Neovascularizacion coroidea secundaria a coroideremia

Campos-Pavón, J.; Torres-Peña, José L.

doi:10.1016/j.oftal.2014.03.012

Cited by 12 publications

(3 citation statements)

References 5 publications

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“…Although moderate levels of VEGF-A are mandatory to maintain fenestration of choroidal endothelium and to prevent apoptosis of endothelial cells [9,10,80], high levels of VEGF-A can cause serious harm: high levels of VEGF-A cause choroidal neovascularization leading to abundant ingrowth of vessels from the choroid through Bruch's membrane into the subretinal space. This has also been reported in chorioderemia, and could be treated with anti-VEGF-A therapy [81][82][83][84][85]. A comparable picture has been drawn from analysis of RPE cells from choroidal neovascular membranes isolated from patients with age-related macular degeneration.…”

Section: Discussionsupporting

confidence: 56%

Rab27a GTPase modulates L-type Ca2+ channel function via interaction with the II–III linker of CaV1.3 subunit

Reichhart

Markowski

Ishiyama

et al. 2015

Cellular Signalling

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Section: Discussionsupporting

confidence: 56%

Rab27a GTPase modulates L-type Ca2+ channel function via interaction with the II–III linker of CaV1.3 subunit

Reichhart

Markowski

Ishiyama

et al. 2015

Cellular Signalling

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“…Two follow-up visits (at 6 and 12 months after presentation) showed stability of his visual acuity and complete resolution of intraretinal fluid on repeat OCT testing was observed. A recent report had also highlighted the spontaneous regression of CNV in a patient with choroideremia [11]. …”

Section: Discussionmentioning

confidence: 99%

Spontaneous Regression of Choroidal Neovascularization in a Patient with Pattern Dystrophy

Anastasakis

Goleni

Livir-Rallatos

et al. 2016

Case Reports in Ophthalmological Medicine

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Purpose. To present a case of a patient with pattern dystrophy (PD) associated choroidal neovascularization (CNV) that resolved spontaneously without treatment. Methods. A 69-year-old male patient was referred to our unit, for evaluation of a recent visual loss (metamorphopsias) in his left eye. Fundus examination, fundus autofluorescence imaging, and fluorescein angiography showed a choroidal neovascular membrane in his left eye. Since visual acuity was satisfactory the patient elected observation. Clinical examination and OCT testing were repeated at 6 and 12 months after presentation. Results. Visual acuity remained stable at the level of 0.9 (baseline BCVA) during the follow-up period (12 months). Repeat OCT testing showed complete spontaneous regression of the choroidal neovascular membrane without evidence of intra- or subretinal fluid in both follow-up visits. Conclusions. Spontaneous regression of choroidal neovascularization can occur in patients with retinal dystrophies and associated choroidal neovascular membranes. The decision to treat or observe these patients relies strongly on the presenting visual acuity, since, in isolated instances, spontaneous resolution of choroidal neovascularization may occur.

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“…Moreover, a few articles have reported examples of female CHM carriers with areas of chorioretinal atrophy in the retinal periphery, highlighting that also carriers have clinical heterogenicity 27,28…”

Section: Clinical Diagnosismentioning

confidence: 99%

<p>Choroideremia: Update On Clinical Features And Emerging Treatments</p>

Brambati¹,

Borrelli²,

Sacconi³

et al. 2019

OPTH

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Choroideremia (CHM) is an X-linked chorioretinal dystrophy characterized by progressive degeneration of the choroid, retinal pigment epithelium and retina. This disease is caused by mutations in the X-linked CHM gene encoding a Ras-related GTPase Rab escort protein (REP)-1, which is extremely important for the retinal function. Clinically, male-affected patients have a progressive reduction in visual acuity. This disease is formally considered incurable, although new promising treatments have been recently introduced. In this article, a review of the salient pathogenetic features of choroideremia, essential for the proper interpretation of therapeutic approaches, is followed by a discussion of the fundamental clinical features of this hereditary disease. Finally, relevant new therapeutic approaches in this disease will be discussed, including gene therapy, stem cells, small molecules, and retinal prosthesis.

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Neovascularizacion coroidea secundaria a coroideremia

Cited by 12 publications

References 5 publications

Rab27a GTPase modulates L-type Ca2+ channel function via interaction with the II–III linker of CaV1.3 subunit

Rab27a GTPase modulates L-type Ca2+ channel function via interaction with the II–III linker of CaV1.3 subunit

Spontaneous Regression of Choroidal Neovascularization in a Patient with Pattern Dystrophy

<p>Choroideremia: Update On Clinical Features And Emerging Treatments</p>

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