erifoveal telangiectasia, alsoreferred to as macular telangiec-tasia type 2, idiopathic macularteleangiectasia type 2 and juxtafoveo-lar retinal telangiectasis group 2A, area slowly progressive, usually bilateralmacular disease, characterized bydilated, tortuous capillaries in theperifoveolar region (Gass & Blodi1993; Yannuzzi et al. 2006; CharbelIssa et al. 2008; Clemons et al. 2008,2010; Gamulescu et al. 2008; Gillieset al. 2009). They usually becomesymptomatic in the fifth to seventhdecade with a slow and progressivedecrease in visual acuity and meta-morphopsia. Typical findings in fluo-rescein angiography are parafovealectatic capillaries and a late-stage dif-fuse leakage, mainly temporal to thefovea. Imaging with optical coherencetomography shows intraretinal hypo-reflective spaces in the foveal area(Yannuzzi et al. 2006; Gillies et al.2009). In a subset of patients, neovas-cular membranes as well as the devel-opment of macular holes, either fullthickness or lamellar, may lead to fur-ther functional damage. Gillies andcolleagues reported on the occurrencewith diabetes, arterial hypertensionand coronary artery disease (Gillieset al. 2009). So far, no therapy hasbeen proved to benefit idiopathic mac-ular teleangiectasia. The intravitrealuse of triamcinolone and bevaci-zumab and the application of photo-dynamic therapy have been previouslyreported. Because vascular endothelialgrowth factor (VEGF) plays an inte-gral part in the formation of abnor-mal blood vessels and increasingvascular permeability in many patho-logic conditions, and because intravi-treal inhibition of VEGF was shownto be effective for a variety of oculardiseases with destabilized blood–retinabarrier or pathologic growth of newvessels and because it has recentlybeen hypothesized that VEGF alsomay play an essential role in the path-ogenesis of macular telangiectasia(Charbel Issa et al. 2007; Kovach RCarl Zeiss Meditec, Oberkochen, Ger-many), criteria for the diagnosis ofnonproliferative type 2 idiopathicmacular telangiectasias were dilated,tortuous capillaries in the perifoveolarregion accompanied by cystoid macu-lar oedema and visual symptoms suchas decreased central visual acuity andmetamorphopsias. In none of thepatients, neovascularisations weredetected. All patients had complainedof a progressive loss of vision from avisual acuity level of 20⁄20 to the pre-senting visual acuity measured atbaseline of the study. The loss ofvision had been observed by thepatients in a period of several monthsprior to attending the hospital. Exclu-sion criteria were any signs for dia-betic retinopathy or retinal veinocclusions. All patients signed aninformed consent describing the off-label use of intravitreal bevacizumab.Eyes were prepared for an intravitrealinjection using standard protocol thatemployed a sterile lid speculum andtopical 5% povidone–iodine. The in-travitreal dose of bevacizumab was1.5 mg delivered in 0.05 ml through apars plana injection. All eyes receivedthree bevacizumab injections in inter-vals of 2 months. After that loadingdosage, injections were repeated inintervals ranging between 2 and5 months.Ten eyes of nine patients (threewomen) were identified by the sameexaminer (JBJ). After treatment, fol-low-up ranged from 6 to 36 months.The mean best-corrected visual acuityat baseline (0.43 ± 0.43 LogMAR)improved slightly, although, not sta-tistically significantly (p = 0.09) tothe mean best-corrected visual acuityat 6 months follow-up (0.37 ± 0.39LogMAR; p = 0.09). At 12 monthsfollow-up, mean best-corrected visualacuity was 0.33 ± 0.34 LogMARwith no significant (p = 0.49) differ-ence to the baseline examination. In asimilar manner, mean macular thick-ness decreased slightly, although, notstatistically significantly (p = 0.28),from 322 ± 90 to 276 ± 67 lmat6 months follow-up and to 264 ±106 lm at 12 months follow-up.Taking into account that all patientsreported a progressive loss of visionbefore start of the treatment, the resultsindicate that in nonproliferative type2 idiopathic macular telangiectasias,therapy with repeated intravitreal injec-tions of intravitreal bevacizumab wasassociated with a stabilization of func-tion and structure. It confirms previousstudies by Charbel Issa and colleaguesand Kovach and Rosenfeld (CharbelIssa et al. 2007; Kovach & Rosenfeld2009). Despite the limitations of ourstudy, namely the design as a retrospec-tive hospital-based case series studywithout control group, the findingssuggest a therapeutically positive effectof intravitreal bevacizumab to at leasttemporarily arrest the progression ofthe disease. Because the therapy withbevacizumab is specific to VEGF A,future studies may examine whetherother anti-angiogenic drugs bindingto a variety of growth factors includ-ing broader VEGF molecules andplacental growth factor may have atherapeutic effect superior to the oneby bevacizumab.
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Mar 3, 2014
Mete Güler + 6
Open Access