Clinical spectrum and management options in Vogt–Koyanagi–Harada disease

Abstract

Purpose
The aim of this study was to describe the clinical features, treatment options, and visual outcome of Vogt–Koyanagi–Harada (VKH) disease patients over a 9-year period.

Method
A retrospective chart analysis of 32 patients with VKH, from January 2007 to December 2015, at a tertiary care government medical college eye hospital in South India.

Results
A total of 32 patients were diagnosed with VKH. The mean age at diagnosis was 32.03±8.8 years. There were 24 patients (42 eyes) with acute VKH and eight patients (16 eyes) with recurrent/chronic VKH. The mean baseline best-corrected visual acuity on presentation in the acute VKH group was 5/60 (1.114±0.565) and at last follow-up it was 6/9 (0.225±0.157). Intravenous methyl prednisolone (IVMP) was administered for 3 days to all patients with acute and recurrent VKH, followed by posterior subtenon triamcinolone (40 mg/mL) and oral azathioprine.

Conclusion
VKH-related uveitis is more common in the female gender in this South Indian population. Posterior uveitis is the most common initial manifestation. Initial aggressive treatment with IVMP, peribulbar long-acting corticosteroids, and immunosuppressives, avoiding side effects of systemic steroids, gives a good visual outcome without recurrences. Cases of unilateral VKH, seen in six patients, are the initial manifestations in the natural course of the disease, which if managed aggressively at the acute stage prevents recurrence in the other eye.

Full text

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Clinical Ophthalmology 2017:11 1399–1406
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ORIGINAL RESEARCH
open access to scientific and medical research
Open Access Full Text Article
http://dx.doi.org/10.2147/OPTH.S134977
Clinical spectrum and management options in
Vogt–Koyanagi–Harada disease
Sikander AK Lodhi
JM Lokabhi Reddy
Venkataratnam Peram
Department of Ophthalmology,
Osmania Medical College/Sarojini
Devi Eye Hospital, Hyderabad,
Telangana, India
Purpose: The aim of this study was to describe the clinical features, treatment options, and
visual outcome of Vogt–Koyanagi–Harada (VKH) disease patients over a 9-year period.
Method: A retrospective chart analysis of 32 patients with VKH, from January 2007 to
December 2015, at a tertiary care government medical college eye hospital in South India.
Results: A total of 32 patients were diagnosed with VKH. The mean age at diagnosis was
32.03±8.8 years. There were 24 patients (42 eyes) with acute VKH and eight patients (16 eyes) with
recurrent/chronic VKH. The mean baseline best-corrected visual acuity on presentation in the acute
VKH group was 5/60 (1.114±0.565) and at last follow-up it was 6/9 (0.225±0.157). Intravenous
methyl prednisolone (IVMP) was administered for 3 days to all patients with acute and recurrent
VKH, followed by posterior subtenon triamcinolone (40 mg/mL) and oral azathioprine.
Conclusion: VKH-related uveitis is more common in the female gender in this South Indian
population. Posterior uveitis is the most common initial manifestation. Initial aggressive treat-
ment with IVMP, peribulbar long-acting corticosteroids, and immunosuppressives, avoiding side
effects of systemic steroids, gives a good visual outcome without recurrences. Cases of unilateral
VKH, seen in six patients, are the initial manifestations in the natural course of the disease,
which if managed aggressively at the acute stage prevents recurrence in the other eye.
Keywords: Vogt–Koyanagi–Harada disease, female, posterior uveitis, retinal detachment,
triamcinolone, azathioprine
Introduction
Vogt–Koyanagi–Harada (VKH) is a multisystem autoimmune inflammatory disorder
with ophthalmic, auditory, dermatologic, and neurologic manifestations.1 The preva-
lence of this disease varies with ethnicity. VKH characteristically affects pigmented
groups, such as Hispanics, Asians, people from the Middle East, and Asian Indians,
but not the blacks of sub-Saharan African descent.2 The extraocular manifestations
appear in different phases of the disease and show ethnic variations.3–5 VKH disease
accounts for 8% of uveitis in Japan, 2.9% in the Middle East, 1.2% in Europe, and
1%–4% in the USA.6,7 In a study from a referral eye care center in South India, the
prevalence is reported as 1.4%–3.5%.8 VKH is seen more frequently in an adult
population, and women are more frequently affected.9 VKH disease usually manifests
as four distinct clinical phases: prodromal, acute uveitic, convalescent, and chronic
recurrent.1 The prodromal phase features neurologic and auditory manifestations,
including a headache, tinnitus, neck stiffness, and hearing loss. The acute uveitic
phase shows diffuse choroiditis with exudative retinal detachment (RD) and optic
disc swelling. A variable amount of anterior chamber and vitreous inflammation may
be seen. In the acute phase, anterior uveitis seen in some patients usually presents as
low-grade non-granulomatous anterior uveitis, while in the chronic recurrent phase,
Correspondence: Sikander AK Lodhi
“Hill View,” 10-3-300/3, /Sarojini Devi
Eye Hospital, Hyderabad 500028,
Telangana, India
Tel +91 98 4802 0497
Email sikanderlodhi@gmail.com
Journal name: Clinical Ophthalmology
Article Designation: Original Research
Year: 2017
Volume: 11
Running head verso: Lodhi et al
Running head recto: Clinical spectrum and management options
DOI: http://dx.doi.org/10.2147/OPTH.S134977
Number of times this article has been viewed
This article was published in the following Dove Press journal:
Clinical Ophthalmology
7 August 2017

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Lodhi et al
patients present with recurrent granulomatous anterior
uveitis. “Sunset glow fundus,” due to depigmentation of the
choroid, is the hallmark of the convalescent phase. Recurrent
episodes of anterior uveitis are characteristic of the chronic
recurrent phase.
In a study by Rao et al, in an ethnically and geographically
diverse group of patients, it is revealed that there are two
clinical signs which are highly specific to VKH – exudative
RD during the acute phase and sunset glow fundus during
the chronic phase of the disease.3
Imaging technology has allowed a better visualization
and understanding of the disease process in VKH. The first
international workshop on VKH disease proposed criteria to
make diagnosis.2 According to the revised diagnostic criteria,
VKH disease can be complete, incomplete, and probable. All
the three categories have the absolute requirement of bilateral
eye disease; however, a unilateral or delayed involvement of
the other eye can occur in rare cases.10–13 Complete disease
represents the involvement of ocular, neurologic/auditory,
and integumentary systems. Incomplete disease is an eye
disease with either neurological/auditory or integumentary
signs. Probable VKH is uveitis consistent with VKH, without
any extraocular manifestations.
Multiple treatment regimens have been tried for VKH
disease, including intravenous, oral, regional corticosteroid,
cyclosporine, antimetabolites, and alkylating agents.14
Improper and inadequate immunosuppressive therapy during
initial-onset acute VKH disease will lead to chronic recurrent
VKH disease manifesting as granulomatous anterior uveitis
with sunset glow fundus. Vision threatening complications
like secondary glaucoma and cataract occur in the chronic
recurrent phase. Early and high-dose systemic corticosteroids,
followed by slow tapering, are mandatory to suppress the
inflammation in the acute posterior uveitis stage. Adding
immunomodulatory agents can improve the outcome and
can reduce the risk of integumentary involvement. High-dose
corticosteroids are associated with side effects such as hyper-
glycemia, hypertension, immunodeficiency, and secondary
glaucoma. Posterior subtenon triamcinolone (PST) acetonide
injection is a safe and more convenient treatment compared
with systemic steroid administration, avoiding the systemic
side effects and patient compliance. Most of the recurrences
of RD and inflammation are due to noncompliance or a very
rapid tapering of systemic corticosteroids.
The aim of this study was to analyze the demographic
characteristics, clinical features, efficacy of subtenon triamci-
nolone acetonide injection with immunomodulatory therapy
(ITP), and visual outcome in VKH patients referred to a
medical college tertiary eye care center in South India.
Methods
This is a retrospective, nonrandomized, noncomparative
interventional study. Patients diagnosed with VKH disease,
attending the retina/uvea outpatient department of a medical
college tertiary eye hospital, between January 2007 and
December 2015, were included in the study. Informed con-
sent was obtained from all the patients included in the study,
and the study adhered to the tenets of the Declaration of
Helsinki. Institutional ethics committee (Ethics Committee
of Osmania Medical College) approval was obtained for a
retrospective chart review. Retrospective chart review was
performed for 32 patients (58 eyes) diagnosed with VKH
for demographic data, clinical signs, investigations, treat-
ment received, complications, and visual outcome (Tables 1
and 2). All patients underwent a comprehensive ophthalmic
examination, including measurement of best-corrected visual
acuity (BCVA) with Snellen charts, applanation tonometry,
slit lamp examination, ophthalmoscopy, and fundus photog-
raphy. Ultrasound examination of the eye and fundus fluo-
rescein angiography (FFA) were performed in all the cases,
and optical coherence tomography (OCT) was performed
whenever possible. A general examination was done to look
for any integumentary findings. The clinical presentation and
its confirmation on FFA formed the basis for the diagnosis of
VKH disease. Previous history of any trauma was ruled out in
all the cases. Investigations were done to rule out tuberculosis
(Mantoux test, chest X-ray) and syphilis (venereal disease
research laboratory [VDRL] test). Revised diagnostic criteria
for VKH disease by Read et al2 were used for classifying the
cases into complete, incomplete, or probable VKH. Cases
with unilateral involvement were diagnosed to have VKH
Table 1 Demographic and clinical prole
Variables Number
Mean age (years) 31.16 (range 16–60)
Gender
Male
Female
13 (40.6)
19 (59.37)
Laterality
Bilateral 26 (81.25)
Anatomical classication
Panuveitis
Posterior uveitis
16 eyes (27.6)
42 eyes (72.4)
Clinical types
Probable
Incomplete
Complete
47 eyes (81.03)
7 eyes (12.06)
4 eyes (6.9)
Course
Acute
Chronic
Recurrent
24 (42.85)
7 (12.5)
8 (14.28)
Note: Data presented as n (%), unless otherwise stated.

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Clinical spectrum and management options
when all the characteristic ocular manifestations were present
because unilateral or delayed involvement of the other eye
can occur in rare cases. A uniform protocol was followed
in treating all the cases. All acute cases and recurrent cases
on presentation (31 patients) were treated with intravenous
methyl prednisolone (IVMP) 1 g for 3 days followed by PST
acetonide 40 mg/mL in the affected eyes. Simultaneously,
oral azathioprine 1–2 mg/kg was started and continued for
6–9 months. Patients were followed-up at monthly intervals.
PST was used in 44 eyes. PST was repeated after 3 months,
if required. Continuing inflammation or recurrence was
monitored by BCVA, signs of inflammation, and OCT. PST
was required to be repeated in 4 eyes. In our earlier cases
(not included in this study), we used IVMP followed by oral
corticosteroids for 1 year. The compliance with oral steroids
was very poor, and therefore, the strategy was modified
to use PST combined with the immunosuppressive agent
azathioprine. Patients with anterior segment inflammation
were treated with topical corticosteroids and cycloplegics
in addition to systemic treatment. Any case that had raised
intraocular pressure (IOP) was managed with medical ther-
apy. Use of azathioprine was monitored by complete blood
count and liver function tests. Complications such as cataract,
glaucoma, and choroidal neovascular membrane were noted,
and any extraocular manifestations were recorded in addition
to chronic stage features such as sunset glow fundus and
chorioretinal atrophy patches. For statistical analysis, visual
acuity data were converted to logMAR values. The data
were entered in an Excel 2007 spreadsheet and statistically
analyzed with SPSS software.
Results
A total of 32 patients were seen during the study period.
The average age of the patients was 31.16 years (range
16–60 years). There were 13 male and 19 female patients
(Table 1). The average follow-up was 18 months (range
2–84 months). All patients were from South Indian states
of Telangana and Andhra Pradesh. Twenty-six patients had
a bilateral presentation and six patients had only unilateral
VKH. The type of VKH, according to diagnostic criteria,
was classified as complete in 2 patients, incomplete in
5 patients, and probable in 25 patients. We have classified
our patients into two groups depending on the stage of the
disease at presentation (Table 2). At presentation, there were
24 patients (75%) with acute VKH and 8 patients (25%) with
chronic recurrent VKH disease. This amounts to 42 eyes
with acute VKH and 16 eyes with chronic recurrent VKH,
and all patients with unilateral VKH were in the acute stage.
Comparisons between acute and chronic VKH with respect
to clinical features at presentation, clinical evaluation, and
follow-up are presented in Table 2. Meningism and headache
were the most common systemic associations in the acute
stage (Table 3). Three patients in chronic VKH had alopecia
Table 2 Comparison of results between acute and chronic
recurrent Vogt–Koyanagi–Harada (VKH)
Characteristics Clinical presentation
Acute VKH Chronic/
recurrent
VKH
P-value
Patients (n) 24 (75%) 8 (25%)
Eyes (n) 42 (72.4%) 16 (27.6%)
Mean age (years) 30.54±6.64 36.5±12.96 0.247
Gender: female 13 (54.16%) 6 (75%) 0.299
Initial visual acuity
Mean BCVA (logMAR) 1.1148±0.56576 1.3125±0.57140 0.248
6/12 or better 5 (11.9) –
6/18 to 6/36 6 (14.3) 3
6/60 or worse 31 (73.8) 13
Final visual acuity
Mean BCVA (logMAR) 0.2257±0.15756 0.8138±0.63316 0.002
6/12 or better 38 3
6/18 to 6/36 4 9
6/60 or worse – 4
Late complications
Glaucoma 8 1 0.218
Cataract 4 14 #0.0001
CNVM – 3 0.004
Band keratopathy – – –
Recurrences (n, %) 4 11 #0.0001
Notes: Data presented as n (%), unless otherwise stated. For both categories mean
visual acuity is given.
Abbreviations: BCVA, best-corrected visual acuity; CNVM, choroidal neovascular
membrane.
Table 3 Incidence of systemic and ocular manifestations
Systemic manifestations Number (%)
Headache 15 patients (47)
Meningismus 5 patients (15)
Alopecia 3 patients (9)
Hearing disturbance 3 patients (9)
Poliosis 3 patients (9)
Tinnitus 2 patients (6)
Vitiligo 1 patient (3)
Anterior segment manifestations
Circumciliary congestion 6 eyes (10.3)
Keratic precipitates (KPs)
Fine KPs
Mutton fat KPs
10 eyes (17)
4 eyes (7)
Iris nodules 6 eyes (10.3)
Flare 10 eyes (17)
Cells 10 eyes (17)
Posterior segment manifestations
Vitreous cells 38 eyes (65)
Disc hyperemia 55 eyes (95)
Disc edema 26 eyes (45)
Exudative retinal detachment 52 eyes (91)
Sunset glow fundus 24 eyes (41)
Dalen–Fuchs nodules 17 eyes (29)

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Lodhi et al
and poliosis, and three patients had a hearing disturbance.
Clinically, 16 eyes presented with panuveitis and 42 eyes pre-
sented with posterior uveitis. Slit lamp examination showed
keratic precipitates in 14 eyes and flare and cells in 10 eyes.
All the 24 cases in the acute stage presented with posterior
segment manifestations, and the most common finding was
multiple serous RDs in the posterior pole in all the 42 eyes.
Vitreous cells were seen in 38 eyes. Disc hyperemia was seen
in 55 eyes and disc edema in 26 eyes. Sunset glow fundus
was seen in 24 eyes (which includes chronic VKH cases on
presentation and acute VKH cases in convalescence on fol-
low-up; Table 3). FFA (Figures 1–3) performed in all patients
(except one) showed multiple pinpoint hyperfluorescent
leaks in 54 eyes and late pooling in serous RDs in 42 eyes.
Late disc staining was seen in 46 eyes. 10 MHz ultrasonog-
raphy showed a diffuse choroidal thickening in all the acute
cases, which was most marked in the juxta papillary region
(Figures 1 and 2). OCT in acute cases showed multilobular
RDs, subretinal septa, retinal pigment epithelium undula-
tions, and choroidal thickening (Figures 1 and 2).
Twenty-five cases of acute VKH were treated with the
above-mentioned strategy. Four cases were lost to follow-up
after 2 months. Twenty cases completed follow-up from
6 months to 5 years. One case had multiple recurrences
over a follow-up period of 1.5 years and was treated with
a combination of immunosuppressives (azathioprine and
methotrexate). We found six cases of unilateral VKH in this
study. All these cases clinically showed uniocular multiple
serous detachments in the posterior pole, with angiographic
features of choroidal delay, multiple pinpoint hyperfluo-
rescent leaks, and pooling in the serous elevations by late
phases. Ultrasound examination showed choroidal thickening
in all these cases. All these cases were treated aggressively
with IVMP, PST acetonide, and immunosuppression with
Figure 1 (A) A 30-year-old female. BCVA 20/200 in both eyes. Serous retinal detachments, pinpoint leaks, disc hyperourescence, and pooling of dye. (B) Ultrasonography
shows choroidal thickening and serous retinal detachment. (C) OCT – shows large serous retinal detachments with subretinal septae and RPE undulation. (D) Two and a
half months after initiating treatment, the retina is reattached. BCVA is RE 20/20 and LE 20/25.
Abbreviations: BCVA, best-corrected visual acuity; RPE, retinal pigment epithelium; OCT, optical coherence tomography; RE, right eye; LE, left eye.

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Clinical spectrum and management options
Figure 2 A 25-year-old female with unilateral VKH. (A) RE shows serous retinal detachment and optic nerve head hyperemia. LE fundus is normal. FFA shows RE late leakage
and pooling of the dye. (B) RE OCT demonstrates the presence of subretinal uid and septae, LE OCT is normal. (C) Ultrasonography reveals RE showing a diffuse choroidal
thickening and LE showing a normal posterior segment.
Abbreviations: BCVA, best-corrected visual acuity; OCT, optical coherence tomography; FFA, fundus uorescein angiography; VKH, Vogt–Koyanagi–Harada; RE, right
eye; LE, left eye.
azathioprine for 6–9 months. One other case presented with
unilateral VKH in the right eye (RE) and treated with IVMP
followed by PST was lost to follow-up. After 3 years, she
presented with acute VKH in the left eye (LE) with BCVA
RE 6/24 and LE 6/60. She was treated with the same pro-
tocol; 6 months later, she had BCVA RE 6/24 and LE 6/9
(Figure 2). Once the inflammation has subsided, RDs have
resolved, and with no disc hyperemia, the fundus had a near
normal appearance in 21 patients and sunset glow fundus
in 6 patients of acute VKH and 6 patients with chronic and
recurrent uveitis.
In this series, visual acuity of 6/12 or better was main-
tained in 38 eyes that presented with acute VKH. Of these,
21 eyes had a BCVA better than 6/12 after at least 1-year
follow-up without recurrences (Table 2). Chronic and
recurrent VKH cases had a poor visual outcome, ,6/60.
Complicated cataract was seen in 14 eyes, one chronic VKH
patient had raised IOP, and eight patients with acute VKH had
secondary glaucoma after PST injection. All these cases were
managed with medical therapy. The choroidal neovascular
membrane was seen in 3 eyes and chronic vitritis in 6 eyes
of chronic VKH cases (Table 2).
Discussion
This retrospective study investigated patients with VKH
disease over a 9-year period. Demographic features in the
present case series are almost similar to those studied in
other countries.1,7,8,15–18 Most of the studies show female
preponderance. In accordance with the published literature,
we also found that 59.37% of the cases were females. In this
series, majority of the cases presented with posterior uveitis
in the acute stage, and therefore, as per the revised diagnostic
criteria, 25 patients (78.12%) are in the probable category.
Compared to studies from Japan,19,20 we have a higher propor-
tion of probable VKH. A study by Arevalo et al from Saudi
Arabia also shows a higher proportion (58.4%) of probable
VKH cases.21 Extraocular signs such as poliosis, alopecia,
vitiligo, and hearing loss develop during the course of VKH
disease and are seen mainly in the chronic stage of the dis-
ease.4 In a multicenter study by Rao et al, in ethnically and
geographically diverse study groups, exudative RD was the
most statistically significant feature of the acute disease.3
They report that robust positive and negative predictive
values and likelihood ratios of various documented clinical
findings indicate that in acute uveitis, the presence of bilateral
exudative RDs in a patient with bilateral intraocular inflam-
mation strongly suggests acute VKH. In the present study,
exudative RD and disc hyperemia were the most common
posterior segment findings in the acute cases, and sunset glow
fundus was the most common finding in chronic/convalescent
cases. Ancillary testing supports the clinical diagnosis of
VKH disease. FFA performed in all cases showed multiple
hyperfluorescent pinpoint leaks in 56 eyes (96.55%) and
late pooling in serous RDs in 54 eyes (93.1%). Rao et al,
in their multiethnic diverse study, reported one or more
angiographic findings (choroidal delay, multifocal leaks,
subretinal pooling of dye) in 83% of VKH cases.3 Another
test that supported the diagnosis was ultrasound examination,
performed in all cases, which showed choroidal thickening
in all acute cases.

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To the best of our knowledge, the number of cases of
unilateral VKH seen in this study is more than that reported
by any other study (Figures 2 and 3). As has been observed
by Rao et al,3 from multiple papers proposing or evaluating
diagnostic criteria for VKH,2,22,23 a definitive set of criteria has
not been universally agreed upon. This is mainly because of
the multiphasic nature of VKH, with varying clinical features
in different stages of the disease as well as due to ethnic
variation in disease manifestations. What we are seeing as
unilateral VKH may be the early phase of the disease which
if not treated aggressively in the initial stages may occur in
the other eye in due course. All the six cases of unilateral
VKH did not have a recurrence because of early aggressive
and prompt treatment and continuation of immunosuppres-
sive therapy for a sufficient period of time. The one case of
unilateral VKH that was lost to follow-up and was not suf-
ficiently treated in the early phase had a recurrence in the
other eye after 3 years.
Prompt and aggressive treatment with corticosteroids
with slow tapering over a period of 6 months is recom-
mended to avoid recurrence and complications.24,25 Sys-
temic corticosteroids are associated with possible side
effects like hyperglycemia, hypertension, gastritis, and
rising IOPs. Compliance with the use of systemic corti-
costeroids is usually poor. Recurrences are usually due
to early and abrupt discontinuation of corticosteroids.
Rubsamen and Gass reported recurrences in 43% and 52%
of their patients occurring in the first 3 and 6 months of
the disease, associated in most cases with rapid tapering
of corticosteroids.26 Ocular manifestations of VKH can be
Figure 3 (A and B): Unilateral VKH. A 31-year-old female patient with BCVA RE 20/400 and LE 20/20 shows multiple serous retinal detachments, with multiple pinpoint
leaks and subretinal pooling of dye. LE shows normal fundus with normal FFA. (C) Follow-up after 40 months shows both eyes normal fundus with BCVA RE 20/25 and
LE 20/20.
Abbreviations: BCVA, best-corrected visual acuity; FFA, fundus uorescein angiography; RE, right eye; LE, left eye.

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Clinical spectrum and management options
managed by local administration of steroids.27–29 Moreker
and Lodhi, from their study on the use of intravitreal tri-
amcinolone acetonide (IVTA) in VKH, have concluded that
IVTA, when used as an adjuvant, can induce remission in
the acute stage of VKH and help avoid the long-term use
of systemic corticosteroids.27 Hosoda et al demonstrated
that isolated PST is a useful primary treatment option for
patients with acute VKH without systemic disorders. In
77.8% of patients, they achieved complete resolution of
serous RD without recurrence after PST therapy.30 Paredes
et al31 reported their outcomes in 13 patients with VKH
disease and suggested that immunomodulatory therapy as
a first-line therapy for VKH is associated with a superior
outcome when compared to steroid as monotherapy or with
delayed addition of immunomodulatory drugs.
To overcome the problem of compliance, side effects, and
recurrences, we have used a combination of PST acetonide
and systemic immunosuppression with azathioprine. Aza-
thioprine is shown to be effective for the treatment of chronic
uveitis, usually in combination with corticosteroids.32–34
Azathioprine may show some adverse side effects, such
as myelosuppresson, and serious side effects are unusual
with the low dose (1–2 mg/kg/day) compared to high dose
of azathioprine. A visual acuity of 6/12 or better was main-
tained in 44 eyes that presented with acute VKH that had no
recurrences in the follow-up. Periocular injection of depot
steroids likely induces the IOP to rise. In our study, 8 eyes of
four patients showed ocular hypertension (IOP .21 mmHg)
after the injection. The IOP was controlled by topical
medications only, and no additional glaucoma treatment was
required. In a recent review by Rao et al it was concluded that,
“The initial treatment is with high dose corticosteroids, then
steroid-sparing therapy, with a focus on getting the inflam-
matory response under control to prevent the development of
sequelae such as a sunset glow fundus, cataracts, glaucoma,
and choroidal neovascularization.”14
Conclusion
This study shows that in acute VKH, initial aggressive corti-
costeroid treatment with IVMP, followed by peribulbar depot
steroids in combination with systemic immunosuppression,
is effective in treating the ocular inflammation with rare
recurrences.
Disclosure
The authors report no conflicts of interest in this work.
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