|Year : 1992 | Volume
| Issue : 5 | Page : 331-333
Comparative histopathology of vitiligo and contact depigmentation
RR Mittal, JS Jassal, R Popli, D Kumar
R R Mittal
Source of Support: None, Conflict of Interest: None
Fifteen cases of vitiligo and 12 cases of contact depigmentation were compared histopathologically. Incontinence of melanin in dermis was seen in 33% cases of contact depigmentation and 6.6% cases of vitiligo. Mononuclear infiltrate was more in contact depigmentation and had lichenoid character at places. Vasculitis with perivascular mononuclear infiltrate was seen in all cases of contact depigmentation. It is proposed that chemicals responsible for contact destruction of melanocytes.
Keywords: Contact depigmentation, Vitiligo
|How to cite this article:|
Mittal R R, Jassal J S, Popli R, Kumar D. Comparative histopathology of vitiligo and contact depigmentation. Indian J Dermatol Venereol Leprol 1992;58:331-3
|How to cite this URL:|
Mittal R R, Jassal J S, Popli R, Kumar D. Comparative histopathology of vitiligo and contact depigmentation. Indian J Dermatol Venereol Leprol [serial online] 1992 [cited 2019 May 22];58:331-3. Available from: http://www.ijdvl.com/text.asp?1992/58/5/331/3839
| Introduction|| |
Both vitiligo and contact depigmentation (CD) clinically present with depigmented macules. Some cases of vitiligo develop CD and vice versa. Melanin is absent in vitiligo lesions and dopa stain or silver stain show absence of melanocytes.  Borders of vitiligo patches may show large melanocytes  or melanocyte degeneration.  Dermal lymphocytic infiltration of the border of vitiligo patches has been reported.  Complete lack of melanin in depigmented areas and its marked reduction in dopa positive melanocytes in CD has been reported. , Melanin incontinence into superficial dermis and the absence of inflammatory infiltrate in CD has been observed. 
| Material and Methods|| |
Twenty eight patients of vitiligo and 27 patients of CD were selected for this study. Detailed history was taken and clinical examination was done. Patch tests were applied in 27 cases of contact depigmentation for 72 hours and 96 hours. Histopathological study was carried out in 15 cases of vitiligo and 12 cases of CD under light microscope. Haematoxylin and eosion stain was used.
Twelve case of CD were due to bindi and patch tests were applied with offending brands of bindi. Fifteen cases of CD were due to chappals or shoes and were patch tested at 2 sites with scrapings from shoes or chappals which were minced into small pieces with scissors and were soaked in 4 drops of distilled water of petrolatum for 15 minutes before application and third control patch was with petrolatum alone.
| Results|| |
Patch tests were positive in 17 out of 27 cases. [Table - 1] shows that 8 of 12 were positive cases of CD due to bindi and 9 of 15 were due to shoes or chappals. Sixteen positive path tests occurred after 72 hours and 19 after 96 hours while 2 patients, one each due to bindi and shoes, had both positive patch test and depigmentation. [Table - 2] shows histopathological changes in vitiligo and CD.
Melanin in basal layers was absent in 12 of 15 cases of vitiligo and 10 of 12 cases of CD. Melanin in dermis was seen in 1 of 15 cases of vitiligo and 4 of 12 cases of CD thus melanin in dermis was present in 6.6% of vitiligo and 33% cases of CD. Mononuclear infiltrate was not localized to margins of depigmented spots in either condition. Mononuclear infiltrate was more intense in CD and had lichenoid character at a number of places. Most significant difference was that all cases of CD had vasculitis with fibrinoid deposits and prominent perivascular 'mononuclear infiltrate and it was absent in all cases of vitiligo.
| Comments|| |
CD has been reported as a toxic effect on melanocytes after contact with chemicals such as monobenzyl ether of hydroquinone, paratertiary butyl phenol, paratertiary amyl phenol, 4-isopropylcatechol, and tertiary butyl catechol. In the present study vasculitis with perivascular mononuclear infiltrate, lichenoid character of mononuclear infiltrate, and the resultant incontinence of melanin were seen in CD. It could be concluded that most probably CD resulted from immunological reaction to chemicals which ultimately resulted in melanocyte destruction rather than due to a direct toxic effect of chemicals on the melanocytes.
| References|| |
|1.||Brown J, Winkelmann RK, Wolf K. Langerhans cells in vitiligo. J Invest Dermatol 1967; 49: 849-53. |
|2.||Morohashi M. Hasimoto K, Goodman TJR, et al. Ultrastructural studies of vitiligo, VogtKoyanagi syndrome and incontinentia pigmenti achromians. Arch Dermatol 1977; 113: 756-66. |
|3.||Bazex A, Balas D, Bazan J. Maladie de Vogt Koyanagi-Harada. Ann Dermatol Venereol 1977; 104: 849-53. |
|4.||Bleehen SS. Pathak MA, Heri Y, et al. Depigmentation of skin with 4-isopropylcatechol, mercaptoamines and othor compounds. J Invest Dermatol 1968; 50: 103-17. |
|5.||Kahn G. Depigmentation caused by phenolic detergentgermicides. Arch Dermatol 1970; 102: 177-87. [PUBMED] |
|6.||Mathias CGT, Maibach HI, Contant MA. Perioral leukoderma simulating vitiligo from use of a toothpaste containing cinnamic aldehyde. Arch Dermatol 1980; 116: 1172-3. |
[Table - 1], [Table - 2]