key: cord-1043153-52sgn3lm
authors: Anthony, Eliza; Rajamani, Archana; Baskaran, Prabu; Rajendran, Anand
title: Vogt Koyanagi Harada disease following a recent COVID-19 infection
date: 2022-01-27
journal: Indian J Ophthalmol
DOI: 10.4103/ijo.ijo_2550_21
sha: 87510992a76c6b28b0e62bd1bf603ac300146b2d
doc_id: 1043153
cord_uid: 52sgn3lm

A 23-year-old female presented with a 3-day history of bilateral (OU) diminution of vision 3 weeks after COVID-19 infection. Best corrected visual acuity (BCVA) was 20/30 in right eye and 20/40 in left eye. Anterior segment showed OU 1+ cells in anterior chamber and anterior vitreous face. Fundus OU showed disc hyperemia and multiple pockets of subretinal fluid (SRF), confirmed on optical coherence tomography. Fundus fluorescein angiography showed multiple pin point leaks suggestive of Vogt Koyanagi Harada disease. Oral corticosteroids 1 mg/kg/day were started. At 2-months’ follow-up, her BCVA improved to 20/25 OU with complete resolution of SRF.

Vogt Koyanagi Harada disease (VKH) is an autoimmune condition, where T-cell-mediated immune response is triggered against melanocyte rich tissues in our body namely eye, ear, skin, and brain. In eye, VKH mainly manifests as chronic, bilateral, granulomatous panuveitis. [1] The global pandemic caused by COVID-19 is caused by severe acute respiratory syndrome coronavirus-2 virus (SARS-CoV-2). It is a multifaceted disease and various ocular conditions have been reported in association with COVID-19 infection like follicular conjunctivitis, acute anterior uveitis, panuveitis, optic neuritis, and vascular occlusions. [2, 3] However, various infective triggers for VKH like Epstein-barr virus, cytomegalovirus, influenza A, and mycoplasma pneumonia have been reported earlier in literature. [1, 4] We report a case of a young female with features of VKH, probably triggered by SARS-CoV-2 virus, post COVID-19 infection, which, to the best of our knowledge, is not previously reported in India.

A 23-year-old female presented with headache and bilateral diminution of vision for 3 days. She had no history of tinnitus. This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. 

She was infected with COVID-19 3 weeks before, confirmed with a positive reverse transcriptase-polymerase chain 

Santamaria et al. [10] VKH post COVID-19 Saraceno et al. [11] VKH post COVID-19 Vaccıne Saraceno et al. [11] Age ( computed tomography (HRCT) of chest was normal at this stage and her repeat RT-PCR for COVID-19 was negative. As she already had a positive RT-PCR report for COVID -19 done at the time of COVID-19 infection, SARS-COV-2 antibody test wasn't done. All other infectious etiologies were ruled out. She was diagnosed as probable VKH, as she didn't have any neurological or integumentary findings. The patient was started on oral prednisolone 1 mg/kg/day with weekly tapering. At 1-month's follow-up, her BCVA improved to 20/25 OU, with complete resolution of SRF. At 2-months' follow-up, her BCVA was stable with no recurrence of inflammation on OCT [ Fig. 3a and b] and fundus examination [ Fig. 3c and d] .

We report a unique case demonstrating SARS-CoV-2 virus as a possible trigger for VKH. VKH is characterized by bilateral serous retinal detachment and disc hyperemia. [1, 5] Our patient had a recent COVID-19 infection, following which she developed VKH, with characteristic clinical and imaging features and showed a good response to oral corticosteroids. She was classified as probable VKH as per revised international diagnostic criteria for VKH, as she didn't have neurological or integumentary findings. [6] VKH is known autoimmune inflammatory condition targeting the melanocyte-rich antigen particularly tyrosinase peptide, through a CD4+ T-cell-mediated response, in genetically susceptible individuals. Expression of HLA-DQA1*0301 and HLA-DQB1*0401 has been identified as a predisposing factor for genetic susceptibility for VKH. [7] Autoimmune response elicited by COVID-19 viral antigen is supported by elevated acute phase reactants like ESR and CRP. Various viral triggers have been reported in causation of VKH especially in genetically susceptible individuals. [1] The onset and exacerbation of VKH by infective triggers like Epstein-barr virus, cytomegalovirus, influenza A, and mycoplasma pneumonia due to molecular mimicry and cross reactivity have been reported earlier. [1, 4] Expression of HLA DRB1*0405, HLA-DQA1*0301 and HLA-DQB1*0401 also makes an individual genetically susceptible to develop autoimmune inflammations following exposure to viral triggers. [7, 8] These viral triggers exhibit molecular mimicry, which induces autoimmune response mediated by mononuclear cells including the T cells that cross reacts with melanocyte self-antigens. Homology between the viral antigen peptides and melanocyte self-antigen peptides is responsible for the cross reactivity and molecular mimicry involved in pathogenesis of VKH. [9] Strong association of HLA-DR4 in the pathogenesis of VKH post-viral infections has been demonstrated. HLA-DR4 acts by facilitating antigen presentation to T cells. [1] Post-viral infections, microbial antigens also hypothesized to initiate an innate immune response through toll-like receptors identified in the uveal tact. [10] So far, two cases of VKH developing post-COVID-19 infection have been reported in literature and SARS-CoV-2 has been identified as a possible trigger factor for VKH. Inflammatory events in these reported cases occurred 2 weeks following COVID-19 infection [ Table 1 ]. [10, 11] COVID-19 infection is known to trigger several autoimmune and inflammatory disorders, usually in pediatric age group and rarely in adults. [12] In pediatric age group, autoimmune disorders like Kawasaki disease has been reported in 2-15-year-old children between 18 and 79 days post-COVID-19 infection. [12] In adults, autoimmune diseases like Guillian--Barre syndrome, idiopathic thrombocytopenic purpura, and autoimmune hemolytic anemia have been reported early in course, usually 4-13 days from the onset of COVID-19 symptoms. [12] Our patient developed ocular symptoms after 3 weeks following COVID -19 infection. To the best of our knowledge, incidence of VKH following a recent COVID-19 infection has not been reported in the Indian population yet.

COVID-19 infection could be a possible trigger factor for VKH. However, further studies are needed to unveil the exact pathogenesis and association. Early initiation of treatment with corticosteroids helps in faster visual recovery in these patients.

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Nil.

There are no conflicts of interest.

Vogt-Koyanagi-Harada disease associated with influenza A virus infection

Panuveitis and optic neuritis as a possible initial presentation of the Novel coronavirus disease 2019 (COVID-19)

Central retinal vein occlusion with COVID-19 infection as the presumptive etiology

Vogt-Koyanagi-Harada disease presenting secondary to a post-infectious Mycoplasma pneumoniae autoimmune response

OCTA Study Group. Bacillary layer detachment in acute Vogt-Koyanagi-Harada disease: A novel swept-source optical coherence tomography analysis

Vogt-Koyanagi-Harada disease diagnostic criteria

Association of human leukocyte antigen (HLA)-DQ and HLA-DQA1/DQB1 alleles with Vogt-Koyanagi-Harada disease: A systematic review and meta-analysis

Vogt-Koyanagi-Harada disease: Review of a rare autoimmune disease targeting antigens of melanocytes

Cross-reaction between tyrosinase peptides and cytomegalovirus antigen by T cells from patients with Vogt-Koyanagi-Harada disease

SARS-CoV-2 among the potential viral triggers for Vogt-Konayagi-Harada disease: First case report and literature review

Koyanagi-Harada syndrome following COVID-19 and ChAdOx1 nCoV-19 (AZD1222) vaccine

Autoimmune and inflammatory diseases following COVID-19