CAIs In Macular Edema Macular Degeneration And Related Ocular Pathologies

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Optic nerve blood flow is diminished in the eyes of primary open-angle glaucoma suspects and patients (Pilts-Seymour et al. 2001). Because sulfonamides with CAI properties act as vasodilators (Supuran and Scozzafava 2000), this might explain the use of such drugs for treating retinal edema and age-related macular degeneration. In consequence, these pharmacological agents represent a new approach for improving visual function. Retinal edema (also referred to as cystoid macular edema) consists of a swelling process within the critically important central visual zone, and might develop in association with a variety of ocular conditions, such as diabetic retinopathy, ischemic retinopathies, intraocular surgery (such as cataract procedures) or laser photocoagulation (Cox et al. 1988; Grover et al. 1997; Sponsel et al. 1997; Barnes et al. 2000). It is also common in patients affected by retinitis pigmentosa, a hereditary disorder leading to total blindness (Orzalesi et al. 1993). The precise mechanism by which the swelling process is triggered is uncertain, but natural metabolic toxins might play a role in this disease (Sponsel et al. 1997). Macular degeneration is characterized by fluid accumulation in the outer retina, accompanied by lipofuscin (a metabolic waste product) accumulation between photoreceptors and the villi of the retina pigment epithelium. These catabolic waste products (also called drusen) are generally cleared by the blood in the healthy retina, but with aging they tend to accumulate and coalesce, so that vast areas of the retinal photoreceptors become disengaged from their neighboring retinal pigment epithelial villi (Cox et al. 1988; Grover et al. 1997; Sponsel et al. 1997; Barnes et al. 2000). As a consequence of drusen confluencing in the foveal area, the affected sections of the retina become blind, which can trigger a macular degenerative disease with dramatic loss of the visual function. No satisfactory therapy for this condition is currently known (Sponsel et al. 1997; Barnes et al. 2000).

The use of CAIs to treat macular edema is based on the important observation of Cox et al. (1988) that acetazolamide 8.1 (as sodium salt) is effective in treating this condition when administered systemically. A similar efficiency has also recently been reported for dorzolamide (Grover et al. 1997; Sponsel et al. 1997) after topical administration (without the side effects of the systemic inhibitor 8.1). It is generally assumed that the disappearance of the edema and the improvement of visual function are independent of the hypotensive activity of the sulfonamide, being due to direct effects of the drug on the circulation in the retina (Sponsel et al. 1997). Practically, acetazolamide, dorzolamide or brinzolamide act as local vasodilators (Supuran and Scozzafava 2000) and improve blood flow in this organ, thereby clearing metabolic waste products, drusen, etc. The improvement of visual function after such a treatment (in early phases of the disease) seems to be very good (Sponsel et al. 1997).

It has also been reported that acetazolamide (375 mg/d) is effective in treating serous retinal detachment of various etiologies (this disease is also generally not amenable to treatment) (Gonzalez 1992). Additional studies are needed to establish whether the topically acting sulfonamide CAIs might be also used in this serious medical problem.

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