Destruction of melanocytes in vitiligo is caused by combination of immunological and cytotoxic mechanisms. In addition to cutaneous melanocyte, melanin-containing cells of leptomeninges, inner ear and eyes might be destroyed. With regards to eye changes, it should be recalled that two distinct populations of pigment-bearing cells exist: the uveal melanocytes and pigment epithelium (
8). Destruction of uveal melanocytes and pigment epithelium in patients with vitiligo was first documented by Albert et al. (
9), who reported various abnormalities in 112 patients, including uveitis, retinal pigment epithelial hypopigmentation, choroidal scars, pigment clumping and transillumination defects. In the same year, Rosenbaum et al. (
10) reported a case of bilateral retinal pigment epithelial changes associated with periorbital vitiligo and seizure. Four years later, Albert et al. (
9) found asymptomatic and symptomatic retinal pigment epithelium atrophy in 27% of 223 patients with vitiligo; this was the only controlled study so far that compared ocular findings in patients with vitiligo and psoriasis and demonstrated a significant increase in retinal pigment epithelium atrophy or hypopigmentation in patients with vitiligo. In a subsequent study by Cowan et al. (
11) ocular inflammation was not found as a major feature in patients with vitiligo and 40% of patients showed some degree of fundal pigment findings including pigment clump, focal hypo pigmented spots, and choroidal nevi. The most common ocular findings in our study were peripapillary atrophy around the optic nerve, atrophy of retinal pigment epithelium and diffuse and focal hypopigmented spots on the retina. During 2006, a study done on 45 patients with vitiligo examined for ocular findings (
5) in addition to evaluation of demographic features including age, gender, duration of vitiligo, association with autoimmune disease and anatomical distribution of depigmented macules to evaluate any probable association with ocular abnormalities. The results showed ocular abnormalities including iritis, peripapillary atrophy, pigmented epithelium atrophy and focal hypopigmented spots in ten (22.23%) patients (
5). Anatomical localization, primarily periorbital, and to a lesser extent vitiligo of the genitalia were reported to be the most probable alerting features for ocular findings. Another study performed on 150 patients with vitiligo during 2007, revealed 24 (16%) cases of ocular problems including uveitis and pigment abnormalities in iris and retinas in which 18 patients had hypothyroidism, diabetes mellitus or alopecia as an autoimmune disease. The ocular findings of our study were similar to those of the literature and were not associated with any other abnormalities.
It is evident that multiple ocular abnormalities might be found in patients with vitiligo. Many ocular abnormalities are non-specific in character and distribution; however, they might be ascribed mostly to immunological processes in vitiligo. In this study, we aimed to determine any features that might be related to ocular findings. Our study revealed a significant association between age and duration of vitiligo with ocular findings and showed that positive family history was an important risk factor for patients presenting ocular problems. The prevalence of ocular findings was significantly higher in patients with autoimmune diseases. Our findings were similar to recent studies and showed that with increasing age and duration of vitiligo, the risk of ocular findings was greater. In addition, having a positive family history and autoimmune disease were important risk factors that increased ocular findings. This study showed that ocular problems are important and assessable findings in patients with vitiligo. In addition, aging and duration of vitiligo can increase the risk of ocular abnormalities and patients with a positive family history and autoimmune disease should be on priority of screening.