Mai-Jun - Sociedade Brasileira de Oftalmologia

196Veloso CER, Almeida LNF, De Marco LA, Vianna RNG, Nehemy MBshown that there is no statistical significant differenceamong the genotypes in response to PDT. (62,65) However,Sakurada et al. have recently shown that there is apharmacogenetic association between the LOC387715A69S variant and the long-term results after PDT in eyeswith polypoidal choroidal vasculopathy (PCV). In thisstudy, PDT was repeated every 3 months until thedisappearance of angiographic signs of active lesions in71 eyes of 71 patients with PCV who were followed-upfor at least 12 months. There was a statistically significantdifference in the visual acuity both at the 12-month andfinal visits (p = 0.002 and P < 0.001, respectively) withthe poorer acuity in patients with the higher T-allelefrequency. (66) Immonen et al. have evaluated VEGF genepolymorphism and the outcome after PDT and showed astrong relationship between this gene and the treatmentresults. The VEGF gene polymorphic SNPs at rs699947and rs2146323 were strong determinants of the anatomicoutcome after PDT, but the SNPs studied were notassociated with the presence of exudative AMD or withthe CNV lesion size or configuration. (67) However,Tsuchihashi et al. did not show any association betweenVEGF rs 699947 SNP and the response to PDT. (68) Othergenetic polymorphisms and its relationship with theresponse to PDT were evaluated but showed nostatistically significant results. (62,67)Recently, two studies have demonstrated theassociation between gene polymorphisms and theresponse to intravitreal injections of the antivascularendothelial growth factor (anti-VEGF) agentsbevacizumab and ranibizumab. (69,70) Brantley et al.conducted a study in which eighty-six patients withexudative AMD undergoing treatment with 1.25 mgintravitreal bevacizumab in one eye were enrolled.Intravitreal injections were performed at 6-weekintervals until there was no longer evidence of activeneovascularization. Each patient was followed for aminimum of 6 months. The authors showed that postbevacizumabVA was significantly worse in the CFH CCgenotype than for the CFH TC or TT genotypes (p=0.016).However, there was no significant difference in responseto this drug according to the LOC387715 genotypes. (69)The other pharmacogenetic study published three yearslater was conducted to determine whether CFHgenotypes had an effect on the treatment of exudativeAMD with ranibizumab. A total of 178 patients werestudied and, for each patient, an intravitreal injection of0.5 mg of ranibizumab was performed at the initialpresentation of an active choroidal neovascular complex.Subsequent injections were performed as needed andpatients were followed for a minimum of 9 months. Inthis retrospective study, Lee et al. found no difference inVA outcomes after ranibizumab treatment among thedifferent CFH genotypes, in contrast to the previous studywith bevacizumab. Nevertheless, over 9 months, patientswith both risk alleles received approximately 1 moreintravitreal injection. (70)There is only one study with a large number ofpatients that addresses the preventive treatment of dryAMD related to the genetic polymorphisms. As we canobserve, the majority of published articles about thetherapeutic response of exudative AMD are related thephotodynamic therapy and many of them arecontroversial. Only two papers consider the intravitrealresponse to anti-VEGF agents according to the geneticpolymorphisms. Since antiangiogenic therapy is nowconsidered the gold standard treatment of exudative AMD,there is a long way to be traversed until treatment couldbe indicated according to the genetic profile of the patient.Additional studies with a larger number of patients, longerfollow-up period and including more SNPs are importantto establish a definite correlation between genepolymorphism and the therapeutic response in AMD. Onlythen may the treatment of this disease be recommendedor modified based on genetic findings.REFERÊNCIAS1. Seddon JM, Chen CA. Epidemiology of age-related maculardegeneration. In: Ryan SJ. Retina. 4th ed. Philadelphia:Elsevier; 2006.2. Donoso LA, Kim D, Frost A, Callahan A, Hageman G. Therole of inflammation in the pathogenesis of age-related maculardegeneration. Surv Ophthalmol. 2006;51(2):137-52. Commentin: Surv Ophthalmol. 2006;51(5):532; author reply 532.3. 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Complement factor H variant increases the risk of agerelatedmacular degeneration. Science. 2005;308(5720):419-21.Comment in: Science. 2005;308(5720):362-4.9. Klein RJ, Zeiss C, Chew EY, Tsai JY, Sackler RS, Haynes C,et al. Complement factor H polymorphism in age-relatedmacular degeneration. Science. 2005;308(5720):385-9. Commentin: Science. 2005;308(5720):362-4.Rev Bras Oftalmol. 2012; 71 (3): 194-8