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.