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Diamox (Acetazolamide)
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Diamox

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:
Acemit, Acemox, Acetadiazol, Acetak, Acetamide, Acetazolam, Acetazolamid, Acetazolamida, Acetazolamidum, Acetazoleamide, Ak-zol, Azomid, Carbinib, Dazamide, Defiltran, Diacarb, Diazomid, Diluran, Diuramid, Edemox, Ederen, Edimox, Glaumox, Glaupax, Huma-zolamide, Oculten, Shalak, Storzolamide, Uramox, Vetamox

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Also known as: Acetazolamide.

Description

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.

Dosage

Diamox is available in tablets.

The dosage depends on the disease and its prescribed treatmen.

Glaucoma treatment:

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.

Epilepsy treatment:

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.

Overdose

If you overdose Diamox and you don't feel good you should visit your doctor or health care provider immediately.

Storage

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.

Side effects

The most common side effects associated with Diamox are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

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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A comparative study on the performance of two RPLC modes on the separation of 18 diuretics with diverse acid-base behaviour (acetazolamide, althiazide, amiloride, bendroflumethiazide, benzthiazide, bumetanide, canrenoic acid, chlorothiazide, chlorthalidone, ethacrynic acid, furosemide, hydrochlorothiazide, piretanide, probenecid, spironolactone, triamterene, trichloromethiazide and xipamide) was carried out. A conventional octadecylsilane column and acidic acetonitrile-water mobile phases, in the absence and presence of micelles of the anionic surfactant sodium dodecyl sulphate (SDS), were used. The effects of pH and the modifiers acetonitrile and SDS on peak asymmetry, efficiency, selectivity, resolution and analysis time, were examined. The comparison of both RPLC modes (aqueous- and micellar-organics) was done using the same processing tools, applying several polynomial and mechanistic equations to describe the retention. The best separations were obtained by maximising the product of peak purities, considering a wide range of experimental conditions. The study illustrates that, despite the theoretical and practical complexity of the problem, the predicted optimal chromatograms can be reproduced experimentally with great accuracy. None of the examined RPLC modes was able to yield baseline separation of the 18 diuretics. However, their selectivity was complementary, being appropriate for different combinations of a smaller number of the assayed diuretics.

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Primary hypokalemic periodic paralysis (HOKPP) is an autosomal dominant disorder manifesting as recurrent periodic flaccid paralysis and concomitant hypokalemia. HOKPP is divided into type 1 and type 2 based on the causative gene. Although 2 different ion channels have been identified as the molecular genetic cause of HOKPP, the clinical manifestations between the 2 groups are similar. We report the cases of 2 patients with HOKPP who both presented with typical clinical manifestations, but with mutations in 2 different genes (CACNA1Sp.Arg528His and SCN4A p.Arg672His). Despite the similar clinical manifestations, there were differences in the response to acetazolamide treatment between certain genotypes of SCN4A mutations and CACNA1S mutations. We identified p.Arg672His in the SCN4A gene of patient 2 immediately after the first attack through a molecular genetic testing strategy. Molecular genetic diagnosis is important for genetic counseling and selecting preventive treatment.

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Using a constant perfusion technique, sodium and bicarbonate absorption was studied in human subjects. The following observations were made on sodium absorption from saline solution: (a) the rate of sodium absorption is markedly influenced by bulk water flow, (b) when net water flow is zero, sodium absorption is zero if there are no concentration gradients between plasma and lumen that favor net NaCl diffusion; and (c) the PD between abraded skin and jejunal lumen is near zero when saline is perfused and does not change with partial substitution of sulfate or bicarbonate for chloride. Based on these observations, we conclude that sodium absorption from saline is entirely passive in the human jejunum. On the other hand, in the presence of bicarbonate sodium is absorbed actively against electrochemical gradients. The mechanism of the link between bicarbonate and sodium absorption was studied in normal subjects and in 11 patients with pernicious anemia; the latter were chosen because they do not secrete gastric acid which can react with bicarbonate in the jejunal lumen. We observed that bicarbonate absorption (a) occurs against steep electrochemical gradients, (b) does not generate a potential difference between abraded skin and jejunal lumen, (c) is inhibited by acetazolamide, and (d) generates a high CO2 tension in jejunal fluid. These observations suggest that bicarbonate absorption is mediated by active hydrogen secretion, rather than by bicarbonate ion transport per se, and that the link between sodium and bicarbonate transport is best explained by a sodium-hydrogen exchange process.

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The stability of acetazolamide in an extemporaneous suspension compounded from tablets was studied. Acetazolamide 25-mg/mL suspension was prepared by levigating the comminuted 250-mg tablets with 70% sorbitol solution. The mixture was incorporated into a suspension vehicle containing magnesium aluminum silicate and carboxymethylcellulose sodium. Appropriate sweeteners, flavoring agents, preservatives, humectants, and pH adjusters were then added. The suspension was stored in amber glass bottles at 5, 22, 30, 40, and 50 degrees C. Samples were analyzed for the concentration of acetazolamide by stability-indicating high-performance liquid chromatography on days 3, 7, 11, 18, 24, 32, 42, 54, and 79. For batches stored at 5, 22, and 30 degrees C, the initial acetazolamide concentration was maintained during the entire 79 days of the study. However, the concentrations in the batches stored at 40 and 50 degrees C were below 90% of the initial value after 79 and 32 days, respectively. The Arrhenius plot was used to predict a shelf life of the suspension at room temperature of 371 days. Acetazolamide oral suspension 25 mg/mL was stable for at least 79 days at 5, 22, and 30 degrees C. The formulation should be maintained at pH 4-5 and stored in amber glass bottles.

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A 34-year-old man presented with severe headache and diplopia after a motor vehicle accident. Clinical examination demonstrated severe papilledema and bilateral abducens palsy. Imaging findings demonstrated a DCF over the posterior third of the SSS and absent flow distal to the fracture with dilated cortical venous drainage.

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These data clearly establish the specificity of EA2 mutations compared with SCA-6 and familial hemiplegic migraine. Detailed clinical analysis of the mutation carriers showed the highly variable penetrance and expression of this disorder: Several of the carriers did not show any clinical symptom; others displayed atypical or permanent neurologic symptoms (such as recurrent, transient diplopia or severe, permanent, and isolated cerebellar ataxia).

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Retrospective review of patients undergoing endoscopic endonasal repair of spontaneous CSF leaks. All participants had a lumbar catheter placed for 24-hour continuous preoperative pressure monitoring, and 24 hours of continuous monitoring starting 48 hours after repair. In addition to patient characteristics, mean and peak CSFP, pulse waveform amplitudes (PWAs), and related parameters were calculated.

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Hereditary paroxysmal cerebellar ataxia (HPCA) is an autosomal dominant disorder characterized by the recurrence of intermittent attacks of vestibulocerebellar ataxia lasting from 15 minutes to a few days. The number of attacks is often significantly decreased by acetazolamide treatment. Neurological examination shows a permanent gaze-evoked nystagmus, as well as a mild cerebellar ataxia in most patients. The paroxysmal feature of this condition is shared by another autosomal dominant neurological condition, familial hemiplegic migraine (FHM), a condition in which permanent cerebellar signs have also been reported in some families. Although hemiplegic migraine has never been reported in patients with HPCA, we hypothesized, based on the latter observations, that HPCA and FHM may be allelic disorders. We previously mapped a gene responsible for FHM on the short arm of chromosome 19. We performed linkage analysis with 6 markers spanning the FHM interval on a large HPCA family. Significant lod scores were obtained with 3 markers: D19S244 (LS = 3.71), D19S221 (3.60), and D19S226 (3.54) at theta = 0. Haplotype and multipoint linkage analysis established that the most likely location was the same interval of 30 cM encompassing the chromosome 19 FHM locus.

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Combination therapy with a loop diuretic and an aldosterone antagonist can produce normokalemic hypochloremic alkalosis, a complication not previously documented in the literature. This report describes 74 patients who had severe congestive heart failure treated with a combination of furosemide and spironolactone in whom this complication developed. Acetazolamide corrected the metabolic abnormality. The combination of furosemide and spironolactone with intermittent courses of acetazolamide was very effective in the treatment of severe congestive heart failure complicated by normokalemic hypochloremic alkalosis.

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All 6 patients achieved relief of their symptoms, with decreased incidence of occurrence and duration of Floxin Prices episode if not complete resolution.

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Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Avapro Generic Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment.

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The Augmentin Generic effects of exogenous adenosine 3':5'-cyclic monophosphate (cyclic AMP), parathyroid hormone (PTH) and acetazolamide (Az) on renal calcium and phosphate excretion of the isolated perfused rat kidney were compared. Both PTH and Az evoked an early increase in urinary cyclic AMP excretion followed by a later more prolonged increase in phosphate excretion. All of the increased urinary cyclic AMP was derived from renal cells. Calcium excretion decreased with PTH but was unchanged with Az. Sodium and potassium excretion increased with Az but not PTH. Transitory urinary cyclic AMP excretion rates following bolus additions of exogenous cyclic AMP to perfusate were up to twentyfold greater than those evoked by PTH or Az but unassociated with changes in calcium, phosphate, sodium or potassium excretion. Sustained perfusate levels (above 0.5 microM) and excretion rates of cyclic AMP induced phosphaturia proportional to the perfusate cyclic AMP concentrations achieved up to 2.0 microM. Clearances of exogenous cyclic AMP exceeded inulin clearance at perfusate concentrations greater than 1.0 microM. Aminophylline evoked a small phosphaturia which increased further on addition of cyclic AMP to 5 microM. Glomerular filtration was not affected by any of the agents except Az. Since increased phosphate excretion could be evoked only at perfusate concentrations exceeding either plasma or intracellular concentrations observed in vivo, it is concluded that circulating cyclic AMP at levels in vivo is unlikely to mediate a significant fraction of the renal effects of PTH.

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The Ocusert-pilocarpine devides with seven days' therapeutic duration were compared with pilocarpine eye drops for efficacy and ocular tolerance in the management of glaucoma in 16 patients. Magnitude of pressure reduction with release rates of 20 mcg. and 40 mcg. of pilocarpine per hour were as effective in the treatment of glaucoma as 2 per cent and 4 per cent pilocarpine eye drops, respectively. Ocular tolerance and retention in the human eyes were good. There were no appreciable side effects other than the occasional sudden leakage phenomenon encountered. Further refinement of the Ocusert-pilocarpine device to reduce the incidence of leakage would not only ensure precision in the rate of Cialis Online Generic drug release, but would also expand its clinical application.

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Acetazolamide, a carbonic anhydrase (CA) inhibitor, was used to normalize metabolic alkalemia. A dosage of acetazolamide for normalizing metabolic alkalemia has not yet been experimentally determined. The dosage of acetazolamide for this purpose is experimentally calculated in this paper. The correlation between various concentration of acetazolamide mixed with blood and the base excess (BE) levels in blood at the start of normalizing metabolic alkalosis was studied in vitro. The change rate of the BE level was calculated from BE levels noted before and after Cheap Cialis Guestbook tonometry of the blood with and without acetazolamide. A dosage of acetazolamide which can cause the change rate of the BE level to decrease is considered to be an effective dosage. Metabolic alkalosis in vitro was produced by adding bicarbonate into the blood. An effective dosage of acetazolamide for metabolic alkalemia of which the BE range was from 0 to + 30 mEq/liter was calculated. CA activities in the kidney and the blood of dogs administered acetazolamide were examined. The effective dosage of acetazolamide obtained from in vitro experiments inhibited the CA activities not only in the blood but also in the kidneys. An effective dosage of acetazolamide to normalize a BE of + 10 mEq/liter in vitro was converted into about 7-12 mg/kg in vivo. This dosage inhibited the red blood cell carbonic anhydrase (RCA) activity to 20-40%, whereas the normal physiological variation range is 25%. An effective dosage of acetazolamide in the blood did not proportionally increase with an increase of HCO3- during severe alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

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We compared the acetazolamide Cymbalta Cost Canada challenge test using 99mTc-ECD SPECT and 123I-IMP SPECT images in patients with chronic occlusive cerebrovascular disease. We also evaluated the usefulness of linearization correction for acetazolamide challenge test of 99mTc-ECD SPECT.

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Based on clinical experiments with fluorophotometry, several observations can be made about aqueous flow through the chambers of the human eye. 1. The rate of flow is 2.75 +/- 0.63 microliters/min in normal subjects, as derived from measurements averaged during normal office hours. The normal range (95%) is 1.8 to 4.3 microliters/min. 2. There is a circadian rhythm of flow, with the highest rates during morning hours, slightly lower rates during afternoon hours, and rates during sleep that are approximately one half of those during the morning. The hormonal basis for this rhythm is unknown, but it is known to be present in both eyes of persons with unilateral Horner's syndrome. 3. A slight decline of the rate occurs after age 10 yr--3.2% per decade. There is no significant difference in aqueous flow between men and women. 4. Of the hundreds of drugs that are used clinically, most are unlikely to have a significant effect on aqueous flow. Exceptions are the beta-adrenergic agonists that, under certain circumstances, are able to increase flow, the corticosteroids that may have a stimulating effect on flow, and three classes of drugs that have therapeutically useful suppressing effects on flow: carbonic-anhydrase inhibitors, beta-adrenergic antagonists, and alpha 2-selective adrenergic agonists. 5. Timolol, which has a remarkably Zovirax Prescription Cost consistent suppressing effect on flow during the day, has no effect on the flow of sleeping subjects. By contrast, acetazolamide and apraclonidine are able to reduce the flow of sleeping subjects. 6. Acute doses of beta-adrenergic antagonists and alpha 2-agonists are not additive, but beta-adrenergic antagonists and carbonic-anhydrase inhibitors are partly additive. 7. The eye adapts partly to the chronic use of timolol and recovers from its effects when it is discontinued. 8. The rate of disappearance of the effect of beta-adrenergic antagonists is longer for the noncardioselective agents, such as timolol and levobunolol, but is relatively short for the cardioselective agent, betaxolol. 9. The rate of aqueous flow is insensitive to moderate changes of intraocular pressure. Clinical studies can provide suggestive leads for more basic investigations or test specific hypotheses. Biochemical, biologic, and pharmacologic approaches in simpler, more controlled experimental conditions are necessary to determine the fundamental processes that bring about aqueous formation in the living eye. The combination of many disciplines (eg, studying molecules, cells, tissues, organs, and the intact living system) has the best chance of furthering our understanding of the aqueous circulation.

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Paroxysmal movement disorders are of sudden onset, paroxystic Azulfidine Generic or intermittent, with normality or at least absence of abnormal movements between episodes. They are uncommon conditions with high familial incidence. The commonest form is paroxystic dystony. Paroxystic ataxia and paroxystic tremor are much rarer.

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A patient with paroxysmal dystonic choreoathetosis also had familial ataxia. His brother was similarly affected but had rare paroxysmal episodes. No secondary or symptomatic forms of this type of paroxysmal dyskinesia have ever been reported. Episodes were briefly controlled with acetazolamide and were almost completely eliminated by clonazepam therapy.

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Cerebrovascular reactivity is compromised early in TgNotch3R90C mice. The data show an impaired autoregulation and are suggestive of a decreased relaxation or increased resistance of cerebral vessels. Our findings indicate that vascular dysfunction is an early pathogenic event that may promote the subsequent development of brain ischemia in CADASIL.

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We measured titratable acid (TA) and NH4 excretion by isolated rat kidneys perfused either with conventional bicarbonate-containing solutions or with solutions in which bicarbonate was replaced by propionate. Rates of TA excretion by bicarbonate-perfused kidneys were similar to in vivo values, 0.27 +/- 0.04 mueq.ml GF-1 (0.21 mueq.min-1.g-1), and increased significantly under bicarbonate-free conditions to 0.70 +/- 0.12 mueq.ml GF-1 (0.42 mueq.min-1.g-1). At the same time the perfusate/urine pH difference (delta pH) increased significantly, from 0.63 +/- 0.06 to 0.92 +/- 0.06. Carbonic anhydrase inhibition by 5 X 10(-4) M acetazolamide alkalinized the urine of bicarbonate-perfused kidneys, while in the bicarbonate-free preparation the urine remained acid (delta pH = 0.27 +/- 0.04) and titratable acid continued to be excreted, though at a reduced rate, 0.19 +/- 0.04 mueq.ml GF-1. Under these same bicarbonate-free carbonic anhydrase-inhibited conditions, lowering the perfusate pH from 7.4 to 7.1 increased delta pH to 0.36 +/- 0.02 and caused total acid excretion (TA + NH4) to rise from 0.29 +/- 0.04 to 0.45 +/- 0.06 mueq.ml GF-1, and increasing the perfusate [HPO4] from 2.4 to 9.6 mM increased TA to 0.80 +/- 0.09 mueq.ml GF-1.