Pegaptanib sodium for acute retinal necrosis-induced macular oedema.

35-year-old immunocompromisedwoman with umbilical cordblood transplantation for adult lym-phoma presented with a 2-week his-tory of redness and blurred vision inboth eyes following initial herpes zos-ter encephalitis. Examination revealedvitritis, retinal whitening (Fig. 1), vas-culitis and optic nerve head oedema.Best-corrected visual acuity (BCVA)was 20⁄40 right eye (OD) and 20⁄60left eye (OS). Optical coherencetomography (OCT) showed no cystoidmacular oedema (CMO).Polymerase chain reaction testing ofthe aqueous ﬂuid revealed varicellazoster virus and the patient was diag-nosed with bilateral acute retinalnecrosis (ARN).The retinitis was controlled withoral valacyclovir and intravitrealfoscarnet (2.4 mg) every 3 days,followed 10 days later by pars-planavitrectomy and endolaser in both eyes.BCVA improved to 20⁄25 OD and20⁄20 OS with no signs of ocularinﬂammation.One month later, the clinical coursewas complicated by severe CMO inthe right eye with a central fovealthickness of 410 lm and a BCVA of20⁄60, with no signs of ocular inﬂam-mation.After discussion of periocularand⁄or intravitreal use of steroids, thepatient refused to have this treatmentbecause of his family history of glau-coma and the increased potential riskof cataract formation. After a lengthydiscussion of the potential risks andbeneﬁts of off-label intravitreal bev-acizumab or intravitreal pegaptanibsodium use, the patient requestedintravitreal pegaptanib sodium.An intravitreal injection of pegap-tanib sodium (Macugen; Eyetech⁄Pﬁzer, New York, NY, USA) wasadministered in the right eye withoutcomplication. Two weeks after injec-tion, OCT demonstrated a markedimprovement of the macular oedema,with a central foveal thickness of 197lm and a BCVA of 20⁄25 in theright eye (Fig. 2). Three months aftertreatment, there was no ocularinﬂammation and the OCT revealedno CMO.Acute retinal necrosis (ARN) syn-drome is a distinct infectious retinitiscaused by members of the herpes virusfamily that can impair vision. Itoccurs mostly in adult patients,especially those severely immunocom-promised, in association with a reacti-vation of a herpes virus infection (Lauet al. 2007).Active vasculitis is characterized byvascular sheathing and perivascularintraretinal haemorrhages. Vesselobstruction affects the central retinalartery more often than the vein and isa contributing factor to severe visionloss (Chang & Young 2007). Retinalischaemia is the major trigger ofvascular endothelial growth factor(VEGF) over-expression; it can leadto chronic inﬂammation and thedevelopment of retinal neovasculari-zation (Nishijima et al. 2007).Active inﬂammation secondary toARN progresses despite antiviraltreatment. High-dose systemic cortico-steroid therapy improves intraocularinﬂammation and improves vitreousopacity (Chang & Young 2007).However, some patients have CMOthat is resistant or non-responsive tosteroids.Bevacizumab is an anti-VEGFmonoclonal antibody that blocksall VEGF isoforms. Intravitrealbevacizumab has been used success-fully for the treatment of uveitic-resistant CMO (Cordero Coma et al.2007) with short-term improvementin BCVA and decreased OCT retinalthickness in a considerable propor-tion of patients. However, VEGF-Ais a survival factor for retinal neu-rons and a critical neuroprotectantduring the adaptative response toischaemic injury (Nishijima et al.2007).Pegaptanib sodium is a selectiveRNA aptamer that inhibits VEGF-165, the VEGF isoform primarilyresponsible for pathological ocularneovascularization and vascular per-meability, while sparing the physiolog-ical isoform VEGF-121. Retrospectivedata suggest that pegaptanib may pro-vide therapeutic beneﬁt for patientswith diabetic macular oedema, prolif-erative diabetic retinopathy and reti-nal vein occlusion (Ng & Adamis2006).