Failure of acetazolamide to decrease intraocular pressure in patients with carbonic anhydrase II deficiency.
The effect of the carbonic anhydrase inhibitor acetazolamide on intraocular pressure was studied in two patients with carbonic anhydrase II deficiency and in six control subjects. The deficient patients had the autosomal recessive syndrome of osteopetrosis with renal tubular acidosis and cerebral calcification. A dose of 125 mg of intravenous acetazolamide caused a significant (P less than .01) decrease in intraocular pressure from baseline (15.0 +/- 1.5 mm Hg) in the control subjects one hour (11.3 +/- 1.5 mm Hg) and four hours (13.8 +/- 1.2 mm Hg) after drug administration. In contrast, the patients with carbonic anhydrase deficiency showed no such decrease in intraocular pressure; baseline intraocular pressure (19.2 +/- 0.2 mm Hg) was significantly unchanged (P greater than .5) at one hour (20.0 +/- 0.1 mm Hg) and four hours (19.2 +/- 0.2 mm Hg).
D000086:Acetazolamide / Q000494:pharmacology* / Q000627:therapeutic use; D000141:Acidosis, Renal Tubular / Q000188:drug therapy / Q000235:genetics; D000328:Adult; D001927:Brain Diseases / Q000188:drug therapy / Q000235:genetics; D002114:Calcinosis / Q000188:drug therapy / Q000235:genetics; D002256:Carbonic Anhydrases / Q000172:deficiency*; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D007429:Intraocular Pressure / Q000187:drug effects*; D010022:Osteopetrosis / Q000188:drug therapy / Q000235:genetics; D013577:Syndrome; D013997:Time Factors
D002256:Carbonic Anhydrases; D000086:Acetazolamide