Choroidal Thickness in Convalescent Vogt–koyanagi–harada Disease

Abstract

The thinner choroid and larger PPA areas were correlated with the degree of depigmentation or disease duration and might be caused by latent choroidal inflammation in the convalescent stage of Vogt-Koyanagi-Harada disease.

Analysis of choroidal folds in acute Vogt–Koyanagi–Harada disease using high-penetration optical coherence tomography

“…In addition, the frequency of a sunset glow fundus at the 6-month evaluation was significantly higher in eyes with CFs than in those without CFs. These results agreed with previous studies that have reported that the choroidal tissue thinned in eyes with a sunset glow fundus [19,24]; and a sunset glow fundus develops primarily in patients with longstanding uveitis [24,25]. Patients with VKH disease with CFs may have a longer disease duration than those without CFs, which is similar to a study that reported that patients with CFs had a longer disease duration at the first visit than those without CFs [7].…”

Changes in Central Macular Thickness and Retinal Nerve Fiber Layer Thickness in Eyes with Vogt-Koyanagi-Harada Disease: A 2-Year Follow-Up Study

“…Nazari et al [8] reported a loss of choroidal tissue including the choriocapillaris layer in the convalescent stage of VKH disease and a correlation with an increased duration of disease, lower visual acuity, and structural changes in the retina such as photoreceptor disruption or external limiting membrane disruption. Takahashi et al [4] evaluated the subfoveal choroidal thickness in the convalescent stage of VKH disease and concluded that a thinner choroid was correlated with the disease duration and might be caused by latent choroidal inflammation in the convalescent stage. These findings suggest that the changes in the CMT in the present study may have been caused by inflammation, cytokines, and loss of choroidal tissue including the choriocapillaris layer in the convalescent stage of VKH disease.…”

“…Ocular findings such as bilateral granulomatous panuveitis, multifocal serous retinal detachment, and optic disc swelling are common in the acute phase of VKH disease [1,3]. Histopathological examinations and indocyanine green angiographic findings in eyes with VKH disease suggested that inflammatory manifestations of VKH disease might result from an autoimmune reaction to melanocytes, and the choroid is the main site of disease-related inflammation [1,2,[4][5][6].…”

Vogt−Koyanagi−Harada disease

“…Both patients achieved disease control after the first infusion of rituximab, with stable, long-lasting remission. One of the patients also recovered some hearing as well [24]. Given that rituximab is a B-cell-targeted therapy, and that VKH is believed to be a primarily T-cell-driven disease, this response to rituximab raises interesting questions about the pathogenesis of VKH disease, and how we might use rituximab and other similar drugs to treat VKH in the future.…”

“…Thus, they postulate that the RPE undulation index may be useful in assessing disease severity. In addition, ED-OCT has demonstrated that choroidal thickness decreases with treatment [22] and is thinner in eyes with chronic disease [23,24].…”