The effects of dorzolamide on choroidal and retinal perfusion in non-exudative age related macular degeneration.

AIM: To comprehensively evaluate the effects of dorzolamide on the choroidal and retinal circulation in patients with age related macular degeneration (AMD). METHODS: In this randomised, double masked, parallel study, 36 non-exudative AMD patients were randomised in a 2 to 1 fashion to placebo versus topical dorzolamide and underwent assessment of their choroidal and retinal circulation. Scanning laser ophthalmoscope indocyanine green angiograms (ICGA) were analysed by a new area dilution analysis technique. Four areas in the perifoveal region and two areas in the temporal peripapillary region were evaluated by plotting intensity of fluorescence of each area over time. The means of the choroidal filling times and the heterogeneity of the filling times were assessed. Scanning laser ophthalmoscope fluorescein angiography (FA) was evaluated for retinal arteriovenous passage (AVP) times by plotting intensity of fluorescence of retinal vessels over time. Assessment was performed at baseline and at 4 months. RESULTS: Compared to placebo, AMD patients treated with dorzolamide showed a significantly increased rapidity of choroidal filling in the superior and inferior peripapillary regions (p=0.007, p=0.02, respectively). No significant difference in choroidal filling times was found in any of the perifoveal areas (p=0.9). Also, on FA assessment, treatment with dorzolamide showed no statistical differences in AVP times (p=0.19). CONCLUSIONS: Dorzolamide may increase peripapillary choroidal perfusion in non-exudative AMD patients. Further studies are merited.

Presumed ocular histoplasmosis syndrome: update on epidemiology, pathogenesis, and photodynamic, antiangiogenic, and surgical therapies.

Presumed ocular histoplasmosis involves the classic triad of discrete atrophic choroidal scars in the macula or midperiphery known as histo spots, peripapillary atrophy, and choroidal neovascularization, which leads to severe loss of central vision. The histo spots from which the choroidal neovascularization develop do not show active inflammation but do represent focal defects in Bruch membrane that could facilitate development of choroidal neovascularization. The macular photocoagulation studies unequivocally show the benefit of photocoagulation compared with observation in reducing the risk of vision loss in patients with presumed ocular histoplasmosis, well defined extrafoveal or juxtafoveal choroidal neovascularization, and choroidal neovascularization in the peripapillary area. However, laser treatment itself causes an absolute scotoma correlating with the site of the laser photocoagulation scar, and subfoveal choroidal neovascularization is not amenable to laser photocoagulation because this would cause a blinding central scotoma. Consequently, other treatments have been sought. The Verteporfin in Ocular Histoplasmosis study evaluated photodynamic therapy for subfoveal choroidal neovascularization caused by presumed ocular histoplasmosis and demonstrated stabilization of the choroidal neovascularization and visual acuity benefit. In addition to photodynamic therapy, antiangiogenic compounds are being developed for choroidal neovascularization caused by age-related macular degeneration, and these agents will likely be of benefit in presumed ocular histoplasmosis associated choroidal neovascularization. Finally, submacular surgery for the removal of subfoveal choroidal neovascularization has promising results. The results of these research efforts will produce more effective therapeutic approaches in the future.