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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High altitude headache (HAH) is the most common neurological complaint at altitude and the defining component of acute mountain sickness (AMS). However, there is a paucity of literature concerning its prevention. Toward this end, we initiated a prospective, double-blind, randomized, placebo-controlled trial in the Nepal Himalaya designed to compare the effectiveness of ibuprofen and acetazolamide for the prevention of HAH.
The authors sought to determine risk for stroke in individuals with symptomatic carotid stenosis or occlusion based upon an assessment of cerebral blood flow (CBF) reserves. Vascular reserve was assessed by two consecutive xenon/computerized tomography (Xe/CT) CBF studies with intravenous acetazolamide introduced 20 minutes prior to the second study. Patients were assigned to one of two vasoreactivity groups. Group 2 included individuals who experienced a CBF reduction of more than 5% in at least one vascular territory and had a baseline flow of 45 cc/100 gm/min or less. Group 1 included all other individuals. Any territory with volume loss on CT of more than 50% was eliminated from analysis. Sixty-eight individuals were followed at 6-month intervals for a mean of 24 months. In Group 1 two strokes were observed contralateral to the side with lowest reserve, for a stroke incidence of 4.4%; in Group 2 eight strokes were observed ipsilateral to the side with lowest reserve, for a stroke incidence of 36%. The latter group had a 12.6 times greater chance of stroke (p = 0.0007). History of stroke, history of transient ischemic attacks, baseline CBF, and degree of stenosis were not associated with an increased stroke rate. In this study, significantly compromised vascular reserves accompanied by relatively low initial flow identified individuals who subsequently demonstrated a significantly increased rate of ipsilateral stroke.
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Level II, moderate degree of clinical certainty. Recommendation Concerning Surgical Temporizing Measures: II. The evidence demonstrates that VSG shunts reduce the need for daily CSF aspiration compared with VADs.
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Although dual PLD methods may not be a completely alternative test for (123)I-iodoamphetamine single-photon emission computed tomography with acetazolamide loading, it is a feasible, simple, noninvasive, and repeatable technique for assessing CVR, even when employed in a routine clinical setting.
A series of experiments were performed to demonstrate the presence of and characterize the Na-H exchanger on rabbit ileal brush border with a vesicle preparation. An outwardly directed proton gradient (pH 5.5 inside, pH 7.5 outside) stimulated Na uptake, and a fourfold "overshoot" was observed. Conversely, an inwardly directed proton gradient (pH 7.5 inside, pH 5.5 outside) inhibited Na uptake. This stimulation/inhibition of Na uptake could not be accounted for by a proton diffusion potential, because Na uptake was found to be potential insensitive. Amiloride and harmaline inhibited pH-stimulated Na uptake, but other transport inhibitors (acetazolamide, DIDS, SITS, furosemide, and bumetanide) had no effect. Amiloride also inhibited Na efflux in the presence and absence of a pH gradient. Proton gradient-stimulated Na uptake was saturable with a Km of 16.2 mM and a Vmax of 129 nmol X min-1 X mg protein-1. Tetramethylammonium did not affect pH-stimulated Na uptake, but other cations tested inhibited Na uptake, with NH4+ and Li+ causing greater inhibition than K+ or Cs+. Using the fluorescent probe acridine orange, an inwardly directed Na gradient was shown to stimulate proton efflux from the vesicles and an outwardly directed Na gradient stimulated proton influx.
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This study was designed to test the hypothesis that the antikaliuresis caused by trimethoprim could be diminished by alkalinizing the luminal fluid in the CCD, thereby converting trimethoprim from its cationic, active form to an electroneutral, inactive, form. Trimethoprim-induced inhibition of transepithelial Na+ transport was examined in A6 distal nephron cells by analysis of short circuit current. The voltage-dependence of the trimethoprim-induced block of Na+ channels was examined with patch clamp recordings of A6 cells. The antikaliuretic effect of trimethoprim was examined in vivo in rats pretreated with deoxycorticosterone and with NH4Cl to lower urine pH, and in rats also receiving acetazolamide to raise urine pH. We found that the concentration of trimethoprim required to inhibit the amiloride sensitive component of short circuit current by 50% (IC50) was 340 microM (at pH 8.2) and 50 microM (at pH 6.3). The IC50S of protonated trimethoprim were similar (34 microM at pH 8.2 and 45 microM at pH 6.3). The mean time open for the high selectivity, Na+ channel was reduced from 1679 +/- 387 msec to 502 +/- 98 msec with addition of 10-5 M trimethoprim to patch pipette solution at the resting membrane potential (-Vpipette = 0 mV). further decreases in mean time open were observed as -Vpipette was reduced (that is, apical membrane hyperpolarization) to -40 mV (mean time open = 217 +/- 85 msec) and to -80 mV (mean time open = 69 +/- 13 msec). In vivo, trimethoprim caused a > 50% reduction in potassium (K+) excretion due primarily to a fall in the [K+] in the lumen of the terminal CCD. This effect of trimethoprim was markedly attenuated in an alkaline urine induced by acetazolamide. We conclude that it is the charged, protonated species of trimethoprim which blocks epithelial Na+ channels. Increasing urinary pH decreases the concentration of the charged species of trimethoprim and minimizes its antikaliuretic effect.
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We performed a randomized, double-blind, controlled study to investigate the effect of a 3-month course of 300 mg allopurinol once daily vs. placebo on CVR in individuals with recent (within 6 months) subcortical stroke. Participants were randomized on a 1:1 basis. CVR was defined as the percentage change in middle cerebral artery flow velocity following an intravenous injection of 15 mg kg(-1) of acetazolamide. Our primary end-point was the CVR difference between baseline and 3 months. Secondary end-points included measures of peripheral vascular reactivity and blood markers of inflammation and endothelial activation.
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Multicenter, randomized, controlled, double-blind study, with COPD or OHS patients with MV < 72 h and initial bicarbonate >28 mmol/L and pH > 7.35. Test-treatment, ACTZ 500 mg or placebo, was daily administered if pH > 7.35 and bicarbonate >26 mmol/L. Clinical, respiratory and laboratory parameters were recorded.
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Previous studies have shown that patients at high risk for stroke can be identified with quantitative CBF methods. This study shows that the important subgroup cannot be accurately defined with qualitative methodology. The implications of using the more reliable methodology are important for individual patient management and for designing clinical trials.
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Candida albicans was the most common fungus responsible for mycotic keratitis in our series from a northern climate, as opposed to southern climates where other fungi were more common. Pimaricin was effective in our patients with Candida infections and in one patient with Aspergillus infection that had been unresponsive to previous amphotericin B.
Highland population (HA) from the Andes, living above 3000 m, have a blunted ventilatory response to increasing hypoxia, breathe less compared to acclimatized newcomers, but more, compared to sea-level natives at sea level. Subjects with chronic mountain sickness (CMS) breathe like sea-level natives and have excessive erythrocytosis (EE). The respiratory stimulation that arises through the peripheral chemoreflex is modestly less in the CMS group when compared with the HA group at the same P(ET(O2)). With regard to CO(2) sensitivity, CMS subjects seem to have reset their central CO(2) chemoreceptors to operate around the sea-level resting P(ET(CO2)). Acetazolamide, an acidifying drug that increases the chemosensitivity of regions in the brain stem that contain CO(2)/H(+) sensitive neurons, partially reverses this phenomenon, thus, providing CMS subjects with the possibility to have high CO(2) changes, despite small changes in ventilation. However, the same type of adjustments of the breathing pattern established for Andeans has not been found necessarily in Asian humans and/or domestic animals nor in the various high altitude species studied. The differing time frames of exposure to hypoxia among the populations, as well as the reversibility of the different components of the respiratory process at sea level, provide key concepts concerning the importance of time at high altitude in the evolution of an appropriate breathing pattern.
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A gas chromatography-mass spectrometry (GC-MS)-based screening procedure was developed for the detection of diuretics, uricosurics, and/or their metabolites in human urine after extractive methylation. Phase-transfer catalyst remaining in the organic phase was removed by solid-phase extraction on a diol phase. The compounds were separated by GC and identified by MS in the full-scan mode. The possible presence of the following drugs and/or their metabolites could be indicated using mass chromatography with the given ions: m/z 267, 352, 353, 355, 386, and 392 for thiazide diuretics bemetizide, bendroflumethiazide, butizide, chlorothiazide, cyclopenthiazide, cyclothiazide, hydrochlorothiazide, metolazone, polythiazide, and for canrenoic acid and spironolactone; m/z 77, 81, 181, 261, 270, 295, 406, and 438 for loop diuretics bumetanide, ethacrynic acid, furosemide, piretanide, torasemide, as well as the uricosurics benzbromarone, probenecid, and sulfinpyrazone; m/z 84, 85, 111, 112, 135, 161, 249, 253, 289, and 363 for the other diuretics acetazolamide, carzenide, chlorthalidone, clopamide, diclofenamide, etozoline, indapamide, mefruside, tienilic acid, and xipamide. The identity of positive signals in such mass chromatograms was confirmed by comparison of the peaks underlying full mass spectra with reference spectra. This method allowed the detection of the abovementioned drugs and/or their metabolites in human urine samples, except torasemide. The limits of detection ranged from 0.001 to 5 mg/L in the full-scan mode. Recoveries of selected diuretics and uricosurics, representing the different chemical classes, ranged from 46% to 99% with coefficients of variation of less than 21%. After ingestion of the lowest therapeutic doses, furosemide was detectable in urine samples for 67 hours, hydrochlorothiazide for 48 hours, and spironolactone for 52 hours (via its target analyte canrenone). The procedure described here is part of a systematic toxicological analysis procedure for acidic drugs and poisons.
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A 43-year-old man had been suffering from exertional headache for 10 years. Sagittal sections on magnetic resonance imaging showed a Chiari type 1 malformation and a cerebellar arachnoid cyst. This syndrome, named hindbrain hernia headache, disappeared with oral acetazolamide. This treatment should be tried in patients with hindbrain hernia headache prior to considering surgical decompression of the foramen magnum.
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The visual prognosis is generally better for this age group compared to adults and no risk factors for visual sequelae were identified. A standardized protocol for management of IIH was proposed.
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We report on the feasibility of hemodynamic monitoring during occlusive neuro-endovascular procedures. The cerebrovascular reserve capacity as assessed by transcranial Doppler sonography was chosen as the hemodynamic parameter. A standardized stimulation of cerebral blood flow was achieved by a bolus injection of 100 mg acetazolamide (Diamox) i.v. Ten minutes after injection, the middle cerebral artery blood flow velocity of 54 arteries in 33 normal persons increased by 41% +/- 17.5 (mean +/- standard deviation). The lower threshold value was therefore set to 6% increase (mean minus 2 standard deviations). An application in a case of endovascular test- and permanent occlusion of an internal carotid artery is described.
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To describe the prognosis and the neurosonological features in a series of patients with BCAO.
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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.
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MCT1-4 expression of rabbit endothelium was examined by Western blotting and immunofluorescence staining. Lactate-induced acidification (LIA) was measured in perfused CE in the presence and absence of HCO₃⁻ and acetazolamide (ACTZ) using tissue treated with siRNA specific to MCT1, 2, and 4. Corneal thickness and lactate concentration were measured in New Zealand White rabbits treated with the topical CA inhibitor Azopt, and from eyes that were injected intracamerally with ouabain, disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS), and shRNA specific to the 1Na⁺:2HCO₃⁻ cotransporter NBCe1.
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In the treatment of CRAO, an aggressive systematic regimen including medical and mechanical means may reestablish retinal circulation and improve visual outcome. The cause of arterial occlusion, the nature of occlusive emboli, and the duration of retinal ischemia may determine the visual outcome, but a larger series is warranted to verify the effectiveness of the treatment and the prognostic factors.
A 21-year-old male presented with severe throbbing headache, nausea, vomiting and progressive visual loss. Clinical examination revealed bilateral papilledema and left abducens nerve palsy. MRI showed findings consistent with dural sinus thrombosis. Combinging the clinical findings, MRI and a positive pathergy test, the patient was diagnosed with dural sinus thrombosis associated with Behçet's disease (BD). Despite acetazolamide, prednisone, azathioprine and repeated lumbar punctures, his signs and symptoms of intracranial hypertension gradually worsened. Therefore, lumboperitoneal shunting was planned after which rapid resolution of intracranial hypertension was observed. After reviewing similar reports, we suggest that lumboperitoneal shunt placement can be an effective treatment for patients with BD with medically refractory intracranial hypertension associated with dural sinus thrombosis.
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Linear regression analyses revealed highly significant correlations (P < .001) between CBV (r, 0.98; slope, 0.96), CBF (r, 0.89; slope, 0.87), and MTT (r, 0.80; slope, 0.76) values calculated with the ICA and the noncarotid inputs. The CT-derived patient data correlated well with ancillary clinical and neuroradiologic findings.
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Systemic juvenile idiopathic arthritis (SJIA) is one of the most severe forms of arthritis that affects children younger than 16 years of age at onset. SJIA often requires corticosteroids to control the inflammation. However, long-term corticosteroid use may have adverse effects, including intracranial hypertension (IH). Biologic therapies have been used as corticosteroid sparing agents. We report the first case of a child with steroid-dependent SJIA treated with tocilizumab, an IL-6 receptor monoclonal antibody, who developed fulminant IH, bilateral papilloedema and vision loss when oral prednisone was weaned from 2 to 1 mg per day. Despite repeated lumbar punctures and high dose acetazolamide, he required urgent unilateral optic nerve sheath fenestration (ONSF). This endoscopic surgical intervention released the pressure exerted by the cerebrospinal fluid on the optic nerve and stopped the progression of vision loss. Nine weeks after the diagnosis of bilateral papilloedema, his vision was completely restored in one eye and partially recovered in the contralateral one. Long-term treatment with corticosteroids even at very low dose and tocilizumab may predispose to severe IH, papilloedema and vision loss. The role that tocilizumab might have played in this case in unclear. Early recognition and prompt treatment of papilloedema is crucial in avoiding permanent vision loss. Fulminant papilloedema in an immunocompromised child carries additional significant challenges. Early ONSF is a safe and effective intervention in refractory papilloedema. Children with severe papilledema secondary to IH should be managed by a multidisciplinary team in tertiary centres.
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