Contact vitiligo: etiology and treatment

Introduction

Contact vitiligo is an acquired leukoderma that occurs as a result of repeated topical or systemic exposure to a variety of chemicals.[1] These chemicals are mainly alkyl phenols and catechols. They are used in the manufacturing of plastics, resins, synthetic rubber, paints, petrolatum products, deodorants, pesticides, disinfectants, germicides photographic chemicals, printing ink, varnishes[1] etc. These chemicals are also present in certain objects of our daily use eg. foot wear, plastic watch strap, purse and bindis.[1],[2],[3]

The present study was conducted to find out the cause of contact vitiligo with patch testing and to evaluate the response of treatment with PUVASOL along with topical corticosteroids.

Materials and Methods

All patients were assessed on a prescribed proforma regarding clinical history, occupation, family history of vitiligo, duration of illness, sites of depigmentation, spread of disease and duration of contact with offending agent.

Following base line investigations were carried out like Hemoglobin, TWBC,DLC, TEC,VEC,LFT, and other relevant tests suggested by clinical examination. All patients were patch tested with offending agent as such or their scraping as mentioned by Bajaj et al.[3],[4] Reaction of patch testing was observed on 4th and 7th day and delayed reaction was observed on 15th and 21 r days. After patch test all patients were advised to avoid the use of object responsible for contact vitiligo. Oral trisoralen 0.6 mg/kg body weight was given on alternate day 2 hours before sun exposure along with topical betamethasone dipropionate 0.05%. These patients were followed up every month for 6 months and response of treatment was observed as:

No response -No change in vitiligo lesion

Mild response-Appearance of erythema in lesions

Good response-Appearance of pigmented spots in lesions

Excellent response-Disappearance of vitiligo patch.

Any side effect observed during treatment was also noted.

Results

Total 166 cases of contact vitiligo were included but only 50 cases could complete 6 month follow up. This included 4 males and 46 females, with age between 14 to 60 years. In 24 patients etiolological agent was sticking bindi alone, while bindi along with other etiological agents (purse, foot wear, watch strap and tooth paste) was found in 12 patients. Other etiological agents were found in 14 ( 28%) patients. These were purse in one case, foot wear in 8 cases , plastic watch strap in one case, tooth paste in 2 cases and lipstick in one case, and purses chappal both in one case [Table - 1].

Duration of contact with suspected agent was 10 days to 40 years with mean duration of 13.6 years. Duration of illness was between 15 days to 10 years with the mean of 2.14 years. 14 patients were having depigmentation at distant area along with contact site. Out of 50 patients positive patch test reactivity with suspected chemical was observed in 18(36%) cases [Table - 2]. Eleven (22%) patients showed positive reaction with bindi out o which depigmentation was observed in 3 (6%) case after 21 days of patch testing. 2 (4%) patient showed positive reaction with both bindi and purse while depigmentation was seen in one (2%) case at the site of bindi patch testing. 3(6%) case showed positive reaction with scraping of foot wear and one (2%) case with scraping of purse. One (2%) patient showed positive reaction with purse and tooth paste both, but there was no depigmentation.

25 (50%) patients had duration c diseases less than 1 year and they showed exceller response of treatment 7(14%), mild to goo( response in 15(30%) while no response in 3 (6% patients. Out of 20 (40%) patients with duratioi of disease 1-5 years,excellent response was sees in 3 (6%), mild to good response in 12 (24% while 5(10%) patients showed no response t( treatment. 5(10%) patients had duration of diseas, more than 5 year, in this group only one (2% patient showed excellent response and one (2% showed mild response while 3(6%) cases showe no response [Table - 3].

Discussion

Vitiligo is mostly idiopathic but certai chemicals have been documented to caus depigmentation eg. Hydroq- uinone, monomethy monoethyl and monobezyl ether of hydroquinone paratertiary butyl phenol, paratertiary amylphenc and paratertiary butyl catechol.[6] The chemical requirement for depigmenting activity is a hydroxyl group in the 4th position and a non-polar side group in the one position of organic ring.[7]

Non-occupational substances which can produce contact vitiligo are sticking bindis, shoes, adhesive tapes, wrist watch straps, rubber products and germicidal phenolic detergents. 1-3

In our clinic most of the cases of contact vitiligo are due to bindi, purse, footwear and plastic watch strap.

The exact mechanism of chemical induced depigmentation is not clear, several theories have been proposed for melanocyte destruction via.[8],[9],[10]

· The immune system in contact sensitized skin (post inflammatory hypopigmentation).

· Free radical formation induced by the depigmenting agent.

· Inhibition of the synthesis of the tyrosinase.

· Interference with transfer of melanosomes from melanocytes to keratinocytes.

Bajaj et al[4] studied 100 cases of bindi depigmentation. On analysis they found bindi contains 80% free paratertiary butyl phenol (PTBP) and purse contains monobenzyl ether of hydroquinone. Angelini[11] described allergic contact dermatitis and depigmentation of the lip margin from PTBP in a lip liner. Mathias et al[12] reported contact leucoderma due to cinnamic aldehyde in tooth paste.

In our study majority of patients (92%) were females because in majority of patients etiological agent was bindi which is used only by female. The averge duration of contact with probable etiological agent was 13.6 years. It shows that prolonged duration of contact is needed to induce depigmentation.

In this study 28% of cases had depigmentation at other sites. In all these cases depigmentation initially developed at the site of exposure and then subsequently at other sites. The phenomenon of depigmentation away from the site of exposure is not fully understood, but it is thought to be immunologic response resulting from sensitization of lymphocytes after exposure to melanocytic antigen showing melanocyte destruction. Subsequently the lymphocytes attack melanocytes at distant location.[13]

In our study etiological agent was found to be bindi alone in 48% (24) cases, while bindi along with other etiological agents (purse, rubber chappol, toothpaste, watch strap) in 28% (14) cases. All these agents were used by many people butdepigmentation developed only in a few cases. This could be either individual susceptibility to develop vitiligo or due to constant use for a prolonged period.

Depigmentation at the site of patch testing is diagnostic for contact depigmentation. We have found significant positive patch test reactivity with offending agent in 18 (36%) and depigmentation was seen in 4 (8%) cases after 21 days of patch testing. According to Fitzpatrick′ early localized cases may be reversed by avoidance of cause and if necessary by topical or oral PUVA, as with vitiligo. In the present study 25 (50%) patients having duration of disease less than 1 year, out of which excellent results of treatment was observed in 7(14%) patients, mild to good response in 15(30%) patients, while no response in 3 (6%) cases.

Out of 20 patients with duration of disease 1-5 years, excellent result was seen in 3(6%), mild to good response in 12 (24%), while 5 (10%) patients showed no response. In patients with duration of disease more than 5 years, only one patient showed excellent response while 3(6%) showed no response.