Assumere nicotina rappresenta un fattore di rischio molto importante per lo sviluppo della maculopatia degenerativa.
Questo studio sperimentale, effettuato su animali di laboratorio, stabilisce che l’esposizione alla nicotina esercita un’azione negativa anche sull’evoluzione della malattia e sulla risposta alle terapie con inibitori del VEGF (Avastin, Lucentis). Nelle cavie esposte alla nicotina, la terapia con antiVEGF non riusciva a ridurre le dimensioni delle lesione neovascolare, mentre negli animali non esposti alla nicotina la lesione risultava ridotta, in seguito a terapia, del 61-86%. I ricercatori hanno anche rilevato che il fattore di crescita vascolare (VEGF) tornava ad essere presente in concentrazioni più elevate negli occhi delle cavie esposte alla nicotina 14 giorni dopo il trattamento.

Questo lavoro consente di comprendere l’importanza dell’esposizione alla nicotina nell’evoluzione della maculopatia degenerativa e la sua influenza nell’ottenere una migliore risposta alle terapie. E’ importante, quindi, cessare l’abitudine del fumo, non solo a scopo preventivo, ma anche una volta che la malattia si è presentata in fase essudativa.



Retina the journal of retinal and vitreous diseases
The Effect of Nicotine on Anti–Vascular Endothelial Growth Factor Therapy in A Mouse Model of Neovascular Age-Related Macular Degeneration

Davis, Stephen J. MD; Lyzogubov, Valeriy V. PhD; Tytarenko, Ruslana G. MS; Safar, Ammar N. MD; Bora, Nalini S. PhD; Bora, Puran S. PhD

Retina
June 2012 – Volume 32 – Issue 6 – p 1171–1180



Purpose: The purpose of this article is to evaluate the effect of nicotine on anti–vascular endothelial growth factor therapy in the treatment of neovascular age-related macular degeneration.

Methods: One group of mice received nicotine in drinking water and the other group received water only. Choroidal neovascularization (CNV) was induced with a laser. Nicotinic acetylcholine receptor-α7 (nAChRα7) expression was evaluated by immunohistochemistry. Bevacizumab or adiponectin peptide II (APNpII) was injected intravitreally on Day 7 postlaser, and the effects were evaluated on Days 14 and 21. α-Bungarotoxin was injected intraperitoneally on Days 2 to 5, and its effect was evaluated on Day 14.

Results: Expression of nAChRα7 was 2 to 7 times higher between Days 3 and 7 postlaser compared with naive mice. In water-fed mice, APNpII, bevacizumab, and α-bungarotoxin significantly reduced CNV size. In nicotine-fed mice, treatment with APNpII or bevacizumab did not significantly reduce CNV size, whereas α-bungarotoxin did have an effect. Comparing water- and nicotine-fed mice, CNV size was 61% to 86% smaller in water-fed mice except for the α-bungarotoxin group, where there was no difference. Platelet-derived growth factor and vascular endothelial growth factor expression was 1.5- to 2.5-fold higher at Day 14 in nicotine-treated mice.

Conclusion: Nicotine significantly blocks the effect of anti–vascular endothelial growth factor therapy in the treatment of laser-induced neovascular age-related macular degeneration. nAChRα7 is significantly upregulated during the formation of CNV, and treatment with an nAChRα7 antagonist decreases CNV size irrespective of nicotine administration.