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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Acetazolamide-challenged perfusion MRI is feasible for evaluating CVR in symptomatic patients with severe MCA stenosis quantitatively.
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Eleven patients had type 1 RLVD. In these patients, preoperative T2-weighted MR images showed no hyperintense areas, and angiographic evidence showed flow into more than one venous sinus. The other 11 patients had type 2 RLVD. In these patients, preoperative SPECT demonstrated hypoperfused areas that coincided with hyperintense areas on T2-weighted MR images. After treatment, the hyperintense areas disappeared, and symptoms improved in seven of these patients (type 2a). Their preoperative SPECT studies demonstrated preservation of vasoreactivity after an acetazolamide challenge. In the other four patients (Type 2b), the hyperintense areas and symptoms persisted after treatment. Their preoperative SPECT studies revealed a marked disturbance of vasoreactivity.
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To present a case of retrobulbar optic nerve and chiasm sarcoidosis that mimicked pseudotumor cerebri.
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Calcium (Ca2+) and Magnesium (Mg2+) reabsorption along the renal tubule is dependent on distinct trans- and paracellular pathways. Our understanding of the molecular machinery involved is increasing. Ca2+ and Mg2+ reclamation in kidney is dependent on a diverse array of proteins, which are important for both forming divalent cation permeable pores and channels, but also for generating the necessary driving forces for Ca2+ and Mg2+ transport. Alterations in these molecular constituents lead to profound effects on tubular Ca2+ and Mg2+ handling. Diuretics are used to treat a large range of clinical conditions, but most commonly for the management of blood pressure and fluid balance. The pharmacological targets of diuretics generally directly facilitate sodium (Na+) transport, but also indirectly affect renal Ca2+ and Mg2+ handling, i.e. by establishing a prerequisite electrochemical gradient. It is therefore not surprising that substantial alterations in divalent cation handling can be observed following diuretic treatment. The effects of diuretics on renal Ca2+ and Mg2+ handling are reviewed in the context of the current understanding of basal molecular mechanisms of Ca2+ and Mg2+ transport. Acetazolamide, osmotic diuretics, NHE3 inhibitors and antidiabetic SGLT blocking compounds, target the proximal tubule, where paracellular Ca2+ transport predominates. Loop-diuretics and ROMK inhibitors block thick ascending limb transport, a segment with significant paracellular Ca2+ and Mg2+ transport. Thiazides target the distal convoluted tubule, however, their effect on divalent cation transport is not limited to that segment. Finally, potassium-sparing diuretics, which inhibit electrogenic Na+ transport at distal sites, can also affect divalent cation transport.
We assessed 10 patients who had experienced a stroke at least 6 months earlier; they received low-dose (5 mg) simvastatin. Using our triple-injection technetium 99m-ethylcysteinate dimer method, we determined their cerebral blood flow and cerebrovascular reactivity. A second assessment of at-rest cerebral blood flow and cerebrovascular reactivity was performed 4 or more months (mean 6 months) after the start of statin administration. We used acetazolamide (1 g) as the vasodilator. The region of interest was the middle cerebral artery territory on a 3-dimensional stereotaxic region of interest template.
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The physiological role of carbonic anhydrase III in slow-twitch skeletal muscle was investigated using isolated mouse soleus (N = 30) contracting once every 1.7 min for 75 min in Krebs-Henseleit solution gassed with either 95% oxygen - 5% carbon dioxide (normocapnia) or 90% oxygen - 10% carbon dioxide (hypercapnia). Each contraction was 500 ms in duration at 50 Hz. When muscles contracted in normocapnic solution (pH 7.42), the developed tension decreased an average of 6.1 +/- 0.8% over 25 min. For the next 50 min, 15 muscles remained normocapnic, while the remainder contracted in hypercapnic solution (pH 7.20). Tension decreased significantly more with hypercapnia. For the last 25 min, both normocapnic and hypercapnic muscles were divided into three treatment groups (N = 5). One group continued in the same environment, while acetazolamide (final concentration of 10(-5) M) was added to the bath of the second and sodium cyanate (final concentration of 10(-5) M) was added to the bath of the third group. Acetazolamide had no effect on tension in either carbon dioxide environment. Sodium cyanate significantly decreased tension from the hypercapnic control but had no effect in normocapnia. Thus carbonic anhydrase III inhibition with sodium cyanate increased the effect of hypercapnia implying that carbonic anhydrase III assists in the regulation of free hydrogen ion concentration in slow-twitch skeletal muscle.
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In a system for ventriculocisternal perfusion of the choroid plexus, the rate of formation of new cerebrospinal fluid was measured by changes in dilution of an impermeant dye in the perfusate. Norepinephrine added to the perfusate decreased formation of cerebrospinal fluid in rats as was previously demonstrated in rabbits. The dose-response relationship for rats was determined. The formation rate was decreased 42% by 10(-3) M norepinephrine. Acetazolamide, 50 mg/kg i.v., caused a decrease of 46%. Given together, these drugs decreased formation 79%, demonstrating essentially full addition between the regulatory mechanisms involved. Addition of equal magnitude occurred when intraventricular nialamide, an inhibitor of monoamine oxidase, and i.v. acetazolamide were given together. This demonstrates addition between acetazolamide and endogenous norepinephrine (or other catecholamines present) in which metabolic breakdown is prevented by the inhibitor. The degree of reduction in cerebrospinal fluid formation seen in these experiments exceeds that reported for numerous other trials of single drugs.
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Of 131 women with hormonally related migraines unresponsive to standard medication, 67 (51.1%) noted profound relief after a 12-month, phased study using danazol for migraine prevention. The first three phases consisted of two-month cycles: dietary control and acetazolamide, the addition of danazol and danazol discontinuation. Eighty-three women (63.36%) reported control of their hormonal migraines while using danazol. In phase IV, 81 women whose headaches were controlled by danazol restarted danazol for an additional six months. Sixty-seven (82.7%) reported continued success with this medication. Danazol proved highly successful in the control of women's cyclic migraine. Its effectiveness remained consistent throughout the treatment course. In the prophylactic treatment of women's hormonal migraine, 400 mg of danazol administered daily for 25 days each month can prove effective when standard medical therapy fails. Furthermore, the response to danazol supported the concept that hormonal migraine should be treated as a distinct clinical entity.
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Cerebral blood flow (CBF) was studied by 133Xe inhalation dynamic single photon emission computer tomography in 8 members of a climbing expedition to the Himalayas. With one exception they had all previously climbed at high altitudes. All stayed above 6,500 m for approximately 3 weeks, and 5 reached the summit of Mt. Everest. CBF was measured in Oslo before, immediately after, and one year after the completion of the expedition. Measurements were made at rest and following the injection of 1 g acetazolamide intravenously. As reference group was used 13 healthy male subjects of similar age from the hospital staff. Ten age-matched male diving instructors formed a second control group. In the climbers a small, but not significant reduction in CBF was seen after the expedition. On the other hand, they had significantly lower CBF than reference subjects already before the expedition. The flow difference was most pronounced corresponding to the perfusion territory of the middle cerebral artery. One year after the completion of the expedition the average CBF in climbers was still more than 15% lower than in the reference group. The climbers had higher relative flow increase after acetazolamide injection than the reference subjects, showing that the functional capacity of the microvascular system of the brain was intact. Whether neuronal activity or number of neurones is reduced in climbers proportional to the decrease in flow, or maintained at normal level by increased oxygen and glucose extraction, cannot be answered by the present data.
The combination of hyperostosis and hyperphosphatemia is very rare. In this case report, we present a boy with a combination of diffuse hyperostosis and hyperphosphatemia. We evaluated most possible known causes of hyperphosphatemia and hyperostosis. He had normal renal function and serum parathormone level. Concerning some few similar cases, most of them from Middle Eastern countries, we present this combination (diffuse hyperostosis and hyperphosphatemia) as a new syndrome to be discussed in pediatric textbooks.
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Previous studies have demonstrated that carbonic anhydrase inhibition with acetazolamide reduces exercise capacity. The mechanism responsible for this early fatigue is unclear, but may be partly mediated by impaired respiratory muscle function. Inspiratory muscle strength and endurance were assessed in seven healthy men (age 28 ± 5 yrs, ±SD) by measuring maximal inspiratory pressure (MIP) and time to task failure during a constant-load breathing test (CLBT), respectively, under control (CON) and acetazolamide (ACZ; 500 mg/8 h po for 3 days) conditions that were separated by two weeks and randomized between subjects. In addition, MIP was measured before and after moderate-intensity cycling exercise to fatigue while pulmonary gas exchange, plasma pH, and ventilation were measured during exercise. ACZ did not alter pulmonary function (FVC, FEV1, MVV) or MIP measured at rest (CON, -157 ± 47 vs. ACZ, -154 ± 45 cmH(2)O, p>0.05), but decreased time to task failure during the CLBT (CON, 1340 ± 820 vs. ACZ, 698 ± 434 s; p=0.01). Exercise duration during cycling exercise was reduced (p=0.003) with ACZ (1090 ± 254 s) compared to CON (1944 ± 532 s) in the presence of a significantly lower plasma pH and higher ventilation compared to control (p<0.05). Compared to resting values, MIP was reduced (p=0.03) in ACZ but not CON at exhaustion. In conclusion, carbonic anhydrase inhibition with ACZ is associated with impaired respiratory muscle function at rest and following constant load cycling which may contribute to reduced exercise tolerance with carbonic anhydrase inhibition.
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It is well established that the gills of teleost fish contain substantial levels of cytoplasmic carbonic anhydrase (CA), but it is unclear which CA isozyme(s) might be responsible for this activity. The objective of the current study was to determine if branchial CA activity in rainbow trout was the result of a general cytoplasmic CA isozyme, with kinetic properties, tissue distribution and physiological functions distinct from those of the red blood cell (rbc)-specific CA isozyme. Isolation and sequencing of a second trout cytoplasmic CA yielded a 780 bp coding region that was 76% identical with the trout rbc CA (TCAb), although the active sites differed by only 1 amino acid. Interestingly, phylogenetic analyses did not group these two isozymes closely together, suggesting that more fish species may have multiple cytoplasmic CA isozymes. In contrast to TCAb, the second cytoplasmic CA isozyme had a wide tissue distribution with high expression in the gills and brain, and lower expression in many tissues, including the red blood cells. Thus, unlike TCAb, the second isozyme lacks tissue specificity and may be expressed in the cytoplasm of all cells. For this reason, it is referred to hereafter as TCAc (trout cytoplasmic CA). The inhibitor properties of both cytoplasmic isozymes were similar (Ki acetazolamide 1.21+/-0.18 nmol l(-1) and 1.34+/-0.10 nmol l(-1) for TCAc and TCAb, respectively). However, the turnover of TCAb was over three times greater than that of TCAc (30.3+/-5.83 vs 8.90+/-1.95 e4 s(-1), respectively), indicating that the rbc-specific CA isoform was significantly faster than the general cytoplasmic isoform. Induction of anaemia revealed differential expression of the two isozymes in the red blood cell; whereas TCAc mRNA expression was unaffected, TCAb mRNA expression was significantly increased by 30- to 60-fold in anaemic trout.
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Freshwater bivalves maintain a Na steady state in artificial pondwater: JiNa = 1.2 +/- 0.1 mumol/g dry tissue per h. Na uptake is Cl independent. The affinity (KS) of the Na transport system is 0.15-0.23 mmol Na/1. Sodium influx is coupled to H and/or NH4 exchange. Salt depletion stimulates JiNa 300% relative to nondepleted animals with no change in Ks. Injected ammonium ion stimulates JiNa. Sodium transport is inhibited 84% by 0.5 mM amiloride but is not affected by 4 mM NH4 or 1 mM furosemide in the bathing solution or injection of acetazolamide (0.26 mumol/ml blood).
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To characterize ivy sign on FLAIR images in Moyamoya disease and compare this finding with hemodynamic alterations on perfusion single-photon emission CT (SPECT) obtained before and after bypass surgery.
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A 14-year-old girl presented with a history of left-sided headache and acute bilateral blurred vision. She had a remote history of oral tetracycline use for the treatment of acne vulgaris, which had been discontinued for 1 month. The patient was diagnosed with drug-induced intracranial hypertension (IH) and treated with oral acetazolamide with subsequent resolution of symptoms. IH, a known rare complication of the tetracycline class of antibiotics, can also have a delayed presentation after discontinuation of the medication.
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Complete clamping of the contralateral kidney results in a rapid and significant increase in the fractional excretion of Na, K, and bicarbonate by the remaining kidney during bicarbonate loading. Similar studies were performed in dogs after administration of diuretics with different major sites of action to localize the adaptive excretory response to acute reduction in renal mass. Volume expansion was carefully avoided. In experiments with the loop inhibitor, furosemide, contralateral kidney clamping rapidly and significantly increased fractional excretion of Na and bicarbonate. A more delayed and smaller response was observed in dogs given hydrochlorothiazide. Acetazolamide, a potent inhibitor of proximal Na bicarbonate reabsorption, completely blocked the excretory response to contralateral kidney clamping. The enhanced response with furosemide and its blockade with acetazolamide indicates a proximal site of adaptation to acute contralateral kidney exclusion. The overall natriuretic response depends on the level of inhibition of loop reabsorption.
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Prospective study conducted at our hospital from June 1994 to March 1996, with 45 patients who had chronic respiratory acidosis and metabolic alkalosis. After a previous stabilization of the patient and eventually the discontinuation of diuretic or corticosteroid drugs fro 24-48 hours, 500 or 750 mg of acetazolamide were administered daily for 48 hours. Later, variations both in arterial gasometry and venous electrolytes were analyzed by comparing two means of paired data.
Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a 133Xe-clearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity.
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Twelve patients were treated with acetazolamide for IIH during pregnancy, and there were no adverse pregnancy outcomes. A critical review of the English language literature on the subject failed to demonstrate any convincing evidence for any adverse effect on pregnancy for acetazolamide.
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We searched the Cochrane Neuromuscular Disease Group Trials Register, MEDLINE (from January 1966 to July 2007), and EMBASE (from January 1980 to July 2007) and any other available international medical library sources from the University of Milan for randomised trials.
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Acetazolamide-related hypophosphatemia leading to cardiac arrest is extremely rare. Herein we report a 78-year-old female glaucoma patient who developed general weakness and acute respiratory failure, followed by cardiac arrest 1 day after taking acetazolamide. The patient was successfully weaned from the ventilator after correction of hypophosphatemia and fully recovered. As acetazolamide was shown to have the potential to cause a lethal side effect in stable glaucoma, the risk of hypophosphatemia should be kept in mind by ophthalmologists. An examination of serum metabolic panels may be indicated in patients at risk of hypophosphatemia.
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Cimetidine, a substrate of the H+/organic cation antiporter, and aminoglycoside antibiotics did not affect trientine excretion, while acetazolamide and furosemide, which increase the concentration of sodium ions in renal proximal tubules, increased the excretion of trientine. However, trichlormethiazide, which acts in renal distal tubules, did not affect trientine excretion. Acetazolamide and furosemide did not directly affect the Na+/spermine transporter because these diuretics had no effect on the uptake of spermine into the rat renal brush-border membrane vesicles.
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1. Alkaline extracellular pH transients evoked by afferent stimulation, and local pressure ejection of glutamate and gamma-aminobutyric acid (GABA), were studied in the CA1 region of rat hippocampal slices. Amino acid-evoked responses were obtained by use of a dual micromanipulator, with the tip of a double-barreled pH-sensitive microelectrode positioned 50 microns from a pressure ejection pipette. 2. At 31 degrees C, in Ringer solutions buffered with 26 mM HCO3- and 5% CO2, mean extracellular pH in submerged 300-microns slices was 7.15 +/- 0.12 (n = 27 slices), at a tissue depth of approximately 150 microns. In Ringer buffered with 35 mM HCO3- and 5% CO2, extracellular pH was 7.29 +/- 0.10 (n = 19 slices). 3. Repetitive stimulation of the Schaffer collaterals caused an extracellular alkaline shift in stratum oriens, pyramidale, and radiatum, averaging 0.05 +/- 0.03 pH units among all regions (n = 138), with a maximum response of 0.16 pH units. Alkaline transients of similar appearance were obtained by local ejection of glutamate (0.01-0.12 pH units, n = 110) and GABA (0.01-0.18 pH units, n = 137). Control ejection of these amino acids into dilute agar caused only small acid shifts. 4. Superfusion of 100 microM picrotoxin abolished the GABA-evoked alkaline shift but failed to inhibit the Schaffer collateral- and glutamate-evoked alkalinizations. 5. Superfusion of 10(-5)-10(-3) M acetazolamide acidified the baseline by 0.05-0.10 pH units and amplified the Schaffer collateral- and glutamate-evoked alkaline shifts.(ABSTRACT TRUNCATED AT 250 WORDS)
All cases were idiopathic. Ten patients had a positive familial history. Three patients suffered from ICCA syndrome. Some atypical features were seen, such as the association of kinesigenic and nonkinesigenic attacks and the presence of migraine, ataxia, seizures and myoclonus. Acetazolamide responsiveness was seen in two patients.
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