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      Occlusive retinal vasculitis: novel insights into causes, pathogenesis and treatment

      Author(s): ,
      Publication date (Electronic):
      Journal: Current Opinion in Ophthalmology
      Publisher: Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          Purpose of review

          Occlusive retinal vasculitis (ORV) has a large differential diagnosis and varied therapeutic approaches. This review highlights existing and novel causes and treatment options for ORV.

          Recent findings

          Mutations in CAPN5, TREX1, and TNFAIP3 have been associated with dominantly inherited forms of ORV. Various intraocular therapeutics have been shown to occasionally cause ORV; the most recent medications associated with ORV are vancomycin and brolucizumab. In cases of ORV linked to Behçet's disease, clinical trials support the use of tumor necrosis factor alpha inhibitors.

          Summary

          Identification of the underlying etiology of ORV is critical to help guide treatment. Treatment in ORV involves both treatment any underlying infection or autoimmune condition, cessation of the any offending causative agent and local treatment of neovascular complications.

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          Most cited references70

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          Is Open Access

          HAWK and HARRIER: phase 3, multicenter, randomized, double-masked trials of brolucizumab for neovascular age-related macular degeneration

          Pravin Dugel, Adrian Koh, Yuichiro Ogura … (2019)
          Two similarly designed phase 3 trials (HAWK and HARRIER) compared brolucizumab, a single-chain antibody fragment that inhibits vascular endothelial growth factor-A, with aflibercept to treat neovascular age-related macular degeneration (nAMD).
          Article 0 comments Cited 280 times – based on 0 reviews     Review now
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            Secondary infection as a risk factor for dengue hemorrhagic fever/dengue shock syndrome: an historical perspective and role of antibody-dependent enhancement of infection.

            María G Guzmán, Mayling Álvarez, Scott B Halstead (2013)
            Today, dengue viruses are the most prevalent arthropod-borne viruses in the world. Since the 1960s, numerous reports have identified a second heterologous dengue virus (DENV) infection as a principal risk factor for severe dengue disease (dengue hemorrhagic fever/dengue shock syndrome, DHF/DSS). Modifiers of dengue disease response include the specific sequence of two DENV infections, the interval between infections, and contributions from the human host, such as age, ethnicity, chronic illnesses and genetic background. Antibody-dependent enhancement (ADE) of dengue virus infection has been proposed as the early mechanism underlying DHF/DSS. Dengue cross-reactive antibodies raised following a first dengue infection combine with a second infecting virus to form infectious immune complexes that enter Fc-receptor-bearing cells. This results in an increased number of infected cells and increased viral output per cell. At the late illness stage, high levels of cytokines, possibly the result of T cell elimination of infected cells, result in vascular permeability, leading to shock and death. This review is focused on the etiological role of secondary infections (SI) and mechanisms of ADE.
            Article 0 comments Cited 137 times – based on 0 reviews     Review now
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              Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early onset autoinflammatory syndrome

              Qing Zhou, Hongying Wang, Daniella Schwartz … (2015)
              Systemic autoinflammatory diseases are driven by abnormal activation of innate immunity 1 . Herein we describe a new syndrome caused by high penetrance heterozygous germline mutations in the NFκB regulatory protein TNFAIP3 (A20) in six unrelated families with early onset systemic inflammation. The syndrome resembles Behçet’s disease (BD), which is typically considered a polygenic disorder with onset in early adulthood 2 . A20 is a potent inhibitor of the NFκB signaling pathway 3 . TNFAIP3 mutant truncated proteins are likely to act by haploinsufficiency since they do not exert a dominant-negative effect in overexpression experiments. Patients’ cells show increased degradation of IκBα and nuclear translocation of NFκB p65, and increased expression of NFκB-mediated proinflammatory cytokines. A20 restricts NFκB signals via deubiquitinating (DUB) activity. In cells expressing the mutant A20 protein, there is defective removal of K63-linked ubiquitin from TRAF6, NEMO, and RIP1 after TNF stimulation. NFκB-dependent pro-inflammatory cytokines are potential therapeutic targets for these patients.
              Article 0 comments Cited 132 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Current Opinion in Ophthalmology
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1040-8738
                ISSN (Electronic): 1531-7021
                Publication date Created: 2022
                Publication date (Print): May 2022
                Publication date (Electronic): March 2 2022
                Volume: 33
                Issue: 3
                Pages: 147-156
                Article
                DOI: 10.1097/ICU.0000000000000843
                PubMed ID: 35239517
                SO-VID: 61d4e322-01c5-4a71-8261-4ff029adaf4e
                Copyright © © 2022
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