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 Table of Contents  
Year : 2022  |  Volume : 2  |  Issue : 4  |  Page : 909-910

Commentary: Treatment of refractory uveitis with Vogt Koyanagi Harada disease

1 Uveitis Services, Aravind Eye Hospital, Puducherry, India
2 Uveitis Services, Aravind Eye Hospital, Madurai, Tamil Nadu, India

Date of Web Publication11-Oct-2022

Correspondence Address:
Dr. Sivaraman Balamurugan
Uveitis Services, Aravind Eye Hospital, Puducherry - 605 007
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_961_22

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How to cite this article:
Balamurugan S, Anjana S. Commentary: Treatment of refractory uveitis with Vogt Koyanagi Harada disease. Indian J Ophthalmol Case Rep 2022;2:909-10

How to cite this URL:
Balamurugan S, Anjana S. Commentary: Treatment of refractory uveitis with Vogt Koyanagi Harada disease. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Nov 27];2:909-10. Available from: https://www.ijoreports.in/text.asp?2022/2/4/909/358200

Uveitis in Vogt Koyanagi Harada disease presents as granulomatous panuveitis. It is a common clinical entity for uveitis practitioners. It accounts for 15.9% of panuveitis.[1] Systemic corticosteroids are still the mainstay of treatment for VKH. Concurrently, immunomodulatory therapy can be added, as they take weeks to months to show its effect.[2],[3] Immunomodulatory therapy allows early withdrawal of systemic corticosteroids, chronicity, and reduces the severity of complications. It is continued until the remission of the disease.

Early control of intraocular inflammation provides promising results in visual prognosis. However, delay in treatment or inadequate therapy leads to the progression of the disease. Evidence suggests that despite early initiation of treatment and appropriate therapy patients progress to chronic granulomatous uveitis.[4] They develop sunset glow fundus with chorioretinal atrophy in spite of the disease being well controlled. Keino et al.[5] and Chee et al.[6] have reported patients progressing to the chronic stage of VKH in spite of receiving high-dose corticosteroid therapy. Thus, patients with chronic, recurrent, and refractory VKH can develop resistance to conventional therapy. Therefore, refractory uveitis in VKH patients, immunomodulatory drugs, and biological drugs play a key role in controlling inflammation. The advantage of biological drugs is their faster duration of action, thereby leading to early withdrawal of corticosteroids. An expert panel from the American uveitis society has generated guidelines for the use of tumor necrosis factor (TNF) alpha inhibitors in uveitis.[7]

The rationale for the use of adalimumab in VKH disease is related to the Th1 cytokine shown in the peripheral blood mononuclear cells. Th1 cells and inflammatory macrophages produce TNF alpha which plays a master role in the cytokine pathway involved in the disease pathogenesis.[8] In patients with active uveitis, levels of this cytokine are elevated in aqueous humor and serum.[9] Adalimumab is a TNF alpha inhibitor, which binds to TNF alpha, thereby controlling inflammation. The current manuscript (IJO-2902-21R1'The successful efficacy of Adalimumab in Vogt- Koyanagi-Harada disease: a case report) throws light on the effectiveness of adalimumab in refractory VKH.

Yang et al.[10] have reported a prospective study of nine patients refractory to uveitis in VKH patients. The addition of adalimumab helped in the reduction of inflammation, reduction of oral steroid dose, and relapse rate. However, a case report by Kwon et al.[11] reported a case of a 26-year-old female patient with recurrent episodes of inflammation in VKH. Oral steroids, oral methotrexate, and mycophenolate mofetil were not beneficial. However, the use of adalimumab was successful in controlling inflammation with remission of the disease. Su et al.[12] and Jeroudi et al.[13] reported the successful use of adalimumab for refractory uveitis in VKH. Mycophenolate mofetil, intravitreal triamcinolone was not useful in controlling inflammation. Similarly, Jeroudi et al. have reported pediatric VKH with recurrent uveitis despite the use of corticosteroids and methotrexate. This evidence shows that adalimumab can be considered in refractory uveitis in VKH patients. One of the main benefits of adalimumab is the faster onset of action compared to conventional immunomodulatory drugs.

Another valid consideration is the duration of treatment of refractory uveitis in a VKH patient with adalimumab before it is tapered and stopped. Cristobal et al. have reported the recurrence of inflammation within 1 to 3 months of stopping the medication.[14] Nonetheless Yang et al.[10] have had a very low relapse rate and withdrawal of corticosteroids without adverse effects.

A low prevalence of adverse effects is reported with the use of adalimumab in refractory VKH patients. Respiratory infections, urinary tract infections, and mild injection site reactions are the reported adverse effects.[10] However, reactivation of latent tuberculosis, malignancy, congestive heart failure, and opportunistic infections are the adverse effects that should be considered while treating a patient with adalimumab. Patients treated with adalimumab living in a TB endemic country pose a risk factor for the reactivation of tuberculosis.[15] Hence, adequate screening of tuberculosis and treatment of latent tuberculosis is required before initiating treatment with adalimumab.[16] Burmester et al.[17] have reported adverse effects of adalimumab in a large series of patients with various indications.

Studies are focused on adalimumab for refractory VKH patients. Whether adalimumab will be appropriate for the treatment of naïve uveitis in VKH patients is yet to be known and is a definite lacuna in the existing literature. Though adalimumab has been reported to be effective in treating refractory uveitis in VKH, reports involving a larger number of patients with uveitis and refractory uveitis in VKH with regard to the duration of treatment, efficacy, relapse of disease, and safety profile are yet to be known.

  References Top

Yang P, Zhang Z, Zhou H, Li B, Huang X, Gao Y, et al. Clinical patterns and characteristics of uveitis in a tertiary center for uveitis in China. Curr Eye Res 2005;30:943-8.  Back to cited text no. 1
Jabs DA, Rosenbaum JT, Foster CS, Holland GN, Jaffe GJ, Louie JS, et al. Guidelines for the use of immunosuppressive drugs in patients with ocular inflammatory disorders: Recommendations of an expert panel. Am J Ophthalmol 2000;130:492-513.  Back to cited text no. 2
Paredes I, Ahmed M, Foster CS. Immunomodulatory therapy for Vogt-Koyanagi-Harada patients as first-line therapy. Ocul Immunol Inflamm 2006;14:87-90.  Back to cited text no. 3
Herbort CP Jr, Abu El Asrar AM, Takeuchi M, Pavésio CE, Couto C, Hedayatfar A, et al. Catching the therapeutic window of opportunity in early initial-onset Vogt-Koyanagi-Harada uveitis can cure the disease. Int Ophthalmol 2019;39:1419-25.  Back to cited text no. 4
Keino H, Goto H, Usui M. Sunset glow fundus in Vogt-Koyanagi-Harada disease with or without chronic ocular inflammation. Graefes Arch Clin Exp Ophthalmol 2002;240:878-82.  Back to cited text no. 5
Chee S-P, Jap A, Bacsal K. Spectrum of Vogt-Koyanagi-Harada disease in Singapore. Int Ophthalmol. 2007;27:137-42.  Back to cited text no. 6
Levy-Clarke G, Jabs DA, Read RW, Rosenbaum JT, Vitale A, Van Gelder RN, et al. Expert panel recommendations for the use of anti-tumor necrosis factor biologic agents in patients with ocular inflammatory disorders. Ophthalmology 2014;121:785-96.  Back to cited text no. 7
Khera TK, Dick AD, Nicholson LB. Mechanisms of TNFα regulation in uveitis: Focus on RNA-binding proteins. Prog Retin Eye Res 2010;29:610-21.  Back to cited text no. 8
Santos Lacomba M, Marcos Martín C, Gallardo Galera JM, Gómaz Vidal MA, Collantes Estévez E, Ramírez Chamond R, et al. Aqueous humor and serum tumor necrosis factor-alpha in clinical uveitis. Ophthalmic Res 2001;33:251-5.  Back to cited text no. 9
Yang S, Tao T, Huang Z, Liu X, Li H, Xie L, et al. Adalimumab in Vogt-Koyanagi-Harada disease refractory to conventional therapy. Front Med (Lausanne) 2022;8:799427.  Back to cited text no. 10
Kwon HY, Woo SJ. A case of recurrent vogt-koyanagi-harada disease successfully treated with adalimumab in young female adult patient. Korean J Ophthalmol 2020;34:92-3.  Back to cited text no. 11
Su E, Oza VS, Latkany P. A case of recalcitrant pediatric Vogt-Koyanagi-Harada disease successfully controlled with adalimumab. J Formos Med Assoc 2019;118:945-50.  Back to cited text no. 12
Jeroudi A, Angeles-Han ST, Yeh S. Efficacy of adalimumab for pediatric Vogt-Koyanagi-Harada syndrome. Ophthalmic Surg Lasers Imaging Retina 2014;45:332-4.  Back to cited text no. 13
Couto C, Schlaen A, Frick M, Khoury M, LopezM, Hurtado E, et al. Adalimumab treatment in patients with Vogt-Koyanagi-Harada disease. Ocular Immunol Inflamm 2018;26:485-9.  Back to cited text no. 14
Cantini F, Nannini C, Niccoli L, Iannone F, Delogu G, Garlaschi G, et al. Guidance for the management of patients with latent tuberculosis infection requiring biologic therapy in rheumatology and dermatology clinical practice. Autoimmun Rev 2015;14:503-9.  Back to cited text no. 15
Carmona L, Gómez-Reino JJ, Rodríguez-Valverde V, Montero D, Pascual-Gómez E, Mola EM, et al. Effectiveness of recommendations to prevent reactivation of latent tuberculosis nfection in patients treated with tumor necrosis factor antagonists. Arthritis Rheum 2005;52:1766-72.  Back to cited text no. 16
Burmester G, Gordon KB, Rosenbaum JT, Arikan D, Lau WL, Li P, et al. Long-term safety of Adalimumab in 29,967 adult patients from global clinical trials across multiple indications: An updated analysis. Adv Ther 2020;37364-80.  Back to cited text no. 17


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