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Management of Idiopathic Macular Telangiectasia Type 2

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Management of Idiopathic Macular Telangiectasia Type 2 Ophthalmol Ther https://doi.org/10.1007/s40123-019-0170-1 REVIEW Management of Idiopathic Macular Telangiectasia Type 2 Alireza Khodabande . Ramak Roohipoor . Javad Zamani . Masoud Mirghorbani . Hamidreza Zolfaghari . Shahab Karami . Bobeck S. Modjtahedi Received: January 2, 2019 Ó The Author(s) 2019 ABSTRACT toward neuro-protection for the non-prolifera- tive phase of this disease. Carotenoid supple- Macular telangiectasia type 2 (MacTel) is a rel- mentation has had mixed results. Ciliary atively rare disease without established treat- neurotrophic factor (CNTF) has demonstrated ments. Although MacTel was previously some promising early results, but further study considered a primarily vascular condition, the is necessary to determine its actual effect. Some thinking on its pathogenesis has shifted to it structural improvements have been seen in the now being considered principally a neurode- non-proliferative phase with oral acetazolamide generative disease. This has resulted in a subse- but without accompanying functional quent change in the approach to treatment improvement. Anti-vascular endothelial drugs have been studied and not found to have ben- efit in the non-proliferative phase of disease but Enhanced digital features To view enhanced digital have demonstrated significant structural and features for this article go to https://doi.org/10.6084/ m9.figshare.7637177. functional value in the treatment of secondary neovascularization. There is no level I evidence Electronic supplementary material The online for the various proposed MacTel treatments, version of this article (https://doi.org/10.1007/s40123- 019-0170-1) contains supplementary material, which is and efforts need to be directed toward con- available to authorized users. ducting multicenter randomized trials to better understand possible treatments for this A. Khodabande Á R. Roohipoor Á J. Zamani Á condition. M. Mirghorbani (&) Á H. Zolfaghari Á S. Karami Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran e-mail: [email protected] Keywords: Anti-vascular endothelial growth; Macular telangiectasia; Management; Retina B. S. Modjtahedi Department of Ophthalmology, Southern California Permanente Medical Group, Baldwin Park, CA, USA INTRODUCTION B. S. Modjtahedi Eye Monitoring Center, Kaiser Permanente Idiopathic macular telangiectasia type 2 (Mac- Southern California, Baldwin Park, CA, USA Tel) is a rare entity characterized by bilateral B. S. Modjtahedi telangiectasia and dilation of the retinal capil- Department of Research and Evaluation, Southern laries in the juxtafoveal area, located mainly California Permanente Medical Group, Pasadena, CA, USA temporal to the fovea. Patients suffer variable Ophthalmol Ther amounts of bilateral progressive vision loss. OVERVIEW OF MACTEL Other clinical findings include loss of macular transparency, which may often appear in the MacTel was first reported in 1968 as a case of temporal juxtafoveal area, intraretinal crys- macular dysfunction secondary to retinal vas- talline deposits, propagation of brown pigment- cular disease [4]. The first systematic attempt to containing cells along abnormal blood vessels, classify idiopathic macular telangiectasias, an which may represent hyperplasia of retinal ultimately diverse group of diseases, was done pigment epithelium (RPE), and redistribution of in 1982 [4]. In 1993, these conditions were macular pigment with a highly characteristic classified into three groups and several sub- pattern including a loss of pigment temporal to groups [3], and by 2006 a simplified classifica- the fovea without a loss of pigment at or beyond tion was proposed by Yannuzzi et al. in which [ 6.58 [1]. Irregular retinal structural clefts can MacTel patients were classified into two groups: be seen in optical coherence tomography (OCT) aneurysmal telangiectasia (MacTel type I) and and can be mistaken for macular edema. End perifoveal telangiectasia (MacTel type II) [5]. stages of this disease are characterized by outer The latter is the most common type [5]. In this retinal degeneration, atrophy, and scarring. review, the preferred nomenclature for macular Subretinal neovascularization occurs in a telangiectasia type II is MacTel (in accordance minority of patients and is a secondary event with the MacTel Study Group [2]). MacTel that can result in significant loss of vision [2–4]. affects both genders equally [7] and is highly Gass and Blodi categorized macular telangiec- likely to be genetically determined, which tasia into five stages according to disease sever- indicates it would be expected to be present ity [3], but Yannuzzi et al. simplified the from the earliest stages of retinal development classification with a focus on clinical, thera- [8]. The signs and symptoms of MacTel can be peutic, and prognostic relevance: stages 1–4 subtle, especially early in the disease course, and were categorized as a non-proliferative phase patients may not be diagnosed on routine with stage 5 as the proliferative phase with the examination. Initial symptoms have the highest evolution of the subretinal neovascular com- incidence in the 5th and 6th decades [9]. plex [5]. Although subretinal neovasculariza- Patients typically present with difficulty read- tion is classified as stage 5, it can present at any ing, metamorphopsia, and paracentral sco- point during the natural evolution of disease tomas. Vision loss is slowly progressive, and best and is not part of a stepwise progression of in corrected visual acuity is preserved until late in MacTel. the disease [9]. Newer imaging modalities have Treatments for MacTel have gained increas- allowed for earlier detection of MacTel: blue ing interest, which necessitates an updated light fundus reflectance (BLR), dual-wavelength review of the current literature. The manage- autofluorescence (DWAF), optical coherence ment of retinal vascular disease has been revo- tomography (OCT), and optical coherence lutionized by anti-vascular endothelial growth tomography angiography (OCTA) [10]; all rep- factor (anti-VEGF) drugs, which have also been resent important diagnostic tools. Prevalence employed to treat the proliferative phase of data are limited by differences in methodology MacTel; however, treatments for the non-pro- including imaging methods used; however, the liferative phases of MacTel remain elusive [6]. reported prevalence is higher in older age Given increasing knowledge about the patho- groups, which may be due to more easily physiology of MacTel, including the paradigm apparent fundus findings in older cohorts [11]. shift from considering it a vascular disease to a The pathophysiology of MacTel has been the neurogenetic condition, and its translation into subject of debate. Gass et al. initially suggested a possible therapeutic interventions, this review vascular etiology based on the premise that seeks to categorize the recent literature while vascular insufficiency and the consequent considering the level of evidence provided by hypoperfusion of nutrients and oxygen cause each study for both structural and functional retinal tissue injury and atrophy [3]; however, outcomes. Ophthalmol Ther Powner et al. demonstrated that the vasculature Search Methods for Identifying Studies of the deep plexus is dilated abnormally within the affected retina [12] and that these areas Two authors (Sh.K. and H.Z.) searched four suffer from depletion of Muller cells [13]. The databases including MEDLINE, SCOPUS, concept that MacTel is a primarily neurode- EMBASE, and Cochrane, for the following key- generative process was born from imaging words: ‘‘macula*’’, ‘‘parafovea*’’, ‘‘telangiect*’’, studies using OCT and scanning laser ophthal- and ‘‘mactel’’. The search results were confined moscopy (SLO) [14] that suggested that vascular to papers published from 2010 to 2018, and the anomalies were a secondary feature of the dis- literature search was concluded on 1 October ease [13, 15]. Muller cells play a key role in 2018. Although several studies had included MacTel because they provide several critical both MacTel I and II, papers that included functions for retina physiology including patients with type I MacTel were excluded from growth factor secretion, angiogenesis/antian- this analysis because of fundamental differences giogenesis, neurotransmitter metabolism, in the pathophysiologies of these diseases. The synaptogenesis, neuroprotection, and photore- references of selected studies were evaluated to ceptor survival [16]. Although the loss of Muller identify additional publications for review. cells is not exclusively responsible for the initi- ation of retinal injury in MacTel [15], the Study Selection experimental ablation of Muller cells results in the retina undergoing several alterations Studies examining the interventions for MacTel including photoreceptor apoptosis, vascular were included in this review. Papers were telangiectasia formation, and intraretinal neo- screened for relevancy in title and abstract by vascularization, similar to what is seen in Mac- both primary reviewers. In case of disagree- Tel [17]. In the non-proliferative phase, ment, a third reviewer (J.Z.) would evaluate a neurodegeneration is the predominant event, study for suitable for inclusion. The final list of which leads to decreased photoreceptor func- included studies was re-evaluated by J.Z. to tion, loss of inner retina integrity, vascular ensure proper study selection. Only papers with anomalies, fluid leakage, and subsequent slow full texts or abstracts
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