Autoimmune Retinopathy Research Articles

Consensus on the Diagnosis and Management of Nonparaneoplastic Autoimmune Retinopathy Using a Modified Delphi Approach

To develop diagnostic criteria for nonparaneoplastic autoimmune retinopathy (AIR) through expert panel consensus and to examine treatment patterns among clinical experts. Modified Delphi process. A survey of uveitis specialists in the American Uveitis Society, a face-to-face meeting (AIR Workshop) held at the National Eye Institute, and 2 iterations of expert panel surveys were used in a modified Delphi process. The expert panel consisted of 17 experts, including uveitis specialists and researchers with expertise in antiretinal antibody detection. Supermajority consensus was used and defined as 75% of experts in agreement. There was unanimous agreement among experts regarding the categorization of autoimmune retinopathies as nonparaneoplastic and paraneoplastic, including cancer-associated retinopathy and melanoma-associated retinopathy. Diagnostic criteria and tests essential to the diagnosis of nonparaneoplastic AIR and multiple supportive criteria reached consensus. For treatment, experts agreed that corticosteroids and conventional immunosuppressives should be used (prescribed) as first- or second-line treatments, though a consensus agreed that biologics and intravenous immunoglobulin were considered appropriate in the treatment of nonparaneoplastic AIR patients regardless of the stage of disease. Experts agreed that more evidence is needed to treat nonparaneoplastic AIR patients with long-term immunomodulatory therapy and that there is enough equipoise to justify randomized, placebo-controlled trials to determine if nonparaneoplastic AIR patients should be treated with long-term immunomodulatory therapy. Regarding antiretinal antibody detection, consensus agreed that a standardized assay system is needed to detect serum antiretinal antibodies. Consensus agreed that an ideal assay should have a 2-tier design and that Western blot and immunohistochemistry should be the methods used to identify antiretinal antibodies. Consensus was achieved using a modified Delphi process to develop diagnostic criteria for nonparaneoplastic AIR. There is enough equipoise to justify randomized, placebo-controlled trials to determine whether patients with nonparaneoplastic AIR should be treated with long-term immunomodulatory therapy. Efforts to develop a standardized 2-tier assay system for the detection of antiretinal antibodies have been initiated as a result of this study.

Unique epitopes for carbonic anhydrase II autoantibodies related to autoimmune retinopathy and cancer-associated retinopathy

High titers of anti-carbonic anhydrase II (anti-CA II) autoantibodies were detected in sera of patients with autoimmune retinopathies (AR), including cancer-associated retinopathy (CAR) and also in normal population. The goal was to investigate whether unique immunodominant epitopes for anti-CAII autoantibodies occur in AR and CAR. A cohort of 216 patients with symptoms of AR and CAR and healthy controls, seropositive for anti-CA II autoantibodies were analyzed for the prevalence of CAII major domains. Autoantibody titers against CAII in sera were determined by ELISA. Biotinylated 12-mer synthetic peptides, overlapping the entire sequence of CAII, were coated onto a microplate and monospecific sera were tested for their ability to bind specific peptides by ELISA. We identified 3 epitopes common for AR, CAR and control subjects but the key epitopes were significantly different between sera from different groups (p = 0.009). Ninety one percent of AR sera predominantly reacted with the N-terminal epitope 85–90 (p < 0.0001), which corresponded to the catalytic core of the enzyme. The major epitope for 77% of CAR autoantibodies was found to be reactive with the peptide 218–222 (P = 0.0005) clustered within the α-helix. The analysis of epitope position in a 3D structure of the native CAII revealed their partial or full exposure on the protein surface. Anti-CAII autoantibodies from normal healthy controls did not share the major determinants with either group of patients. We also observed an epitope shift in antibody recognition from the AR-like epitope profile to the CAR-like profile in a patient who developed cancer 2 years after initial symptoms of vision loss (p < 0.0001). In conclusion, autoantibodies against CAII recognized different epitopes, depending whether they originated in patients with or without cancer. Also, antibodies targeted different determinates within the molecule during the development of retinopathy from non-paraneoplastic to paraneoplastic, suggesting an intramolecular epitope spreading phenomenon. Accurate distinction between AR and CAR is critical in designing immunotherapies and better diagnosis for those two conditions.

GCAP1, Rab6, and HSP27: Novel Autoantibody Targets in Cancer-Associated Retinopathy and Autoimmune Retinopathy.

PurposeAutoantibodies (AAbs) with different retinal specificities were reported in cancer-associated retinopathy (CAR) and autoimmune retinopathy (AR). The goal was to identify the small retinal proteins of apparent molecular mass of 23-kDa often recognized by patients' AAbs.MethodsSera specific for a 23-kDa retinal protein of 173 patients were investigated retrospectively by Western blotting and double immunofluorescence confocal microscopy. A proteomic analysis revealed new 23-kDa protein candidates, including guanylyl cyclase-activating proteins (GCAPs), heat shock protein 27 (HSP27), and Rab6A GTPase (Rab6A).ResultsAmong the cohort of 173 patients, only 68 had anti-recoverin AAbs and the remaining 105 reacted with 4 unique proteins, which were identified as a Rab6A, HSP27, GCAP1, and GCAP2. Confocal images from a double labeling study confirmed the reactivity of AAbs with different types of cells in human retina, consistent with the target protein's respective cellular functions. Patients (62/173) had been diagnosed with various kinds of cancer, including 20% of patients who had anti-recoverin, 11% anti-Rab6A, and 5% anti-HSP27 AAbs. Only 50% of recoverin-seropositive patients had cancer and the individuals with anti-recoverin AAbs had a significantly higher likelihood to be diagnosed with cancer than patients with other anti-23-kDa AAbs.ConclusionsThe newly discovered retinal autoantigens may be involved in pathogenicity of CAR and AR. The recognition of AAbs against various retinal proteins associated with autoimmune retinal degeneration broadens the group of proteins related with these entities.Translational RelevancePatients with anti-recoverin, anti-GCAP1, anti-Rab6A, and anti-HSP27 AAbs represented diverse clinical phenotypes, so the presence of disease-associated AAbs provides important information for molecular diagnosis.

Choroidal Thickness and En Face Optical Coherence Tomography Imaging in Autoimmune Retinopathy

A 57-year-old white woman developed autoimmune retinopathy (AIR) in both eyes associated with bilateral autoimmune sensorineural hearing loss. Laboratory testing was positive for 68kDa (heat-shock protein) and 136kDa (human interstitial retinoid-binding protein). Extensive cancer screening was negative. Spectral-domain optical coherence tomography enhanced depth imaging demonstrated a markedly thickened choroid in both eyes. En face imaging showed a distinctive pattern of granular hyperreflective foveal dots. The concurrent sensorineural hearing loss was thought to be of autoimmune origin and also responded to immunosuppressive treatment. Eyes with non-paraneoplastic, seropositive AIR may have associated increased choroidal thickness. Audiology testing should be considered.

Assessment of Retinal Structural and Functional Characteristics in Eyes with Autoimmune Retinopathy.

To evaluate the thicknesses of individual retinal layers, and the correlation between structural changes and functional loss using spectral domain optical coherence tomography (SD-OCT) scans and electroretinograms (ERG), in eyes with autoimmune retinopathy (AIR). SD-OCT raster scans of 12 eyes from 6 patients serologically diagnosed with AIR were evaluated. Retinal layers were segmented along a 5 mm horizontal scan passing through the fovea. Retinal layers analyzed include full retinal thickness (FRT), retinal pigment epithelium and Bruch's membrane complex (RPE+BM complex), photoreceptor layer (PRL), inner nuclear layer (INL), combined ganglion cell and inner plexiform layers (GCL+), nerve fiber layer (NFL), and combined GCL+ and NFL layers (GCL+/NFL). Changes in the thicknesses of the layers were assessed in 0.5 mm increments along the B-scan in the central, nasal, and temporal regions. These recorded values were compared to corresponding values of 51 eyes from 51 subjects with no known ocular pathology. Full-field ERGs were obtained at corresponding visits and were interpreted by a grader masked to the diagnoses and OCT findings. The mean age of the patients was 59.5 years (range, 33-83), with 4 males (66.6%). Within the control population of 51 subjects, mean age was 51.5 years (range, 40-75), with 25 males (49%). Eyes with AIR showed a loss of retinal tissue compared to eyes with no known ocular pathology at the fovea. Specifically, the FRT, RPE+BM complex, and PRL exhibited thinning of statistically significance. ERG findings demonstrated a functional deficit which showed a good correlation with structural loss. Fifty (50) percent of eyes experienced central photoreceptor (rod and cone) dysfunction and 75% of eyes displayed peripheral photoreceptor (rod and cone) dysfunction. Eyes with AIR show a loss of retinal tissue compared to eyes with no known ocular pathology. The greatest loss appears to occur in the RPE and PRL. ERG findings correlate strongly with the loss of tissue seen in these layers. Thus, therapeutic options may be targeted to preserve these regions of the retina.

Retinal degeneration in autoimmune polyglandular syndrome type 1: a case series

BackgroundAutoimmune polyglandular syndrome type 1 (APS1) is a rare autosomal recessive disorder due to mutations in the AIRE gene.AimTo report the ocular features and characterise the retinal phenotype in molecularly...

The enigma of autoimmune retinopathy.

Autoimmune retinopathy (AIR) refers to an immunologic process whereby retinal antigens are aberrantly recognized as autoantigens, leading to retinal degeneration. AIR was initially described in 1976 as a paraneoplastic syndrome, termed cancer-associated retinopathy (CAR), secondary to a remote malignancy.1 Laboratory investigations revealed that the serum of patients with CAR contained autoantibodies against the photoreceptor protein recoverin, which are believed to represent the underlying etiology of CAR.2,3 A related syndrome, termed melanoma-associated retinopathy (MAR), was reported in patients with cutaneous malignant melanoma who were found to have autoantibodies to an unknown antigen on bipolar cells.4,5 Since that time, AIR in the absence of neoplasm, termed nonparaneoplastic AIR (npAIR), has been described as well.6 Along with this has come the identification of several novel putative antiretinal autoantibodies. Although all these novel discoveries have expanded our knowledge of AIR, they have also brought with them some confusion. There are numerous excellent reviews of AIR that have recently been published in the literature.7–13 The purpose of this current article is not to provide another review of this topic, but rather to highlight some of the ambiguity and uncertainty that exists in this field. For the purposes of this review, the term AIR will be used to refer to CAR, npAIR, and MAR, as the ocular features and proposed pathogenesis of these entities are essentially the same.

A Case of Nonparaneoplastic Autoimmune Retinopathy

Purpose: To report a case of nonparaneoplastic autoimmune retinopathy diagnosed using serum anti-retinal autoantibodies. Case summary: A 60-year-old female complained of progressive visual loss in both eyes over 3 months. Her best corrected visual acuity was hand motion in the right eye, 0.9 (decimal) in the left eye, and no definite abnormal findings were identified on fundus examinations. Automated visual field test revealed severely depressed visual fields in both eyes. Standard full-field electroretinogram (ERG) revealed nearly extinguished scotopic b-waves and spectral-domain optical coherence tomography (SD-OCT) showed subtle obscuration and interruption of the inner segment/outer segment (IS/OS) junction of the photoreceptors. Using Western blotting with human retinal proteins and the patient’s serum, we diagnosed nonparaneoplastic autoimmune retinopathy and performed posterior subtenon steroid injection in the right eye, systemic corticosteroids, and oral mycophenolate mofetil. Full-field ERG after treatment showed slightly increased amplitude but there was no subjective visual improvement. OCT after treatment did not reveal significant changes in the photoreceptor layer. Conclusions: This is the first reported case of nonparaneoplastic autoimmune retinopathy in Korea diagnosed using Western blotting with anti-retinal autoantibodies. Autoimmune retinopathy should be considered in patients with visual field and ERG impairment without definite fundus abnormalities. J Korean Ophthalmol Soc 2015;56(7):1134-1140

AUTOIMMUNE RETINOPATHY AND ANTIRETINAL ANTIBODIES

To review the current state for diagnosis and management of autoimmune retinopathy. A review of the literature was performed, encompassing autoimmune retinopathy including paraneoplastic retinopathy (cancer-associated retinopathy, melanoma-associated retinopathy, and bilateral diffuse uveal melanocytic proliferation) and non-paraneoplastic autoimmune retinopathy. Based on this review, current principles and techniques for diagnosis and the treatments reported for autoimmune retinopathy are discussed with the aim to clarify some of the confusion that exists regarding this complex entity. Autoimmune retinopathy encompasses a spectrum of retinal degeneration phenotypes. The clinical features, fundus characteristics, and electroretinogram findings for paraneoplastic and non-paraneoplastic retinopathy are reviewed. The different antiretinal antibodies reported in these entities are described. The diagnostic approaches for detecting these antiretinal antibodies and their limitations are covered. The treatments reported for autoimmune retinopathy and their outcomes are reviewed. Among the myriad of antiretinal antibodies reported, challenges persist in determining which antibodies are pathogenic and which are benign and what factors cause antiretinal antibodies to become pathologic. There also remain difficulties in the detection and accurate measurement of antiretinal antibodies, and the response to therapeutic intervention in autoimmune retinopathy is variable.

Autoimmune retinopathy

Autoimmune retinopathy (AIR) is an immune-mediated disorder characterized by progressive visual loss, abnormal electroretinographic and visual field findings in the presence of circulating anti-retinal antibodies. This review highlights advances made toward understanding the pathophysiology, clinical manifestations, and trends in the management of AIR. The pathophysiology of AIR is likely antibody-mediated. AIR serum autoantibodies are variable in their size and retinal tissue they target and can also be present in healthy controls and multiple autoimmune diseases. Rarely, AIR may be associated with dysregulated self-tolerance mechanisms in the thymus. Despite progress in research, our understanding of AIR remains incomplete. Lack of standardized methods for anti-retinal antibody testing continues to challenge the interpretation of seropositivity. Conventional immunosuppressives have been further studied, and promising immunomodulatory therapies, such as targeted B-cell therapy, have been introduced. Newer imaging modalities such as fundus autofluorescence and spectral domain optical coherence tomography may be helpful in diagnosis, monitoring progression of disease and response to treatment. AIR is a rare but vision-threatening disease whose pathogenesis is poorly defined. Lack of standardized clinical or laboratory criteria further complicates the diagnosis and management. Despite recent progress, further basic science research into the autoimmune process is needed. Prospective controlled clinical trials with immunomodulatory therapy can help define future treatment paradigms.

Autoimmune retinopathy associated with carcinoid tumour of the small bowel

Cancer associated retinopathy (CAR) is an immune mediated paraneoplastic condition associated with vision loss. It has been associated with a variety of systemic malignancies. The primary clinical presentation is rapid, progressive vision loss. Rod and cone dysfunction can cause other associated symptoms, such as nyctalopia. Electrophysiological testing and detection of anti-retinal antibodies are used to confirm the diagnosis. To our knowledge we describe the first patient with CAR associated with a carcinoid tumour of the gastrointestinal system. Auto-antibodies against alpha enolase and carbonic anhydrase II were detected with western blotting. Electroretinogram findings were consistent with rod and cone dysfunction.

Unilateral retinopathy secondary to occult primary intraocular lymphoma

The purpose of the study is to report the clinical case of a 53-year-old woman whose presenting manifestation of primary intraocular lymphoma (PIOL) was unilateral retinal degeneration. A case report was created with review of clinical, imaging, electrophysiologic, and pathological investigations. A 53-year-old woman with a distant history of ocular herpes simplex developed progressive central visual loss and intermittent photopsia over 4 years in her right eye. Ophthalmic examination revealed reduced visual acuity OD, central scotoma, and minimal ocular findings. Autofluorescence and infrared imaging revealed mild reflectance changes in the temporal macula, and spectral-domain optical coherence tomography identified mild disruptions of inner segment/outer segment junctions in the subfoveal region of the right eye. A mild window defect was seen on fluorescein angiography. Electrophysiology with multifocal electroretinogram (ERG) revealed evidence of unilateral macular dysfunction. Full-field ERGs revealed progressive global retinal dysfunction over 6 months, with unilateral decreases in amplitude and implicit time shifts, as seen in cases of autoimmune retinopathies. The eye eventually exhibited mild vitreous cellular infiltration on ophthalmoscopic examination, and vitrectomy diagnosed B cell non-Hodgkin's lymphoma. Further evaluation revealed no evidence of central nervous system or systemic disease, consistent with occult PIOL. This case illustrates an atypical presentation of PIOL characterized by unilateral retinal disease presenting with symptoms and signs of macular dysfunction. Clinical and ERG features evolved into an acute zonal occult outer retinopathy (AZOOR)-like phenotype. PIOL should be considered in atypical cases of AZOOR with vitreal reactions, and some cases of AZOOR may be related to B cell lymphocyte disorders.

Autoimmune Retinopathy

To provide a detailed review of current clinical guidelines for the diagnosis, work-up and treatment of autoimmune retinopathy and to preview briefly possible future therapies. Perspective based on literature review and clinical expertise. Interpretation of current literature, relying on the authors' clinical experience. Autoimmune retinopathy is a rare immunologic disease characterized by the presence of circulating antiretinal antibodies along with electroretinographic and visual field abnormalities. An ophthalmic examination can be normal or show minimal findings. The diagnosis of autoimmune retinopathy is made difficult by diagnostic criteria that are both limited and nonstandardized. Currently, the diagnosis is made based on the demonstration of serum antiretinal antibodies and the presence of clinical manifestations (including abnormal electroretinographic findings). The mere presence of these antibodies is not diagnostic. Lack of an accepted gold standard for antiretinal antibodies detection and poor interlaboratory concordance make the diagnosis challenging. There are anecdotal reports of immunosuppressive therapy in autoimmune retinopathy; however, the response to treatment is variable, with more favorable results achieved in paraneoplastic retinopathy, particularly cancer-associated retinopathy, with a combination of chemotherapy and immunosuppression. Whether an earlier attempt to treat nonparaneoplastic autoimmune retinopathy would be more beneficial is unknown. Early treatment attempts are limited by lack of sensitive and specific assays and definitive clinical criteria. Little is known about the clinical course, prognosis and treatment of autoimmune retinopathy. Additional studies should examine the specificity and pathogenicity of antiretinal antibodies and screen for biomarkers, and they should be conducted concurrently with studies seeking to identify appropriate treatment.

Detection of autoantibodies against heat shock proteins and collapsin response mediator proteins in autoimmune retinopathy

BackgroundAutoimmune retinopathy (AR) and Cancer-Associated Retinopathy (CAR) are associated with a diverse repertoire of anti-retinal autoantibodies (AAbs) but not all antigenic targets have been characterized. Identification of new AAbs may help with clinical diagnosis and prognosis of retinal dysfunction in AR. The goal was to identify frequently targeted retinal autoantigens within the 60-70-kDa molecular weight range.MethodsHuman retinal proteins were separated by SDS-PAGE and 2D gel electrophoresis (2-DE) and sera from AR patients with and without cancer were used to identify immunoreactive proteins by Western blotting. Proteins were identified following separation by electrophoresis, Coomassie staining using in-gel trypsin digestion and mass spectrometric analysis. Circulating serum hsp60 and anti-hsp60 antibody levels were determined by quantitative ELISA.ResultsRetrospective evaluation of 819 patients with anti-retinal AAbs showed that 29% patients had AAbs targeted proteins between 60-70-kDa. Shotgun mass spectrometry of human retinal proteins present in 1D-gel found 66 species within this range. To identify the immunoreactive proteins, we performed Western blots of 2-DE gels and showed a group of heat shock proteins (hsps), including hsp60 and CRMP proteins that were frequently recognized by AR patient AAbs, irrespective of cancer status. These results were validated by immunostaining of purified hsp60 and CRMP2 proteins. ELISA results revealed that patients with AR and CAR had significantly increased levels of serum anti-hsp60 antibodies compared to control healthy subjects (p < 0.0001). However, circulating hsp60 protein was not significantly elevated in sera of either patient group.ConclusionsDifferent anti-retinal antibodies frequently co-exist in a single patient, creating antibody-arrays related to the syndrome. Hsps and CRMP-2 are newly identified autoantigens in AR. A frequent co-association of anti-hsp antibodies with other anti-retinal AAbs may augment pathogenic processes, leading to retinal degeneration.

A curious case of glaucoma?

An 84-year-old woman diagnosed with primary open-angle glaucoma was referred because her optic nerve appearance did not account for her visual field deficits. Further evaluation showed loss of color vision and rapid progression of visual field defects. Electroretinography revealed abnormal scotopic and photopic responses. Blood samples were positive for anti-retinal antibodies, but a malignancy work-up was negative, consistent with non-paraneoplastic autoimmune retinopathy.

Autoimmune Retinopathies: A Report of 3 Cases

Purpose: To describe 3 representative cases of autoimmune retinopathy (AIR).Methods: Clinical records of patients with a diagnosis of AIR were analyzed for demographic data, clinical findings, ancillary and laboratory tests, and treatment employed.Results: Three female patients diagnosed with AIR had bilateral reduction of electroretinogram amplitudes and elevation of visual field threshold within the central 30 degrees of the visual field that was disproportionately more severe than the clinical findings of retinal degeneration. The diagnoses were cancer-associated retinopathy, non-neoplastic AIR, and hereditary retinal dystrophy with secondary inflammation. Optic nerve involvement was also present in all cases. The patient with non-neoplastic AIR was successfully treated with systemic corticosteroids and immunomodulatory agents.Conclusion: High index of suspicion is essential for an early diagnosis of AIR. Visual function and electrophysiological tests should be included in the initial workup of patients who present with suggestive clinical signs and symptoms of AIR.

Commensal flora as possible pathogens of autoimmune pancreatitis

High titers of anti-carbonic anhydrase II (anti-CA II) autoantibodies were detected in sera of patients with autoimmune retinopathies (AR), including cancer-associated retinopathy (CAR) and also in normal population. The goal was to investigate whether unique immunodominant epitopes for anti-CAII autoantibodies occur in AR and CAR. A cohort of 216 patients with symptoms of AR and CAR and healthy controls, seropositive for anti-CA II autoantibodies were analyzed for the prevalence of CAII major domains. Autoantibody titers against CAII in sera were determined by ELISA. Biotinylated 12-mer synthetic peptides, overlapping the entire sequence of CAII, were coated onto a microplate and monospecific sera were tested for their ability to bind specific peptides by ELISA. We identified 3 epitopes common for AR, CAR and control subjects but the key epitopes were significantly different between sera from different groups (p = 0.009). Ninety one percent of AR sera predominantly reacted with the N-terminal epitope 85–90 (p < 0.0001), which corresponded to the catalytic core of the enzyme. The major epitope for 77% of CAR autoantibodies was found to be reactive with the peptide 218–222 (P = 0.0005) clustered within the α-helix. The analysis of epitope position in a 3D structure of the native CAII revealed their partial or full exposure on the protein surface. Anti-CAII autoantibodies from normal healthy controls did not share the major determinants with either group of patients. We also observed an epitope shift in antibody recognition from the AR-like epitope profile to the CAR-like profile in a patient who developed cancer 2 years after initial symptoms of vision loss (p < 0.0001). In conclusion, autoantibodies against CAII recognized different epitopes, depending whether they originated in patients with or without cancer. Also, antibodies targeted different determinates within the molecule during the development of retinopathy from non-paraneoplastic to paraneoplastic, suggesting an intramolecular epitope spreading phenomenon. Accurate distinction between AR and CAR is critical in designing immunotherapies and better diagnosis for those two conditions.

Concordance of Antiretinal Antibody Testing Results Between Laboratories in Autoimmune Retinopathy

Concordance of Antiretinal Antibody Testing Results Between Laboratories in Autoimmune Retinopathy

NONPARANEOPLASTIC AUTOIMMUNE RETINOPATHY PRESENTING WITH PERIPHERAL RETINAL VASOOCCLUSION

To report a case of nonparaneoplastic autoimmune retinopathy presenting with severe peripheral retinal vasoocclusion. Interventional case report. A 44-year-old woman complained of blurred vision and photopsia in both eyes. She has no history of cancer or autoimmune disease. Best-corrected visual acuity was 20/40 in the left eye and 20/30 in the right eye. Constriction of the visual field sparing central vision was found. Fluorescein angiography revealed severe peripheral retinal vasoocclusion, panretinal degeneration, and cystoid macular edema. Optical coherence tomography demonstrated intraretinal fluid. Electroretinography showed decreased amplitude of a- and b-waves in both scotopic and photopic tests. The implicit time was generally within normal limits. The amplitude of flicker response was also diminished. Multifocal electroretinography showed declined signal all over the macular region. Systemic workup including whole body positron emission tomography/computed tomography for cancer screening showed negative results. Only antirecoverin antibody was positive. Under the impression of nonparaneoplastic autoimmune retinopathy, systemic and local immunosuppressive therapy was given and showed improvement. Nonparaneoplastic autoimmune retinopathies are uncommon retinal degenerations with visual loss associated with unique clinical symptoms and findings and with serum antiretinal autoantibodies. Severe peripheral retinal vasoocclusion was not reported. Early detection and timely treatment with immunosuppression could result in clinical improvement.

SD-OCT and autofluorescence characteristics of autoimmune retinopathy

AimsTo report abnormal fundus hyperautofluorescence (hyper-AF) and loss of outer retinal layers by spectral domain optical coherence tomography in patients with autoimmune retinopathy (AIR).MethodsRetrospective, observational case series of 14 eyes...