Angioid streaks were first described by Doyne1 in 1889, in a patient with retinal hemorrhages secondary to trauma, and were defined as “irregular peripapillary jagged lines extending from the disk margin to the retinal periphery.” Interestingly, the term “angioid,” which has a Greek origin, was given by Knapp2 in 1892 because the prevalent belief was that the disease had a vascular involvement, while 25 years later, Kopler first determined angioid streaks as a dysfunction at the Bruch membrane level.3
Specifically, angioid streaks are often bilateral and constitute visible, irregular, linear, crack-like dehiscences of a calcified and brittle Bruch membrane, typically emerging as dark reddish brown bands, with borders of variable width.4 Frequently, angioid streaks surround and radiate from the optic disk and the posterior pole toward the retinal periphery, which could be attributed to the mechanical stress, exerted by the extraocular muscles on a fragile, and less flexible posterior pole.4 Although angioid streaks are considered to remain stable, they may increase in length and diameter over time, while new lesions can develop adjacent to older ones.5
In light of the above, the purpose of this review is to stratify the literature on angioid streaks, emphasizing on the epidemiology, pathophysiology, histology, clinical characteristics, imaging, and potential treatment modalities for angioid streaks.
Method of Literature Search
We conducted a comprehensive search of the PubMed database to include articles up to December 31, 2017, using the following terms: angioid streaks OR pseudoxanthoma elasticum. Articles and book chapters cited in the reference lists of articles obtained by this method were reviewed and included when considered appropriate, whereas the retrieved articles were filtered manually to exclude duplicates. There was no language restriction.
Angioid streaks constitute a hereditary retinal disease, showing a familial tendency, although the inheritance pattern has not been recognized yet.6 In 1896, Deschweinitz first described the disease in brothers, while it has also occurred in siblings and family members.7,8 More recently, in 2004, the presence of idiopathic angioid streaks in identical twins without any associated systemic conditions was reported.3
For the time being, no reports for possible presence of the disease in newborns or infants exist, and angioid streaks rarely occur in patients under the age of 10 years.9 In general, the onset of angioid streaks commonly lies between the second and fifth decades, depending also on the underlying systemic disease.10
The incidence of the disease depends on the systemic association. In pseudoxanthoma elasticum, the incidence varies between 59% and 87%, based on whether the pseudoxanthoma was diagnosed clinically or with a skin biopsy. Practically, all patients with pseudoxanthoma elasticum would have developed angioid streaks 20 years after first diagnosis.5 In Paget disease, the incidence ranges from 8% to 15%,11 whereas in patients with sickle cell hemoglobinopathies, the incidence varies between 0.9% and 6%, depending on the sample size of the study.12–16
More than 50% of patients with angioid streaks have a concurrent disease. This is markedly important because some of these diseases are life-threatening, such as the connective tissue disorder pseudoxanthoma elasticum, which can damage the gastrointestinal tract, the great vessels, and especially arteries, resulting in sudden death due to hemorrhage and accelerated atherosclerosis.17 Of note, pseudoxanthoma elasticum is the most common systemic disease associated with angioid streaks.9 Other common systemic associations are Paget disease, Ehlers–Danlos syndrome, Marfan syndrome, hemoglobinopathies, and hypercalcemia, which may have an impact either on the elastic or on the collagenous layers of Bruch membrane.9 Apart from the aforementioned frequently presenting diseases associated with angioid streaks, there is an extended catalog of potential systemic associations, such as acromegaly, a-beta-lipoproteinemia, cutaneous calcinosis, diffuse lipomatosis, microsomia, myopia, hereditary spherocytosis, hemochromatosis, trauma, acquired hemolytic anemia, hypertensive coronary disease, chronic congenital hyperphosphatemia, Sturge–Weber syndrome, neurofibromatosis, diabetes mellitus, epilepsy, and senile elastosis.9 More recently, angioid streaks were described in a patient suffered from the very rare Camurati–Engelmann disease, which is characterized by bilateral symmetric diaphyseal hyperostosis of the long bones with progressive involvement of the metaphysis and bony overgrowth of the orbit and optic canal stenosis.18
The genetics of angioid streaks include genes and polymorphisms, which have been evaluated especially in patients with pseudoxanthoma elasticum. The mutations were localized at ABCCG gene, which code for the transporter protein, multidrug resistance-associated protein six.4 This protein is expressed primarily in the basolateral surface of hepatocytes and has a potential role of an efflux pump transporting anionic small molecular weight conjugates.9,19–21 Single-strand conformation polymorphism of the gene in patients with angioid streaks suffering from pseudoxanthoma elasticum demonstrated a specific base substitution of c.G3803A in exon 27, changing the correspondent codon from CGG to CAG (p.R1268Q), and this missense mutation was considered to reflect the state of angioid streaks.22 In a Japanese subpopulation from the aforementioned study, six more mutations (p.R419Q, p.E422K, c.2542delG, Del_exon23, c.3774-3775insC, and p.E1427K) were identified as potential causes of the disease.23 Other studies in Japanese populations offer new evidence that the ABCCG variants are crucial not only for the pathogenesis of the pseudoxanthoma elasticum, but also for angioid streaks at least for this ethnicity. The authors described 4 variants as highly associated with angioid streaks occurrence, i.e., p.Q378X, p.V848CfsX83, p.R1357W, and p.R419Q, suggesting a different profile of ABCC6 mutations at Asian and European populations.6 Furthermore, more than 300 distinct mutations have been identified in the ABCC6 gene, consisting of premature termination codon, or those affecting the nucleotide-binding folds (NBF1 and NBF2), 2 protein domains critical for the function of ABCC6 as a transmembrane transporter protein.19,24
Bruch membrane is an elastin and collagen-rich membrane, attached to the retinal pigment epithelium (RPE) and involved in the transport of nutrients and metabolites between the RPE and the choriocapillaris. Bruch membrane has also a remarkable mechanical function, separating the choroidal circulation from the outer retina.25 This elastin-rich membrane's mineralization is responsible for the pathogenesis of angioid streaks, especially in patients with pseudoxanthoma elasticum, where the lack of systemic antimineralization factor results in a calcification of connective tissues rich in elastic fibers, as is Bruch membrane, with profound deposition of calcium elements in the Bruch membrane. This effect may cause rupture of blood vessels and subsequent detrimental effects on the visual function.26 Remarkably, the phenotypic appearance of angioid streaks is similar regardless the underlying systemic disease, suggesting the existence of molecular links to the aforementioned antimineralization pathway.10
The pathogenetic pathway for the development of angioid streaks could be as follows: at the early stages, a thickening of Bruch membrane and/or a decrease of the pigment granules, pigment stripping, and mottling or formation of pigment clumps in the RPE exist. These findings can occur with or without concurrent disruption in the overlying layers of the retina and the underlying choriocapillaris.27 The disease can progress to the development of choroidal neovascularization (CNV), emanating from the growth of fibrovascular tissue through the localized defect. Specifically, if the mechanical integrity of Bruch membrane is interrupted, it can result in modification of growth factor agents interacting with a potential communication between the retina and choroid, leading to CNV formation. At the final stage of the disease's natural course, the CNV can result in a disciform scar with detrimental implications for the vision. A remarkable observation is the potential relationship between angioid streaks and peripapillary chorioretinal atrophy or peripapillary choroidal sclerosis because these entities may be precursors of the subsequent development of angioid streaks.3
The hallmark for the determination of angioid streaks was the hypothesis of Kofler, who attributed the disease to splits in the lamina vitrea. Alternative theories for a potential role in the pathogenesis of the disease of hemorrhage or exudation were discarded.28 Only in 1938, Bock confirmed histopathologically that angioid streaks were not vascular in origin, but they represent defects in the Bruch membrane, in 2 patients with pseudoxanthoma elasticum. He used the dyes hematoxylin and eosin, as well as elastic tissue stains to demonstrate the thickening and deep staining of the lamina vitrea, respectively. Lamina vitrea in the samples showed multiple tiny disruptions and breaks in some areas, whereas there are also areas characterized by splitting and fragmentation. The findings were more prominent peripapillary, leaving the ora serrata's region unscathed. Moreover, there were findings suggestive of the nature of the pseudoxanthoma elasticum, like the thickened and disintegrated aorta as well as the presence of degenerations at the tunica elastic of the ciliary and choriocapillaris' arterial network.8 Hagedoorn used the dye orcein and validated the degenerative changes of Bruch membrane in a case of angioid streaks. He found, also, a positive staining of the lamina vitrea for iron with Turnbull's blue reagent.29 Recently, Spaide30 suggested that the confluent area of opacity, which corresponded to diffuse infiltration with calcium, in patients with angioid streaks is the relevant lesion, not the subconfluent zone known as peau d' orange.
The fundoscopic findings of angioid streaks can be defined based on several characteristics. An important finding is that of a mottled fundus (peau d' orange), pathognomonic for the presence of pseudoxanthoma elasticum.30 The color of the lesions may vary between gray, red, mixed, or pigmented, while it seems to be independent from the underlying systemic disease or the fundus defects and the prognosis.31 Regarding the distribution of the streaks, they can be confined only to the peripapillary region, extended to the posterior pole or have more widespread localization. Noticeably, if angioid streaks are not localized at the fovea, the patients remain mainly asymptomatic, and frequently, the disease is an accidental finding. By contrast, if the fovea is involved or if breaks and distortions of the RPE and of the overlying photoreceptors develop, the patients suffer from metamorphopsia, scotomas, or reduced visual acuity.9,10
Retinal or subretinal hemorrhages along the course of angioid streaks are commonly observed mainly at the posterior pole and they are frequently recurrent, resulting in decreased visual acuity.3,4 Other funduscopic manifestations of the disease are paired red spots distributed along streaks, drusen of the optic disk, macular hole, and peripheral focal lesions.31 Interestingly, angioid streaks can coexist with retinal telangiectasis, especially in older patients or in patients with sickle cell hemoglobinopathy.32 A recent finding is the occurrence of polypoidal choroidal vasculopathy secondary to angioid streaks.17,33,34 Moreover, another reason for visual impairment could be a traumatic rupture of the fragile Bruch membrane or a choroidal rupture.10
As it is mentioned above, although the disease may remain stable, the most significant complication, leading to decrease of vision, can occur because of the development of CNV. In this occasion, the initial insult could be with the symptoms of metamorphopsia or of rapid and severe deterioration of vision due to the hemorrhage, exudation, edema, retinal epithelium detachment, and sequential subretinal fibrosis and atrophy after CNV. If left untreated, the prognosis is poor, and the disease can progress to blindness in middle-aged working adults.35
The incidence of CNV secondary to angioid streaks lies between 42% and 86%, while it occurs bilaterally even asymmetrically up to 71%.36 Type 2 CNV is the most prominent form, although Type 1 and a mixed pattern can also exist in up to 16% of patients.25 Mansour et al initially described and later confirmed the correlation of the CNV occurrence with the morphologic characteristics of the streaks. Thus, they found a higher percentage of CNV in wider and longer lesions, and the risk for the occurrence was even higher if the streaks were localized less than one optic disk diameter from the center of the posterior pole.37 In addition, macular involvement from CNV is prominent (with the exception of hemoglobinopathies), especially in patients with pseudoxanthoma elasticum.35
The main problem accompanying the CNV in patients with angioid streaks is the frequent recurrence. Even after years without active disease, new CNV can occur either emerging from a preexisting lesion or as new region with neovascularization away from the initial. The final visual acuity depends mainly on the location of CNV, the age of patients at the initial onset of symptoms, and the coexistence of a systemic disease. An important finding is that the attenuation of vision occurs remarkably earlier in patients with angioid streaks in comparison with them who suffer from wet age-related macular degeneration.10
In the differential diagnosis of angioid streaks, a number of diseases insulting the retina are included, such as macular degeneration, choroidal sclerosis, myopia, histoplasmosis, toxoplasmosis, retinal vasculitis, papilledema, and traumatic hemorrhage.31
A series of diagnostic methods, including infrared and red-free retinography, autofluorescence, optical coherence tomography (OCT), the advanced OCT angiography (OCTA), fluorescein angiography (FA), and indocyanine green (ICG) angiography, are useful to diagnose, evaluate, and monitor angioid streaks.
Infrared imaging demonstrates the brick-red–colored streaks as well-demarcated dark fissures against a lighter background (Figure 1A), even when they passed unnoticed on color imaging.38
Autofluorescence is an alternative tool to confirm the presence and progression of angioid streaks. This imaging modality relies on the light that is emitted from lipofuscin in RPE cells, functioning mainly as a measurement of the metabolic activity of the RPE.39,40 The typical pattern is that of hypoautofluorescent fissures indicative of the attenuated or absent RPE in angioid streaks.41,42 Remarkably, the hypofluorescent region can be expanded during the natural course of the disease.42 Moreover, the area of RPE disturbance depicted by autofluorescence is more widespread in comparison with correspondent fundoscopic or fluorangiographic findings (Figure 1B).43 Alternative pattern of angioid streaks in fundus autofluorescence is a reticular pattern of hyperautofluorescence in the macular area, reminiscent of patterned hypercalcification of the Bruch membrane in the posterior pole or irregular lines with hyperautofluorescence speckled in its interior and edges, or bands with lobulated lesions inside and hyperautofluorescence at the edges.44 Infrared, red-free, and autofluorescence imaging are more sensitive than white-light funduscopy and imaging in recognition of early retinal lesions as angioid streaks in patients suffering from pseudoxanthoma elasticum, and they are also more beneficial in the evaluation of the extent of disruptions.38 Nevertheless, it should be noted that autofluorescence evaluates the metabolic characteristics of RPE; however, the pathogenetic mechanism of angioid streaks is localized at the level of Bruch membrane rendering ICG angiography more valuable in the assessment of angioid streaks.39
Optical Coherence Tomography
Optical coherence tomography can be also used to evaluate angioid streaks and the derived CNV, especially in patients with pseudoxanthoma elasticum, where OCT reveals the characteristic calcium deposits at the Bruch membrane level as localized areas of hyperreflectivity.45,46 En face OCT may locate the lesions at the level of Bruch membrane and has the potential to determine the extent of disruptions at the Bruch membrane and its correlation with CNV.47,48 Furthermore, OCT can delineate the sclerochoroidal boundary and determine a thinner choroid in eyes with CNV because of angioid streaks in patients with pseudoxanthoma elasticum in comparison with the healthy control group.49 Accordingly, Ellabban et al50 using swept-source OCT have found that the choroid in eyes with angioid streaks without CNV was as thick as that in normal controls, but was significantly thinner in eyes with angioid streaks that had developed CNV. Recently, Bruch membrane undulations were described and considered as precursors of Bruch membrane breaks, where subsequently develops CNV. Undulations mainly surround the optic nerve head, and they are believed to result from dense stretching forces around the optic nerve.51
Optical Coherence Tomography Angiography
Optical coherence tomography angiography is an innovative, noninvasive method to depict the flow in the vascular structures of the fundus. Orly Gal was the first who assessed the importance of OCTA in detection and monitoring the CNV development in angioid streaks. Interpreting the relationship between Bruch membrane and CNV with OCTA, there is a profound association of the CNV pattern with the form of Bruch membrane disruptions, supporting the hypothesis for the causal role of Bruch membrane breaks in the pathogenesis of the disease. Moreover, the derived pattern of occult CNV regarding the intervening of the new vessels is similar to the morphology of age-related macular degeneration enhancing the hypothesis for a common pathogenetic pathway.25 Recently, findings using the OCTA imaging modality have demonstrated an irregular vascular network, possibly representing fibrovascular tissue over the crack-like breaks in the Bruch membrane.52,53
Fluorescein angiography shows a specific pattern of an early appearance and late retention of the dye in the lesions of angioid streaks (Figure 1C), which could be attributed to the absence of RPE revealing the underlying choriocapillaris (window defect).54–57 The aforementioned hyperfluorescent pattern is the most common with a number of variants, like the presence of a hyperfluorescent line between fluorescent edges or a depiction with numerous hyperfluorescent spots, while hypofluorescent streaks have been also described. It is worthy to note that the prominent role of FA is to confirm the existence of CNV.54–58
Indocyanine Green Angiography
Indocyanine green angiography shows three different patterns in patients with angioid streaks: fluorescent, hypofluorescent, “track-like,” and mixed. These different depictions may represent distinguishable stages of the disease. Lafaut et al58 confirmed the prominence of the fluorescent pattern; however, 20% of cases funduscopically diagnosed were invisible on ICG angiography, while this imaging modality better visualizes occult CNV. In addition, peau d' orange was seen better and found to be more widespread by ICG angiography compared with FA.58–62
As it is mentioned above, CNV constitutes the most detrimental complication of angioid streaks, resulting in visual impairment in working-age patients' impact.63 Without treatment, the prognosis is discouraging because of eventual development of a disciform scar at the fovea during the fourth or fifth decade of life. As a result, the characteristic nature of the disease does not allow for observation without treatment as an option. Parameters that predispose to a worse final visual outcome constitute the age at the initiation of symptoms, the localization of CNV regarding to the fovea, and the presence of a concomitant eye disease as in the patients with pseudoxanthoma elasticum.4
Various treatment modalities have been used for the treatment of CNV secondary to angioid streaks, including laser photocoagulation, transpupillary thermotherapy, photothrombosis, photodynamic therapy (PDT) with verteporfin and surgical approaches with limited success. The critical enhancement of our therapeutic armamentarium was the induction of anti–vascular endothelial growth factor (anti-VEGF) agents. However, for the time being, the available remedies mainly limit the natural course of the disease without permanent inactivation.
Initial Therapies for Choroidal Neovascularization Due to Angioid Streaks
A conservative procedure used in the past for the elimination of CNV in patients with angioid streaks was photocoagulation, which was beneficial strictly for juxtafoveal and extrafoveal lesions.64,65 The first studies using laser photocoagulation for the treatment of angioid streaks were discouraging, as patients presented retinal hemorrhages, degenerative changes, and loss of central vision after treatment.66 Since then, there are several case series, presenting controversial results.64,65,67–71 In addition, because of the central localization of CNV at the fovea and the parafoveal region, laser treatment may have an immediate destructive impact on the treated area, leading either to a central visual acuity deterioration or to a paracentral scotoma, both of them decompensating the visual function.72 Similar to laser photocoagulation, Malerbi et al investigated the efficacy of ICG-mediated photothrombosis on subfoveal CNV secondary to angioid streaks. The authors found that most eyes achieved at least a steady visual acuity and anatomical improvement at the 12-month follow-up.73
Transpupillary thermotherapy has been also used for the treatment of CNV due to angioid streaks in the past, showing no positive effect on disease progression.74,75 Macular translocation and subretinal extraction have been also proposed for the treatment of CNV due to angioid streaks.76–81 Both techniques may provide short-term stabilization in visual acuity, but recurrences are common and adverse events may occur, such as hemorrhage, epiretinal membrane formation, macular edema, proliferative vitreoretinopathy, and retinal detachment.76–81 Therefore, the application of invasive surgical techniques is not recommended.
Photodynamic therapy with verteporfin has been firstly used for the treatment of CNV due to angioid streaks in 2002. Karacorlu et al82 demonstrated stabilization or increase in visual acuity accompanied by a confinement of leakage in FA in eight eyes with angioid streaks. However, most studies have shown no alteration or slight improvement in visual acuity, even with deceleration in disease progression,83–96 suggesting that the disease may persist because it was proven by increase in lesion size in FA.72 By and large, the use of PDT as monotherapy failed because of the need for multiple interventions leading to additional disruptions in the Bruch membrane and subsequent recurrences.97
It is worthy to mention that most of studies used the treatment protocol of the treatment of AMD with PDT (TAP) study examining the patients every 3 months after baseline and retreating them based on FA findings.98 Because the results were discouraging, some groups applied different protocols, performing more frequent reviews and treatment but having no favorable results.86,89
Current Therapy for Choroidal Neovascularization Due to Angioid Streaks
Although the aforementioned therapeutic approaches seem to provide short-term favorable results regarding visual acuity in patients with CNV secondary to angioid streaks, they were found to be insufficient to limit the high recurrence rate of the disease in the long-term follow-up. A new era in the available remedies emerged with the use of anti-VEGF factors, which were previously successfully used for the treatment of CNV due to age-related macular degeneration and other causes.99,100 The most common anti-VEGF agents, which have been used intravitreally for the treatment of CNV due to angioid streaks, were ranibizumab, aflibercept and off-label bevacizumab.101–127 Most studies have shown that anti-VEGF agents are effective to improve or at least stabilize the visual acuity in a long-term follow-up of patients with CNV due to angioid streaks, irrespective of the underlying disease.101–127 In addition, all anti-VEGF agents seem to provide anatomical improvement, reducing central retinal thickness, even not consistent with the grade of functional improvement.105 Interestingly, all anti-VEGF agents seem to have similar efficacy for both juxtafoveal CNV and subfoveal CNV, and their action takes place rapidly despite the natural course of the disease progression,4,63 while the major advantage of anti-VEGF treatment was the cessation of CNV activity without concomitant transformation of the neovascular membrane into scar.105
It is worthy to note that monitoring of patients receiving anti-VEGF agents for angioid streaks is the key to successful outcomes. Patients should be alert regarding potential recurrence, attending a monthly follow-up until CNV is inactivated.63 In addition, because bilateral insult of CNV in patients with angioid streaks is as high as 70%, the examination of the fellow eye seems to be valuable to achieve an early diagnosis and initiate the treatment on time.119 Alagöz et al125 assessed the potential risk factors, which were correlated with a progressive disease, showing that younger age and concurrence of pseudoxanthoma elasticum predispose to a more aggressive and resistant to treatment disease. However, treatment-naive eyes with good visual acuity could achieve visual stability at 2 years, although they seemed to be more vulnerable to the development of RPE atrophy and disruption of the ellipsoid zone compared with previously treated eyes.107
As far as the safety profile of anti-VEGF agents is concerned, studies demonstrated no correlation of the treatment with postinjection intraocular pressure peaks, hyposphagmas, endophthalmitis, uveitis, intravitreal hemorrhage, lens trauma, retinal tear, or detachment.105 However, a critical point to consider is the specific characteristics of patients with CNV secondary to angioid streaks, who usually have concurrent systemic diseases. Although patients with pseudoxanthoma elasticum present high cardiovascular risk, Savastano et al128 did not notice serious thromboembolic or cardiovascular complications in patients with angioid streaks treated with ranibizumab throughout 6-year follow-up.
Regarding the schedule of intervention, a reasonable approach is an induction scheme of 3 monthly injections, followed by a pro re nata protocol based on clinical evaluation, as well as on FA and OCT findings.105 For the time being, pro re nata scheme has been proven effective regarding anatomical and functional aspects in the short term; however, this efficacy seems to attenuate when a strict follow-up program is not feasible to pursue in the long term. This hypothesis may be indicative of the need for a fixed regimen in patients with angioid streaks.4
Apart from anti-VEGF as monotherapy, combination treatment may be considered as a reasonable alternative for the treatment of CNV secondary to angioid streaks. The first relevant study was conducted in 2007, and the authors demonstrated an improvement of visual acuity and transition of CNV into a fibrotic scar after the addition of bevacizumab in patients treated initially only with PDT.129 Accordingly, Pece et al130 combined PDT with a unique injection of intravitreal triamcinolone to achieve fewer PDT interventions, reporting no superiority over the PDT monotherapy, while cataract development and increase of intraocular pressure remain potential adverse events.
A series of studies tried to combine PDT with anti-VEGF agents, but they failed to demonstrate a remarkable difference in the eventual outcome compared with monotherapy.97 The rationale of the combination treatment is the additional effect derived from both the ability of verteporfin to obstruct the new vessels and the potential of anti-VEGF agents to inhibit CNV growth and confine the neovascular leakage. As a consequence, combination therapy targets to long-term disease inactivity with less requirement for reintervention. However, as in separate PDT or anti-VEGF therapy, strict follow-up is required to decide an appropriate intervention.
Angioid streaks are visible, linear, irregular, crack-like dehiscences of Bruch membrane, which may be unilateral or most commonly bilateral. They often coexist with systemic diseases, such as pseudoxanthoma elasticum, Paget disease, Ehlers–Danlos syndrome, hemoglobinopathies, or other diseases of the collagen. A series of diagnostic methods, including infrared and red-free retinography, autofluorescence, OCT, the advanced OCTA, FA, and ICG angiography, are useful to diagnose, evaluate, and monitor angioid streaks. Regarding treatment, it is worthy to note that because CNV consists a major complication of angioid streaks leading to visual impairment, observation could not be a treatment option. Various treatment modalities have been used, offering promising but short-term results, such as PDT and anti-VEGF agents. However, using the currently available remedies, the disease may be limited but not permanently inactivated.
1. Doyne RW. Choroidal and retinal changes. The results of blows on the eyes. Trans Ophthalmol Soc UK 1889;9:128.
2. Knapp H. On formation of dark angiod streaks as an unusual metamorphosis of retinal hemorrhage. Arch Ophthalmol 1892;21:289.
3. Kumudhan D, Wallace EJ, Roxburgh ST. Angioid streaks
in identical twins. Br J Ophthalmol 2004;88:837–838.
4. Martinez-Serrano MG, Rodriguez-Reyes A, Guerrero-Naranjo JL, et al. Long-term follow-up of patients with choroidal neovascularization due to angioid streaks
. Clin Ophthalmol 2016;11:23–30.
5. Batten RD. Angioid streaks
, and their relation to a form of central choroidal disease. Br J Ophthalmol 1931;15:279–289.
6. Katagiri S, Negishi Y, Mizobuchi K, et al. ABCC6
gene analysis in 20 Japanese patients with angioid streaks
revealing four frequent and two novel variants and pseudodominant inheritance. J Ophthalmol 2017;2017:1079687.
7. Deschweinitz GE. Angioid streaks
in retina. Trans Am Ophthalmol Soc 1896;7:650–654.
8. Keith CG. Angioid streaks
and pseudoxanthoma elasticum. Br J Ophthalmol 1956;40:480–486.
9. Georgalas I, Papaconstantinou D, Koutsandrea C, et al. Angioid streaks
, clinical course, complications, and current therapeutic management. Ther Clin Risk Manag 2009;5:81–89.
10. Myung JS, Bhatnagar P, Spaide RF, et al. Long-term outcomes of intravitreal antivascular endothelial growth factor therapy for the management of choroidal neovascularization in pseudoxanthoma elasticum. Retina 2010;30:748–755.
11. Dabbs TR, Skjodt K. Prevalence of angioid streaks
and other ocular complications of Paget's disease of bone. Br J Ophthalmol 1990;74:579–582.
12. Geeraets WJ, Guerry D III. Angioid streaks
and sickle cell disease. Am J Ophthalmol 1960;49:450–470.
13. Nagpal KC, Asdourian G, Goldbaum M, et al. Angioid streaks
and sickle haemoglobinopathies. Br J Ophthalmol 1976;60:31–34.
14. Bertrand JJ, Hart ML, Voisin J. Angioid streaks
and sickle cell anemia [in French]. Bull Soc Ophtalmol Fr 1970;70:1184–1190.
15. Aessopos A, Voskaridou E, Kavouklis E, et al. Angioid streaks
in sickle-thalassemia. Am J Ophthalmol 1994;117:589–592.
16. Ketner S, Moradi IE, Rosenbaum PS. Angioid streaks
in association with sickle thalassemia trait. JAMA Ophthalmol 2015;133:e141770.
17. Wong JG, Qian KY. Long-term follow-up of polypoidal choroidal vasculopathy secondary to angioid streaks
treated by intravitreal aflibercept
. Case Rep Ophthalmol 2017;8:221–231.
18. Tugcu BL, Sezer T, Elbay A, Özdemir H. Angioid streaks
in a case of Camurati-Engelmann disease. Indian J Ophthalmol 2017;65:628–630.
19. Pfendner EG, Vanakker OM, Terry SF, et al. Mutation detection in the ABCC6 gene and genotype-phenotype analysis in a large international case series affected by pseudoxanthoma elasticum. J Med Genet 2007;44:621–628.
20. Hesse RJ, Groetsch J, Burshell A. Pseudoxanthoma elasticum: a novel mutation in the ABCC6 gene that affects eye manifestations of the disease. Ochsner J 2010;10:13–15.
21. Tan MH, Vanakker OM, Tran HV, et al. Angioid streaks
with severe macular dysfunction and generalised retinal involvement due to a homozygous duplication in the ABCC6 gene. Eye 2012;26:753–755.
22. Mizutani Y, Nakayama T, Asai S, et al. ABCC6 mutation in patients with angioid streaks
. Int J Biomed Sci 2006;2:7–12.
23. Sato N, Nakayama T, Mizutani Y, Yuzawa M. Novel mutations of ABCC6 gene in Japanese patients with Angioid streaks
. Biochem Biophys Res Commun 2009;380:548–553.
24. Li Q, Sadowski S, Uitto J. Angioid streaks
in Pseudoxanthoma Elasticum: role of the p.R1268Q mutation in the ABCC6 gene. J Invest Dermatol 2011;131:782–785.
25. Gal-Or O, Balaratnasingam C, Freund KB. Optical coherence tomography angiography findings of choroidal neovascularization in pseudoxanthoma elasticum. Int J Retina Vitreous 2015;1:11.
26. Booij JC, Baas DC, Beisekeeva J, et al. The dynamic nature of Bruch's membrane. Prog Retin Eye Res 2010;29:1–18.
27. Dreyer R, Green WR. The pathology of angioid streaks
: a study of twenty-one cases. Trans Pa Acad Ophthalmol Otolaryngol 1978;31:158–167.
28. Calhoun FP. Concerning the site of angioid streaks
of the fundus oculi. Trans Am Ophthalmol Soc 1927;25:209–216.
29. Hagedoorn A. Angioid streaks
and traumatic ruptures of Bruch's membrane. Br J Ophthalmol 1975;59:267.
30. Spaide RF. Peau d'orange and angioid streaks
: manifestations of Bruch membrane pathology. Retina 2015;35:392–397.
31. Shields JA, Federman JL, Tomer TL, Annesley WH Jr. Angioid streaks
. I. Ophthalmoscopic variations and diagnostic problems. Br J Ophthalmol 1975;59:257–266.
32. Gandorfer A, Ulbig M, Bechmann M, et al. Retinal telangiectasis and angioid streaks
. Br J Ophthalmol 2000;84:1327–1328.
33. Baillif-Gostoli S, Quaranta-El Maftouhi M, Mauget-Faÿsse M. Polypoidal choroidal vasculopathy in a patient with angioid streaks
secondary to pseudoxanthoma elasticum. Graefes Arch Clin Exp Ophthalmol 2010;248:1845–1848.
34. Cebeci Z, Bayraktar S, Oray M, Kir N. Silent polypoidal choroidal vasculopathy in a patient with angioid streaks
. Arq Bras Oftalmol 2016;79:200–201.
35. Al-Rashaed S, Arevalo JF. Long-term follow-up of choroidal neovascularization secondary to angioid streaks
: case series and literature review. Clin Ophthalmol 2012;6:1029–1034.
36. Shah M, Amoaku WM. Intravitreal ranibizumab
for the treatment
of choroidal neovascularisation secondary to angioid streaks
. Eye (Lond) 2012;26:1194–1198.
37. Mansour AM, Ansari NH, Shields JA, et al. Evolution of angioid streaks
. Ophthalmologica 1993;207:57–61.
38. De Zaeytijd J, Vanakker OM, Coucke PJ, et al. Added value of infrared, red-free and autofluorescence fundus imaging
in pseudoxanthoma elasticum. Br J Ophthalmol 2010;94:479–486.
39. Lee TK, Forooghian F, Cukras C, et al. Complementary angiographic and autofluorescence findings in pseudoxanthoma elasticum. Int Ophthalmol 2010;30:77–79.
40. Sayanagi K, Sharma S, Kaiser PK. Spectral domain optical coherence tomography and fundus autofluorescence findings in pseudoxanthoma elasticum. Ophthalmic Surg Lasers Imaging
41. Shiraki K, Kohno T, Moriwaki M, Yanagihara N. Fundus autofluorescence in patients with pseudoxanthoma elasticum. Int Ophthalmol 2001;24:243–248.
42. Sawa M, Ober MD, Freund KB, Spaide RF. Fundus autofluorescence in patients with pseudoxanthoma elasticum. Ophthalmology 2006;113:814–820.
43. Finger RP, Charbel Issa P, Ladewig M, et al. Fundus autofluorescence in Pseudoxanthoma elasticum. Retina 2009;29:1496–1505.
44. Morillo MJ, Mora J, Soler A, et al. Retinal autofluorescence imaging
in patients with pseudoxanthoma elasticum. Arch Soc Esp Oftalmol 2011;86:8–15.
45. Arvas S, Akar S, Yolar M, et al. Optical coherence tomography (OCT) and angiography in patients with angioid streaks
. Eur J Ophthalmol 2002;12:473–481.
46. Ari Yaylali S, Akcakaya AA, Erbil HH, et al. Optical coherence tomography findings in pseudoxanthoma elasticum. Eur J Ophthalmol 2010;20:397–401.
47. Hanhart J, Greifner H, Rozenman Y. Locating and characterizing angioid streaks
with en face optical coherence tomography. Retin Cases Brief Rep 2017;11:203–206.
48. Sampson DM, Alonso-Caneiro D, Chew AL, et al. Enhanced visualization of subtle outer retinal pathology by en face optical coherence tomography and correlation with multi-modal imaging
. PLoS One 2016;11:e0168275.
49. Dolz-Marco R, Andreu-Fenoll M, Hernández-Martínez P, et al. Automated macular choroidal thickness measurement by swept-source optical coherence tomography in pseudoxanthoma elasticum. Int J Retina Vitreous 2016;2:15.
50. Ellabban AA, Tsujikawa A, Matsumoto A, et al. Macular choroidal thickness and volume in eyes with angioid streaks
measured by swept source optical coherence tomography. Am J Ophthalmol 2012;153:1133–1143.
51. Marchese A, Parravano M, Rabiolo A, et al. Optical coherence tomography analysis of evolution of Bruch's membrane features in angioid streaks
. Eye (Lond) 2017;31:1600–1605.
52. Andreanos KD, Rotsos T, Koutsandrea C, et al. Detection of nonexudative choroidal neovascularization secondary to angioid streaks
using optical coherence tomography angiography. Eur J Ophthalmol 2017;27:140–143.
53. Corbelli E, Carnevali A, Marchese A, et al. Optical coherence tomography angiography features of angioid streaks
. Retina. doi: .
54. Szedélyová L. Fluorescein angiography of angioid streaks
. Cesk Slov Oftalmol 1996;52:88–92.
55. Sato K, Ikeda T. Fluorescein angiographic features of neovascular maculopathy in angioid streaks
. Jpn J Ophthalmol 1994;38:417–422.
56. Hull DS, Aaberg TM. Fluorescein study of a family with angioid streaks
and pseudoxanthoma elasticum. Br J Ophthalmol 1974;58:738–745.
57. Federman JL, Shields JA, Tomer TL. Angioid streaks
. II. Fluorescein angiographic features. Arch Ophthalmol 1975;93:951–962.
58. Lafaut BA, Leys AM, Scassellati-Sforzolini B, et al. Comparison of fluorescein and indocyanine green angiography in angioid streaks
. Graefes Arch Clin Exp Ophthalmol 1998;236:346–353.
59. Atmaca LS, Batioğlu F, Atmaca P. Indocyanine green videoangiography of angioid streaks
. Acta Ophthalmol Scand 1997;75:657–660.
60. Blanco Rivera MC, Gómez Ulla De Irazazábal F, Ferrer Jaureguizar J, Abelenda Pose D. Indocyanine green angiography in angioid streaks
. Arch Soc Esp Oftalmol 2001;76:297–302.
61. Pece A, Avanza P, Introini U, Brancato R. Indocyanine green angiography in angioid streaks
. Acta Ophthalmol Scand 1997;75:261–265.
62. Lafaut BA, Priem H, De Laey JJ. Indocyanine green angiography in angioid streaks
. Bull Soc Belge Ophtalmol 1997;265:21–24.
63. Tilleul J, Mimoun G, Querques G, et al. Intravitreal ranibizumab
for choroidal neovascularization in angioid streaks
: four-year follow-up. Retina 2016;36:483–491.
64. Offret G, Coscas G, Orsoni-Dupont C. Photo-coagulation of angioid striae after fluoresceinic angiography. Arch Ophtalmol Rev Gen Ophtalmol 1970;30:419–422.
65. Brancato R, Menchini U, Pece A, et al. Laser treatment
of macular subretinal neovascularizations in angioid streaks
. Ophthalmologica 1987;195:84–87.
66. Schatz H. Other retinal pigment epithelial diseases. Int Ophthalmol Clin 1975;15:181–197.
67. Esente S, Français C, Soubrane G, Coscas G. Angioid streaks
and subretinal neovessels: retrospective study of the results of photocoagulation with krypton laser and green argon laser. Bull Soc Ophtalmol Fr 1987;87:293–296.
68. Gelisken O, Hendrikse F, Deutman AF. A long-term follow-up study of laser coagulation of neovascular membranes in angioid streaks
. Am J Ophthalmol 1988;105:299–303.
69. Pece A, Avanza P, Zorgno F, et al. Laser treatment
of macular subretinal neovascularization in angioid streaks
. J Fr Ophtalmol 1989;12:687–689.
70. Lim JI, Bressler NM, Marsh MJ, Bressler SB. Laser treatment
of choroidal neovascularization in patients with angioid streaks
. Am J Ophthalmol 1993;116:414–423.
71. Pece A, Avanza P, Galli L, Brancato R. Laser photocoagulation of choroidal neovascularization in angioid streaks
. Retina 1997;17:12–16.
72. Gliem M, Finger RP, Fimmers R, et al. Treatment
of choroidal neovascularization due to angioid streaks
: a comprehensive review. Retina 2013;33:1300–1314.
73. Malerbi FK, Huang SJ, Aggio FB, et al. Indocyanine green-mediated photothrombosis for choroidal neovascularization in angioid streaks
. Arq Bras Oftalmol 2008;71:311–315.
74. Aras C, Başerer T, Yolar M, et al. Two cases of choroidal neovascularization treated with transpupillary thermotherapy in angioid streaks
. Retina 2004;24:801–803.
75. Ozdek S, Bozan E, Gürelik G, Hasanreisoglu B. Transpupillary thermotherapy for the treatment
of choroidal neovascularization secondary to angioid streaks
. Can J Ophthalmol 2007;42:95–100.
76. Roth DB, Estafanous M, Lewis H. Macular translocation for subfoveal choroidal neovascularization in angioid streaks
. Am J Ophthalmol 2001;131:390–392.
77. Ehlers JP, Maldonado R, Sarin N, Toth CA. Treatment
of non age-related macular degeneration submacular diseases with macular translocation surgery. Retina 2011;31:1337–1346.
78. Fujii GY, Humayun MS, Pieramici DJ, et al. Initial experience of inferior limited macular translocation for subfoveal choroidal neovascularization resulting from causes other than age-related macular degeneration. Am J Ophthalmol 2001;131:90–100.
79. Adelberg DA, Del Priore LV, Kaplan HJ. Surgery for subfoveal membranes in myopia, angioid streaks
, and other disorders. Retina 1995;15:198–205.
80. Eckstein M, Wells JA, Aylward B, Gregor Z. Surgical removal of non-age-related subfoveal choroidal neovascular membranes. Eye (Lond) 1998;12:775–780.
81. Thomas MA, Dickinson JD, Melberg NS, et al. Visual results after surgical removal of subfoveal choroidal neovascular membranes. Ophthalmology 1994;101:1384–1396.
82. Karacorlu M, Karacorlu S, Ozdemir H, Mat C. Photodynamic therapy
with verteporfin for choroidal neovascularization in patients with angioid streaks
. Am J Ophthalmol 2002;134:360–366.
83. Shaikh S, Ruby AJ, Williams GA. Photodynamic therapy
using verteporfin for choroidal neovascularization in angioid streaks
. Am J Ophthalmol 2003;135:1–6.
84. Karadimas P, Bouzas EA. Photodynamic therapy
with verteporfin for choroidal neovascularization complicating angioid streaks
. Ophthalmic Surg Lasers Imaging
85. Menchini U, Virgili G, Introini U, et al. Outcome of choroidal neovascularization in angioid streaks
after photodynamic therapy
. Retina 2004;24:763–771.
86. Ladas ID, Georgalas I, Rouvas AA, et al. Photodynamic therapy
with verteporfin of choroidal neovascularization in angioid streaks
: conventional versus early retreatment. Eur J Ophthalmol 2005;15:69–73.
87. Chung AK, Gauba V, Ghanchi FD. Photodynamic therapy
(PDT) using verteporfin for juxtafoveal choroidal neovascularisation (CNV) in angioid streaks
(AS) associated with pseudoxanthoma elasticum: 40 months results. Eye (Lond) 2006;20:629–631.
88. Browning AC, Chung AK, Ghanchi F, et al. Verteporfin photodynamic therapy
of choroidal neovascularization in angioid streaks
: one-year results of a prospective case series. Ophthalmology 2005;112:1227–1231.
89. Heimann H, Gelisken F, Wachtlin J, et al. Photodynamic therapy
with verteporfin for choroidal neovascularization associated with angioid streaks
. Graefes Arch Clin Exp Ophthalmol 2005;243:1115–1123.
90. Arias L, Pujol O, Rubio M, Caminal J. Long-term results of photodynamic therapy
for the treatment
of choroidal neovascularization secondary to angioid streaks
. Graefes Arch Clin Exp Ophthalmol 2006;244:753–757.
91. Shyong MP, Chen SJ, Lee FL, et al. Increased and persisted subretinal haemorrhage after photodynamic therapy
for choroidal neovascularization secondary to angioid streaks
. Eye (Lond) 2006;20:1420–1422.
92. Jurklies B, Bornfeld N, Schilling H. Photodynamic therapy
using verteporfin for choroidal neovascularization associated with angioid streaks
–long-term effects. Ophthalmic Res 2006;38:209–217.
93. Schargus M, Guthoff R, Keilhauer C, Schrader WF. Photodynamic therapy
in classic chorioidal neovascularisation in patients with angioid streaks
[in German]. Klin Monbl Augenheilkd 2006;223:987–992.
94. Lee JM, Nam WH, Kim HK. Photodynamic therapy
with verteporfin for choroidal neovascularization in patients with angioid streaks
. Korean J Ophthalmol 2007;21:142–145.
95. González-Blanco MJ, Blanco-Rivera C, Campos-García S. Treatment
of angioid streaks
with phothodynamic therapy. Arch Soc Esp Oftalmol 2007;82:719–722.
96. Elías-de-Tejada M, Calvo-González C, Reche-Frutos J, et al. Photodynamic therapy
in angioid streaks
. Arch Soc Esp Oftalmol 2007;82:741–746.
97. Artunay O, Yuzbasioglu E, Rasier R, et al. Combination treatment
with intravitreal injection of ranibizumab
and reduced fluence photodynamic therapy
for choroidal neovascularization secondary to angioid streaks
: preliminary clinical results of 12-month follow-up. Retina 2011;31:1279–1286.
98. Harding SP, Tomlin K, Reeves BC, et al. Verteporfin photodynamic therapy
cohort study: report 1: effectiveness and factors influencing outcomes. Ophthalmology 2009;116:1–8.
99. Rosenfeld PJ, Brown DM, Heier JS, et al. Ranibizumab
for neovascular age-related macular degeneration. N Engl J Med 2006;355:1419–1431.
100. Lai TYY, Staurenghi G, Lanzetta P, et al. Efficacy and safety of ranibizumab
for the treatment
of choroidal neovascularization due to uncommon cause: twelve-month results of the MINERVA Study. Retina 2018;38:1464–1477.
101. Kang S, Roh YJ. Intravitreal ranibizumab
for choroidal neovascularisation secondary to angioid streaks
. Eye (Lond) 2009;23:1750–1751.
102. Lazaros K, Leonidas Z. Intravitreal ranibizumab
as primary treatment
for neovascular membrane associated with angioid streaks
. Acta Ophthalmol 2010;88:100–101.
103. Vadalà M, Pece A, Cipolla S, et al. Angioid streak-related choroidal neovascularization treated by intravitreal ranibizumab
. Retina 2010;30:903–907.
104. Ladas ID, Kotsolis AI, Ladas DS, et al. Intravitreal ranibizumab treatment
of macular choroidal neovascularization secondary to angioid streaks
: one-year results of a prospective study. Retina 2010;30:1185–1189.
105. Mimoun G, Tilleul J, Leys A, et al. Intravitreal ranibizumab
for choroidal neovascularization in angioid streaks
. Am J Ophthalmol 2010;150:692–700.
106. Finger RP, Charbel Issa P, Hendig D, et al. Monthly ranibizumab
for choroidal neovascularizations secondary to angioid streaks
in pseudoxanthoma elasticum: a one-year prospective study. Am J Ophthalmol 2011;152:695–703.
107. Zebardast N, Adelman RA. Intravitreal ranibizumab
of choroidal neovascularization secondary to angioid streaks
in pseudoxanthoma elasticum: five-year follow-up. Semin Ophthalmol 2012;27:61–64.
108. Ebran JM, Mimoun G, Cohen SY, et al. Treatment
for choroidal neovascularization secondary to a pseudoxanthoma elasticum: results of the French observational study PiXEL. J Fr Ophtalmol 2016;39:370–375.
109. Ladas DS, Koutsandrea C, Kotsolis AI, et al. Intravitreal ranibizumab
for choroidal neovascularization secondary to angiod streaks. Comparison of the 12 and 24-month results of treatment
-naïve eyes. Eur Rev Med Pharmacol Sci 2016;20:2779–2785.
110. Mimoun G, Ebran JM, Grenet T, et al. Ranibizumab
for choroidal neovascularization secondary to pseudoxanthoma elasticum: 4-year results from the PIXEL study in France. Graefes Arch Clin Exp Ophthalmol 2017;255:1651–1660.
111. Vaz-Pereira S, Collaço L, De Salvo G, van Zeller P. Intravitreal aflibercept
for choroidal neovascularisation in angioid streaks
. Eye 2015;29:1236–1238.
112. Esen E, Sizmaz S, Demircan N. Intravitreal aflibercept
for management of subfoveal choroidal neovascularization secondary to angioid streaks
. Indian J Ophthalmol 2015;63:616–618.
113. Teixeira A, Moraes N, Farah ME, Bonomo PP. Choroidal neovascularization treated with intravitreal injection of bevacizumab (Avastin) in angioid streaks
. Acta Ophthalmol Scand 2006;84:835–836.
114. Bhatnagar P, Freund KB, Spaide RF, et al. Intravitreal bevacizumab for the management of choroidal neovascularization in pseudoxanthoma elasticum. Retina 2007;27:897–902.
115. Neri P, Salvolini S, Mariotti C, et al. Long-term control of choroidal neovascularisation secondary to angioid streaks
treated with intravitreal bevacizumab (Avastin). Br J Ophthalmol 2009;93:155–158.
116. Wiegand TW, Rogers AH, McCabe F, et al. Intravitreal bevacizumab (Avastin) treatment
of choroidal neovascularisation in patients with angioid streaks
. Br J Ophthalmol 2009;93:47–51.
117. Kovach JL, Schwartz SG, Hickey M, Puliafito CA. Thirty-two month follow-up of successful treatment
of choroidal neovascularization from angioid streaks
with intravitreal bevacizumab. Ophthalmic Surg Lasers Imaging
118. Schiano Lomoriello D, Parravano MC, Chiaravalloti A, Varano M. Choroidal neovascularization in angioid streaks
and pseudoxanthoma elasticum: 1 year follow-up. Eur J Ophthalmol 2009;19:151–153.
119. Sawa M, Gomi F, Tsujikawa M, et al. Long-term results of intravitreal bevacizumab injection for choroidal neovascularization secondary to angioid streaks
. Am J Ophthalmol 2009;148:584–590.
120. Teixeira A, Mattos T, Velletri R, et al. Clinical course of choroidal neovascularization secondary to angioid streaks
treated with intravitreal bevacizumab. Ophthalmic Surg Lasers Imaging
121. El Matri L, Kort F, Bouraoui R, et al. Intravitreal bevacizumab for the treatment
of choroidal neovascularization secondary to angioid streaks
: one year of follow-up. Acta Ophthalmol 2011;89:641–646.
122. Finger RP, Charbel Issa P, Schmitz-Valckenberg S, et al. Long-term effectiveness of intravitreal bevacizumab for choroidal neovascularization secondary to angioid streaks
in pseudoxanthoma elasticum. Retina 2011;31:1268–1278.
123. Battaglia Parodi M, Iacono P, La Spina C, et al. Intravitreal bevacizumab for nonsubfoveal choroidal neovascularization associated with angioid streaks
. Am J Ophthalmol 2014;157:374–377.
124. Rosina C, Romano M, Cigada M, et al. Intravitreal bevacizumab for choroidal neovascularization secondary to angioid streaks
: a long-term follow-up study. Eur J Ophthalmol 2015;25:47–50.
125. Alagöz C, Alagöz N, Özkaya A, et al. Intravitreal bevacizumab in the treatment
of choroidal neovascular membrane due to angioid streaks
. Retina 2015;35:2001–2010.
126. Iacono P, Battaglia Parodi M, La Spina C, Bandello F. Intravitreal bevacizumab for nonsubfoveal choroidal neovascularization associated with angioid streaks
: 3-year follow-up study. Am J Ophthalmol 2016;165:174–178.
127. Lekha T, Prasad HN, Sarwate RN, et al. Intravitreal bevacizumab for choroidal neovascularization associated with angioid streaks
: long-term results. Middle East Afr J Ophthalmol 2017;24:136–142.
128. Savastano MC, Minnella AM, Zinzanella G, et al. Successful long-term management of choroidal neovascularization secondary to angioid streaks
in a patient with pseudoxanthoma elasticum: a case report. J Med Case Rep 2014;8:458.
129. Lommatzsch A, Spital G, Trieschmann M, Pauleikhoff D. Intraocular application of bevacizumab for the treatment
of choroidal neovascularization secondary to angioid streaks
. Ophthalmologe 2007;104:325–328.
130. Pece A, Russo G, Ricci F, et al. Verteporfin photodynamic therapy
combined with intravitreal triamcinolone for choroidal neovascularization due to angioid streaks
. Clin Ophthalmol 2010;4:525–530.