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Low-Level Laser Therapy Improves Vision in Macular Degeneration

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Low-Level Laser Therapy Improves Vision in Macular Degeneration ( low-level-laser-therapy-improves-vision-macular-degeneration )

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LLLT IMPROVES VISION IN PATIENTS WITH AMD 245 stage. The improvement in visual function was maintained for up to 36 mo. The results of this retrospective analysis of a case series are encouraging, especially in light of the fact that if un- treated, AMD inevitably leads to irreversible loss of vision. Thus LLLT may, when initiated during the early stages of AMD, help prevent loss of vision. LLLT may also be com- bined with other therapeutic approaches. Although not in- vestigated in this study, it is likely that synergistic effects may be seen (e.g., improved outcome or shorter treatment duration). In addition to the improvement in visual acuity, other pos- itive effects of LLLT were noted. Eye examinations revealed that LLLT diminished pigment accumulations and cystic drusen. Metamorphopsia, acquired impairments of color vi- sion, and relative scotomas improved as well. Moreover, in patients with wet AMD, edema and bleeding were reduced. Treatment with laser energy at a wavelength of 780 nm was not perceived as unpleasant and was well accepted by the patients. No adverse effects were observed. In general, the photochemical effects of light are mediated through the interaction of photons and various cellular ac- ceptor molecules. Thus, photon energy is transformed into biochemical energy, which stimulates metabolic reactions. LLLT may increase cellular metabolism in choroidea, RPE, and in photoreceptors, where the energy is absorbed by pig- ments. Regular metabolic processes may be enhanced and repair processes may be triggered or accelerated. Recently, an increase in the expression of heat shock proteins was found in the retinal and choroidal layers after sub-thermal transpupillary application of laser energy.13 Heat shock pro- teins (or chaperones) are known to stimulate cellular me- tabolism and may help prevent premature cell death. In in vitro experiments, application of laser light was shown to in- crease cellular metabolic activity, the generation of adeno- sine triphosphate, and phagocytosis.14,15 Enhanced lysoso- mal activity and phagocytosis of cell debris and pigments may help to revitalize the retina.16 The detailed cellular and molecular mechanisms underlying the biomedical effects of laser energy in the treatment of patients with AMD have yet to be further elucidated. Conclusion In conclusion, this study of a case series shows that LLLT may be a novel therapeutic option for both early and ad- vanced forms of AMD. This simple and highly effective treat- ment improves visual acuity and may help to prevent loss of vision without adverse side effects. References 1. Pauleikhoff, D., and Holz, F.G. (1996). Age-related macular degeneration. 1. Epidemiology, pathogenesis and differen- tial diagnosis. Ophthalmologe. 93, 299–315. 2. Apte, R.S., Scheufele, T.A., and Blomquist, P.H. (2001). Eti- ology of blindness in an urban community hospital setting. Ophthalmology. 108, 693–696. 3. Evans, J., and Wormald, R. (1996). Is the incidence of regis- trable age-related macular degeneration increasing? Br. J. Ophthalmol. 80, 9–14. 4. Moore, D.J., and Clover, G.M. (2001). The effect of age on the macromolecular permeability of human Bruch’s mem- brane. Invest. Ophthalmol. Vis. Sci. 42, 2970–2975. 5. Liang, F.Q., and Godley, B.F. (2003). Oxidative stress-in- duced mitochondrial DNA damage in human pigment ep- ithelial cells: a possible mechanism for RPE aging-related macular degeneration. Exp. Eye Res. 76, 397–403. 6. Ambati,J.,Ambati,B.K.,Yoo,S.H.,Ianchule,S.,andAdamis, A.P. (2003). Age-related macular degeneration: etiology, pathogenesis, and therapeutic strategies. Surv. Ophthalmol. 48, 257–293. 7. Hooper, C.Y., and Guymer, R.H. (2003). New treatments in age-related macular degeneration. Clin. Experiment. Oph- thalmol. 31, 376–391. 8. AREDS Report No. 8 (Age-Related Eye Disease Study Re- search Group). (2001). A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular de- generation and vision loss. Arch. Ophthalmol. 119, 1417– 1436. 9. Evans, J.R. (2002). Antioxidant vitamin and mineral supple- ments for age-related macular degeneration. Cochrane Data- base Syst. Rev. CD000254. 10. Holz, F.G., and Miller, D.W. (2003). Pharmacological ther- apy for age-related macular degeneration. Current devel- opments and perspectives. Ophthalmologe. 100, 97–103. 11. Holz, F.G., and Pauleikhoff, D. (1996). Age-related macular degeneration. 2. Therapeutic approaches. Ophthalmologe. 93, 483–506. 12. Rosenfeld, P.J., Brown, D.M., Heier, J.S., Boyer, D.S., Kaiser, P.K., and Chung Kim, R.Y. (2006). Ranbizumab for neovas- cular age-related macular degeneration. N. Engl. J. Med. 14, 1419–1431. 13. Desmettre, T., Maurage, C.A., and Mordon, S. (2003). Transpupillary thermotherapy (TTT) with short duration laser exposures induce heat shock protein (HSP) hyperex- pression on choroidoretinal layers. Lasers Surg. Med. 33, 102–107. 14. Mester, E., Mester, A.F., and Mester, A. (1985). The bio- medical effects of laser application. Lasers Surg. Med. 5, 31–39. 15. Karu, T.I. (1987). Photobiological fundamentals of low- power laser therapy. IEEE J. Quantum Electronics. 10, 1703–1717. 16. Chen,L.,Yang,P.,andKijlstra,A.(2002).Distribution,mark- ers, and functions of retinal microglia. Ocul. Immunol. In- flamm. 10, 27–39. Address reprint requests to: Dr. Boris T. Ivandic, M.D. University of Heidelberg Otto-Meyerhof Centre Im Neuenheimer Feld 350 69120 Heidelberg, Germany E-mail: boris.ivandic@med.uni-heidelberg.de

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