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Acetazolamide (Diamox) Therapy in Chronic GlaucomaA Three-Year Follow-Up Study
CELSO A. de CARVALHO, M.D.;
CARTARET LAWRENCE, M.D.;
HOWARD H. STONE, M.D.
AMA Arch Ophthalmol. 1958;59(6):840-849.
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Since 1954, when acetazolamide ( Diamox) * became available as an additional therapeutic agent for the management of glaucoma, several reports dealing with longterm acetazolamide therapy in chronic glaucoma have been published.1-8 A variety of hypotheses have been advanced concerning the mode of action of this drug.9-15 At the present time, all that can be said with certainty is that acetazolamide is a specific carbonic anhydrase inhibitor, that it lowers intraocular pressure of human and animal eyes, and that it does so by a partial inhibition of aqueous humor formation. The mechanism of action of this drug as well as its exact locus of action still remains to be demonstrated. Since carbonic anhydrase is known to be present in lens epithelium, ciliary body, and retina, it became of immediate interest to study two main problems: (a) Does long-term administration of acetazolamide interfere with the metabolic processes of ocular tissues? (b
. . . [Full Text PDF of this Article]
Author Affiliations
Baltimore
From The Wilmer Ophthalmological Institute of The Johns Hopkins University and Hospital.
Footnotes
Received for publication Sept. 3, 1957.
Presented in part at the Clinical Meeting of the Wilmer Resident's Association, April 5, 1957.
This study was supported in part by the Kellogg Foundation and the Isabella C. Chalfant Fund for the study of Glaucoma.
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