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How Does Acetazolamide Cause Metabolic Acidosis

Acetazolamide For Metabolic Alkalosis In Ventilated Patients

Acetazolamide For Metabolic Alkalosis In Ventilated Patients

Topf , Acetazolamide , AcidBase , Electrolytes Patients in the ICU with pulmonary disease primarily have respiratory acidosis and/or metabolic alkalosis. The respiratory acidosis is due to the primary disease and the metabolic alkalosis is due to our attempts to manage that disease, in this case with diuretics. Compensation for metabolic alkalosis is suppression of respiration to allow the carbon dioxide to accumulate reducing the change in pH. Suppressing respiration is obviously a concern in patients on the vent. One option in this situation is to treat the metabolic alkalosis. Although I have read about giving hydrochloric acid infusions, that is a bit nuts. The conventional choice is to cause a drug induce proximal (Type 2) RTA with acetazolamide. The proximal tubule reabsorbs the vast majority of filtered bicarbonate, but it does it through a complex process, where bicarbonate is metabolized to CO2 and water (catalyzed by carbonic anhydrase). The carbon dioxide diffuses into the proximal tubule cell where bicarbonate is reconstituted (again catalyzed by carbonic anhydrase) and then secreted into the circulation. So bicarbonate is destroyed in the tubules and reformed in the tubule cells. Carbonic anhydrase inhibitors slow this and cause the patient to pee bicarbonate. The loss of bicarbonate causes metabolic acidosis, or alternatively, improvement in pre-existing metabolic alkalosis. The carbonic anhydrase inhibitor of choice is acetazolamide. Other carbonic anhydrase inhibitors include Methazolamide,Dorzolamide,Brinzolamide,Topiramate. The pomegranate contains natural carbonic anhydrase activity. This is a nice theory but in February JAMA published a clinical trial to provide empiric data for this time honored strategy. This is a multi center, double-blind, paral Continue reading >>

Acetazolamide Side Effects

Acetazolamide Side Effects

Applies to acetazolamide : oral capsules, oral tablets, parenteral powder for injection Paresthesias, hearing dysfunction or tinnitus , anorexia, altered taste, nausea , vomiting , diarrhea , polyuria, drowsiness, confusion. Applies to acetazolamide: compounding powder, injectable powder for injection, intravenous powder for injection, oral capsule extended release, oral tablet Adverse reactions occurring early in therapy have included paresthesias, tinnitus, nausea, vomiting, diarrhea, and drowsiness.[ Ref ] Frequency not reported: Anaphylactic/anaphylactoid reactions including shock and fatalities[ Ref ] Frequency not reported: Blood dyscrasias such as aplastic anemia , agranulocytosis, leucopenia, thrombocytopenia , and thrombocytopenia purpura[ Ref ] Frequency not reported: Loss of appetite, electrolyte disturbances, metabolic acidosis and hypokalemia with long term therapy, hyponatremia osteomalacia with long-term therapy, hyper/ hypoglycemia [ Ref ] Frequency not reported: Skin reactions, Stevens-Johnson syndrome, toxic epidermal necrolysis , urticaria , rash including erythema multiforme[ Ref ] Frequency not reported: Nausea, vomiting, diarrhea, melena[ Ref ] Frequency not reported: Abnormal liver function, cholestatic jaundice , fulminant hepatic necrosis, hepatitis[ Ref ] Very common (10% or more): Paresthesias (up to 20%) Frequency not reported: Drowsiness, headache , dizziness , taste alteration, ataxia, flaccid paralysis, convulsions, sensory disturbances[ Ref ] Frequency not reported: Confusion, irritability, depression , excitement, reduced libido[ Ref ] Frequency not reported: Transient myopia[ Ref ] Frequency not reported: Renal colic , increased risk of nephrolithiasis , renal failure[ Ref ] Frequency not reported: Polyuria, polydipsia, crystalluria, r Continue reading >>

Acetazolamide: Mechanism Of Action

Acetazolamide: Mechanism Of Action

Home / ABA Keyword Categories / A / Acetazolamide: mechanism of action Acetazolamide is a reversible inhibitor of the carbonic anhydrase enzyme that results in reduction of hydrogen ion secretion at the renal tubule and an increased renal excretion of sodium, potassium, bicarbonate, and water. It can be used as a diuretic or to treat glaucoma as it prevents excessive build up of aqueous humor. It also inhibits carbonic anhydrase in the central nervous system to minimize abnormal and excessive discharge from CNS neurons. Acetazolamide can be administered to patients with a metabolic alkalosis to promote retention of hydrogen ions at the level of the renal tubule. Mechanism of action: for the reduction of Intraocular pressure Acetazolamide inactivates carbonic anhydrase and interferes with the sodium pump, which decreases aqueous humor formation and thus lowers IOP. Systemic effects however include increased renal loss of sodium, potassium, and water secondary to the drugs renal tubular effects. Arterial Blood gases may show a mild hyperchloremic metabolic acidosis. Continue reading >>

Diuretic_pharm [tusom | Pharmwiki]

Diuretic_pharm [tusom | Pharmwiki]

Diuretics are among the most commonly prescribed drugs, and play an important role in the treatment of heart failure and hypertension. They exert most of their therapeutic effects through inhibiting the reabsorption of sodium at different sites along the nephron of the kidney. Diminished reabsorption of sodium results in increased urinary loss of both sodium and water, leading to a reduction in plasma volume, and a reduction of blood pressure. Thiazide diuretics also exert an additional vasodilator effect on arterial smooth muscle by a still poorly understood mechanism. Figure 1. Overview of the transport systems in the renal nephron, and major sites of action of diuretics. ADH: antidiuretic hormone; ENaC: epithelial Na channel. Acetazolamide is the most commonly used carbonic anhydrase inhibitor (taken systemically) that affects the kidney. Figure 2. Mechanism of action of carbonic anhydrase inhibitor diuretics. Bicarbonate absorption by the proximal tubule is dependent on the activity of carbonic anhydrase (CA) which converts bicarbonate (HCO3-) to CO2 and H2O. CO2 rapidly diffuses across the cell membrane of proximal tubule cells where it is rehydrated back to H2CO3 by carbonic anhydrase. H2CO3 dissociates to HCO3- and H+ which are transported out of the cell on the basolateral side by different transporters. Bicarbonate absorption is therefore dependent on the activity of carbonic anhydrase. Inhibition of carbonic anhydrase by acetazolamide results in an increased urinary loss of bicarbonate. This also interferes with the reabsorption of Na and Cl. The basolateral Na/K ATPase (found in most epithelial cells lining the nephron) maintains a low intracellular Na concentration, which is necessary for reabsorption of Na, and in the proximatl tubule also facilitates the Continue reading >>

Carbonic Anhydrase Inhibitor

Carbonic Anhydrase Inhibitor

Carbonic anhydrase inhibitors are a class of pharmaceuticals that suppress the activity of carbonic anhydrase . Their clinical use has been established as anti- glaucoma agents, diuretics , antiepileptics , in the management of mountain sickness , gastric and duodenal ulcers , idiopathic intracranial hypertension , neurological disorders , or osteoporosis . [1] [2] [3] Carbonic anhydrase inhibitors are primarily used for the treatment of glaucoma. They may also be used to treat seizure disorder and acute mountain sickness . Because they encourage solubilization and excretion of uric acid, they can be used in the treatment of gout. [4] Acetazolamide is an inhibitor of carbonic anhydrase . It is used for glaucoma, epilepsy (rarely), idiopathic intracranial hypertension , and altitude sickness . For the reduction of intraocular pressure (IOP), acetazolamide inactivates carbonic anhydrase and interferes with the sodium pump, which decreases aqueous humor formation and thus lowers IOP. Systemic effects include increased loss of sodium, potassium, and water in the urine, secondary to the drugs effects on the renal tubules , where valuable components of filtered blood are re-absorbed in the kidney. Arterial Blood gases may show a mild hyperchloremic metabolic acidosis . [5] Methazolamide is also a carbonic anhydrase inhibitor. It has a longer elimination half-life than acetazolamide and is less associated with adverse effects to the kidney . [6] [7] [8] Dorzolamide is a sulfonamide and topical carbonic anhydrase II inhibitor. It is indicated for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension and who are insufficiently responsive to beta-blockers . Inhibition of carbonic anhydrase II in the ciliary processes of the ey Continue reading >>

3ddesign Bmw F30 328i N20b20a , 3ddesign

3ddesign Bmw F30 328i N20b20a , 3ddesign

3DDesign BMW F30 328i N20B20A , 3DDesign [3DDesign]BMW F30 328i(N20B20A), 3DDesign SWAGE-LINE 30mm 250SB, 250SB SWAGE-LINE CARB531GOODRIDGE Z2, Z2 GOODRIDGE 20671350 :ET-1057 H24/5H28/12 5 , ELEVEN FY 187.0J 53 114.3-5 3HSMC, DR17V AT 2015.03, AWESOME317 VRX-2 155 55R14 4 14 4 155 55R14 1993 YFM400 Kodiak ATV Carburetor Repair (), 1993 YFM400 Kodiak ATV Carburetor Repair () SWAGE-LINE 100mm GSX-R750, GSX-R750 SWAGE-LINE PARB402TOYO OBSERVE GARIT GIZ 215/55R17 ( ) 1, 1TOYO OBSERVE GARIT GIZ 215/55R17 P24055C 733-0634 () 2X4 55mm, sw :ET-0296 H18/6H20/12 8 , ELEVEN TM Ignite REV DY5W DY5R :ED-0689 H20/8H24/3 4 , ELEVEN Brembo AUDI Q5 8RCTVF 12/11 P85 099S , T.M. Designworks Dirt Polifibar Rear Guide - RCG-SRM-YL (), T.M. Designworks Dirt Polifibar Rear Guide - RCG-SRM-YL ()FUJITSUBO/ AUTHORIZE S DAA-AVV50 H26.09 360-24461, FUJITSUBO/ AUTHORIZE S DAA-AVV50 H26.09 360-24461 [H20.05H28.08] 3, [H20.05H28.08] Fit CVT MT GK 12 2 19:00 12 7 1:59 MPVH11.06H15.10LW#W 02P05Nov16, CAN AM DOO DECAL-WINDSCREEN GENUINE OEM 204901373 (), CAN AM DOO DECAL-WINDSCREEN GENUINE OEM 204901373 ()CMS KNUCKLERH, CMS 391860004[3DDesign]BMW F11 528i(N20B20A), SSR Professor MS1R 7.0J-16 1, SSR & H22A H27A Microlon 32oz946cc, Microlon Continue reading >>

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis and Acetazolamide This form of renal tubular acidosis decreases the strong ion difference by interfering with bicarbonate resorption in the proximal tubule; the mechanism is analogous to the action of acetazolamide. Bicarbonate handling in the proximal tubule Behold, the familiar activity of carbonic anhydrase in the proximal tubule. Carbonic anhydrase converts the filtered bicarbonate into easily resorbed CO2, and then traps it again inside the cell. The filtered bicarbonate is essentialy completely reabsorbed. The concentration of chloride in the tubule is therefore expected to increase- if the bicarbonate has been reabsorbed, more chloride must remain in the tubule to maintain electroneutrality. However, the failure of carbonic anhydrase results in bicarbonate remaining trapped in the urine. This, of course, means that electroneutrality of the tubule is maintained without the excretion of any further chloride. Thus, the chloride which would otherwise be excreted, is retained. There is an excellent article which discusses the mechanisms of chloride retention in acetazolamide-intoxicated patients with metabolic alkalosis. Particularly, it contains a graph of urinary strong ion diference over time, after the administration of 500mg of acetazolamide. It looks a little like this : Causes of proximal renal tubular acidosis Isolated congenital Type 2 RTA is very rare, and would likely form a part of of a syndrome , being associated with a series of other tubular defects, or forming a part of a whole-proximal-tubule problem like Fanconi syndrome. Anong the elderly, a new onset of Type 2 RTA without any new medication changes can be due to a monoclonal gammopathy , where ligh chains selectively damage the proximal tubule. Similarly, amyloidosis Continue reading >>

Use Of Acetazolamide In Copd Patients

Use Of Acetazolamide In Copd Patients

I'm a doctor in Ho Chi Minh City, Vietnam. In my department (Pulmonology), some doctors prescribe acetazolamide for the patients with COPD who have edema and chronic respiratory failure. What is the role of acetazolamide in these patients? Response from Christine Campbell Reardon, MD Some patients with chronic obstructive pulmonary disease (COPD) develop carbon dioxide (CO2) retention and hypoxemia. There are multiple factors that lead to the development of CO2 retention. One of the major factors is an alteration of ventilation and perfusion matching leading to an increase in dead space. The diaphragm may function at an anatomical disadvantage in patients with COPD. In the setting of hyperinflation caused by airflow obstruction, the diaphragm is flattened and generates less pressure than what would occur under normal circumstances. In addition, hypercapnic patients demonstrate a breathing pattern characterized by a lower tidal volume and higher respiratory rate, which increases dead space. The lower tidal volume is caused by a shorter inspiratory time rather than a decrease in respiratory drive. It had previously been thought that hypercapnic COPD patients had a blunted central respiratory drive and this was the major cause of CO2 retention. From this idea, the use of carbonic anhydrase inhibitors -- such as acetazolamide for hypercapnic COPD patients -- developed. Reversible inhibition of carbonic anhydrase results in the reduction of hydrogen ion secretion at the renal tubule and an increased renal secretion of sodium, potassium, bicarbonate, and water. Acetazolamide will block the conversion of CO2 into bicarbonate, which will acutely increase the levels of carbon dioxide in the tissues and blood. The induction of a metabolic acidosis by acetazolamide will increase Continue reading >>

Carbonic Anhydrase Inhibitor

Carbonic Anhydrase Inhibitor

Acetazolamide, the prototype Carbonic Anhydrase Inhibitors, inhibits carbonic anhydrase and in doing so reduces renal bicarbonate resorption in the proximal tubule. This leads to a direct increase in urinary bicarbonate excretion and secondarily to mild increases in sodium and potassium excretion. Because of its mild effects on electrolytes acetazolamide is a largely safe drug with few adverse side effects but in consequence is rarely used for its diuretic capacity. The pharmacological effects of acetazolamide are due to its inhibitory effect on carbonic anhydrase in the proximal tubule. As discussed in Renal Bicarbonate Excretion , luminal and intracellular pools of carbonic anhydrase in the proximal tubule are critical for resorbing filtered bicarbonate and thus administration of acetazolamide results in significant increases in renal bicarbonate excretion. Because bicarbonate acts as a weak base this can lead to significant increases in urinary pH. Additionally, because bicarbonate is the primary weak base of the bicarbonate buffer , its wasting leads to a non-gap metabolic acidosis . As discussed in renal bicarbonate excretion , bicarbonate resorption utilizes a luminal Na-H+ antiporter and in consequence the net process of bicarbonate resorption is linked to sodium resorption. Given this linkage between bicarbonate and sodium resorption, acetazolamide yields significant reductions in proximal tubule sodium resorption. However, the vast majority of this sodium is resorbed by later parts of the nephron and thus urinary sodium excretion is increased only mildly. The increased distal nephron sodium delivery caused by acetazolamide results in increased potassium secretion and thus carbonic anhydrase inhibitors typically result in moderate increases of urinary potassium Continue reading >>

Treatment Of Metabolic Alkalosis

Treatment Of Metabolic Alkalosis

INTRODUCTION Metabolic alkalosis is characterized by a primary rise in the plasma bicarbonate concentration, which leads to an increase in arterial pH. Two factors are required for the genesis and then maintenance of metabolic alkalosis: a process that raises the plasma bicarbonate concentration and a process that prevents excretion of the excess bicarbonate in the urine [1,2]. Treatment of metabolic alkalosis should be aimed at reversing these two factors. This topic will provide a brief overview of the pathogenesis of metabolic alkalosis followed by a discussion of how to treat affected patients. The pathogenesis of metabolic alkalosis is reviewed in more detail elsewhere. (See "Pathogenesis of metabolic alkalosis".) The etiology and evaluation of patients with metabolic alkalosis are discussed separately. (See "Causes of metabolic alkalosis" and "Clinical manifestations and evaluation of metabolic alkalosis".) OVERVIEW OF THE PATHOGENESIS The genesis and the maintenance of metabolic alkalosis are distinct processes. Initially, a process that raises the plasma bicarbonate concentration occurs, and then another process prevents excretion of the excess bicarbonate in the urine [1,2]. Factors that increase plasma bicarbonate — Several mechanisms can increase the plasma bicarbonate concentration. They include (table 1) (see "Causes of metabolic alkalosis"): Continue reading >>

Mechanisms Of Action Of Acetazolamide In Prophylaxis And Treatment Of Acute Mountain Sickness

Mechanisms Of Action Of Acetazolamide In Prophylaxis And Treatment Of Acute Mountain Sickness

What are the 3 major classes of high altitude disease? 1)Acute mountain sickness (10% at 3500m, 75% at 4500) What are the multitude of systemic effects that make acteozolamide effective besides inducing metabolic acidosis (inducing chemoreceptors to respond more to hypoxic stimuli at high altitude? -Improvements in ventilation through, tissue respiratory acidosis -improvements in sleep quality from carotid body CA inhibition What are the two hypothesis that causes of AMS? ;What is the problem with these hypothesis?What is the agreement of symptoms caused by? 1) Hypoxia-mediated mild cerebral edema and increased cranial pressure; brain morphological changes don't correlate with symptoms of AMS 2)Vasogenic Edema: rupture of blood brain barrier, Free radical damage barrier function under hypoxic conditions don't support pathophysiology of AMS -HYPOXIA not hypobaria. Oxygen therapy also effective treatment Ambiguity of causes of AMS,but what is the relative agreement of symptoms? What txt is consistent with this? caused predominantly by hypoxia and not hypobaria --oxygen therapy is an effective treatment for AMS How did acetazolamide significantly increased minute ventilation by 50%? Mechanism is still poorly understood. due to predominantly to increase in TV not due to frequency Improves arterial PO2 and oxyhemoglobin saturation (during sleep increased from 72%-79%. What is the most commonly cited explanation for drug enhancement? At high altitude, reduced barometric pressure and partial pressure of PIO2=>hypoxemia which drives minute ventilation. Hyperventilation causes respiratory alkalosis->leads to symptoms of AMS acetozolamide generates metabolic acidosis and reduce the limit of increased ventilation reduce the effects of alkalosis and improve AMS Hypercapnia ventila Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt Continue reading >>

Acetazolamide - Wikipedia

Acetazolamide - Wikipedia

Not to be confused with acetohexamide or methazolamide . Common side effects include numbness, ringing in the ears , loss of appetite, vomiting, and sleepiness. [2] It is not recommended in those with significant kidney problems , liver problems , or who are allergic to sulfonamides . [2] [4] Acetazolamide is in the diuretic and carbonic anhydrase inhibitor families of medication. [2] It works by decreasing the amount of hydrogen ions and bicarbonate in the body. [2] Acetazolamide came into medical use in 1952. [5] It is on the World Health Organization's List of Essential Medicines , the most effective and safe medicines needed in a health system . [6] Acetazolamide is available as a generic medication . [2] The wholesale cost in the developing world is about 1.40 to 16.93 USD per month. [7] In the United States the wholesale cost is about 125.34 USD per month. [8] It is used in the treatment of glaucoma , drug-induced edema , heart failure-induced edema, epilepsy and in reducing intraocular pressure after surgery. [9] [10] It has also been used in the treatment of altitude sickness , [11] Mnire's disease , increased intracranial pressure and neuromuscular disorders. [12] In epilepsy, the main use of acetazolamide is in menstrual-related epilepsy and as an add on to other treatments in refractory epilepsy. [9] [13] It has been demonstrated in drug trials to relieve symptoms associated with dural ectasia in individuals with Marfan's Syndrome . [14] A 2012 review and meta-analysis found that there was "limited supporting evidence" but that acetazolamide "may be considered" for the treatment of central (as opposed to obstructive) sleep apnea . [15] It has also been used to prevent methotrexate -induced kidney damage by alkalinalizing one's urine, hence speeding up methot Continue reading >>

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