Makoto Araie, MD., Ph.D.

Department of Ophthalmology, University of Tokyo Graduate School of Medicine
At present, lowering IOP is the only option we have for treatment of open angle glaucoma (OAG). Tow recently published longitudinal cohort or RCT studies, however, showed that lower ocular perfusion pressure as well as higher IOP are deninete risk factors for development or progression of OAG.,(Leske & BES group. Ophtalmology, 2008; .Leske & EMGT group. Ophthalmology 2007) which suggested that nonIOP-dependent damaging factors should deserve to be treated. In fact, we have demonstrated that systemic calcium antagonists such as brovincamine or nalvadipine significantly retarded progression of visual field damage in NTG patients without affecting the IOP.(Koseki et al. J Glaucoma, 1999; Koseki et al. Ophthalmology, 2008)

  We also reported that the estimated MD in NTG eyes prospectively followed over 3 years was  0.1 and  0.34 dB/yr for the timolol- and latanoprost-group, , whereas IOP was 14.0 and 13.0 mmHg, respectively.(Tomita et al. Eye, 2004) The fact that the estimated MD slope in the timolol-group tended to be less negative than that in the latanoprost-group in spite of higher IOP during 3-year follow-up may deserve attention. Recently, we have completed 3-year prospective follow-up of about 150 NTG patients treated with a topical beta-blocker (timolol or nipradilol), and found that the estimated MD slope was also about  0.1 dB/yr with average IOP during the follow-up of 13.0 mmHg.(Araie et al. Jpn J Ophthalmol, 2008) The value,  0.1 dB/yr tended to be less negative than that of NTG patients who were left untreated with IOP of about 13.0 mmHg,  0.3 - 0.8 dB/yr.(Koseki et al. J Glaucoma, 1999; Koseki et al. Ophthalmology, 2008) These results suggest that topical timolol or nipradilol might influence the visual field progression not only by slightly lowering IOP, but also by modifying nonIOP-dependent damaging processes in OAG, and in vitro studies demonstrated neuroprotective effects of timolol or nipradilol at concentrations of 0.1  M. (Mizuno et al. IOVS, 2001; Goto et al. Brain Res, 2002; Chen et al. Brain Res, 2007)

  Effects of a calcium antagonist, especially nilvadipine, and topical timolol or nipradilol on the nonIOP-dependent damaging processes in OAG deserve future studies.

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