Therapeutic benefit of melatonin in refractory central serous chorioretinopathy

Gramajo, Ana L.; Marquez, Gabriel E.; Torres, Víctor Eduardo; Juárez, Cecilia P.; Rosenstein, Ruth E.; Luna, José D.

doi:10.1038/eye.2015.104

Cited by 36 publications

(25 citation statements)

References 51 publications

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“…As a whole, these have had poor evidence, including: rifampin, 18 Helicobacter Pylori treatment, 19–21 carbonic anhydrase inhibitors 22,23 , finasteride 24 , beta-blockers, 25 antioxidants, 26–28 aspirin. 29 Mineralocorticoid receptor antagonists appear to be the most promising of the systemic medications used in the management of CSCR.…”

Section: Management Of Chronic Diseasementioning

confidence: 99%

Diagnosed a Patient with Central Serous Chorioretinopathy? Now What?: Management of Central Serous Chorioretinopathy

Goldhagen

Goldhardt

2017

Curr Ophthalmol Rep

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Purpose of review: What is the goal of your paper? What questions did you seek to answer? The goal of this paper is to provide a comprehensive review of the management options for central serous chorioretinopathy (CSCR). Recent findings: Summarize the latest research on your topic The majority of cases of acute CSCR may be managed with observation and cessation of corticosteroids, if possible, as well as life-style modifications including stress reduction and control of hypertension. The management of chronic disease is more challenging and may include either medication or laser-based treatment. Summary: What answers did you find? What are the major takeaways/conclusions of your examination? What’s the impact on future research? Management of CSCR necessitates an individualized and selective treatment approach. There is overall poor evidence for the use of systemic and intravitreal medications. From this class of treatments, mineralocorticoid receptor antagonists appear to have the greatest potential. Although conventional thermal photocoagulation may be used in select cases, the most promising treatment options at this time for chronic CSCR are photodynamic therapy, either half-dose or half-fluence, and non-damaging (subthreshold) retinal laser therapy.

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Section: Management Of Chronic Diseasementioning

confidence: 99%

Diagnosed a Patient with Central Serous Chorioretinopathy? Now What?: Management of Central Serous Chorioretinopathy

Goldhagen

Goldhardt

2017

Curr Ophthalmol Rep

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“…Besides the pineal gland, melatonin is also biosynthesized in the retina, where it behaves as an endogenous neuromodulator . Melatonin may act as a protective agent in ocular conditions such as photo‐keratitis, cataract, retinopathy of prematurity, and ischemia/reperfusion injury , as well as human refractory central serous chorioretinopathy . Moreover, we have previously shown the beneficial effect of melatonin against retinal glaucomatous , uveitic , and type 2 diabetic damage.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of melatonin in experimental optic neuritis in rats

Aranda

Fleitas

Laurentiis

et al. 2016

Journal of Pineal Research

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Optic neuritis (ON) is an inflammatory, demyelinating, and neurodegenerative condition of the optic nerve, which might induce permanent vision loss. Currently, there are no effective therapies for this disorder. We have developed an experimental model of primary ON in rats through a single microinjection of 4.5 μg of bacterial lipopolysaccharide (LPS) into the optic nerve. Since melatonin acts as a pleiotropic therapeutic agent in various neurodegenerative diseases, we analyzed the effect of melatonin on LPS-induced ON. For this purpose, LPS or vehicle were injected into the optic nerve from adult male Wistar rats. One group of animals received a subcutaneous pellet of 20 mg melatonin at 24 hr before vehicle or LPS injection, and another group was submitted to a sham procedure. Melatonin completely prevented the decrease in visual evoked potentials (VEPs), and pupil light reflex (PLR), and preserved anterograde transport of cholera toxin β-subunit from the retina to the superior colliculus. Moreover, melatonin prevented microglial reactivity (ED1-immunoreactivity, P < 0.01), astrocytosis (glial fibrillary acid protein-immunostaining, P < 0.05), demyelination (luxol fast blue staining, P < 0.01), and axon (toluidine blue staining, P < 0.01) and retinal ganglion cell (Brn3a-immunoreactivity, P < 0.01) loss, induced by LPS. Melatonin completely prevented the increase in nitric oxide synthase 2, cyclooxygenase-2 levels (Western blot) and TNFα levels, and partly prevented lipid peroxidation induced by experimental ON. When the pellet of melatonin was implanted at 4 days postinjection of LPS, it completely reversed the decrease in VEPs and PLR. These data suggest that melatonin could be a promising candidate for ON treatment.

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“…Evidence strongly supports that melatonin and its metabolites act both as direct and indirect antioxidants by free radicals scavengers, antioxidant enzymes stimulators and other antioxidants activities enhancers . Melatonin may also act as a shield in other ocular afflictions such as cataract, photokeratitis, prematurity retinopathy and injury due to ischaemia/reperfusion, as well as refractory central serous chorioretinopathy in humans . We have previously exposed the benefits of the treatment with melatonin against glaucoma, uveitis, type‐2 diabetes mellitus‐induced retinal damage and optic neuritis .…”

Section: Introductionmentioning

confidence: 99%

Melatonin protects the retina from experimental nonexudative age‐related macular degeneration in mice

Dieguez

Fleitas

Aranda

et al. 2020

Journal of Pineal Research

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Nonexudative age‐related macular degeneration (NE‐AMD) represents the leading cause of blindness in the elderly. Currently, there are no available treatments for NE‐AMD. We have developed a NE‐AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces the disease hallmarks. Several lines of evidence strongly support the involvement of oxidative stress in NE‐AMD‐induced retinal pigment epithelium (RPE) and outer retina damage. Melatonin is a proven and safe antioxidant. Our aim was analysing the effect of melatonin in the RPE/outer retina damage within experimental NE‐AMD. The treatment with melatonin starting 48 h after SCGx, which had no effect on the ubiquitous choriocapillaris widening, protected visual functions and avoided Bruch´s membrane thickening, RPE melanin content, melanosome number loss, retinoid isomerohydrolase (RPE65)‐immunoreactivity decrease, and RPE and hotoreceptor ultrastructural damage induced within experimental NE‐AMD exclusively located at the central temporal (but not nasal) region. Melatonin also prevented the increase in outer retina/RPE oxidative stress markers and a decrease in mitochondrial mass at 6 weeks post‐SCGx. Moreover, when the treatment with melatonin started at 4 weeks post‐SCGx, it restored visual functions and reversed the decrease in RPE melanin content and RPE65‐immunoreactivity. These findings suggest that melatonin could become a promising safe therapeutic strategy for NE‐AMD.

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Therapeutic benefit of melatonin in refractory central serous chorioretinopathy

Cited by 36 publications

References 51 publications

Diagnosed a Patient with Central Serous Chorioretinopathy? Now What?: Management of Central Serous Chorioretinopathy

Diagnosed a Patient with Central Serous Chorioretinopathy? Now What?: Management of Central Serous Chorioretinopathy

Neuroprotective effect of melatonin in experimental optic neuritis in rats

Melatonin protects the retina from experimental nonexudative age‐related macular degeneration in mice

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