OSLI Retina

December 2016

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December 2016 · Vol. 47, No. 12 1161 our case study, the largest lesion was almost 750 µm, consistent with MCP despite the absence of anterior or vitreous inflammation. Spaide et al. concluded that it is difficult to differentiate MCP from PIC with the current imaging examinations. 16 Further research to investigate whether OCTA can distinguish PIC from MCP is needed. It has been reported that anti-VEGF therapy is effective for CNV secondary to PIC. 6,17 Previous cases of PIC received three intravitreal injections of bevacizumab, and all cases showed regression of CNV resulting in visual improvement. 6,17 In our case study, the patient only received one injection of bevacizumab because we could confirm CNV regression at the outer retina with visual improvement. Importantly, intravitreal anti-VEGF therapy has been reported to induce several side effects such as ocular pain, endophthalmitis, cardiac infarction, and cerebral stroke. Therefore, OCTA could possibly prevent excessive administration of anti-VEGF therapy. Furthermore, anti-VEGF therapy did not affect the neovascular plexus at the choroidal capillary level for up to 2 months after the treatment. Hypoperfusion of the choriocapillaris, as reported in a recent publication, could be observed adjacent to the neovascular complex. 7 In our case study, OCTA enabled visualization of a similar hypoperfusion around CNV. Interestingly, this hypoperfusion gradually diminished during a longer follow-up with OCTA. VEGF inhibition may cause reperfusion of choroidal vessels. This observation could indicate remodeling of choroidal capillaries after anti-VEGF therapy. However, it is not clear as to whether this phenomenon is observed all cases of anti-VEGF therapy. As PIC lesions occur in the macula, OCTA could be extremely useful for the follow-up and evaluation of therapeutic strategies used to treat PIC, although FA has been imperative for showing the disease activity and leakiness of abnormal capillaries in the early stages of this disease. However, OCTA has certain disadvantages, including a limited field of view, inability to view leakage, increased potential for artifacts (blinks, movement, vessel ghosting), and the inability to detect blood flow below the slowest detectable flow. Carlo et al. also reported the sensitivity and specificity of CNV detection by OCTA to be 50% and 91%, respectively. 8 Therefore, it is important to evaluate the pathogenesis of PIC with multimodal imaging. 16 It is also imperative that we increase the power of the study for future clinical significance even though CNV secondary to PIC is a rare disease. REFERENCES 1. Watzke RC, Packer AJ, Folk JC, Benson WE, Burgess D, Ober RR. Punctate inner choroidopathy. Am J Ophthalmol. 1984;98:572-584. 2. Brown J Jr., Folk JC, Reddy CV, Kimura AE. Visual prognosis of multifocal choroiditis, punctate inner choroidopathy, and the diffuse subretinal fibrosis syndrome. Ophthalmology. 1996;103(7):1100- 1105. 3. Levy J, Shneck M, Klemperer I, Lifshitz T. Punctate inner choroidopathy: resolution after oral steroid treatment and review of the literature. Can J Ophthalmol. 2005;40(5):605-608. 4. Brouzas D, Charakidas A, Rotsos T, et al. Choroidal neovascularization due to punctate inner choroidopathy: long-term follow-up and review of literature. Clin Ophthalmol. 2010;4:871-876. 5. Olsen TW, Capone A Jr., Sternberg P Jr., Grossniklaus HE, Martin DF, Aaberg TM Sr. Subfoveal choroidal neovascularization in punctate inner choroidopathy. Surgical management and pathologic findings. Ophthalmology. 1996;103(12):2061-2069. 6. Chan WM, Lai TY, Liu DT, Lam DS. Intravitreal bevacizumab (avastin) for choroidal neovascularization secondary to central serous chorioretinopathy, secondary to punctate inner choroidopathy, or of idiopathic origin. Am J Ophthalmol. 2007;143(6):977-983. 7. Kuehlewein L, Bansal M, Lenis TL, et al. Optical coherence tomography angiography of type 1 neovascularization in age-related macular degeneration. Am J Ophthalmol. 2015;160(4):739-748.e2. 8. de Carlo TE, Bonini Filho MA, Chin AT, et al. Spectral-domain optical coherence tomography angiography of choroidal neovascularization. Ophthalmology. 2015;122(6):1228-1238. 9. Spaide RF. Optical coherence tomography angiography signs of vascular abnormalization with antiangiogenic therapy for choroidal neovascularization. Am J Ophthalmol. 2015;160(1):6-16. 10. Ishibazawa A, Nagaoka T, Takahashi A, et al. Optical coherence tomography angiography in diabetic retinopathy: a prospective pilot study. Am J Ophthalmol. 2015;160(1):35-44.e1. 11. Spaide RF, Klancnik JM Jr., Cooney MJ. Retinal vascular layers imaged by fluorescein angiography and optical coherence tomography angiography. JAMA Ophthalmol. 2015;133(1):45-50. 12. Liang FQ, Godley BF. Oxidative stress-induced mitochondrial DNA damage in human retinal pigment epithelial cells: a possible mechanism for RPE aging and age-related macular degeneration. Exp Eye Res. 2003;76(4):397-403. 13. Tiffin PA, Maini R, Roxburgh ST, Ellingford A. Indocyanine green angiography in a case of punctate inner choroidopathy. Br J Ophthalmol. 1996;80(1):90-91. 14. Moult E, Choi W, Waheed NK, et al. Ultrahigh-speed swept-source OCT angiography in exudative AMD. Ophthalmic Surg Lasers Imaging Retina. 2014;45(6):496-505. 15. Kedhar SR, Thorne JE, Wittenberg S, Dunn JP, Jabs DA. Multifocal choroiditis with panuveitis and punctate inner choroidopathy: comparison of clinical characteristics at presentation. Retina. 2007;27(9):1174-1179. 16. Spaide RF, Goldberg N, Freund KB. Redefining multifocal choroiditis and panuveitis and punctate inner choroidopathy through multimodal imaging. Retina. 2013;33(7):1315-1324. 17. Vossmerbaeumer U, Spandau UH, V Baltz S, Wickenhaeuser A, Jonas JB. Intravitreal bevacizumab for choroidal neovascularisation secondary to punctate inner choroidopathy. Clin Exp Ophthalmol. 2008;36(3):292-294.

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