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.
diamox generic brand
We report on a 24-year old woman with bilateral FAME.
diamox pediatric dose
compared with preadministration values, the R(2)* value did not change significantly in either the cortex or medulla in the control and mannitol groups but decreased significantly in the saline group; the R(2)* value significantly decreased in the medulla but did not change significantly in the cortex in the furosemide group; and the R(2)* value significantly increased in the medulla and significantly decreased in the cortex in the acetazolamide group.
Mutations in the SLC13A5 gene that codes for the Na(+)/citrate cotransporter, NaCT, are associated with early onset epilepsy, developmental delay and tooth dysplasia in children. In the present study we identify additional SLC13A5 mutations in nine epilepsy patients from six families. To better characterize the syndrome, families with affected children answered questions about the scope of illness and treatment strategies. There are currently no effective treatments, but some anti-epileptic drugs targeting the GABA system reduce seizure frequency. Acetazolamide, a carbonic anhydrase inhibitor and atypical anti-seizure medication decreases seizures in 4 patients. In contrast to previous reports, the ketogenic diet and fasting produce worsening of symptoms. The effects of the mutations on NaCT transport function and protein expression were examined by transient transfections of COS-7 cells. There was no transport activity from any of the mutant transporters, although some of the mutant transporter proteins were present on the plasma membrane. The structural model of NaCT suggests that these mutations can affect helix packing or substrate binding. We tested various treatments, including chemical chaperones and low temperatures, but none improve transport function in the NaCT mutants. Interestingly, coexpression of NaCT and the mutants results in decreased protein expression and activity of the wild-type transporter, indicating functional interaction. In conclusion, our study has identified additional SLC13A5 mutations in patients with chronic epilepsy starting in the neonatal period, with the mutations producing inactive Na(+)/citrate transporters.
1. The contribution of Li+ reabsorption in the loop of Henle to lithium clearance (CLi) and the possible mechanism(s) involved were assessed in healthy volunteers. Four mechanisms were considered: (a) passive reabsorption in the thin ascending limb, (b) solvent drag in the thin descending limb, (c) the Na+, K+, 2Cl- transporter in the thick ascending limb and (d) paracellular movement in the thick ascending limb. 2. Since alterations in the corticomedullary osmolal concentration gradient produced by fluid restriction (500 ml day-1) and subsequent water loading (15 ml kg-1) did not affect either CLi (28.5 +/- 2.1 vs. 28.2 +/- 1.9 ml min-1) or fractional lithium clearance (FELi; 23.5 +/- 2.0 vs. 23.0 +/- 1.9%), it is unlikely that substantial Li+ reabsorption occurs in the thin limbs by either passive movement or solvent drag. 3. Increasing plasma Li+ with unchanged plasma Na+ in salt-replete volunteers was associated with only small reductions in CLi (32.8 +/- 1.3 ml min-1, P less than 0.05) and FELi (27.3 +/- 1.8 vs. 25.3 +/- 2.0%, P less than 0.05). This suggests that substantial Li+ reabsorption on the Na+, K+, 2Cl- transporter does not occur. 4. Bumetanide increased FELi in salt-depleted (LS) and salt-replete (HS) volunteers and abolished the pre-diuretic difference in FELi between salt intakes (LS, 16.6 +/- 1.5 vs. 38.7 +/- 2.3%, P less than 0.001; HS, 30.1 +/- 1.5 vs. 40.5 +/- 2.0%, P less than 0.001). Changes in CPO4 and CHCO3 were not detected. Acetazolamide produced comparable increases in FELi (LS, 16.6 +/- 1.5 vs. 38.7 +/- 2.2%, P less than 0.001; HS, 30.1 +/- 1.5 vs. 43.1 +/- 2.4%, P less than 0.01); and CPO4 and CHCO3 were increased. When tubular flow to the loop of Henle was increased by acetazolamide, the bumetanide-induced increases in FELi were reduced (LS, 38.7 +/- 2.2 vs. 48.7 +/- 2.3%, P less than 0.001; HS, 43.1 +/- 2.4 vs. 48.1 +/- 2.6%, P less than 0.001). 5. These data are consistent with the view that (a) Li+ is reabsorbed by a bumetanide-sensitive mechanism in the loop of Henle, (b) approximately 20 and 10% of the filtered load, respectively, is reabsorbed in the loop in salt-depleted and salt-replete volunteers, (c) flow-dependent, voltage-driven paracellular movement in the thick ascending limb is the likely mechanism and (d) this mechanism could account for the difference in Li+ reabsorption between low and high salt intakes.
diamox and alcohol
A 14 year-old Caucasian boy with idiopathic intracranial hypertension (IIH) presented with blurred vision in his left eye. Visual acuity was 20/20, right eye, and 20/80, left eye, and funduscopy revealed bilateral papilledema. In addition, there was peripapillary choroidal neovascular membrane (PPCNVM) in the left eye. Oral acetazolamide improved the symptoms and signs of IIH, but seven weeks later, acuity remained 20/80, left eye, with an increase in subretinal hemorrhage. Two weeks following an intravitreal injection of bevacizumab, visual acuity on the left had improved to 20/30 with resolution of subretinal hemorrhage and fibrosis of PPCNVM. After an additional 2 weeks, visual acuity improved to 20/20, and there has been no sign of recurrence over 3.5 years of follow-up.
diamox vs generic
A close correlation between hemispheric CVR and OEFR was observed. Two hemispheres from two different patients showed an increase in OEF to acetazolamide challenge despite a normal baseline OEF. The two hemispheres showing an increase in OEF in response to acetazolamide were also associated with the lowest CVR and severest white matter hyperintensities.
Carbonic anhydrase IX (CAIX) is expressed in many solid tumors in response to hypoxia and plays an important role in tumor acid-base homeostasis under these conditions. It is also constitutively expressed in the majority of renal cell carcinoma. Its functional inhibition with small molecules has recently been shown to retard tumor growth in murine models of cancer, reduce metastasis and tumor stem cell expansion. Additionally, CAIX is a promising antigen for targeted drug delivery approaches. Initially validated with anti-CAIX antibodies, the tumor-homing capacity of high-affinity small-molecule ligands of CAIX has recently been demonstrated. Indeed, conjugates formed of CAIX ligands and potent cytotoxic drugs could eradicate CAIX-expressing solid tumors in mice. These results suggest that CAIX is a promising target for the development of novel therapies for the treatment of solid tumors.
diamox generic cost
Trabeculectomy is among the first choice surgical treatments for glaucoma. Antimetabolites, especially mitomycin C, have improved the success rate. The aim of this study is to present the results of trabeculectomy with 5-fluorouracil (5-FU).
diamox drug interaction
The identification of small molecule ligands is an important first step in drug development, especially drugs that target proteins with no intrinsic activity. Toward this goal, it is important to have access to technologies that are able to measure binding affinities for a large number of potential ligands in a fast and accurate way. Because ligand binding stabilizes the protein structure in a manner dependent on concentration and binding affinity, the magnitude of the protein stabilization effect elicited by binding can be used to identify and characterize ligands. For example, the shift in protein denaturation temperature (Tm shift) has become a popular approach to identify potential ligands. However, Tm shifts cannot be readily transformed into binding affinities, and the ligand rank order obtained at denaturation temperatures (≥60°C) does not necessarily coincide with the rank order at physiological temperature. An alternative approach is the use of chemical denaturation, which can be implemented at any temperature. Chemical denaturation shifts allow accurate determination of binding affinities with a surprisingly wide dynamic range (high micromolar to sub nanomolar) and in situations where binding changes the cooperativity of the unfolding transition. In this article, we develop the basic analytical equations and provide several experimental examples.
Spinocerebellar ataxia type 6 (SCA6), episodic ataxia type 2 (EA2) and familial hemiplegic migraine (FHM) have been known as allelic disorders, which are caused by the alteration of the alpha1A voltage-dependent calcium channel subunit. Expansions of the CAG repeat in the CACNA1A gene on the short arm of the chromosome 19 induce SCA6, and point mutations in the same gene are responsible for EA2 and FHM. In recent studies, both SCA6 and EA2 have been concurrently found in families with 26 CAG repeats without previously reported point mutations either in coding sequences or in intron-exon junctions. We describe a Korean family with CAG26 repeats in the CACNA1A gene. Some of the affected family members had progressive ataxia typical of SCA6 whereas others had episodic vertigo responsive to acetazolamide typical of EA2. Our family support that SCA6 and EA2 are allelic disorders with a high phenotypic variability.
diamox drug interactions
Ballooning and procoagulant spreading of platelets are driven by fluid entry into the cells, and are important for the amplification of localized coagulation in thrombosis.
Ten nonobese, healthy elderly adults (M = 73.3 years) were monitored polygraphically during sleep for sleep state changes, breathing, and the development of cardiac arrhythmias. All participated in 2 baseline nights and 1 night of flurazepam 30 mg ingestion; six underwent 1 night of sleep deprivation; four received ethyl alcohol (.6 mg/kg); and four whose apnea worsened significantly with flurazepam 30 mg were pretreated for 3 days with acetazolamide, taking acetazolamide and flurazepam 30 mg on the fourth night. Elderly adults with an Apnea Index (the number of apneas per sleep hour) between 5 and 7 at baseline experienced a worsening of their apnea with each manipulation. Acetazolamide did not protect individuals whose Apnea Index increased after flurazepam ingestion. One person developed premature ventricular contractions in conjunction with an increased Apnea Index after each manipulation.
diamox 25 mg
A 16-year-old patient with multiple sclerosis (MS) showed paroxysmal movement disorders during a recurrence of the disease. The paroxysms took the form ot brief unilateral dystonic posturings of the right body suggestive of paroxysmal dystonia (PD); they completely receded with acetazolamide. A single episode of a high amplitude, rythmic slow and coarse generalized tremor, present at rest and increasing with movement, particularly involving the head in a no-no movement, occurred soon after recovery from PD and lasted three hours. The present report provides evidence that MS has to be considered in the diagnostic approach to symptomatic childhood PD and underlines the efficacy of acetazolamide in the treatment of PD attacks. It also describes a rare paroxysmal movement disorder, defined as paroxysmal dystonic tremor, that can be considered as falling within the spectrum of PD.
diamox dose glaucoma
The intracellular Cl concentration ([Cl]i) in rat cardiac ventricular muscle, measured with double-barreled microelectrodes in vitro, was 21.3 +/- 1.5 (SD) mM [number of observations (n) = 46]. With the Na-K-Cl cotransport inhibitor bumetanide (10 microM), it fell to 13.4 +/- 1.4 mM (n = 27), and with 1 mM acetazolamide, it fell further, to 7.2 +/- 1.5 mM (n = 5), close to equilibrium with the membrane potential. In the absence of Na, [Cl]i was 15.9 +/- 1.4 mM (n = 8), and with 1 mM acetazolamide, it fell to 6.5 +/- 0.6 mM (n = 4), again close to equilibrium. The bumetanide- and Na-insensitive components of inward Cl pumping were inhibited by chlorothiazide and ethacrynic acid but were unaffected by the Na-Cl cotransport inhibitor metolazone. There was inhibition of Na-K-Cl cotransport by chlorothiazide = acetazolamide > metolazone. The anion exchange inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and HCO3 had no effect on [Cl]i in any condition. Thus Cl accumulation in the rat ventricle is fully accounted for by two systems, namely, Na-K-Cl cotransport and an Na-independent, possibly primary active, process.
Our previous studies demonstrated that thrombin is an important factor in brain injury after intracerebral and intraventricular hemorrhage. This study examined the effect of acetazolamide, a carbonic anhydrase inhibitor, on thrombin-induced hydrocephalus. There were two parts in this study. First, rats had an injection of either 50 μl saline or 3 U thrombin into the right lateral ventricle. Second, rats had an injection of 3 U thrombin into the right lateral ventricle and were treated with either vehicle or acetazolamide (30 mg/kg, intraperitoneally (IP)) at 1 h after thrombin infusion. Lateral ventricle volumes were measured in magnetic resonance imaging T2 images and the brains were used for histology analysis at 24 h later. Intraventricular injection of thrombin induced significantly larger ventricle volume (27.8 ± 3.7 vs 8.5 ± 1.3 mm(3), n = 6, p < 0.01) and more ventricular wall damage (the breakdown of the ependymal layer, 20.2 ± 3.1 vs 2.4 ± 0.8 %, n = 6, p < 0.01) compared with saline injection. Acetazolamide treatment (30 mg/kg, IP) markedly attenuated thrombin-induced hydrocephalus (16.1 ± 4.2 mm(3) vs 29.5 ± 5.3 mm(3), n = 6, p < 0.01). These results suggest decreasing CSF production by acetazolamide attenuated thrombin-induced hydrocephalus in rats.
Prospective, double blind, randomised, placebo controlled trial.
diamox cost uk
Because of the similarity in clinical presentation of CVST and IIH, it is important to differentiate distinguishing characteristics of these diseases for correct diagnosis and prompt treatment.
acetazolamide diamox medication
Both surface pH (pHs) and intracellular pH (pHi) were measured using single- and double-barreled pH-sensitive microelectrodes in isolated sheep cardiac Purkinje strands, rabbit and cat papillary muscle, and mouse and rat soleus muscle. Superfusion of the preparations with a relatively low buffered solution (containing 5 mM HEPES buffered to control pH) causes surface acidosis that correlates with efflux of metabolically produced acids in the unstirred layer of fluid surrounding the tissue. Acidification of the surface layer induces a slower acid change of pHi and depresses the rate of proton extrusion following an imposed intracellular acid load. In cardiac preparations, the lowering of pHi correlates with depression of twitch tension. Transient changes of pHs and pHi are seen when a weak acid or base is suddenly added to, or removed from the superfusion solution. Indirect evidence of the presence of carbonic anhydrase in the extracellular surface layer is obtained from analysis of transient pHs changes in presence and absence of acetazolamide.
diamox dosage pediatrics
The anticancer drug cisplatin has been known to produce severe renal lesions characterized by high levels of blood urea nitrogen (BUN), toxic nephrosis, and platinum (Pt) retention in the kidney. The effect of IV pretreatment with acetazolamide (ACZ) 30 min before or mannitol (MAN) immediately prior to IP administration of 5 mg/kg cisplatin on Pt excretion, tissue distribution, and nephrotoxicity was investigated in male F344 rats. ACZ pretreatment reduced the cisplatin-induced nephrotoxicity, as indicated by only a slight elevation of BUN, a milder histopathologic lesion, and a more rapid recovery of renal function and structure. Although MAN-pretreated animals exhibited similar changes in BUN to ACZ-pretreated animals, the renal damage was similar to that seen in animals treated with cisplatin alone. A reduction of kidney Pt content was observed with both diuretics, although there was significantly less retention after ACZ pretreatment. The diuretic ACZ was more effective than MAN in reducing the renal lesions induced by cisplatin and it might be clinically useful in preventing cisplatin nephrotoxicity.
Carbonic anhydrase activity in mucosa of the sheep rumen wall was completely inhibited by acetazolamide and ethoxyzolamide. This inhibition significantly reduced ammonia flux across mucosal discs in vitro but was ineffective if short-chain fatty acids were present in the bathing solution. The findings are discussed in relation to the mechanism of ruminal ammonia absorption.
diamox with alcohol
Carotid balloon test occlusion (BTO) is used to assess the collateral circulation and cerebrovascular reserve in patients in whom carotid artery occlusion is contemplated. Eight patients in whom the test was successful were evaluated with perfusion computed tomography (CT) in the resting state and after acetazolamide challenge. Three of the patients showed symmetric blood flow and normal response to acetazolamide. One of them underwent permanent carotid occlusion and did not develop any delayed ischemic stroke. The remaining five patients showed asymmetric blood flow. One of them had markedly low blood flow and abnormal response to acetazolamide. The patient developed ipsilateral hemispheric stroke following permanent carotid occlusion after the superficial temporal artery to middle cerebral artery bypass graft occluded. In the other four patients, the steal phenomenon was seen in ipsilateral and contralateral hemispheres. Although definitive quantitative values for perfusion CT are not yet standardized, it may be feasible to predict that the patients with symmetric blood flow and normal acetazolamide-enhanced challenge test results will do well after permanent carotid occlusion. Patients with asymmetric blood flow and abnormal response to the acetazolamide challenge test may require a revascularization procedure to protect them from delayed ischemic stroke.
|Target Point||Shipping Method||Tracking||Delivery Time||Price|
|Not trackable||14-21 business days||USD 20.00 per order|
|Trackable, where available||5-9 business days||USD 30.00 per order|
Delivery time is:
no signature is required on delivery.
EMS - 5-9 business days, prices - USD 30.00, signature is required on delivery.
Your order will be packed safe and secure and dispatched within 24 hours.
This is exactly how your parcel will look like (pictures of a real shipping item). It has a look of a regular private letter and does not disclose its contents. Size - 9.4x4.3x0.3 inches (24x11x0.7cm).