Suboptimal therapy controls clinically apparent disease but not subclinical progression of Vogt-Koyanagi-Harada disease

Abstract

Submaximal doses of inflammation suppressive therapy are sufficient to suppress clinically apparent disease but not the underlying lesion process. This explains the propensity for sunset glow fundus in seemingly controlled disease.

Vogt-Koyanagi-Harada Disease

“…5 Indocyanine green angiography (ICGA) appears to be especially useful for detecting suboptimal or incomplete control of choroidal inflammation in patients with longstanding or chronic/recurrent disease. 21,22 Two original articles 23,24 and two letters to the editor 25,26 in this issue of Ocular Immunology & Inflammation present important findings relevant to the pathogenesis, clinical presentation, diagnosis and management of VKH disease.…”

Catching the therapeutic window of opportunity in early initial-onset Vogt–Koyanagi–Harada uveitis can cure the disease

“…This shows that the standard corticosteroid monotherapy is indeed suppressing clinically apparent disease, but is insufficient to suppress choroidal inflammation [32]. Subclinical evolution of choroidal inflammation has also been clearly documented by several groups investigating smoldering disease with the help of ICGA [28][29][30][31][32][33], explaining that the development of SGF despite corticosteroid therapy results from the progressive loss of stromal melanocytes due to the ongoing insufficiently controlled immunological process [19,32].…”

“…This shows that the standard corticosteroid monotherapy is indeed suppressing clinically apparent disease, but is insufficient to suppress choroidal inflammation [32]. Subclinical evolution of choroidal inflammation has also been clearly documented by several groups investigating smoldering disease with the help of ICGA [28][29][30][31][32][33], explaining that the development of SGF despite corticosteroid therapy results from the progressive loss of stromal melanocytes due to the ongoing insufficiently controlled immunological process [19,32]. This is a strong incentive to maintain sufficiently dosed therapy including first-line nonsteroidal immunosuppressive drugs, even in the subacute phase and during the corticosteroid tapering process, to be sure to eradicate choroidal inflammation [24][25][26][27][28][29][30][31][32][33].…”

“…Subclinical choroiditis is the reason for chronic evolution and is clearly identified by ICGA, uncovering active choroidal inflammation in an apparently quiescent eye during follow-up while monitoring corticosteroid tapering [28][29][30][31][32][33]. This shows that the standard corticosteroid monotherapy is indeed suppressing clinically apparent disease, but is insufficient to suppress choroidal inflammation [32].…”

Differentiating Vogt-Koyanagi-Harada syndrome from recurrent optic neuritis: a case report and review of the literature concerning Hispanic patients

“…According to the misdiagnosis, a suboptimal dose of steroid was administered at that time, which can at least partially explain the subsequent propensity for recurrence [11].…”