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Photodynamic Therapy Opinion Since late last year we have all heard a lot about verteporfin photodynamic therapy for macular degeneration. Industry, through its media network and by means of financial support for study investigators, made sure that the country and most ophthalmologists knew about this potential promise for relief of macular degeneration. Certainly the concept of photodynamic therapy is innovative and potentially promising, welcomed by patients and physicians alike. The treatment relies on the intravenous injection of a specific dye (Visudyne) which is allowed to circulate systemically and which therefore also enters the area of subretinal neovascularization in AMD. When a specific wavelength laser light of low intensity, not strong enough to burn tissue by itself, is directed at any location where the dye is found, absorption of the energy occurs to such a degree that a "burn" occurs of the vasculature where the dye is located. Enough damage is done at that site to destroy the vessels without destroying any surrounding tissues. Theoretically therefore, this is a low-energy treatment which destroys subretinal neovascularization while saving the anatomy of overlying retina and underlying tissues. It should therefore be ideal for treating subfoveal neovascularization, for which it was specifically approved by the FDA in April 2000. Several studies have now been done, mostly supported by industry, to find out how much and which patients benefit from this treatment. Since November 1999, we have also participated in these studies, so that we are able to gain experience before FDA approval. That experience so far, with about 40 patients, has not resulted in any improvement in any patient and has not stabilized vision better than 20/200 in any patient either. However, we know that our small experience is not statistically significant. Instead we should pay more attention to the statistics of larger studies, which are now available. They suggest that verteporfin treatment be offered to all patients with at least 50% of subretinal neovascularization involving the fovea. The results indicate that the visual acuity is stabilized at or near the treatment level, as compared to the further progression of visual loss in eyes not treated. From these data, it looks like the number of patients in which this treatment may work is small. In the first place, only a small percentage of ARMD patients have the "wet" variety. Of that group, only a small percentage have the ARMD centrally located and of the classic type. Secondly, most patients with ARMD, treated or not, stabilize at some level of visual acuity. This is particularly true for patients treated with conventional laser, even when the center of the fovea is treated when stabilization often occurs between 20/200 and 20/400, at which time low vision aids are used to help patient function. Visudyne-treated study patients are stabilized at approximately 20/120. In our own small group of patients, the stabilized visual acuity was 20/200 or worse with treatment. Thus it seems, for stabilization to be significantly better with treatment, very early treatment (when vision is still relatively good) should be done. Then at least we give this therapy its best chance of saving vision. As I think about the stabilization of vision, I ask myself the question whether patients with 20/120 vision are significantly better able to function than patients with 20/200 vision. Clearly, both groups of patients cannot drive and cannot read without aids. My experience also suggests that these patients have difficulty telling the difference between those levels of vision. This is so because macular degeneration produces, as one of my mentors stated, "fractured vision" and visual acuity measurements in a doctor's office, testing one eye at a time and encouraging a patient to find a paracentral area of best vision, is relatively meaningless in the real world. Thus the question needs to be asked whether society should be willing to pay the estimated $1.5 billion each year to obtain a stabilization of vision at a level which may still not be very useful to patients. For the ophthalmologist, verteporfin may also pose another problem. He/she is used to a high degree of success in medical and surgical treatments. Cataract surgery is now close to 100%successful and even retinal surgery is about 94% successful for rhegmatogenous retinal detachment. These numbers are higher than in most other surgical specialties. Now comes a therapy which does not improve vision but stabilizes it at an unacceptable level. For most ophthalmologists this is foreign territory. This does not mean we should abandon verteporfin treatment, or that we should not continue the research which has established its use. However this is not a panacea, and research must go on in an accelerated fashion, so that we get beyond this specific treatment to something which will work better and earlier. Perhaps it will be a modified form of verteporfin therapy. W.A.J.
van Heuven, M.D. is Professor and Chairman of
Ophthalmology
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