Zwyrodnienie plamki związane z wiekiem. Część II: metody leczenia – chirurgiczne, monoterapia i terapie złożone
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mar 31, 2015
Słowa kluczowe:
nowe terapie AMD, leczenie chirurgiczne, terapie złożone w AMD, glikokortykosteroidy, radioterapia, plazmafereza, lentiwirusy
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Abstrakt
Zwyrodnienie plamki związane z wiekiem jest najczęstszą przyczyną utraty widzenia centralnego. Proces chorobowy obejmuje region plamkowy siatkówki i prowadzi do znacznego pogorszenia ostrości wzroku, a co za tym idzie – jakości życia. Chory traci możliwość uprawiania dotychczas wykonywanego zawodu, czytania, oglądania telewizji czy prowadzenia samochodu. Schorzenie to jest wyraźnie związane z procesami starzenia się i degeneracji tkanek i zazwyczaj pojawia się po 50. r.ż. Dopiero kilka lat temu wprowadzono środki farmakologiczne i inne metody terapeutyczne, które zdecydowanie poprawiły szanse na zachowanie użytecznej ostrości wzroku. Przełomowym odkryciem było klinicznie potwierdzone zahamowanie endotelialnego czynnika wzrostu, powodującego neowaskularyzację, co skutkowało brakiem wzrostu nieprawidłowych naczyń i w efekcie chroniło nie tylko przed spadkiem ostrości wzroku, ale nawet tę funkcję poprawiało. To była prawdziwa rewolucja w okulistyce, która dała pacjentom nadzieję na całkowite wyleczenie. Jednak czy jest ono możliwe? Jak wskazują doświadczenia kliniczne i doniesienia badaczy, walka o zahamowanie rozwoju choroby trwa. Leczenie chirurgiczne, leki podawane miejscowo i ogólnie, plazmafereza, wirusy wektorowe, radioterapia to tylko niektóre sposoby w walce o zachowanie widzenia centralnego. Arsenał terapeutyczny stale i intensywnie się poszerza i daje nadzieję na powstrzymanie rozwoju schorzenia.
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Jarmak A. Zwyrodnienie plamki związane z wiekiem. Część II: metody leczenia – chirurgiczne, monoterapia i terapie złożone. Ophthatherapy [Internet]. 31 marzec 2015 [cytowane 17 maj 2024];2(1):31-5. Dostępne na: https://journalsmededu.pl/index.php/ophthatherapy/article/view/615
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3. Ferrara N, Henzel WJ. Pituitary follicular cells secrete a novel heparin-binding growth factor specific for vascular endothelial cells. Biochem Biophys Res Commun. 1989; 161: 851-8.
4. Ferrara N, Gerber HP, LeCouter J. The biology of VEGF and its receptors. Nat Med. 2003; 9(6): 669-76.
5. Houck KA, Ferrara N, Winer J et al. The vascular endothelial growth factor family: identification of a fourth molecular species and characterization of alternative splicing of RNA. Mol Endocrinol. 1991; 5: 1806-14.
6. Olsson AK, Dimberg A, Kreuger J et al. VEGF receptor signalling – in control of vascular function. Nat Rev Mol Cell Biol. 2006; 7(5): 359-71.
7. Sheikpranbabu S, Kalishwaralal K, Venkataraman D et al. Silver nanoparticles inhibit VEGF- and IL-1beta-induced vascular permeability via Src dependent pathway in porcine retinal endothelial cells. J Nanobiotechnology. 2009; 7: 8.
8. Allen WR, Gower S, Wilsher S. Immunohistochemical localization of vascular endothelial growth factor (VEGF) and its two receptors (Flt-I and KDR) in the endometrium and placenta of the mare during the oestrous cycle and pregnancy. Reprod Domest Anim. 2007; 42(5): 516-26.
9. Witmer AN, Vrensen GF, Van Noorden CJ et al. Vascular endothelial growth factors and angiogenesis in eye disease. Prog Retin Eye Res. 2003; 22(1): 1-29.
10. Hiroshima K, Ng YS, Zhong L et al. Vascular endothelial growth factor-A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury. Am J Pathol. 2007; 171(1): 53-67.
11. Ablonczy Z, Crosson CE. VEGF modulation of retinal pigment epithelium resistance. Exp Eye Res. 2007; 85(6): 762-71.
12. Takahashi H, Shibuya M. The vascular endothelial growth factor (VEGF)/VEGF receptor system and its role under physiological and pathological conditions. Clin Sci (Lond). 2005; 109(3): 227-41.
13. Slomiany MG, Rosenzweig SA. Autocrine effects of IGF-I-induced VEGF and IGFBP-3 secretion in retinal pigment epithelial cell line ARPE-19. Am J Physiol Cell Physiol. 2004; 287(3): C746-53.
14. Funatsu H, Noma H, Mimura T et al. Association of vitreous inflammatory factors with diabetic macular edema. Ophthalmology. 2009; 116(1): 73-9.
15. Tsai DC, Charng MJ, Lee FL et al. Different plasma levels of vascular endothelial growth factor and nitric oxide between patients with choroidal and retinal neovascularisation. Ophthalmologica. 2006; 220(4): 246-51.
16. Boulton ME, Cai J, Grant MB. Gamma-Secretase: a multifaceted regulator of angiogenesis. J Cell Mol Med. 2008; 12(3): 781-95.
17. Chappelow AV, Kaiser PK. Neovascular age-related macular degeneration: potential therapies. Drugs. 2008; 68(8): 1029-36.
18. Michels S, Schmidt-Erfurth U, Rosenfeld PJ. Promising new treatments for neovascular age-related macular degeneration. Expert Opin Investig Drugs. 2006; 15(7): 779-93.
19. Leung E, Landa G. Update on current and future novel therapies for dry age-related macular degeneration. Expert Rev Clin Pharmacol. 2013; 6(5): 565-79.
20. Steinbrook R. The price of sight – ranibizumab, bevacizumab, and the treatment of macular degeneration. N Engl J Med. 2006; 355(14): 1409-12.
21. Bakri SJ, Snyder MR, Reid JM et al. Pharmacokinetics of intravitreal ranibizumab (Lucentis). Ophthalmology. 2007; 114(12): 2179-82.
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