayed, with corresponding delays in urinary excretion of primidone and metabolites. Plasma and urine concentrations of the two metabolites, phenylethylmalonamide and phenobarbital, were also studied.

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PubMed1978

Acetazolamide in the treatment of pyruvate dysmetabolism syndromes.

Two children with periodic weakness beginning in infancy were demonstrated to have abnormalities in pyruvate metabolism by the production of lactic acidosis following a glucose load. Daily oral doses of acetazolamide reduced the frequency of attacks and reversed the abnormal response to glucose loading. The mechanism of action of acetazolamide in these patients is not clear.

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PubMed1977

Short-term dose response characteristics of acetazolamide in man.

Nine patients with ocular hypertension each randomly received on separate days 0, 63, 125, 250, and 500 mg of acetazolamide (Diamox). In a double masked manner, acetazolamide plasma levels and intraocular pressure were monitored for seven hours following administration. Plasma levels increased linearly with dose, reaching 30 microgram/ml with the 500-mg dose. Maximum plasma levels occurred at one hour, and the minimum IOP was at two hours. The maximum IOP effect was a 30% to 35% fall. The IOP response was related to dose and plasma level, up to a 63-mg dose, which produced an average fall of 8.2 mm Hg. Little further average effect was documented at higher doses or plasma levels. The duration of response was slightly prolonged by 250 mg, but 500 mg showed no greater response. Thus, a 63-mg dose or a plasma level of 4 to 5 microgram/ml was as effective in lowering IOP as higher doses that produced plasma levels of 10 microgram/ml or more.

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PubMed1980

Acetazolamide dosage forms in the treatment of glaucoma.

Patients with chronic glaucoma had a carefully scheduled series of intraocular pressure measurements before and after taking acetazolamide for one week at the following dosages: none, 500 mg of sustained-release capsules once a day, 500 mg of capsules twice a day, and 250 mg of tablets four times a day. A capsule taken once a day, which is better tolerated than one taken twice a day by some patients, offers a substantial pressure-lowering effect that lasts at least 23 hours, although the magnitude of the pressure lowering is less than with higher dosages. One capsule twice a day appears to be as effective in the regulation of IOP as one tablet four times a day. The 45% reduction in outflow pressure is achieved with an acetazolamide serum concentration in the range of 15 to 20 micrograms/mL.

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PubMed1981

Determination of acetazolamide compliance in patients with glaucoma.

In an objective test to determine compliance with acetazolamide regimens by patients with glaucoma, treated inpatients had lower carbon dioxide levels (less than or equal to mEq/L) than untreated patients (greater than or equal to 25 mEq/L). The test results may be inaccurate in some obese diabetic patients with hyperglycemia and in some patients with obstructive lung disease, such as asthma and emphysema. In an outpatient clinic population, the test showed that 35% (30/87) of the patients did not seem to be taking acetazolamide and 22% (19/87) seemed to be taking it less frequently.

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PubMed1983

Effect of acetazolamide on the differential threshold.

Following the oral administration of three 250-mg doses of acetazolamide sodium to nine patients with glaucomatous visual-field defects, a statistically significant improvement in the differential threshold was observed, whereas in 16 glaucoma suspects, no change could be detected. The greatest improvements following acetazolamide administration occurred in younger patients and in those with the greatest disturbances of the visual field.

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PubMed1985

Experimental retinal detachment. X. Effect of acetazolamide on vitreous fluorescein disappearance.

Retinal detachments were created in one eye of each of eight cynomolgus monkeys. Total vitrectomy was performed in the fellow eyes. Fluorophotometry was used to study the rate of disappearance of fluorescein injected into the vitreous cavity. The rate of fluorescein loss via the anterior chamber accounted for only 1% to 3% of the total rate of vitreous fluorescein loss in eyes with retinal detachment or in fellow eyes. Posterior loss of fluorescein (presumably across the retinal pigment epithelium) increased by 25% following intravenous acetazolamide in eyes with retinal detachment and 22% in fellow eyes. It is concluded that acetazolamide increases the rate of fluid absorption across the retinal pigment epithelium.

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PubMed1988

Treatment of chronic macular edema with acetazolamide.

In a prospective study, 41 patients with documented chronic macular edema of various causes were entered into a therapeutic trial of acetazolamide sodium, a carbonic anhydrase inhibitor. Each patient received a five-cycle cross-over regimen of treatment/no treatment with a further two cycles of cross-over with another diuretic, cyclopenthiazide, which does not inhibit carbonic anhydrase. At each cross-over patients were examined for evidence of macular edema. Sixteen of 41 patients showed a reproducible response to acetazolamide with partial or complete resolution of edema and improvement of visual acuity. The therapeutic effect occurred in more than half of the patients with inherited outer retinal disease or uveitis, but in none with primary retinal vascular disorders. There was no correlation between the response to treatment and the extent or duration of the edema. No influence of cyclopenthiazide on macular edema was detected.

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PubMed1989

Acetazolamide for treatment of chronic macular edema in retinitis pigmentosa.

Twelve patients with retinitis pigmentosa and chronic macular edema were prospectively treated for 2-week periods with acetazolamide or a placebo in a masked, crossover study. Ten of the 12 patients had both subjective and objective improvement in visual acuity when treated with acetazolamide. Improvement was seen even in patients with an acuity as good as 20/25 at baseline as well as in patients with macular edema present for more than a decade. A dosage of 500 mg/d was found to be more effective than 250 mg/d. Six patients (50%) showed lessening of their macular edema on fluorescein angiography. This angiographically demonstrated improvement was predominantly due to less detectable leakage from retinal capillaries rather than from choroidal capillaries through the retinal pigment epithelium. Improvement in visual acuity was seen in some patients without a detectable change in the amount of angiographic fluorescein leakage.

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PubMed1998

De novo mutation in CACNA1A caused acetazolamide-responsive episodic ataxia.

With the recent report of mutations in the calcium channel gene CACNA1A in two families with episodic ataxia type 2, we investigated a patient with nonfamilial episodic vertigo and ataxia responsive to acetazolamide for similar mutations. Single-strand conformation polymorphism (SSCP) analysis of exon 23 identified an extra band in the patient that was not present in other relatives or in normal controls. Exon 23 of the patient showed a spontaneous C to T substitution at position 4410 resulting in an early stop codon. Patients with nonfamilial episodic ataxia may respond to acetazolamide and may have mutations in CACNA1A.

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PubMed1999

Noninvasive magnetic resonance imaging evaluation of cerebral blood flow with acetazolamide challenge in patients with cerebrovascular stenosis.

To evaluate the utility of using magnetic resonance imaging (MRI) of cerebral blood flow (CBF) in conjunction with pharmacologic flow augmentation, the authors imaged 14 patients with ischemic symptoms referable to large artery cerebrovascular stenosis of the anterior circulation. CBF was measured by using continuous arterial spin labeling (CASL) both at rest and 10 minutes after 1 g intravenous acetazolamide on a commercial 1.5 Tesla scanner. Quantitative CBF images were calculated along with augmentation images showing the effects of acetazolamide. Interpretable studies were obtained from all patients. Based on the image data as well as a region of interest analysis of CBF changes in middle cerebral artery distributions, varying patterns of augmentation were observed that suggested differing mechanisms of ischemic symptomatology. The ability to obtain this information in conjunction with a structural MRI examination extends the diagnostic potential for MRI in cerebrovascular disease and allows the value of augmentation testing in clinical management to be assessed more widely. J. Magn. Reson. Imaging 1999;10:870-875.

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PubMedDate not supplied

Detection and metabolism of fencamfamine and the influence of acetazolamide on its urinary excretion.

A gas-chromatographic (g.l.c.) method with electron-capture (e.c.) detection is described for the simultaneous quantitative determination of nanogram concentrations of 2-ethylamino-3-phenyl-norbornane (Fencamfamine, REACTIVAN) and its metabolite 2-amino-3-phenylnorbornane in urine. The renal excretion of fencamfamine and its metabolite after oral administration to humans was followed over a period of several days. The excretion of both substances was affected by urinary pH. Excretion peaks were obtained 2-4 h after ingestion and the total amount excreted during 80 h varied from 11.9 to 33.2 per cent. Based on urinary values, the biological half life of fencamfamine was 16 h. The intake of acetazolamide shortly after fencamfamine resulted in a decrease of the fencamfamine excretion and a suppression of the metabolite output during at least 10 h. Acetazolamide did not influence the percentage of the doses excreted during 80 h. No changes occurred in urinary fencamfamine or metabolite concentrations during storage of urine at -18 degrees for 6 weeks.

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PubMedDate not supplied

Determination of acetazolamide in dosage forms by high performance liquid chromatography.

A high performance liquid chromatographic assay for the quantitation of acetazolamide in both tablet and injection form is described. Acetazolamide is extracted with 0.005 M NaOH solution containing 0.3 mg/mL sulphadiazine (internal standard). A commercially available mu-Bondapak C18 cartridge column was used for the separation together with a mobile phase made of acetonitrile, methanol and sodium acetate buffer mixture (10:2:88) (pH 4) at a flow-rate of 4 mL/min. Retention times of about 2.50 and 3.36 min were obtained for the drug and the internal standard, respectively.

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