Ocular Abnormalities Occurring with Vitiligo

Albert, Daniel M.; Nordlund, James J.; Lerner, Aaron B.

doi:10.1016/s0161-6420(79)35413-6

Cited by 99 publications

(77 citation statements)

References 26 publications

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“…Eye defects reported in vitiligo patients include uveitis, retinal pigment epithelium hypopigmentation, chorioretinal scars, pigment clumping and iris transillumination defects (Albert et al, 1979). Conversely, a high incidence of vitiligo has been found in patients with idiopathic uveitis (Wagoner et al, 1983).…”

Section: Is Vitiligo a Systemic Disease Involvingmentioning

confidence: 99%

Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

140

107

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Vitiligo is a puzzling disorder characterized by a disappearance of epidermal and/or follicular melanocytes by unknown mechanisms. This very common disorder involving 1-4% of the world population is thus of great importance for the practicing dermatologist. The cellular and molecular mechanisms leading to the destruction of melanocytes in this disorder have not yet been elucidated, making it of major interest for the cell biologist involved in melanocyte research.Recent advances in this field, due largely to the availability of techniques for culturing normal human melanocytes, opened new perspectives in the underitanding of vitiligo. Although vitiligo has long been considered a disorder confined to the skin, there is now good evidence that it also inwlves the extracutaneous compartment of the "melanocyte organ." It is also clear that vitiligo is not only a melanocyte disorder, but that it also involves cells, such as keratinocytes and Langerhans cells, found in the epidermis and follicular epithelium.The three prevailing theories of the pathogenesis of vitiligo are the immune hypothesis, the neural hypothesis, and the self-destruct hypothesis. New hypotheses suggest that vitiligo may be due to (1) a deficiency in an unidentified melanocyte growth factor, (2) an intrinsic defect of the structure and function of the rough endoplasmic reticulum in vitiligo melanocytes, (3) abnormalities in a putative melatonin receptor on melanocytes and (4) a breakdown in free radical defense in the epidermis. None of these hypotheses has been demonstrated, and according to the available data, it is likely that the loss of epidermal and follicular melanocytes in vitiligo may be the result of several different pathogenetic mechanisms.

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Section: Is Vitiligo a Systemic Disease Involvingmentioning

confidence: 99%

Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

140

107

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“…Various recent clinical and animal experimental studies [3][4][5] support the premise that the pathogenetic mechanisms of Vitiligo could be systemic events as vitiligo is associated with ocular [6][7][8][9] and auditory abnormalities and other autoimmune disorders [2,3,9,10]. There have been few studies in India on the ocular and otic abnormalities and the presence of other autoimmune disorders in association with vitiligo [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Audiological and Electrophysiological Changes in Patients with Vitiligo

Arya

Munjal

Panda

et al. 2015

Indian J Otolaryngol Head Neck Surg

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The study was conducted to evaluate the audiological and electrophysiological findings in patients with Vitiligo and to compare the findings with otologically and audiologically normal controls. Study group included 50 subjects (25 Males, 25 Females) with Vitiligo (Mean age-27.4 years) and control group contained 40 age-matched normal hearing subjects. Pure tone audiometry (PTA) with extended high frequency audiometry, Otoacoustic emissions (OAEs), Tympanometry, Auditory brainstem responses (ABR) and Middle latency responses (MLR) were conducted in all subjects. Comparison of the study group with the control group showed statistically significant differences (p \ 0.05) on PTA, in Transient otoacoustic emissions (TOAEs) at 1, 2, 3, 4 kHz and in distortion product otoacoustic emissions (DPOAEs) at 357, 499, 704, 1003 Hz. On ABR, statistically significant differences were observed between the groups in wave I (p \ 0.01) in both ears, wave V (p \ 0.05) in left ear and on interpeak latency of I-III (p \ 0.01, p \ 0.05), III-V (p \ 0.01 in left ear) and I-V (p \ 0.01, p \ 0.05) in left and right ears respectively. When patients with localized vitiligo were compared with generalized vitiligo, the SNR of TOAEs was highly significant in both ears at 2 KHz (p \ 0.05), 3 kHz (p \ 0.01) and 4 kHz (p \ 0.05). PTA average of 2 KHz, 4 and 8 kHz (PTA2) showed a significant difference (p \ 0.01) when localized vitiligo was compared to generalized vitiligo. Results support possible auditory and electrophysiological changes in Vitiligo patients along with decreased cochlear function.

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“…These symptoms involve tissues in which MCs are present. Eye defects reported in vitiligo patients include uveitis, retinal pigment epithelium hypopigmentation, chorioretinal scars, pigment clumping and iris transillumination defects [4]. Cowan et al [17] reported choroidal abnormalities in up to 30% and evidence of iritis in 5% of patients.…”

Section: Vitiligo and MC Organ Involvementmentioning

confidence: 99%

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

2002

J Biomed Sci

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Melanocytes (MCs) are melanin-producing cells of the skin that are derived from neural crest cells. Vitiligo vulgaris is a common depigmentation disorder resulting from the destruction of functional MCs in the affected skin. The three prevailing pathomechanisms of vitiligo are the immune hypothesis, the neural hypothesis and the autocytotoxic hypothesis. None of these mechanisms has been conclusively proven. Melanoblasts (MBs) in the outer root sheath of the hair follicles are the reservoir cells for repigmentation. Recovery from vitiligo is initiated by activation and proliferation of these MBs, followed by upward migration to the nearby epidermis that forms perifollicular pigmentation islands. Migration, proliferation and differentiation of MCs and MBs are regulated by keratinocyte-derived factors and some coat color genes. Any therapy for vitiligo must explain not only the repopulation of MCs but also their functional development. In patients with vitiligo, MCs are destroyed in the skin, the eyes, and possibly the ears. However, the concept of vitiligo as a systemic disease will be clearly established only when the mechanisms involved in vitiligo are identified. Recent advances in the fields of neural crest cell culture and molecular genetics have opened new perspectives in the understanding of vitiligo. Not only will this result in better treatments for vitiligo patients, but possibly will also provide a key to triggering nerve cell regrowth in other nervous diseases.

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Ocular Abnormalities Occurring with Vitiligo

Cited by 99 publications

References 26 publications

Vitiligo: Where Do We Stand?

Vitiligo: Where Do We Stand?

Audiological and Electrophysiological Changes in Patients with Vitiligo

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

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