Ocular disturbances in vitiligo

Cowan, Claude L.; Halder, Rebat M.; Grimes, Pearl E.; Chakrabarti, Siba G.; Kenney, John A.

doi:10.1016/s0190-9622(86)70136-9

Cited by 71 publications

(43 citation statements)

References 12 publications

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“…An increased release of leukocyte migration inhibition factor from patient's lymphocytes has been reported suggesting an hyperfunctioning of these cells in vitiligo (Zaman et al, 1992). Other studies showed abnormalities including elevated numbers of peripheral monocytes (OKM5) (Baumer et al, 1990) or depressed interleukin2 activity (Halder et al, 1986).…”

Section: Is Vitiligo An Autoimmune Disease?mentioning

confidence: 98%

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Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

138

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 An Autoimmune Disease?mentioning

confidence: 98%

“…Conversely, a high incidence of vitiligo has been found in patients with idiopathic uveitis (Wagoner et al, 1983). Other studies found that ocular inflammation is not the main manifestation of ocular vitiligo, but noted fundal pigment disturbances in a high percentage of patients (Cowan et al, 1986).…”

Section: Is Vitiligo a Systemic Disease Involvingmentioning

confidence: 99%

Vitiligo: Where Do We Stand?

Ortonne

Bose

1993

Pigment Cell Research

138

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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“…[1][2] Only a small number of cases have been reported with widespread hypopigmentation of both choroid and retinal pigment epithelium (RPE). [1][2][3] Our two patients with vitiligo had extensive choroidal hypopigmentation without signs or a previous history of ocular inflammation. They both had normal visual function, and additional fluorescein angiogram and electrodiagnostic tests in case 1 were normal.…”

mentioning

confidence: 85%

“…We describe an unusual case of tuberculous (TB) dacryocystitis, a rare secondary cause of nasolacrimal duct obstruction, 3,4 diagnosed with the aid of out-patient nasal endoscopy.…”

Section: Correspondencementioning

confidence: 99%