Dataset Information

Ocular Manifestations of Spondyloarthritis.

ABSTRACT:

Introduction

Ocular manifestations are seen in several autoimmune disorders including spondyloarthritis (SpAs). Though acute anterior uveitis (AAU) is the hallmark of SpAs, episcleritis and scleritis are also seen. Genetic and geographical factors impact the prevalence of AAU; however, available evidence support that HLA-B27 positivity is closely associated with it.

Objective

The current narrative review is focused on clinical features of AAU and its management.

Methods

For the purpose of this narrative review; literature search covered MEDLINE, Google scholar and EMBASE databases and included articles published in English language from January 1980 till April 2022 using the following keywords: "Ankylosing spondylitis", "Spondyloarthritis", "Eye manifestations", "Ocular", "Uveitis" and "Arthritis".

Conclusion

Patients with SpA may suffer from different ocular complications with uveitis being the most common one. Biological therapy is a promising medical strategy enabling in achieving therapeutic goals with minimal adverse effects. An effective management strategy for patients with AAU associated with SpA could be formulated by the collaboration between ophthalmologists and rheumatologists.

SUBMITTER: Pandey A

PROVIDER: S-EPMC10201097 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Ocular Manifestations of Spondyloarthritis.

Pandey Akshat A Ravindran Vinod V

Mediterranean journal of rheumatology 20230331 1

<h4>Introduction</h4>Ocular manifestations are seen in several autoimmune disorders including spondyloarthritis (SpAs). Though acute anterior uveitis (AAU) is the hallmark of SpAs, episcleritis and scleritis are also seen. Genetic and geographical factors impact the prevalence of AAU; however, available evidence support that HLA-B27 positivity is closely associated with it.<h4>Objective</h4>The current narrative review is focused on clinical features of AAU and its management.<h4>Methods</h4>For ...[more]

PMID: 37223599

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Project description:ObjectiveTrichothiodystrophy (TTD) is a rare, autosomal recessive disorder characterized by sulfur-deficient brittle hair and multisystem abnormalities. Many TTD patients have a defect in known DNA repair genes. This report systematically evaluates the ocular manifestations of the largest-to-date cohort of TTD patients and xeroderma pigmentosum (XP)/TTD patients.DesignCase series.ParticipantsThirty-two participants, ages 1 to 30 years, referred to the National Eye Institute for examination from 2001 to 2010; 25 had TTD and 7 had XP/TTD.MethodsComplete, age- and developmental stage-appropriate ophthalmic examination.Main outcome measuresVisual acuity (VA), best-corrected VA, ocular motility, state of the ocular surface and corneal endothelial cell density, corneal diameter, and lens assessment.ResultsDevelopmental abnormalities included microcornea (44% TTD), microphthalmia (8% TTD, 14% XP/TTD), nystagmus (40% TTD), and infantile cataracts (56% TTD, 86% XP/TTD). Corrective lenses were required by 65% of the participants, and decreased best-corrected VA was present in 28% of TTD patients and 71% of XP/TTD patients. Degenerative changes included dry eye (32% TTD, 57% XP/TTD) and ocular surface disease identified by ocular surface staining with fluorescein (32% TTD) that usually are exhibited by much older patients in the general population. The 2 oldest TTD patients exhibited clinical signs of retinal/macular degeneration. Four XP/TTD patients presented with corneal neovascularization.ConclusionsThese TTD and XP/TTD study participants had a wide variety of ocular findings including refractive error, infantile cataracts, microcornea, nystagmus, and dry eye/ocular surface disease. Although many of these can be ascribed to abnormal development--likely owing to abnormalities in basal transcription of critical genes--patients may also have a degenerative course.Financial disclosure(s)Proprietary or commercial disclosures may be found after the references.

Project description:Central insulin resistance, the diminished cellular sensitivity to insulin in the brain, has been implicated in diabetes mellitus, Alzheimer's disease and other neurological disorders. However, whether and how central insulin resistance plays a role in the eye remains unclear. Here, we performed intracerebroventricular injection of S961, a potent and specific blocker of insulin receptor in adult Wistar rats to test if central insulin resistance leads to pathological changes in ocular structures. 80 mg of S961 was stereotaxically injected into the lateral ventricle of the experimental group twice at 7 days apart, whereas buffer solution was injected to the sham control group. Blood samples, intraocular pressure, trabecular meshwork morphology, ciliary body markers, retinal and optic nerve integrity, and whole genome expression patterns were then evaluated. While neither blood glucose nor serum insulin level was significantly altered in the experimental or control group, we found that injection of S961 but not buffer solution significantly increased intraocular pressure at 14 and 24 days after first injection, along with reduced porosity and aquaporin 4 expression in the trabecular meshwork, and increased tumor necrosis factor α and aquaporin 4 expression in the ciliary body. In the retina, cell density and insulin receptor expression decreased in the retinal ganglion cell layer upon S961 injection. Fundus photography revealed peripapillary atrophy with vascular dysregulation in the experimental group. These retinal changes were accompanied by upregulation of pro-inflammatory and pro-apoptotic genes, downregulation of anti-inflammatory, anti-apoptotic, and neurotrophic genes, as well as dysregulation of genes involved in insulin signaling. Optic nerve histology indicated microglial activation and changes in the expression of glial fibrillary acidic protein, tumor necrosis factor α, and aquaporin 4. Molecular pathway architecture of the retina revealed the three most significant pathways involved being inflammation/cell stress, insulin signaling, and extracellular matrix regulation relevant to neurodegeneration. There was also a multimodal crosstalk between insulin signaling derangement and inflammation-related genes. Taken together, our results indicate that blocking insulin receptor signaling in the central nervous system can lead to trabecular meshwork and ciliary body dysfunction, intraocular pressure elevation, as well as inflammation, glial activation, and apoptosis in the retina and optic nerve. Given that central insulin resistance may lead to neurodegenerative phenotype in the visual system, targeting insulin signaling may hold promise for vision disorders involving the retina and optic nerve.

Dataset Information

Ocular Manifestations of Spondyloarthritis.

Introduction

Objective

Methods

Conclusion

Publications

Ocular Manifestations of Spondyloarthritis.

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