Diamox is an FDA-approved medication used to treat certain types of glaucoma, congestive heart failure, certain types of seizures. Diamox also prevents altitude sickness.
Other names for this medication:
Also known as: Acetazolamide.
Diamox contains an active ingredient Acetazolamide, which belongs to class of drugs called carbonic anhydrase inhibitors.
Diamox effectively treats certain types of glaucoma (excessive pressure in the eyes) by reducing the amount of fluid in the eye, and thereby decreases pressure inside the eye.
Acetazolamide acts also as a diuretic ("water pill") and inhibits the protein in the body called carbonic anhydrase. This leads to reducing the build-up of certain fluids in the body, significantly alleviating the symptoms of congestive heart failure.
Acetazolamide is also used to treat certain types of seizures, and to treat or prevent altitude sickness.
Diamox is available in tablets.
The dosage depends on the disease and its prescribed treatmen.
250 mg to 1 gram per 24 hours in 2 or more smaller doses.
In secondary glaucoma and before surgery in acute congestive (closed-angle) glaucoma, the usual dosage is 250 mg every 4 hours or, in some cases, 250 mg twice a day.
The daily dosage is 8 to 30 mg per 2.2 pounds of body weight in 2 or more doses. Typical dosage may range from 375 to 1,000 mg per day.
Congestive Heart Failure treatment:
The usual dosage is 250 mg to 375 mg per day or 5 mg per 2.2 pounds of body weight, taken in the morning.
Diamox can be used by children.
If you want to achieve most effective results do not stop taking Diamox suddenly.
If you overdose Diamox and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Diamox are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Diamox if you are allergic to Diamox components.
Be careful with Diamox if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not take Diamox if your sodium or potassium levels are low.
Do not take Diamox if you have kidney or liver disease, including cirrhosis.
Be careful with Diamox if you suffer from or have a history of emphysema or other breathing disorders.
Be careful with Diamox if you take high doses of aspirin.
Be careful with Diamox if you are taking Amitriptyline, Cyclosporine, Lithium, Methenamine, oral diabetes drugs such as Glyburide, Quinidine.
Do not use potassium supplements or salt substitutes.
If you want to achieve most effective results without any side effects it is better to avoid alcohol.
Do not stop taking Diamox suddenly.
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In light of the competition between microneurosurgery and alternative methods such as stereotactic radiosurgery, we tested the hypothesis that changes in the cerebral circulation after microneurosurgery are common among patients without evidence of cerebrovascular or neoplastic disease.
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A 75-year-old man without Fuchs dystrophy underwent cataract extraction on his right eye in 2007, and 5 years later, Descemet membrane endothelial keratoplasty was performed for pseudophakic edema in the same eye at another center. On presentation at our institution, a graft that is partially folded over on itself was observed in the right eye, leaving about 2/3 of donor endothelium correctly exposed. The graft was only attached in the lower part of the cornea. We observed progressive clearance of the entire cornea within 7 months with reendothelialization of the entire cornea. Good visual acuity was achieved, with no evidence of recurrent corneal edema.
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A prospective, randomized, investigator-masked, parallel study compared the capability of five different intraocular pressure (IOP) lowering agents to prevent acute IOP elevations following argon laser trabeculoplasty. Two hundred sixty eyes (patients) received either apraclonidine 1% (125 eyes), pilocarpine hydrochloride 4% (37 eyes), timolol maleate 0.5% (35 eyes), dipivefrin 0.1% (32 eyes), or acetazolamide 250 mg (31 eyes) both 1 hour before and immediately following 360-degree argon laser trabeculoplasty. Apraclonidine was the only medication that significantly decreased mean IOP from baseline. Only 4 (3%) of the apraclonidine-treated eyes had IOP rises greater than 5 mm Hg. This frequency was significantly lower than that found in eyes treated with acetazolamide (39%), dipivefrin (38%), pilocarpine (33%), or timolol (32%).
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All four CAIs decreased bovine Isc (% change in Isc: acetazolamide, -21.0 ± 9.5, n = 8; brinzolamide, -35.5 ± 13.5, n = 9; dorzolamide, -33.6 ± 7.2, n = 8; ethoxzolamide, -35.3 ± 12.9, n = 8). That decrease was not present in humans (% change in Isc: acetazolamide, 16.2 ± 20.1, n = 3; brinzolamide, 6.7 ± 13.9, n = 3; dorzolamide, 8.0 ± 20.4, n = 3; ethoxzolamide, -4.8 ± 10.3, n = 2). Despite no functional effect of CAIs on Isc, both carbonic anhydrase II and IV were present in human corneal endothelium by immunofluorescence microscopy. Histochemical analysis of human corneal endothelium revealed functionally active carbonic anhydrase activity inhibited by brinzolamide.
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Baseline BFV and CRC both were significantly reduced in HIV-infected patients as compared with control subjects (P<0.05, Student's t test). These findings did not correlate with duration of seropositivity, helper cell count, or other clinical, rheumatological, and neuroradiological findings.
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Retrospective review of patients with nonproliferative cystoid changes associated with MacTel seen at the University of Iowa between 2009 and 2012. Carbonic anhydrase inhibitors were used in 8 patients with MacTel Type 2. Five patients with MacTel Type 2 were observed during this period. Initial and final visual acuities were documented. The presence of cystic spaces and the retinal thickness were measured with spectral-domain optical coherence tomography.
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In four patients with periodic hypokalemic paralysis paralytic attacks were induced in the untreated state and later, after the patients had been treated with acetazolamide. There was a distinct, clinically favourable effect of acetazolamide upon the length as well as the severity of paralysis. The maximum fall in serum potassium was less marked during acetazolamide therapy. After treatment all four patients showed significantly reduced serum levels of glucose and insulin during induced attacks of paralysis as compared with the levels obtained during paretic attacks in the untreated state. These findings indicate that the prophylactic effect of this drug does not relate merely to metabolic acidosis. The hypothesis is advanced that the lower serum insulin and glucose levels might represent reduced absorption which would amount to an indirect prophylactic action.
The use of substances that inhibit root resorption may be an alternative for cases of unsuccessful reimplants. Hence, the purpose of this study was to test a solution of acetazolamide, a resorption inhibitor, as an intracanal therapeutic agent for late reimplanted teeth. Thirty rat maxillary right central incisors were avulsed and kept dry for 30 min. The teeth were instrumented, and the root surfaces treated with 1% hypochlorite solution followed by application of 2% sodium fluoride. Thereafter, the teeth were divided into two groups according to the intracanal dressing: Group I, solution of acetazolamide and Group II, calcium hydroxide paste. Teeth were then reimplanted in their respective sockets. The animals were killed at 15, 30, and 60 days after reimplantation and the samples processed for morphometric and microscopic analysis. The results showed that calcium hydroxide paste limited root resorption, even though not avoiding it. In contrast, no root resorption was observed after 60 days in the acetazolamide group, confirming the efficacy of the substance in inhibiting root resorption.
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A total of 77 (31 males, 46 females, age 6.6+/-3.2 years) patients with postoperative pediatric moyamoya disease who underwent basal/acetazolamide stress brain perfusion SPECT 6 to 12 months after revascularization surgery and who were followed-up >12 months after SPECT were included. Mean follow-up period after SPECT was 36+/-19 months. Sixty-two patients underwent bilateral ribbon encephaloduroarteriosynangiosis (EDAS), 14 bilateral EDAS, and 1 unilateral EDAS. Ordinal logistic regression analysis using 5 independent variables (infarction on preoperative MRI, age at the first operation, highest Suzuki stage on cerebral angiography, and regional cerebrovascular reserve on postoperative SPECT) against postoperative clinical outcomes was performed.
Twelve patients (mean age 63.2+/-2.3 years) completed the protocol. There was no treatment order effect. Cerebral vasomotor reactivity was significantly greater after perindopril treatment (percent change from baseline +18.8+/-10.1% after perindopril, -4.6+/-4.1% after placebo; P=0.032). Dosing with perindopril did not affect resting cerebral blood flow velocity (percent change from baseline +3.1+/-9.5% after perindopril, -0.6+/-5.4% after placebo), nor was there a change in resting blood pressure (+1.8 mm Hg+/-3.1 after perindopril, +1.4 mm Hg+/-2.5 after placebo).
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A double-blind placebo-controlled study was performed in three groups of patients from Cerro de Pasco, Peru (4,300 m), treated orally for 3 weeks with placebo (n = 10), 250 mg of acetazolamide (n = 10), or 500 mg of acetazolamide (n = 10), daily.
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Improvements in MD continued from month 6 to month 12 of the IIHTT in all treatment groups -most marked in the placebo group tapered off study drug. Adding ACZ to the placebo group significantly improved papilledema grade, headache and QoL measures.
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Human erythrocyte carbonic anhydrase isozyme B was measured by a specific and immunological method. The levels of carbonic anhydrase B were determined in normal subjects, patients with hyperthyroidism, and patients with chronic obstructive lung disease and patients with epilepsy under treatment with acetazolamide, using the rapid assay method of single radial immunodiffusion. The levels of carbonic anhydrase B showed a decrease in hyperthyroidism, and increased in chronic obstructive lung diseases and epilepsies. Closely negative correlations were observed between carbonic anhydrase B and T3 resin sponge uptake or protein bound iodine (PBI) levels in hyperthyroidism. Simultaneously, carbonic anhydrase B-dependent esterase activity (active carbonic anhydrase B enzyme) was determined kinetically using the immunoadsorbent method in the above-mentioned patients. The results were compared with the total enzyme protein (active and inactive carbonic anhydrase B enzyme), estimated by the single radial immunodiffusion technique. In patients treated with acetazolamide, the "true" specific activity of the carbonic anhydrase B (carbonic anhydrase B-dependent esterase activity/total carbonic anhydrase B protein) decreased remarkably. In chronic obstructive lung disease, no remarkable changes were observed. On the other hand the specific activity was elevated in hyperthyroidism to 2 times higher than that of normal subjects. The clinical significance of these active enzymes is discussed.
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Vasospasm in aneurysmal subarachnoid hemorrhage results in proliferative vasculopathy. Systemic hypertension also causes vascular hypertrophy. Both of these histological changes can lead to rigidity of the cerebrovascular system, reducing its autoregulatory capacity.
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Intracellular pH (pHI) of intact rat renal cortex was estimated using [14C]-5,5-dimethyl-2,4-oxazolidinedione and 22Na+ under conditions of metabolic acidosis and alkalosis, potassium depletion and carbonic anhydrase inhibition. In metabolic acidosis and alkalosis, pHI and bicarbonate concentration changed in the same direction as occurred in plasma. In potassium depletion, systemic acid-base balance was unaltered but a marked intracellular acidosis developed. Carbonic anhydrase inhibition with acetazolamide was associated with an extracellular respiratory acidosis and a rise in intracellular bicarbonate concentration. Another carbonic anhydrase inhibitor, benzolamide, caused no change in systemic acid-base state but produced a decrease in intracellular bicarbonate concentration. When appropriate corrections were made for predicted change in tubular fluid bicarbonate and for intracellular sodium, modification in the absolute values of the above changes occurred but the directions of the changes in pHI and bicarbonate concentration were unaltered.
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This clinical prospective study included 32 consecutive patients (32 eyes) with diffuse diabetic macular edema. All patients had visual acuity, fluorescein angiogram, and optical coherence tomography performed at the initial visit (baseline). Single triamcinolone acetonide injection was applied intravitreally in different high doses using sterile technique followed by timolol-maleate 0.5%/acetazolamide fixed combination eyedrops twice a day for 6 consecutive months. Macular edema, intraocular pressure, and best-corrected distance visual acuity were reviewed after 5 days and 1, 3, and 6 months.
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In this report, we describe the case of a 34-year-old woman with moyamoya disease who suddenly developed headache and jacksonian seizure. Plain computed tomographic scans on admission revealed SAH localized over the left frontal cortex. The patient was diagnosed with moyamoya disease on cerebral angiography. However, no aneurysm was found on cerebral angiography. Positron emission tomography showed the reduction of CBF and its reactivity to acetazolamide and the elevation of CBV in the left hemisphere. She underwent STA to MCA anastomosis and indirect synangiosis. Intraoperative observations revealed that the pial arterioles were markedly dilated on the brain surface. The CBF in the left hemisphere significantly improved after surgery. The patient has experienced no further episode of cerebral ischemia or intracranial bleeding.
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Acute mountain sickness (AMS) is caused by exposure to altitudes exceeding 2500 m and often resolves by acclimatization without further ascent. Statistical models of AMS score and the probability of an AMS diagnosis were developed to allow the combination of dissimilar exposures for simultaneous analysis. The study population was 302 trekkers from a previous investigation who provided self-reported symptoms upon arrival at 3840 m during hikes through altitudes of 1500 to 6200 m. AMS score (Hackett scale) was estimated by linear regression and the probability of an AMS diagnosis (Lake Louise criteria) by logistic regression. AMS score or probability was significantly associated with exposure day and altitude. Increased altitude over the prior 3 days resulted in higher estimated AMS score or probability and decreased altitude in lower score or probability. The odds ratio (OR) of AMS was 3.6 if not on acetazolamide. Females appeared slightly more susceptible than males (1.5 OR). The approach offers the advantages of (1) improved statistical power by combining exposures, (2) insight into the dose-response relationship of altitude exposure and AMS risk, (3) quantitative tests for the significance of factors that might affect AMS susceptibility, and (4) practical tools to track individual climbers and plan operational ascents.
To investigate whether type of glaucoma or use of acetazolamide are associated with main cause of death and comorbidity.
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Studies were performed to examine the possible effects of carbonic anhydrase (CA) inhibition on the glomerulotubular balance for bicarbonate in anesthetized dogs. Maximal CA inhibition was achieved by acetazolamide infusion and glomerular filtration rate (GFR) was reduced in a stepwise fashion by progressive clamping of the left renal artery. A close relationship (R equals 0.973) was maintained between the amount of filtered and reabsorbed bicarbonate in normal dogs with CA inhibition. A similar relationship was observed between GFR and bicarbonate reabsorption during CA inhibition in normal dogs (R equals 0.957) as well as in sodium bicarbonate loaded dogs (R equals 0.867). In these two groups, GFR in the clamped kidney was reduced to values ranging respectively from 99 to 5% and from 96 to 3%. Distal tubular blockade with ethacrynic acid and chlorothiazide, performed in normal dogs and in sodium bicarbonate loaded dogs, did not abolish glomerulotubular balance for bicarbonate during CA inhibition. This study demonstrates that the glomerulotubular balance for bicarbonate is maintained during CA inhibition whether or not distal tubular blockade is superimposed. A proportionate decrease in both fractions of bicarbonate reabsorption, either CA dependent or not mediated by CA, or an adaptive increase in the fraction of bicarbonate reabsorption not mediated by CA can explain the maintenance of glomerulotubular balance for bicarbonate.
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Twelve young adults with healthy eyes were studied under normocapnic and hypercapnic (6% CO2, 94% O2 tanked gas) conditions after receiving either placebo or 1,000 mg acetazolamide (3 h before study). Color Doppler imaging was used to measure peak systolic and end-diastolic velocities (PSV and EDV) in the internal carotid, middle cerebral, ophthalmic, and central retinal arteries under each condition.
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