Outcomes of Vogt-Koyanagi-Harada Disease: A Subanalysis From a Randomized Clinical Trial of Antimetabolite Therapies

Abstract

Purpose To report outcomes of Vogt-Koyanagi-Harada (VKH) disease from a clinical trial of antimetabolite therapies. Design Subanalysis from an observer-masked randomized clinical trial for non-infectious intermediate, posterior, and pan- uveitis. Methods Setting clinical practice at Aravind Eye Hospitals, India Patient Population Forty-three of 80 patients enrolled (54%) diagnosed with VKH. Intervention Patients were randomized to either 25mg oral methotrexate weekly or 1g mycophenolate mofetil twice daily, with a corticosteroid taper. Main outcome measures Primary outcome was corticosteroid-sparing control of inflammation at 5 and 6 months. Secondary outcomes included visual acuity, central subfield thickness, and adverse events. Patients were categorized as acute (diagnosis ≤3 months prior to enrollment) or chronic (diagnosis >3 months prior to enrollment). Results Twenty-seven patients were randomized to methotrexate and 16 to mycophenolate mofetil; 30 had acute VKH. The odds of achieving corticosteroid-sparing control of inflammation with methotrexate were 2.5 times (95% CI: 0.6, 9.8; P=0.20) the odds with mycophenolate mofetil, a difference which was not statistically significant. The average improvement in visual acuity was 12.5 Early Treatment Diabetic Retinopathy Study (ETDRS) letters. On average, visual acuity for patients with acute VKH improved by 14 more ETDRS letters than those with chronic VKH (P<0.001), but there was no difference in corticosteroid-sparing control of inflammation (P=0.99). All 26 eyes with a serous retinal detachment at baseline resolved, and 88% achieved corticosteroid-sparing control of inflammation. Conclusions The majority of patients treated with antimetabolites and corticosteroids were able to achieve corticosteroid-sparing control of inflammation by 6 months. Although patients with acute VKH gained more visual improvement than those with chronic VKH, this did not correspond with a higher rate of controlled inflammation.

Intravitreal methotrexate and fluocinolone acetonide implantation for Vogt-Koyanagi-Harada uveitis

“… 10 In VKH, systemic methotrexate has resulted in some success when combined with systemic corticosteroids. 15 However, the use of intravitreal methotrexate in VKH has not been previously reported, and, to our knowledge, this may be the first case of intravitreal methotrexate therapy in a patient with VKH.…”

Guidance on Noncorticosteroid Systemic Immunomodulatory Therapy in Noninfectious Uveitis

“…The grade C recommendation for the use of mycophenolate derivatives (alone or with cyclosporine) reflects the low-level evidence for this drug combination. Mycophenolate mofetil also has been evaluated in acute Vogt-Koyanagi-Harada (VKH) disease, 99 and in a comparative study (vs. methotrexate) in patients with acute or chronic VKH disease 100 in combination with high-dose oral corticosteroids. These studies support the use of mycophenolate mofetil and methotrexate for control of inflammation and maintenance of VA, with no evidence of superiority of one drug over the other (grade C recommendation).…”

Long-Term Efficacy of Dexamethasone Intravitreal Implant in the Treatment of Vogt-Koyanagi-Harada (VKH) Disease Relapsing Posterior Uveitis

“…All patients had been previously treated with systemic steroid regimen (at 1.5-2 mg/kg/day) and Azathioprine (at 1-2.5 mg/kg/day) for at least 6 months. [7,8] All patients had systemic steroid and/or immunosuppressive comorbidity, dependency, and non-compliance. The diagnosis and classi cation of VKH disease were established according to the criteria of the International Workshop of Vogt-Koyanagi-Harada Disease.…”

“…Long-term high-dose systemic corticosteroid and immune-modulating therapy might result in systemic side effects such as hypertension, diabetes mellitus, osteoporosis, and long-term risks for cancer and mortality. [5][6][7][8][9] Chronic recurrent VKH disease and the relapse of the ocular in ammation may re ect improper, insu cient, delay initiation, rapid tapering of immune-modulator therapy, or subclinical choroiditis.…”