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Acetazolamide dosage

Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase-independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. Nevertheless, carbonic anhydrase inhibition causes significant bicarbonate losses and hyperchloremic metabolic acidosis. Because of this and the fact that HCO3" depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, the diuretic efficacy of acetazolamide decreases significantly with use over several days. [Pg.355]

Berson FG, Epstein DL, Grant WM, et al. Acetazolamide dosage forms in the treatment of glaucoma. Arch Ophthalmol 1980 98 1051-1054. [Pg.170]

Acetazolamide is a diuretic whose main action is the inhibition of carbonic anhydrase (see Chapter 15). Mild acidosis in the brain may be the mechanism by which the drug exerts its antiseizure activity alternatively, the depolarizing action of bicarbonate ions moving out of neurons via GABA receptor ion channels may be diminished by carbonic anhydrase inhibition. Acetazolamide has been used for all types of seizures but is severely limited by the rapid development of tolerance, with return of seizures usually within a few weeks. The drug may have a special role in epileptic women who experience seizure exacerbations at the time of menses seizure control may be improved and tolerance may not develop because the drug is not administered continuously. The usual dosage is approximately 10 mg/kg/d to a maximum of 1000 mg/d. [Pg.526]

Z. S. Gomaa, Determination of acetazolamide in dosage forms by HPLC, Biomed. Chromatogr., 7 134(1993). [Pg.402]

In humans, 90% to 95% of acetazolamide in the blood binds to plasma proteins. Therefore relatively large dosages of acetazolamide are required to produce a significant plasma level of the unbound drug. At plasma pH (7.4), half the unbound acetazolamide (pK = 7.4) exists in the un-ionized form, which is the form that penetrates tissues and inhibits carbonic anhydrase. [Pg.160]

In the treatment of elevated lOP, oral acetazolamide is often reserved for short-term lOP reduction only. The development of topical dosage forms of CAIs and the availability of safer ocular hypotensive agents provide a more attractive therapeutic alternative for long-term administration. Acetazolamide produces an additional decrease in lOP when added to drug regimens inclnding miotics, P-blockers, and prostaglandins. [Pg.160]

A 9-year-old girl and two teenage boys, all of them taking the highest dosages of carbamazepine tolerable (without adverse effects), developed signs of toxicity after taking acetazolamide 250 to 750 mg daily. Their serum carbamazepine levels were found to have increased by about 25 to 50%. In one instance toxicity appeared within 48 hours. ... [Pg.518]

The seizure control of 54 children with grand mal and temporal lobe epilepsy was improved when acetazolamide 10 mg/kg daily was added to carbamazepine. Serum carbamazepine levels rose by 1 to 6 mg/L in 60% of the 33 patients sampled. Adverse effects developed in 10 children, and in 8 children this was within 1 to 10 days of starting the acetazolamide. The adverse effects responded to a reduction in the carbamazepine dosage. ... [Pg.518]

The documentation of all of these interactions is very limited, and their incidence is uncertain. Concurrent use should be monitored for the possible development of osteomalacia or altered antiepileptic levels and steps taken to accommodate them. Withdraw the acetazolamide if necessary, or ad-just the dosage of the antiepileptic appropriately. In the case of the children with rickets the acet olamide was withdrawn and high doses of vitamin D was given. It seems possible that other carbonic anhydrase inhibitors may behave like acetazolamide. [Pg.518]

Information seems to be limited to these reports but it seems that the concurrent use of cielosporin and acetazolamide should be closely monitored, being alert of the need to reduce the cielosporin dosage. The interaction can apparently develop very rapidly. [Pg.1011]

A 75-year-old-man developed abdominal cramps and constipation after taking acetazolamide 125 mg bd and prednisone 25 mg/day for 2 days. He stopped taking the acetazolamide, and the symptoms resolved in 3 days. Later he started to take acetazolamide again in a dosage of 250 mg/day, and within 24 hours the symptoms returned. Acetazolamide was withdrawn and the symptoms resolved within 48 hours. [Pg.438]

Urinary tract Methotrexate-induced renal damage appears to be physicochemical in nature. Both the parent compound and its major metabolite, 7-hydroxymethotrexate, are less soluble at acidic pH values, increasing the risk of precipitation in the kidneys, particularly at high dosages. An amorphous yellow material—very probably methotrexate—has been isolated in the kidneys of patients who died as a result of methotrexate-induced renal dysfunction. For physicochemical reasons, it is recommended that the urine be alkalinized (target urinary pH above 7.5) before intensive methotrexate regimens are started. Supportive agents include sodium bicarbonate orally or intravenously, acetazolamide 500 mg qds, or both in combination [1805, 18F, 182 ]. If there is acute renal insufficiency despite appropriate urinary alkalinization, one may need to use carboxypeptidase G2 as an antidote, which is also appropriate in cases of accidental intrathecal overdose of methotrexate [183", 184 ]. [Pg.950]


See other pages where Acetazolamide dosage is mentioned: [Pg.328]    [Pg.328]    [Pg.574]    [Pg.1559]    [Pg.159]    [Pg.823]    [Pg.2222]    [Pg.96]    [Pg.135]    [Pg.283]    [Pg.82]   
See also in sourсe #XX -- [ Pg.915 ]




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