Discussion
Although many factors have been blamed for the pathogenesis of vitiligo,
the etiology is not yet fully known. Antibodies against melanocytes are
known to be destructive to melanocytes in the vast majority of patients
(1).
Evidence of the destruction of uveal melanocytes and retinal pigment
epithelium in vitiligo patients was first reported by Albert et al (11).
In some studies, hypopigmentation of the choroid was also detected in
vitiligo patients (12, 13). Bülbül et al. , in their study which
examined ocular findings in 45 vitiligo patients, found peripapillary
atrophy around the optic nerve in seven patients, atrophy of the retina
pigment epithelium in two patients, diffuse in the retina in one
patient, focal hypopigmented spots in one patient. Their study also
found that ocular findings were significantly observed in patients with
periorbital and to a lesser degree genital vitiligo (6). Biswas et al.
found pigment change in iris and anterior chamber in 41 of 100 vitiligo
patients, retinal pigment epithelial hypopigmentation in 9 of them,
uveitis in 5 of them, chorioretinal degeneration in 11 of them, and
reported no ocular findings in 34 of them, indicating a strong
association between vitiligo and ocular disorder (3). Karadağ et al.
found abnormal retinal findings in 24 out of 122 eyes in 122 vitiligo
patients; determined Tigroid retina in 11 eyes, oblique disc in 3 eyes,
peripapillary atrophy in 3 eyes, drusen in 2 eyes, choroidal nevus in 1
eye, myelinated nerve fiber in 1 eye, cage degeneration in 1 eye (2). In
our study, we found ocular fundus findings such as peripapillary atrophy
in three patients, focal hypopigmentation in two patients and widespread
hypopigmentation in one patient.
Studies on the choroidal tissue in vitiligo patients have been limited,
especially in-vivo study of the choroid with the EDI form of the SD-OCT
device has helped to understand the diagnosis and pathogenesis of some
diseases more clearly. The choroidal thickness is known to be affected
by age, sex and ax (14). In our study, there were no significant
differences between age, gender, and ax among the groups.
The choroid is among the most vascularized tissues in the body, covering
the outer retina. A pathology that can occur in the choroidal structure
for any reason can result in decreased vision as a result of
degenerative changes in photoreceptors. The stroma of the choroidal
layer contains a high number of melanocytes (4). A low choroidal
thickness may be expected in vitiligo where melanocyte loss is observed.
Foveal hypoplasia was found in several studies in patients with albinism
(15, 16). In patients with oculocutaneous albinism with melanocyte
deficiency, the choroidal thickness in the subfoveal region was
significantly lower than in the control group and there was no
difference in the peripapillary region compared to the control group
(17). Demirkan et al. determined that the choroidal thickness in
vitiligo patients was significantly thin compared to the control group
in all values except optic nerve area measurements, and it was indicated
that choroidal thickness may be affected by melanocyte loss in vitiligo.
The absence of differences between vitiligo patients and the control
group in optic nerve regions was linked to less space coverage of
melanocytes in histological structure in optic nerve regions. It was
also stated that periorbital involvement had no effect on the choroidal
thickness (18).
Vogt-Koyanagi-Harada (VKH) syndrome is a disease characterized by a T
cell-mediated autoimmune process aimed at melanocytic antigens. Ocular
symptoms of the disease include severe bilateral panuveitis associated
with exudative retinal detachment. Retinal edema, choroidal thickening,
bilateral vitritis, papillitis and retinal detachment are seen. As
exudation is not observed in vitiligo patients, increase in the
choroidal thickness is not expected despite melanocyte destruction as in
VKH (20). We also determined that even though visual acuity of vitiligo
patients was at the same level as the control group, the mean macular
choroidal thickness was thinner. We found no significant changes in the
choroidal thickness in patients with periocular attitude. We found a
negative correlation between the choroidal thickness and the duration of
the disease. Also, in our study, although there was significant decrease
in the choroidal thickness of N1, T1, T2, T3 in vitiligo patients, there
was no significant change in N2, N3, and this may indicate that the
choroidal thickness changed slightly in this region due to the less
dense melanin cells around the optic disc.
In the diagnosis of glaucoma, the determination of thickness thinning of
OCT and RNFL is considered the most specific test for objective
detection of damage (21). In the studies of Rogosic et al., the age of
the patient and the duration of vitiligo were significantly correlated
with primary open-angle glaucoma. In their study, the RNFL thickness was
measured to gauge neuroretinal damage (8).
Dertlioglu et al. reported in their studies that normotensive glaucoma
was seen in 18.4% of vitiligo group and that there was a statistically
significant difference compared to control group. They found no
correlation between periocular involvement and glaucoma (22). Duplancić
et al. reported that the prognostic value of hemodynamic changes
determined by color Doppler imaging in the ophthalmic artery and that
there was a positive correlation between vitiligo and POAG (23). In many
sources, it was that glaucoma seen in vitiligo is a secondary
complication, a direct result of corticosteroid therapy (24, 25).
Studies of Khurrum et al. demonstrated that patients with vitiligo and
periorbital topical steroids did not have an increased risk of glaucoma
or cataracts (26). Örnek et al., in their study, reported no significant
differences between vitiligo patients and control groups in the upper,
lower, nasal and temporal quadrants in the topographic distribution of
RNFL, and concluded that the RNFL thickness was not affected in vitiligo
patients (5).
Electroretinography (ERG) and visual evoked potentials (VEP), which are
electrophysiological tests, are useful tests for determining retinal
ganglion cell and RNFL dysfunction (27). Shoeibi et al. reported that
overall retinal electrophysiological function in vitiligo patients
decreased significantly compared to the normal population regardless of
age and sex (9). Perossini et al. identified abnormal VEP and
electrooculography (EOG) in patients with severe vitiligo. They found
more pronounced negative ocular electrophysiological results in patients
with greater skin involvement and longer duration of disease (10). In an
animal study, abnormal flash ERG findings secondary to histopathological
abnormalities were reported in mutant mice with vitiligo, and the
apopitosis of photoreceptors in these mice was demonstrated in
morphological and biochemical studies (28). Aydın et al., in their
studies on vitiligo patients, found that the photoreceptor segment was
preserved in ”SD-OCT”, while in multifocal electroretinography (mfERG),
there was a decrease in central retinal function, indicating a potential
decrease. This study showed that even with normal fundus appearance and
SD-OCT findings, there may be a potential decline in central retinal
function in vitiligo patients. Their study also noted that there was no
statistically significant difference in the entire retinal layer
thickness between the vitiligo and the control group (29).
Since the choroidal thickness is affected by many factors and diurnal
choroidal thickness changes occur at 30-60 µm (14), we found it
appropriate to measure the choroidal thickness values in a limited time
period (between 09: 00 and 12:00 hours). Low case count, short follow-up
time, the fact that factors which can affect the choroidal thickness
measurements such as smoking and caffeine use are not studied, and
manual measurement of the choroidal thickness are limited aspects of our
study. Studies with a longer follow-up period and broader participation
investigating all factors that may affect the choroidal and the RNFL
thickness in vitiligo patients may provide greater clarity on this
issue.
As far as we know, this study is the first to examine the choroidal
thickness and the RNFL thickness with SD-OCT in vitiligo patients,
analyzing its correlation with disease duration. In our study, it was
determined that mean macular choroidal thickness decreased significantly
in vitiligo patients, while the RNFL thickness did not change. Negative
correlation was found between the choroidal thickness and the duration
of the disease. There was no significant correlation between the
choroidal and the RNFL thickness in vitiligo patients with periocular
involvement. We are of the opinion that close monitoring of the vitiligo
patients by the eye diseases department, the non-invasive OCT screening
for posterior ocular segment disorders, and OCT-EDI examinations for the
choroidal thickness containing dense melanin may be much more
beneficial.