Acta Ophthalmologica 2011
Intravitreal bevacizumab for perifoveal telangiectasia Jost B. Jonas,1 Teodosio Libondi,2 Stefan von Baltz1 and Sven Beutelspacher1 1
Department of Ophthalmology, Medical Faculty Mannheim of the Ruprecht-KarlsUniversity of Heidelberg, Germany 2 Department of Ophthalmology, Faculty of Medicine, II University of Naples, Italy doi: 10.1111/j.1755-3768.2010.02007.x
Editor, erifoveal telangiectasia, also referred to as macular telangiectasia type 2, idiopathic macular teleangiectasia type 2 and juxtafoveolar retinal telangiectasis group 2A, are a slowly progressive, usually bilateral macular disease, characterized by dilated, tortuous capillaries in the perifoveolar region (Gass & Blodi 1993; Yannuzzi et al. 2006; Charbel Issa et al. 2008; Clemons et al. 2008, 2010; Gamulescu et al. 2008; Gillies et al. 2009). They usually become symptomatic in the fifth to seventh decade with a slow and progressive decrease in visual acuity and metamorphopsia. Typical findings in fluorescein angiography are parafoveal ectatic capillaries and a late-stage diffuse leakage, mainly temporal to the fovea. Imaging with optical coherence tomography shows intraretinal hyporeflective spaces in the foveal area (Yannuzzi et al. 2006; Gillies et al. 2009). In a subset of patients, neovascular membranes as well as the development of macular holes, either full thickness or lamellar, may lead to further functional damage. Gillies and colleagues reported on the occurrence with diabetes, arterial hypertension and coronary artery disease (Gillies et al. 2009). So far, no therapy has been proved to benefit idiopathic macular teleangiectasia. The intravitreal use of triamcinolone and bevacizumab and the application of photodynamic therapy have been previously reported. Because vascular endothelial growth factor (VEGF) plays an integral part in the formation of abnormal blood vessels and increasing
P
vascular permeability in many pathologic conditions, and because intravitreal inhibition of VEGF was shown to be effective for a variety of ocular diseases with destabilized blood–retina barrier or pathologic growth of new vessels and because it has recently been hypothesized that VEGF also may play an essential role in the pathogenesis of macular telangiectasia (Charbel Issa et al. 2007; Kovach & Rosenfeld 2009), we conducted the present study to assess the effect of an intravitreal anti-VEGF therapy of Idiopathic macular teleangiectasia Type 2. The retrospective, clinical interventional study included all patients who attended the hospital for diagnosis and treatment of nonproliferative type 2 idiopathic macular telangiectasias in the study period from 2007 to 2009. On the basis of ophthalmoscopy, fluorescein angiography and optical coherence tomography (Stratus OCT; Carl Zeiss Meditec, Oberkochen, Germany), criteria for the diagnosis of nonproliferative type 2 idiopathic macular telangiectasias were dilated, tortuous capillaries in the perifoveolar region accompanied by cystoid macular oedema and visual symptoms such as decreased central visual acuity and metamorphopsias. In none of the patients, neovascularisations were detected. All patients had complained of a progressive loss of vision from a visual acuity level of 20 ⁄ 20 to the presenting visual acuity measured at baseline of the study. The loss of vision had been observed by the patients in a period of several months prior to attending the hospital. Exclusion criteria were any signs for diabetic retinopathy or retinal vein occlusions. All patients signed an informed consent describing the offlabel use of intravitreal bevacizumab. Eyes were prepared for an intravitreal injection using standard protocol that employed a sterile lid speculum and topical 5% povidone–iodine. The intravitreal dose of bevacizumab was 1.5 mg delivered in 0.05 ml through a pars plana injection. All eyes received three bevacizumab injections in intervals of 2 months. After that loading dosage, injections were repeated in intervals ranging between 2 and 5 months. Ten eyes of nine patients (three women) were identified by the same
examiner (JBJ). After treatment, follow-up ranged from 6 to 36 months. The mean best-corrected visual acuity at baseline (0.43 ± 0.43 LogMAR) improved slightly, although, not statistically significantly (p = 0.09) to the mean best-corrected visual acuity at 6 months follow-up (0.37 ± 0.39 LogMAR; p = 0.09). At 12 months follow-up, mean best-corrected visual acuity was 0.33 ± 0.34 LogMAR with no significant (p = 0.49) difference to the baseline examination. In a similar manner, mean macular thickness decreased slightly, although, not statistically significantly (p = 0.28), from 322 ± 90 to 276 ± 67 lm at 6 months follow-up and to 264 ± 106 lm at 12 months follow-up. Taking into account that all patients reported a progressive loss of vision before start of the treatment, the results indicate that in nonproliferative type 2 idiopathic macular telangiectasias, therapy with repeated intravitreal injections of intravitreal bevacizumab was associated with a stabilization of function and structure. It confirms previous studies by Charbel Issa and colleagues and Kovach and Rosenfeld (Charbel Issa et al. 2007; Kovach & Rosenfeld 2009). Despite the limitations of our study, namely the design as a retrospective hospital-based case series study without control group, the findings suggest a therapeutically positive effect of intravitreal bevacizumab to at least temporarily arrest the progression of the disease. Because the therapy with bevacizumab is specific to VEGF A, future studies may examine whether other anti-angiogenic drugs binding to a variety of growth factors including broader VEGF molecules and placental growth factor may have a therapeutic effect superior to the one by bevacizumab.
References Charbel Issa P, Holz FG & Scholl HP (2007): Findings in fluorescein angiography and optical coherence tomography after intravitreal bevacizumab in type 2 idiopathic macular telangiectasia. Ophthalmology 114: 1736–1742. Charbel Issa P, Helb HM, Holz FG & Scholl HP; MacTel Study Group (2008): Correlation of macular function with retinal thickness in nonproliferative type 2 idiopathic macular telangiectasia. Am J Ophthalmol 145: 169–175.
e607
Acta Ophthalmologica 2011
Clemons TE, Gillies MC, Chew EY, Bird AC, Peto T, Figueroa M, Harrington MW; Macular Telangiectasia Research Group (2008): The National Eye Institute visual function questionnaire in the Macular Telangiectasia (MacTel) project. Invest Ophthalmol Vis Sci 49: 4340–4346. Clemons TE, Gillies MC, Chew EY, Bird AC, Peto T, Figueroa MJ, Harrington MW; MacTel Research Group (2010): Baseline characteristics of participants in the natural history study of macular telangiectasia (MacTel) MacTel Project Report No. 2. Ophthalmic Epidemiol 17: 66–73. Gamulescu MA, Walter A, Sachs H & Helbig H (2008): Bevacizumab in the treatment of
e608
idiopathic macular telangiectasia. Graefes Arch Clin Exp Ophthalmol 246: 1189– 1193. Gass JD & Blodi BA (1993): Idiopathic juxtafoveolar retinal telangiectasis: update of classification and follow-up study. Ophthalmology 100: 1536–1546. Gillies MC, Zhu M, Chew E et al. (2009): Familial asymptomatic macular telangiectasia type 2. Ophthalmology 116:2422–2429. Kovach JL & Rosenfeld PJ (2009): Bevacizumab (avastin) therapy for idiopathic macular telangiectasia type II. Retina 29: 27–32. Yannuzzi LA, Bardal AM, Freund KB, Chen KJ, Eandi CM & Blodi B (2006): Idio-
pathic macular telangiectasia. Arch Ophthalmol 124: 450–460.
Correspondence: Dr. J. Jonas Universita¨ts-Augenklinik Theodor-Kutzer-Ufer 1-3 68167 Mannheim Germany Tel: 49 621 383 2242 Fax: 49 621 383 3803 Email:
[email protected]
