RESUMO
PURPOSE: To study the choroidal thickness (CT) and central macular thickness (CMT) in post-fever retinitis (PFR) and their correlation with visual acuity and treatment. METHODS: A retrospective, observational study of patients presenting with PFR from 2013 to 2021 and with spectral domain optical coherence tomography (SD-OCT) (Heidelberg®, SpectralisTM, Heidelberg, Germany) images were included. The CT and CMT were measured at presentation and at the final visit. The CT was measured subfoveally and at points 2000 µm superior, inferior, medial, and lateral from the fovea using the caliper tool. RESULTS: Seventy-nine eyes of 65 patients were included for this study. The mean age was 39.03 (±16.00) years with female preponderance of 53.84% (n = 35). Mean follow-up duration was 30 days. Mean CT at presentation and at follow-up was 254.12 µm and 241.51 µm, respectively. CT was decreased in majority of the eyes 67.1% (n = 53) from their baseline value. Mean CMTs at presentation and final visit were 454.8 µm and 223.7 µm, respectively. Best corrected visual acuity had a positive correlation with CMT (r = 0.340; P = 0.002) and negligible correlation with CT. A significant decrease in the mean CT was noted in patients who received doxycycline either alone or in combination with a steroid as compared to those who did not receive any treatment (P < 0.001). The significance of which is unknown presently. CONCLUSION: CMT has a greater role in determining the final visual outcome than CT. CT can be reduced post-treatment with no effect on vision.
Assuntos
Corioide , Macula Lutea , Retinite , Tomografia de Coerência Óptica , Acuidade Visual , Humanos , Feminino , Estudos Retrospectivos , Masculino , Tomografia de Coerência Óptica/métodos , Adulto , Corioide/patologia , Corioide/diagnóstico por imagem , Acuidade Visual/fisiologia , Macula Lutea/patologia , Macula Lutea/diagnóstico por imagem , Retinite/diagnóstico , Retinite/tratamento farmacológico , Retinite/fisiopatologia , Seguimentos , Pessoa de Meia-Idade , Infecções Oculares Bacterianas/diagnóstico , Infecções Oculares Bacterianas/tratamento farmacológico , Adulto Jovem , Antibacterianos/uso terapêutico , AdolescenteRESUMO
OBJECTIVE: We documented an older female with Coronavirus(CoV) Disease 2019 (COVID-19) and concomitant acquired monocular blindness. We examined this phenomenon in order to understand COVID-19 better. METHODS: We observed an older female with COVID-19 and concomitant acquired monocular blindness. The following indicators were monitored during the course of the disease: ocular examinations, flash visual evoked potential examination, a blood test for COVID-19 IgM antibodies, as well as nasopharyngeal swab and tear sample tests for COVID-19 nucleic acid. RESULTS: The patient's visual acuity for the left eye was NLP and the intraocular pressure was 51 mmHg. Keratic precipitates similar to mutton-fat were spread over the corneal endothelium of the left eye. The funduscopic examination of the patient's left eye revealed severe retinal arterial ischemia, and the color of the retina was off-white. Compared to the right eye, the flash visual evoked potential examination revealed a moderate decrease in P2 wave amplitude for the left eye. A blood test was positive for COVID-19 IgM antibodies, and a nasopharyngeal swab test taken for COVID-19 nucleic acid was positive on May 4, 2020. A sample of the patient's tears was taken, and the nucleic acid test for COVID-19 was still positive two weeks later. CONCLUSIONS: Our study was the first to find that acute viral retinitis could occur in patients with COVID-19 and severe blindness could be associated with SARS-CoV-2 infection. Therefore, physicians should consider the possibility of coronavirus infection in patients with an abnormal fundus or suddenly vision loss.
Assuntos
Cegueira/diagnóstico , COVID-19/diagnóstico , Infecções Oculares Virais/diagnóstico , Retinite/diagnóstico , SARS-CoV-2/isolamento & purificação , Idoso , Cegueira/virologia , COVID-19/virologia , Teste de Ácido Nucleico para COVID-19 , Teste Sorológico para COVID-19 , Potenciais Evocados Visuais/fisiologia , Infecções Oculares Virais/virologia , Feminino , Angiofluoresceinografia , Humanos , Imunoglobulina M/sangue , Estimulação Luminosa , Retina/fisiopatologia , Retinite/fisiopatologia , Retinite/virologia , SARS-CoV-2/genética , SARS-CoV-2/imunologia , Acuidade VisualRESUMO
Purpose: To study treatment outcomes with and without oral corticosteroids in epidemic retinitis (ER).Method: A retrospective, observational study of 35 eyes of 29 patients diagnosed as ER. Days taken for resolution of macular edema and retinitis lesions were compared in patients treated with oral antibiotics (Group 1) and with corticosteroids-antibiotics combination (Group 2).Result: Eighteen eyes of 14 patients and 17 eyes of 15 patients formed Groups 1 and 2, respectively. At the presentation, mean best-corrected visual acuity (BCVA) was 40 and 44 letters and mean central macular thickness was 648 (±243) and 626 (±256) microns in Groups 1 and 2, respectively. Macular edema resolved in 30.83 and 31.94 days; retinitis lesions resolved in 36.71 and 41.41 days in Groups 1 and 2, respectively. BCVA improved to 74 and 77 letters in Groups 1 and 2, respectively.Conclusion: ER with macular edema can be well managed without corticosteroids.
Assuntos
Glucocorticoides/administração & dosagem , Edema Macular/tratamento farmacológico , Retinite/tratamento farmacológico , Administração Oral , Adolescente , Adulto , Idoso , Antibacterianos/uso terapêutico , Feminino , Humanos , Edema Macular/diagnóstico , Edema Macular/fisiopatologia , Masculino , Pessoa de Meia-Idade , Retinite/diagnóstico , Retinite/fisiopatologia , Retinite/virologia , Estudos Retrospectivos , Resultado do Tratamento , Acuidade Visual/fisiologia , Adulto JovemRESUMO
N-Methyl-D-aspartate (NMDA)-induced neuronal cell death is involved in a large spectrum of diseases affecting the brain and the retina such as Alzheimer's disease and diabetic retinopathy. Associated neurological impairments may result from the inhibition of neuronal plasticity by Nogo-A. The objective of the current study was to determine the contribution of Nogo-A to NMDA excitotoxicity in the mouse retina. We observed that Nogo-A is upregulated in the mouse vitreous during NMDA-induced inflammation. Intraocular injection of a function-blocking antibody specific to Nogo-A (11C7) was carried out 2 days after NMDA-induced injury. This treatment significantly enhanced visual function recovery in injured animals. Strikingly, the expression of potent pro-inflammatory molecules was downregulated by 11C7, among which TNFα was the most durably decreased cytokine in microglia/macrophages. Additional analyses suggest that TNFα downregulation may stem from cofilin inactivation in microglia/macrophages. 11C7 also limited gliosis presumably via P.Stat3 downregulation. Diabetic retinopathy was associated with increased levels of Nogo-A in the eyes of donors. In summary, our results reveal that Nogo-A-targeting antibody can stimulate visual recovery after retinal injury and that Nogo-A is a potent modulator of excitotoxicity-induced neuroinflammation. These data may be used to design treatments against inflammatory eye diseases.
Assuntos
Células Amácrinas/efeitos dos fármacos , Anti-Inflamatórios/farmacologia , Anticorpos Neutralizantes/farmacologia , Proteínas Nogo/antagonistas & inibidores , Células Ganglionares da Retina/efeitos dos fármacos , Retinite/prevenção & controle , Visão Ocular/efeitos dos fármacos , Idoso , Idoso de 80 Anos ou mais , Células Amácrinas/metabolismo , Células Amácrinas/patologia , Animais , Retinopatia Diabética/metabolismo , Modelos Animais de Doenças , Feminino , Humanos , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Microglia/metabolismo , N-Metilaspartato , Plasticidade Neuronal/efeitos dos fármacos , Proteínas Nogo/metabolismo , Fosforilação , Recuperação de Função Fisiológica , Células Ganglionares da Retina/metabolismo , Células Ganglionares da Retina/patologia , Retinite/induzido quimicamente , Retinite/metabolismo , Retinite/fisiopatologia , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais , Fator de Necrose Tumoral alfa/metabolismoAssuntos
Infecções Oculares Parasitárias/cirurgia , Terapia a Laser , Recuperação de Função Fisiológica/fisiologia , Retinite/cirurgia , Acuidade Visual/fisiologia , Doença Aguda , Infecções Oculares Parasitárias/diagnóstico por imagem , Infecções Oculares Parasitárias/fisiopatologia , Feminino , Humanos , Retinite/diagnóstico por imagem , Retinite/fisiopatologia , Tomografia de Coerência Óptica , Adulto JovemRESUMO
Angiotensin II and aldosterone are the main effectors of the renin-angiotensin aldosterone system (RAAS) and have a central role in hypertension as well as cardiovascular and renal disease. The localization of RAAS components within the retina has led to studies investigating the roles of angiotensin II, aldosterone and the counter regulatory arm of the pathway in vision-threatening retinopathies. This review will provide a brief overview of RAAS components as well as the vascular pathology that develops in the retinal diseases, retinopathy of prematurity, diabetic retinopathy and neovascular age-related macular degeneration. The review will discuss pre-clinical and clinical evidence that modulation of the RAAS alters the development of vasculopathy and inflammation in the aforementioned retinopathies, as well as the emerging role of aldosterone and the mineralocorticoid receptor in central serous chorioretinopathy.
Assuntos
Aldosterona/fisiologia , Angiotensina II/fisiologia , Retinopatia Diabética/fisiopatologia , Vasos Retinianos/fisiologia , Retinite/fisiopatologia , Retinopatia da Prematuridade/fisiopatologia , Degeneração Macular Exsudativa/fisiopatologia , Inibidores da Enzima Conversora de Angiotensina , Humanos , Receptor Tipo 1 de Angiotensina , Sistema Renina-Angiotensina/fisiologiaRESUMO
[Full article available at http://rimed.org/rimedicaljournal-2019-03.asp].
Assuntos
Retinite/diagnóstico , Toxoplasmose Ocular/diagnóstico , Adulto , Feminino , Humanos , Retinite/parasitologia , Retinite/fisiopatologia , Toxoplasma/isolamento & purificação , Toxoplasmose Ocular/fisiopatologia , Acuidade VisualRESUMO
We have reported the gateway reflex, which describes specific neural activations that regulate immune cell gateways at specific blood vessels in the central nervous system (CNS). Four types of gateway reflexes exist, all of which induce alterations in endothelial cells at specific vessels of the blood-brain barrier followed by inflammation in the CNS in the presence of CNS-autoreactive T cells. Here we report a new gateway reflex that suppresses the development of retinal inflammation by using an autoreactive T cell-mediated ocular inflammation model. Exposure to photopic light down-regulated the adrenoceptor pathway to attenuate ocular inflammation by suppressing breaching of the blood-retina barrier. Mechanistic analysis showed that exposure to photopic light down-regulates the expression of α1A-adrenoceptor (α1AAR) due to high levels of norepinephrine and epinephrine, subsequently suppressing inflammation. Surgical ablation of the superior cervical ganglion (SCG) did not negate the protective effect of photopic light, suggesting the involvement of retinal noradrenergic neurons rather than sympathetic neurons from the SCG. Blockade of α1AAR signaling under mesopic light recapitulated the protective effect of photopic light. Thus, targeting regional adrenoceptor signaling might represent a novel therapeutic strategy for autoimmune diseases including those that affect organs separated by barriers such as the CNS and eyes.
Assuntos
Visão de Cores/fisiologia , Receptores Adrenérgicos alfa 1/metabolismo , Retinite/fisiopatologia , Adrenérgicos/metabolismo , Animais , Doenças Autoimunes/imunologia , Autoimunidade/genética , Autoimunidade/fisiologia , Barreira Hematoencefálica/metabolismo , Barreira Hematorretiniana/metabolismo , Sistema Nervoso Central/metabolismo , Células Endoteliais/metabolismo , Epinefrina/metabolismo , Feminino , Inflamação/metabolismo , Luz , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Neurônios/metabolismo , Norepinefrina/metabolismo , Receptores Adrenérgicos/metabolismo , Gânglio Cervical Superior/metabolismo , Linfócitos T/imunologiaRESUMO
Diabetic retinopathy (DR) and retinopathy of prematurity (ROP) present two examples of proliferative retinopathy, characterized by the same stages of progression; ischemia of the retinal vessels, leads to hypoxia and to correct the problem there is the setting up of uncontrolled angiogenesis, which subsequently causes blindness or even detachment of the retina. The difference is the following; that DR initiated by the metabolic complications that are due to hyperglycemia, and ROP is induced by overexposure of the neonatal retina to oxygen. In this review, we will demonstrate the physiopathological mechanism of the two forms of proliferative retinopathy DR and ROP, in particular the role of the CD40/CD40L axis and IL-1 on vascular complications and onset of inflammation of the retina, the implications of their effects on the onset of pathogenic angiogenesis, thus understanding the link between platelets and retinal ischemia. In addition, what are the therapeutic targets that could slow its progression?
Assuntos
Hipóxia/complicações , Isquemia/complicações , Neovascularização Patológica/complicações , Vasos Retinianos/patologia , Retinite/etiologia , Vitreorretinopatia Proliferativa/etiologia , Animais , Retinopatia Diabética/complicações , Retinopatia Diabética/patologia , Retinopatia Diabética/fisiopatologia , Humanos , Hipóxia/patologia , Hipóxia/fisiopatologia , Isquemia/patologia , Isquemia/fisiopatologia , Neovascularização Patológica/patologia , Neovascularização Patológica/fisiopatologia , Retina/patologia , Vasos Retinianos/fisiopatologia , Retinite/patologia , Retinite/fisiopatologia , Retinopatia da Prematuridade/etiologia , Retinopatia da Prematuridade/patologia , Retinopatia da Prematuridade/fisiopatologia , Vitreorretinopatia Proliferativa/patologia , Vitreorretinopatia Proliferativa/fisiopatologiaRESUMO
Autophagy is a lysosomal degradation process that maintains cellular homeostasis by removing dysfunctional organelles and unfolded proteins. Increasing evidence has shown that autophagy proteins are involved in retinal physiology and pathology and that defective autophagy contributes to retinal degeneration. In retinal diseases, autophagy plays a dual role: promoting retinal cell survival and death. Autophagy at a normal level helps retinal cells defend themselves against harmful stress; however, excessive autophagy results in retinal deterioration. Both synergistic and antagonistic roles of autophagy and apoptosis in the retina have been reported in the literature. In this review, we summarize the roles of autophagy in the development of the retina and retinal diseases. This review highlights the importance of autophagy in retinal diseases, and targeting autophagy may provide a new therapeutic approach for retinal diseases.
Assuntos
Apoptose/fisiologia , Autofagia/fisiologia , Retina/crescimento & desenvolvimento , Retinite/fisiopatologia , Animais , Sobrevivência Celular/fisiologia , Humanos , Inflamação/fisiopatologia , Retina/fisiopatologiaAssuntos
Aneurisma/complicações , Artéria Retiniana/patologia , Vasculite Retiniana/complicações , Retinite/complicações , Adulto , Aneurisma/diagnóstico , Aneurisma/fisiopatologia , Aneurisma/cirurgia , Feminino , Angiofluoresceinografia , Humanos , Fotocoagulação a Laser , Anamnese , Vasculite Retiniana/diagnóstico , Vasculite Retiniana/fisiopatologia , Vasculite Retiniana/cirurgia , Retinite/diagnóstico , Retinite/fisiopatologia , Retinite/cirurgia , Acuidade Visual/fisiologiaRESUMO
Diffuse unilateral subacute neuroretinitis (DUSN) is caused by a subretinal live and mobile nematode. Acute phase: Patients usually present with severe pain, decreased vision, vitritis/papillitis, and tracks of grayish-white lesions-and a live nematode. Late phase: Arterial narrowing, optic atrophy, diffuse disruption of the retinal pigment epithelium (RPE), with severe visual loss.
Assuntos
Infecções Oculares Parasitárias/fisiopatologia , Infecções por Nematoides/fisiopatologia , Retinite/fisiopatologia , Humanos , Epitélio Pigmentado da Retina/parasitologia , Retinite/parasitologiaRESUMO
Changes in permeability of retinal blood vessels contribute to macular edema and the pathophysiology of numerous ocular diseases, including diabetic retinopathy, retinal vein occlusions, and macular degeneration. Vascular endothelial growth factor (VEGF) induces retinal permeability and macular thickening in these diseases. However, inflammatory agents, such as tumor necrosis factor-α (TNF-α), also may drive vascular permeability, specifically in patients unresponsive to anti-VEGF therapy. Recent evidence suggests VEGF and TNF-α induce permeability through distinct mechanisms; however, both require the activation of atypical protein kinase C (aPKC). We provide evidence, using genetic mouse models and therapeutic intervention with small molecules, that inhibition of aPKC prevented or reduced vascular permeability in animal models of retinal inflammation. Expression of a kinase-dead aPKC transgene, driven by a vascular and hematopoietic restricted promoter, reduced retinal vascular permeability in an ischemia-reperfusion model of retinal injury. This effect was recapitulated with a small-molecule inhibitor of aPKC. Expression of the kinase-dead aPKC transgene dramatically reduced the expression of inflammatory factors and blocked the attraction of inflammatory monocytes and granulocytes after ischemic injury. Coinjection of VEGF with TNF-α was sufficient to induce permeability, edema, and retinal inflammation, and treatment with an aPKC inhibitor prevented VEGF/TNF-α-induced permeability. These data suggest that aPKC contributes to inflammation-driven retinal vascular pathology and may be an attractive target for therapeutic intervention.
Assuntos
Permeabilidade Capilar/fisiologia , Proteína Quinase C/antagonistas & inibidores , Vasos Retinianos/fisiologia , Animais , Permeabilidade Capilar/efeitos dos fármacos , Masculino , Camundongos Endogâmicos C57BL , Papiledema/induzido quimicamente , Papiledema/fisiopatologia , Ratos Long-Evans , Proteínas Recombinantes , Traumatismo por Reperfusão/fisiopatologia , Retinite/induzido quimicamente , Retinite/fisiopatologia , Junções Íntimas/química , Junções Íntimas/fisiologia , Fator de Necrose Tumoral alfa/farmacologia , Fator A de Crescimento do Endotélio Vascular/farmacologiaRESUMO
Chikungunya is a systemic viral disease transmitted to humans by infected mosquitoes in endemic areas of Africa, Asia and more recently in the Americas. Chikungunya infection produces a sudden onset of fever, joint pains and erythematous skin eruption. A plethora of ocular manifestations have been described ranging from a non-specific conjunctivitis to exudative retinal detachment. Ocular chikungunya seems to respond well to corticosteroid therapy, and outcomes are usually better if treated early. Our patient acquired this infection on a travel to Mexico jungle. This was confirmed by ReverseTranscriptase-PCR test once she returned to the UK. The peculiarity of the case is the inordinate delay of almost a year in the onset of eye symptoms, from acquiring the viral infection. The ocular inflammation responded to systemic corticosteroid therapy with a favourable visual outcome. She developed a recurrence many months later which again responded well to a course of oral steroids.
Assuntos
Corticosteroides/uso terapêutico , Febre de Chikungunya/diagnóstico , Vírus Chikungunya/isolamento & purificação , Retinite/virologia , Adulto , Febre de Chikungunya/tratamento farmacológico , Febre de Chikungunya/fisiopatologia , Feminino , Humanos , México , RNA Viral/sangue , Recidiva , Retinite/tratamento farmacológico , Retinite/fisiopatologia , Fatores de Tempo , Viagem , Resultado do Tratamento , Reino UnidoRESUMO
Severe macular oedema causing marked loss of vision is seen in cases of retinitis developing postviral fever. The use of antivascular endothelial growth factor agents for macular oedema and submacular fluid secondary to viral retinitis has not been studied or well established in the past. We report a case series of two patients of postviral retinitis with severe macular oedema resistant to steroid therapy, treated with intravitreal bevacizumab. The patients showed significant symptomatic improvement in the visual acuity. The retinitis lesions resolved slowly and macular oedema regressed. Bevacizumab appears to be a safe and useful agent to manage macular oedema subsequent to postviral retinitis. An early resolution of macular oedema helps in the preservation of visual acuity which left untreated can cause severe visual loss.
Assuntos
Inibidores da Angiogênese/uso terapêutico , Bevacizumab/uso terapêutico , Edema Macular/tratamento farmacológico , Retinite/tratamento farmacológico , Febre/virologia , Humanos , Injeções Intravítreas , Edema Macular/fisiopatologia , Masculino , Pessoa de Meia-Idade , Retinite/diagnóstico por imagem , Retinite/fisiopatologia , Retinite/virologia , Resultado do Tratamento , Adulto JovemRESUMO
Chronic low grade inflammation is considered to contribute to the development of experimental diabetic retinopathy (DR). We recently demonstrated that lack of CD40 in mice ameliorates the upregulation of inflammatory molecules in the diabetic retina and prevented capillary degeneration, a hallmark of experimental diabetic retinopathy. Herein, we investigated the contribution of CD40 to diabetes-induced reductions in retinal function via the electroretinogram (ERG) to determine if inflammation plays a role in the development of ERG defects associated with diabetes. We demonstrate that diabetic CD40-/- mice are not protected from reduction to the ERG b-wave despite failing to upregulate inflammatory molecules in the retina. Our data therefore supports the hypothesis that retinal dysfunction found in diabetics occurs independent of the induction of inflammatory processes.
Assuntos
Antígenos CD40/fisiologia , Diabetes Mellitus Experimental/prevenção & controle , Retinopatia Diabética/prevenção & controle , Retina/fisiopatologia , Retinite/prevenção & controle , Animais , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/fisiopatologia , Retinopatia Diabética/genética , Retinopatia Diabética/fisiopatologia , Eletrorretinografia , Feminino , Molécula 1 de Adesão Intercelular/genética , Interleucina-1beta/genética , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Óxido Nítrico Sintase Tipo II/genética , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Retinite/genética , Retinite/fisiopatologia , Fator de Necrose Tumoral alfa/genética , Regulação para CimaRESUMO
Purpose: To accurately evaluate the autoimmune inflammation, we aim to develop three quantitative measurements to monitor the inflammatory changes in the retina: retinal-choroidal thickness, major retinal vessel diameter, and electroretinography amplitudes. Methods: During a 21-day experimental period, eyes were examined by confocal scanning laser ophthalmoscopy, optical coherence tomography, fundus fluorescein angiography, and electroretinography in living mice, which were then subsequently killed for histologic assessments. Results: On day 21 postimmunization, inflammation was observed both in vivo and in vitro. Fold change of retinal-choroidal thickness and major retinal vessel diameter in experimental autoimmune uveoretinitis mice were significantly greater than controls (P < 0.001). Both scotopic and photopic electroretinography amplitudes were significantly attenuated when compared with control mice (P < 0.01). Our results showed that these three quantifiable indicators provided an objective and accurate evaluation of autoimmune inflammation, which are in good correlations with the reported clinical and histopathologic scoring systems (P < 0.05). Conclusions: These three indicators will be useful to detect the small but significant differences in the severity of experimental autoimmune uveoretinitis for future longitudinally therapeutic studies.
Assuntos
Doenças Autoimunes/diagnóstico , Modelos Animais de Doenças , Retina/fisiopatologia , Vasos Retinianos/patologia , Retinite/diagnóstico , Uveíte/diagnóstico , Animais , Autoantígenos , Doenças Autoimunes/imunologia , Doenças Autoimunes/fisiopatologia , Permeabilidade Capilar , Dilatação Patológica , Eletrorretinografia , Proteínas do Olho , Feminino , Angiofluoresceinografia , Camundongos , Camundongos Endogâmicos C57BL , Oligopeptídeos , Oftalmoscopia , Retinite/imunologia , Retinite/fisiopatologia , Proteínas de Ligação ao Retinol , Uveíte/imunologia , Uveíte/fisiopatologiaRESUMO
PURPOSE: To describe the clinical characteristics, macular structure and function, and to document sequential changes over 5 years in a 10-year-old boy with bilateral primary foveomacular retinitis. METHODS: A 10-year-old boy presented with sudden onset scotoma in both eyes, experienced after getting up from bed on a non-eclipse day. He persistently denied direct sun-gazing. He neither had any significant systemic illness, nor was using any medications. In addition to a detailed examination at presentation that included fundus fluorescein angiogram (FFA), electroretinogram (ERG), pattern ERG and electrooculogram (EOG), he was examined periodically for 5 years with Humphrey visual field (HVF), spectral domain optical coherence tomogram (SDOCT), Amsler grid charting and multifocal ERG. The macular structure and functions were analyzed over the years and correlated with the symptoms. RESULTS: All findings were bilaterally symmetrical at each visit. At presentation, his corrected visual acuity was 20/25 with subfoveal yellow dot similar to solar retinopathy, central scotoma with reduced foveal threshold in HVF 24-2, micropsia in Amsler grid, missing of two plates on Ishihara color vision chart, transfoveal full thickness hyper-reflective band on SD OCT, unremarkable FFA and normal foveal peak in mfERG. The flash ERG and EOG were unremarkable. A month later, his VA improved to 20/20, he had relative scotoma in Amsler grid, no scotoma in HVF (10-2), restoration of the inner segment of the photoreceptors with sharp defect involving ellipsoid and photoreceptor interdigitation zone in SDOCT and blunting of foveal peaks in mfERG. Three months later, his corrected VA was 20/20 with relative scotoma in Amsler grid, normal color vision, no scotoma in HVF 10-2 and unchanged SDOCT findings. In subsequent examinations at 6, 9, 14, 29, 39 and 60 months, he was symptomless with VA 20/20, unremarkable fundus, normal Amsler grid and HVF (normal foveal threshold), unchanged SDOCT findings and the reduced foveal peaks on mfERG in both eyes got normalized only at 60 months. CONCLUSION: Presented here is a case of bilaterally symmetrical idiopathic foveomacular retinitis that had a clinical appearance similar to solar retinopathy. The fundus changes persisted for 4 weeks, the symptoms and changes in Amsler grid lasted for 3 months, and the foveal threshold in visual fields normalized within 3 months. Maximum change in the SDOCT defect occurred within a month, and the extrafoveal defect in the ellipsoid and photoreceptor interdigitation line persisted despite resolution of symptoms and resolution of the visual field defect and normal distance vision. Probably, the foveal lesion detected on SDOCT was too small to cause a reduction in the distance visual acuity or show up in the visual field and mfERG later.
Assuntos
Fóvea Central/fisiopatologia , Retinite/fisiopatologia , Escotoma/fisiopatologia , Criança , Eletroculografia , Eletrorretinografia , Angiofluoresceinografia , Seguimentos , Humanos , Masculino , Retinite/diagnóstico , Escotoma/diagnóstico , Estatística como Assunto , Tomografia de Coerência Óptica , Acuidade Visual/fisiologia , Testes de Campo Visual , Campos Visuais/fisiologiaRESUMO
Diabetic macular edema (DME) is caused by blood-retinal barrier breakdown associated with retinal vascular hyperpermeability and inflammation, and it is the major cause of visual dysfunction in diabetic retinopathy. Adrenomedullin (ADM) is an endogenous peptide first identified as a strong vasodilator. ADM is expressed in the eyes and is up-regulated in various eye diseases, although the pathophysiological significance is largely unknown. We investigated the effect of ADM on DME. In Kimba mice, which overexpress human vascular endothelial growth factor in their retinas, the capillary dropout, vascular leakage, and vascular fragility characteristic of diabetic retinopathy were observed. Intravitreal or systemic administration of ADM to Kimba mice ameliorated both the capillary dropout and vascular leakage. Evaluation of the transendothelial electrical resistance and fluorescein isothiocyanate-dextran permeability of an endothelial cell monolayer using TR-iBRB retinal capillary endothelial cells revealed that vascular endothelial growth factor enhanced vascular permeability but that co-administration of ADM suppressed the effect, in part by enhancing tight junction formation between endothelial cells. In addition, a comprehensive PCR array analysis showed that ADM administration suppressed various molecules related to inflammation and NF-κB signaling within retinas. From these results, we suggest that by exerting inhibitory effects on retinal inflammation, vascular permeability, and blood-retinal barrier breakdown, ADM could serve as a novel therapeutic agent for the treatment of DME.
Assuntos
Adrenomedulina/farmacologia , Permeabilidade Capilar/efeitos dos fármacos , Retinopatia Diabética/fisiopatologia , Fator A de Crescimento do Endotélio Vascular/farmacologia , Vasodilatadores/farmacologia , Adrenomedulina/administração & dosagem , Animais , Células Cultivadas , Diabetes Mellitus Experimental/fisiopatologia , Impedância Elétrica , Células Endoteliais/fisiologia , Injeções Intravítreas , Masculino , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , NF-kappa B/metabolismo , Retinite/fisiopatologia , Vasodilatadores/administração & dosagemRESUMO
PURPOSE: To evaluate the features of acute retinal pigment epitheliitis (ARPE) at onset and in the course of recovery by serial spectral-domain optical coherence tomography (SD OCT) and the correlation to visual acuity (VA). DESIGN: Retrospective cohort study. PARTICIPANTS: Consecutive patients with ARPE. METHODS: A review of medical records was performed. MAIN OUTCOME MEASURES: Integrity of SD OCT retinal bands at onset and in the course of disease, time required to achieve each retinal band restoration, corresponding VA change, and final VA. RESULTS: Four patients were included. Initial SD OCT showed a dome-shaped hyper-reflective lesion at the photoreceptor outer segment layer disrupting the ellipsoid zone (EZ) and interdigitation zone (IZ) (100%). In the early phase, there was also upward displacement of the external limiting membrane (ELM) and mild transient thickening of the retinal pigment epithelium (RPE)/Bruch's complex (Bc). Acute retinal pigment epitheliitis resolved in a sequence of (1) a decrease in height of SD OCT hyper-reflective lesion and the upwardly displaced ELM returning to its normal position with irregularity; (2) complete disappearance of the hyper-reflective lesion; (3) restoration of ELM; (4) restoration of EZ; and (5) restoration of IZ. The average time to restore ELM, EZ, and IZ was 4.3±5.2, 7.3±7.2, and 12.5±12.4 weeks, respectively, and the corresponding logarithm of the minimum angles of resolution (logMAR) VAs were 0.24±0.23, 0.09±0.07, and 0.05±0.06, respectively. Visual acuity improved when IZ was restored. CONCLUSIONS: Early SD OCT revealed an inflammatory lesion in the photoreceptor outer segment layer displacing ELM. The RPE was involved only mildly and transiently. Recovery occurred in a sequence of ELM, EZ, and IZ restoration, and VA improved when the IZ was restored. These features suggested that the IZ (i.e., the contact between photoreceptors and RPE) is the primary site of inflammation in ARPE.