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PubMed1984

Simultaneous and independent versus antagonistic inhibition of muscle carbonic anhydrase (CA III) by acetazolamide and cyanate.

The inhibition by cyanate and acetazolamide of pig muscle carbonic anhydrase III (CA III) CO2 hydratase activity was studied in order to explore mechanistic features possibly unique to the muscle isoenzyme. The turnover number for CO2 hydration was found to be 6000 sec-1 with a Km of 83 mM for CO2. Cyanate inhibition (Ki, 3 microM) and acetazolamide inhibition (Ki, 44 microM) were both found to be noncompetitive with respect to CO2. Significantly, acetazolamide and cyanate displayed non-exclusive binding to pig muscle carbonic anhydrase. The similarity of mode and degree of inhibition of muscle carbonic anhydrase by cyanate as compared with the inhibition of the erythrocyte isoenzymes suggests the existence of a similar metal environment. However, the observation that cyanate and acetazolamide bind simultaneously to CA III and the comparatively large Ki for acetazolamide per se appear to be more compatible with a different mode of coordination of the zinc with the sulfonamide, thus supporting a five-coordinate zinc in the catalytic mechanism of CO2 hydration for CA III.

Acetazolamide↗
PubMed1995

Acetazolamide inhibits basal and stimulated HCO3- secretion in the human proximal duodenum.

BACKGROUND/AIMS: Carbonic anhydrase activity plays a role in electrolyte transport in many tissues. This study examined the effect of the carbonic anhydrase inhibitor acetazolamide on human basal and prostaglandin E2- and acid-stimulated duodenal mucosal bicarbonate secretion and transmucosal electrical potential difference. METHODS: Seven healthy volunteers participated in four separate experiments. The variables included oral acetazolamide vs. control test and, as agonists of bicarbonate secretion, either luminal acidification or luminal prostaglandin E2. The proximal 4 cm of the duodenum (i.e., the duodenal bulb) was isolated between balloons as previously described and perfused with an HCO(3-)-containing (24 mmol/L) balanced electrolyte glucose-containing (10 mmol/L) solution. RESULTS: Acetazolamide treatment significantly decreased mean basal HCO3- secretion and basal transmucosal potential difference. After luminal acidification, duodenal mucosal bicarbonate increased significantly after both acetazolamide treatment (mean, 626; 95% CI, 91-1160 mumol.cm-1.h-1) and in the control tests (mean, 868; 95% CI, 652-1084 mumol.cm-1.h-1). However, acetazolamide treatment significantly decreased prostaglandin E2-stimulated HCO3- secretion from 461 (95% CI, 307-615) to 222 (95% CI, 121-324) mumol.cm-1.h-1. CONCLUSIONS: Duodenal mucosal carbonic anhydrase activity has an important function in the regulation of basal and prostaglandin E2-stimulated human duodenal mucosal bicarbonate transport.

Acetazolamide↗
PubMed1988

Ventilatory response to carbonic anhydrase inhibition in cats: effects of acetazolamide in intact vs peripherally chemodenervated animals.

Hyperventilation induced by red cell carbonic anhydrase inhibition (CAI) has been observed frequently; its mechanism, however, is still obscure. In the present study in anaesthetized cats, we have investigated the effect of 50 mg/kg acetazolamide, a carbonic anhydrase inhibitor, on ventilation. In order to determine the role of the peripheral chemoreceptors, we compared the response in peripherally chemodenervated and intact cats. Furthermore, in cats with intact peripheral chemoreceptors, we determined hypoxic sensitivity before and 2 h after i.v. infusion of the drug. In all animals, acetazolamide caused a large increase in ventilation. However, the peripherally chemodenervated animals developed a significantly larger response than the intact animals (respectively about 200 and 100% increases in ventilation). The first group also showed a significantly larger fall in PACO2. In the intact animals studied, acetazolamide virtually abolished the hypoxic sensitivity which existed before infusion of the drug. We conclude that acetazolamide, at the dose studied, causes a decrease in activity of the peripheral chemoreceptors, and also a decrease (c.q. removal) of their sensitivity to PaO2 changes. The increase in ventilation by acetazolamide is probably caused by an action of the drug on the central nervous system, possibly on the central chemoreceptors.

Acetazolamide↗
PubMed2004

The carbonic anhydrase inhibitor acetazolamide exerts antidystonic effects in the dt(sz) mutant hamster.

Previous studies suggested an involvement of gamma-aminobutyric acid (GABA)-mediated excitation by an enhanced efflux of bicarbonate ions in addition to retarded development of GABAergic inhibition in the syndrome of dt(sz) mutant hamsters, a model of paroxysmal dyskinesia in which dystonic episodes occur in response to stress. Acetazolamide blocks bicarbonate regeneration in neurons and can thereby reduce GABA-mediating excitation without affecting GABA-mediated inhibition. In the present study, the effects of acetazolamide (15-60 mg/kg, i.p.) on severity of dystonia were therefore examined in dt(sz) hamsters. Acetazolamide significantly reduced the severity of dystonia at a dose of 60 mg/kg. These data are in line with several case reports from patients with paroxysmal dystonia, suggesting that acetazolamide can be useful in the treatment of this movement disorder. The mechanism of the antidystonic efficacy of acetazolamide has to be examined by further studies.

Acetazolamide↗
PubMed2005

Mapping of the cerebral response to acetazolamide using graded asymmetric spin echo EPI.

Cerebral vascular reactivity in different regions of the rat brain was quantitatively characterized by spatial and temporal measurements of blood oxygenation level-dependent (BOLD)-fMRI signals following intravenous administration of the carbonic anhydrase inhibitor acetazolamide: this causes cerebral vasodilatation through a cerebral extracellular acidosis that spares neuronal metabolism and vascular smooth muscle function, thus separating vascular and cerebral metabolic events. An asymmetric spin echo-echo planar imaging (ASE-EPI) pulse sequence sensitised images selectively to oxygenation changes in the microvasculature; use of a surface coil receiver enhanced image signal-to-noise ratios (SNRs). Image SNRs and hardware integrity were verified by incorporating quality assurance procedures; cardiorespiratory stability in the physiological preparations were monitored and maintained through the duration of the experiments. These conditions made it possible to apply BOLD contrast fMRI to map regional changes in cerebral perfusion in response to acetazolamide administration. Thus, fMRI findings demonstrated cerebral responses to acetazolamide that directly paralleled the known physiological actions of acetazolamide and whose time courses were similar through all regions of interest, consistent with acetazolamide's initial distribution in brain plasma, where it affects cerebral haemodynamics by acting at cerebral capillary endothelial cells. However, marked variations in the magnitude of the responses suggested relative perfusion deficits in the hippocampus and white matter regions correlating well with their relatively low vascularity and the known vulnerability of the hippocampus to ischaemic damage.

Acetazolamide↗
PubMed2004

Low-dose acetazolamide reduces the hypoxic ventilatory response in the anesthetized cat.

Low intravenous dose acetazolamide causes a decrease in steady-state CO(2) sensitivity of both the peripheral and central chemoreflex loops. The effect, however, on the steady-state hypoxic response is unknown. In the present study, we measured the effect of 4 mg x kg(-1) acetazolamide (i.v.) on the isocapnic steady-state hypoxic response in anesthetized cats. Before and after acetazolamide administration, the eucapnic steady-state hypoxic response in these animals was measured by varying inspiratory P(O2) levels to achieve steady-state Pa(O2) levels between hyperoxia Pa(O2) approximately 55 kPa, approximately 412 mmHg) and hypoxia (Pa(O2) approximately 7 kPa, approximately 53 mmHg). The hypoxic ventilatory response was described by the exponential function V(I) = G exp (-DP(o2) + A with an overall hypoxic sensitivity G, a shape parameter D and ventilation during hyperoxia A. Acetazolamide significantly reduced G from 3.057 +/- 1.616 to 1.573 +/- 0.8361 min(-1) (mean +/- S D). Parameter A increased from 0.903 +/- 0.257 to 1.193 +/- 0.321 min(-1), while D remained unchanged. The decrease in overall hypoxic sensitivity by acetazolamide is probably mediated by an inhibitory effect on the carotid bodies and may have clinical significance in the treatment of sleep apneas, particularly those cases that are associated with an increased ventilatory sensitivity to oxygen and/or carbon dioxide.

Acetazolamide↗
PubMed1999

Cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis.

In order to find out the relationship between the cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis, 10 cases of asymptomatic cerebral infarction and 10 age-matched control subjects were studied. The cerebrovascular acetazolamide reactivity was measured using xenon computed tomography method. As markers of platelet function, the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were determined. The cerebrovascular acetazolamide reactivity was significantly lower in the asymptomatic cerebral infarction group than in the control group. The plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were higher in the asymptomatic cerebral infarction group than in the control group. There was a significant negative correlation between the cerebrovascular acetazolamide reactivity and the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2. The low cerebrovascular acetazolamide reactivity is considered to be related to platelet activation in asymptomatic cerebral thrombosis.

Acetazolamide↗
PubMed1998

The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumor cerebri)

OBJECTIVE: To determine the weight loss associated with resolution of papilledema from idiopathic intracranial hypertension (IIH). DESIGN: A retrospective study. PARTICIPANTS: Fifteen consecutive female patients with IIH associated with obesity were studied. INTERVENTION: Patients underwent weight loss and treatment with acetazolamide during a 24-week period. MAIN OUTCOME MEASURES: The severity of papilledema was graded: absent (grade 0), mild (grade 1), moderate (grade 2), and marked (grade 3), based on a predetermined grading system ("gold standard") using stereoscopic photographs and the Frisén classification. RESULTS: The 15 patients, with mean age of 31.3+/-8.8 years, had a mean weight of 110.5+/-28.7 kg and mean body mass index of 40.7+/-13.0 kg/m2. Eleven (73.3%) patients had improved papilledema during the 24-week study period, of which 10 (66.7%) had complete resolution of papilledema within a median time of 8.5 weeks. An average of 3.3% weight loss (+/-0.5% standard error of the mean) was observed among patients having a one-grade change in papilledema. Weight loss of 6.2%+/-0.6% standard error of the mean was associated with a three-grade change in papilledema (i.e., complete resolution of marked papilledema). Nine of the ten patients with complete resolution of papilledema also took acetazolamide. However, none (26.7%) of the four patients without weight loss had improvement in papilledema despite similar treatment with acetazolamide. CONCLUSIONS: Approximately 6% weight loss was associated with resolution of marked papilledema in these authors' patients. The benefit of acetazolamide in IIH is questioned since weight loss, rather than acetazolamide, appeared to have been the catalyst for reducing the severity of papilledema.

Acetazolamide↗
PubMed2000

Formulation and evaluation of ophthalmic preparations of acetazolamide.

The orally administered acetazolamide has a limited use in glaucoma due to the systemic side effects associated with its use. It has been reported to show little effect on the intraocular pressure (IOP) of human and rabbit eyes upon topical application, probably owing to its poor bioavailability and instability at pH >5.0. In order to enhance the bioavailability of the drug, contact time between the drug molecules and the ocular surface was increased using high viscosity, water soluble polymers (PVA, HPMC), and by incorporating acetazolamide into an in situ-forming ophthalmic drug delivery system. Moreover, a penetration enhancer (EDTA) was also used in these formulations to increase the extent of absorption of the drug. Acetazolamide at a concentration of 10% was used and the formulations (eyedrop suspensions) were evaluated for their in vitro release pattern. The effect of these formulations on the IOP in normotensive conscious rabbits was also investigated. These formulations were found to be therapeutically effective with a peak effect at 2 h. A fall in IOP of up to 46.4% was observed with repeated administration of one of the formulation containing PVA, EDTA and Tween 80 (MK-5). Results indicated that a topical effect of acetazolamide can be observed if the formulation, (a) contains a suitable polymer-to increase the residence time; (b) a penetration enhancer-as acetazolamide has a low permeability coefficient i.e. 4. 1x10(-6) cm/s [Duffel, M.W., Ing. I.S., Segarra, T.M., Dixson, J.A., Barfknecht, C.F., Schoenwald, R.D., 1986. J. Med. Chem. 29, 1488-1494]; and (c) pH of the formulation is maintained at the point of maximum stability (pH< or =5.0).

Acetazolamide↗
PubMed1997

Timolol gel versus acetazolamide in the prophylaxis of ocular hypertension after phacoemulsification.

PURPOSE: To compare postoperative intraocular pressure (IOP) after administration of acetazolamide and timolol following phacoemulsification and intraocular lens implantation. SETTING: Ophthalmic Consultants of Long Island, Rockville Centre, New York, USA. METHODS: Sixty patients were included in a prospective, randomized, masked trial. The patients received either two doses of oral, sustained-release acetazolamide (Diamox Sequels) or a single dose of topical timolol 0.5% gel (Timoptic XE). Intraocular pressure was measured by Goldmann applanation tonometry preoperatively and 1 day postoperatively. RESULTS: Mean preoperative IOP was 16.4 mm Hg. One day postoperatively, it was 19.5 mm Hg in the oral acetazolamide group and 15.9 mm Hg in the timolol gel group. One patient in the acetazolamide group developed significant adverse reactions. CONCLUSION: Prophylactic use of topical timolol 0.5% gel for viscoelastic-induced ocular hypertension after cataract extraction appears to offer better IOP control than oral acetazolamide and has potentially fewer adverse systemic effects.

Acetazolamide↗
PubMedDate not supplied

Dissociation between the renal and blood acid-base actions of acetazolamide in restraint-stressed rats.

Subcutaneous injection of acetazolamide (50 or 200 mg/kg) markedly increased the blood H+ and lowered the HCO3- concentrations in a dose-related manner. The urinary pH and HCO3- excretion were elevated. Restraint stress normalized the blood HCO3- levels but not the H+ concentrations; the high levels of urinary pH and the HCO3- content were unaffected in the acetazolamide-treated animals. These findings suggest that acetazolamide induces metabolic acidosis which appears not to be caused by depletion of blood HCO3- through increased urinary HCO3- excretion. Instead, an extra-renal mechanism could be responsible for the increased blood H+ concentration. Restraint stress significantly decreased the respiratory rate, which was prevented by acetazolamide pretreatment. The reversal of restraint-stress-induced respiratory depression by acetazolamide is probably due to the activation of both peripheral and medullary chemoreceptor sites by acidosis.

Acetazolamide↗
PubMed1996

The effect of prophylactic acetazolamide in patients undergoing extensive retinal detachment repair.

Encirclement of the eye as part of a retinal detachment repair is known to raise the post-operative intraocular pressure. We studied the effect of anticipating this pressure rise by giving perioperative acetazolamide to patients having vitrectomy and encirclement procedures. Two groups (9 with acetazolamide and 14 without) were matched for biographic variables, type of detachment and operation variables. The group given acetazolamide had lower day 1 post-operative intraocular pressures (mean 22.11 mmHg vs 36.36 mmHg, p = 0.002) and were able to go home sooner (mean 1.56 days vs 3.29 days, p = 0.001). No adverse effects of short-term acetazolamide use were noted in this study. We conclude that patients having extensive scleral buckling procedures should all receive prophylactic acetazolamide unless it is specifically contraindicated.

Acetazolamide↗
PubMed1992

Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide.

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR (r = 0.69 in VMRTOT versus VMRACE and 0.79 in VMRCO2 versus VMRACE; P less than 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed2000

Gastrotonometry represents dramatic increase in PcO2 after acetazolamide administration.

BACKGROUND: We sought to evaluate the parameters of CO2 transport during the administration of acetazolamide in order to assess the role of carbonic anhydrase in CO2 transport. MATERIALS AND METHODS: The partial pressure of carbon dioxide in tissue (PtCO2), arterial blood (PaCO2) and end-tidal gas (PETCO2) were monitored to study the correlation between PaCO2, PtCO2 and PETCO2 in spontaneously breathing healthy volunteers after the intravenous administration of acetazolamide 6 mg kg-1. RESULTS: At 60 min after the administration of acetazolamide, the PtCO2 peaked at more than 60 mmHg, and although it decreased by 90 min, it then remained stable above the baseline value. The PaCO2 did not change and the PETCO2 decreased significantly. The changes in PtCO2 were greater than those of either PaCO2 or PETCO2. The minute ventilation increased progressively throughout the study. CONCLUSIONS: We concluded that gastrotonometry represents a new method for monitoring the dramatic increase in PtCO2 induced by drugs such as acetazolamide clinically, and that it could be a warning against acetazolamide administration in severe patients without keeping a ventilation and circulation reserve.

Acetazolamide↗
PubMed1992

Acetazolamide and high altitude diseases.

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.

Acetazolamide↗
PubMed1993

[Therapy of cystoid diffuse macular edema after uveitis and cataract surgery with the carbonic anhydrase inhibitor acetazolamide (Diamox)].

BACKGROUND: Observations made by Cox, Bird et al. (1988), who first used acetazolamide (Diamox) for treatment of macular edema of various origin in a higher number of patients, let assume a positive effect of this therapy on fluid accumulation specifically inside the inner retinal layers. Based on these studies 15 patients (20 eyes) with cystoid or cystoid-diffuse macular edema were treated with acetazolamide in a pilot-study. MATERIALS AND METHODS: Eleven patients (fifteen eyes) had postuveitic macular edema, four other patients (five eyes) had cystoid edema following cataract surgery. Patients with additional diseases causing macular edema of retinal vascular origin were excluded. The initial dose was 500 mg daily. In one patient responding to therapy the dose was gradually reduced after three weeks down to a minimum of 125 mg every second day. For evaluation of the therapeutical results fluorescein angiography and visual acuity were taken into account. RESULTS: Eleven patients (fourteen out of twenty eyes) showed a distinct therapeutical effect with decrease of macular edema in repeatedly controlled fluorescein angiography. All these patients had a subjective improvement of vision which correlated with an increase of visual acuity in exactly one half of all patients. Therapy was stopped, when the macular edema had still appeared unchanged in angiography after three weeks or when--in spite of fluid reduction in angiography--no improvement of visual acuity could be obtained in the next two months. The maintenance dose showed large individual variation with a minimum of 125 mg every second day and a maximum of 250 mg per day. Attempts to stop therapy resulted in a early reappearance of the edema of original extension with corresponding deterioration of visual acuity and sensitivity of central visual field. In a few patients even the reduction of the dose below the individual maintenance dose could be demonstrated angiographically. All patients were under continuous internal medical control, permanent side-effects of acetazolamide with the doses used in this study were not seen. CONCLUSIONS: The results show that acetazolamide is a basically effective agent against cystoid macular edema and that a therapeutical trial is justified based on the treatment criteria of this study. The factors limiting the therapeutical effect of acetazolamide cannot yet be evaluated on the basis of the small amount of patients in this pilot-study. Considering the patient data a time factor depending on the period between onset of edema-related symptoms and begin of treatment is likely. In the group of unsuccessfully treated cases we had the patients with the longest period of preexisting edema (more than one year) of the study.

Acetazolamide↗
PubMed2005

Combined treatment potentiates the developmental toxicity of ibuprofen and acetazolamide in rats.

Aspirin (ASA), an irreversible cyclooxygenase (COX) inhibitor, induces ventricular septal defect (VSD) and diaphragmatic hernia (DH) in rat fetuses when administered on gestation days (GDs) 9-10, a critical period for cardiovascular (CV) and midline development. Evaluation of a spectrum of nonsteroidal antiinflammatory drugs (NSAIDs; reversible COX inhibitors) showed that while some NSAIDs induced VSD in rats, none of the NSAIDs evaluated produced DH. In addition to inhibiting COX, ASA also inhibits carbonic anhydrase. The purpose of this study was to determine whether concurrent inhibition of COX and carbonic anhydrase would produce a teratogenic profile that includes both VSD and DH. To inhibit both COX and carbonic anhydrase, ibuprofen (COX inhibitor) and acetazolamide (carbonic anhydrase inhibitor) were coadministered on GDs 9-10. Groups of 20 female Crl:CD(SD)IGS BR rats were given either 300 mg kg(-1) day(-1) ibuprofen, 1000 mg kg(-1) day(-1) acetazolamide, or both (combination of ibuprofen and acetazolamide). Fetuses were evaluated on GD 21 for external and visceral development. Ibuprofen induced VSD in 3.7% of fetuses per litter; no defects in appendicular skeletal development were noted. Acetazolamide induced VSD in 5.9% of the fetuses per litter and appendicular defects in 41% of the fetuses per litter. Coadministration of ibuprofen and acetazolamide produced VSD in 18.7% of the fetuses per litter and appendicular defects in 77% of the fetuses per litter; however, there were no DH. Therefore, while concurrent inhibition of COX and carbonic anhydrase did not produce DH, potentiation was noted for the induction of VSD and appendicular anomalies.

Abnormalities, Drug-Induced↗
PubMed2003

Efficacy of low-dose acetazolamide (125 mg BID) for the prophylaxis of acute mountain sickness: a prospective, double-blind, randomized, placebo-controlled trial.

The objective of this study was to determine the efficacy of low-dose acetazolamide (125 mg twice daily) for the prevention of acute mountain sickness (AMS). The design was a prospective, double-blind, randomized, placebo-controlled trial in the Mt. Everest region of Nepal between Pheriche (4243 m), the study enrollment site, and Lobuje (4937 m), the study endpoint. The participants were 197 healthy male and female trekkers of diverse background, and they were evaluated with the Lake Louise Acute Mountain Sickness Scoring System and pulse oximetry. The main outcome measures were incidence and severity of AMS as judged by the Lake Louise Questionnaire score at Lobuje. Of the 197 participants enrolled, 155 returned their data sheets at Lobuje. In the treatment group there was a statistically significant reduction in incidence of AMS (placebo group, 24.7%, 20 out of 81 subjects; acetazolamide group, 12.2%, 9 out of 74 subjects). Prophylaxis with acetazolamide conferred a 50.6% relative risk reduction, and the number needed to treat in order to prevent one instance of AMS was 8. Of those with AMS, 30% in the placebo group (6 of 20) versus 0% in the acetazolamide group (0 of 9) experienced a more severe degree of AMS as defined by a Lake Louise Questionnaire score of 5 or greater (p = 0.14). Secondary outcome measures associated with statistically significant findings favoring the treatment group included decrease in headache and a greater increase in final oxygen saturation at Lobuje. We concluded that acetazolamide 125 mg twice daily was effective in decreasing the incidence of AMS in this Himalayan trekking population.

Acetazolamide↗