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CONTINUING MEDICAL EDUCATION
Year : 1999  |  Volume : 65  |  Issue : 4  |  Page : 161-167

Etiopathogenesis of vitiligo : Are we dealing with an environmental disorder ?




Correspondence Address:
P N Behl


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Source of Support: None, Conflict of Interest: None


PMID: 20921645

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  Abstract 

The increasing incidence of vitiligo in this part of the world (4.25%), prompted us to study 5000 fresh vitiligo patients. Several triggering factors were elicitable. Malnutrition and intake of junk food were very common in childhood vitiligo. Intercurrent infections as well as intake of antibotics were also significant, immediately preceding the development of depigmented patches in younger age group. Genetic predisposition was uncommon. Autoimmune disorders were infrequent and usually accompanied late onset vitiligo. For management, vitiligo was classified into VI (active), V2 (quiescent) and V3 (improving) stages. The therapy administered varied in each stage. As a common denominator, all out efforts were made to eliminate possible trigger factors in individual cases throughout the period of treatment, and building the general health to prevent recurrence in future. The study strongly points out that vitiligo is a multifactorial disorder. It can be effectively managed after each patient is individually assessed. Elimination of possible triggering factors may form the mainstay of vitiligo therapy along with controlled pharmacological intervention. The improvement of general resistance of body may bring spontaneous repigmentation.



How to cite this article:
Behl P N, Agarwal A, Srivastava G. Etiopathogenesis of vitiligo : Are we dealing with an environmental disorder ?. Indian J Dermatol Venereol Leprol 1999;65:161-7

How to cite this URL:
Behl P N, Agarwal A, Srivastava G. Etiopathogenesis of vitiligo : Are we dealing with an environmental disorder ?. Indian J Dermatol Venereol Leprol [serial online] 1999 [cited 2019 May 23];65:161-7. Available from: http://www.ijdvl.com/text.asp?1999/65/4/161/4798



  Introduction Top


Vitiligo is regarded as a primary acquired idiopathic, depigmentation of the skin and/or mucous membranes. Although a benign cutaneous pigmentary aberration with no influence on physical and intellectual capability of the affected individual or on life span, yet it is a dreaded disease of the pigmented race.[1] It puts tremendous stress on the sufferer and adversely effects his capability and social life. In the developing countries like India, it is frequently confused with leprosy by a lay person.

The fact that at least one percent of the world population has vitiligo speaks boldly for its common occurrence.[2] More over, not so encouraging views expressed by eminent physicians[3] about its treatment disheartens the patient as well as the treating doctor. As little is known about its etiology-being an idiopathic disorder-its treatment regimens widely differ. Thus, the response, subsequent recurrences and damage to the skin are also quite unwarranted. We highly felt that there is always a definite etiology in each case-a group of triggering factors. Unless and until we eliminate these factors we cannot treat a vitiligo patient satisfactorily. Further, if any such triggering stimulus is eliminated, the activity of the disease should stop per se, and spontaneous repigmentation may start. Keeping these facts in mind, our Institute started a detailed clinico-etiologic study of fresh vitiligo patients, spread over the past decade.


  Materials and Methods Top


Five thousand fresh vitiligo patients were included in this study. The parameters in history included age-at-onset, duration, preceding events, history of drug intake, diet, water consumed, geographic area of stay and its surroundings, family history, and systemic illnesses and infections. They were further examined clinically for general assessment of health and nutrition, any overt focus of infection, site of initial affection and its spread, and the affection of mucous membrane and hair. This was followed by routine blood and urine investigation and an immunoglobulin study. In large number of cases, serum elements (copper, molybdinum, manganese, zinc etc.) were also estimated. Stools were examined for ova and cyst of parasites

The treatment was instituted in a systemic way. In the first stage, (VI stage) the above measures along with other conservative measures like phenylalanine, placental extract-topical or systemic (in insidiously spreading VI stage), and ACTH injections (in galloping VI stage), antistress herbal preparations and building up general health of the body will go a long way in its treatment. In stable (V2) stage when no new lesions are appearing, photochemotherapy with psoralens (Ammimajus) can be added. In repigmenting stage (V3) when there is no further pigmentation, surgical measures can be undertaken thus preventing the injudicious use of psoralens. It is equally important to identify the resistant areas which may not repigment even after prolonged use of psoralens, as well as patients with poor response. The findings were recorded on a specially-devised exhaustive proforma. The material thus gathered was assessed at the end of the study, and the results recorded under various heads.


  Observations Top


Age and sex incidence: Of the 5000 patients, 1313 had an age-at-onset below 10 years, and another 708 between 11 and 20 years. There were 2720 males and 2280 females

[Table - 1]

Family history: A positive family history of vitiligo was elicitable in 434 (8.4%) patients. Of these, 243 (4.8%) belonged to first degree relations, while 148 and 43 to second and third degree relations respectively.

Suspected precipitating factors/events: Certain events/factors were found to be clearly preceded or associated with the onset of vitiligo. The most likely event was taken into consideration in every case, wherever such a history was available, to avoid duplication of triggering events. However, there was an overlap in cases with recurrent infections in 200 patients, who also had repeated courses of chemotherapy, as both were regarded significant precipitating events in them [Table - 2]. Most of the cases (130 out of 151) with overt malnutrition also showed associated dull, thin, brown hair with stunted growth, several months/years prior to the onset of vitiligo. Emotional trauma, such as a death in the family, broken marriage, unemployment and other stresses like major operations preceded onset of vitiligo in 70 (3.50%) patients. Among recurrent infections, focal sepsis including chronic tonsillitis/dental sepsis and intestinal amoebiasis were prominent. Broad-spectrum antibiotics especially tetracyclines were found to be the often prescribed medicine for the throat sepsis. Some children, under 8-10 years of age even showed terramycin induced discoloration of the teeth. Amongst topical chemical agents, application of adhesive bindi on the forehead (1.5%) and wearing of rubber foot wear (0.7%) were significant triggering factors.

Trace elemental analysis done in 147 patients of vitiligo is shown in [Table - 3]. Serum copper levels were significantly lower in active stage in 142 of them (96.59%).

Equivocal results were seen in the case of zinc, manganese and selenium.

Serum IgE levels were done in 500 patients. Of them, 241 had a raised IgE level. Majority of patients with raised IgE level had a level of over 500 iu/ml.


  Clinical features Top


The patients were conventionally classified as vitiligo vulgaris, acrofacialis, zosteriformis or mucosae [Table - 4]. Involvement of mucous membrane alone was fairly uncommon (0.35%); however it accompanied other varieties in 110 (10.5%) patients. The variation in the morphology of developing, quiescent and healing lesions, at the time of presentation, were quite distinct, which prompted us to further classify every case as VI (active), V2 (quiescent) and V3 (improving), VI stage patients were still developing new lesions, and the individual lesions were showing activity, with ill-defined, advancing borders. V2 patients had developed no lesions for past few months and had well demarcated skin lesions with hyperpigmented borders. V3 patients had no lesions for the past many months or years, with skin lesions well-defined with variable amount of healing within the patch. [Table - 5].


  Treatment administered Top


VI patients were given a conservative treatment along with elimination of the predisposing cause(s). V2 and V3 patients were given more active treatment, using psoralens to stimulate the melanocytes. However, V3 patients who appeared to have no further chance of repigmentation, were advised to undergo surgery.


  Discussion Top


The possible etiological factors and their interactions is summarised in the following diagram [Figure - 1]. Despite efforts to precisely pinpoint the exact cause of vitiligo, no breakthrough has been achieved. The present study has thus made another attempt to shed some light on the disease.

Various workers from all over the globe have found different incidences of vitiligo [Table:8.] One salient feature appears to be that the incidence of vitiligo is on the rise especially in the developing countries like India. Over the past four decades, several camps have been conducted by us in the remote areas of India [Table - 7]. Certain areas in proximity to industries showed an alarming rise in incidence of vitiligo, possibly due to industrial wastes contaminating the ground water with vegetation grown in such water being consumed by natives. Correlation of number of patients of vitiligo with different age groups in childhood onset vitiligo showed a rise in the incidence of vitiligo as the age advanced (Fig.2). Certain experiments involving the feeding of guinea pigs on different water collected from various such industrial towns showed depigmentation of hair of these animals.

Much has been said about the age and sex incidence of vitiligo.[4][5][6][7][8] An alarming observation made in our study was the conspicuous affliction of children below 10 years of age. As much as 34.2 percent had the age-at-onset less than 10 years. On scrutinizing their records, we found a large number of these children had some or the other predisposing/triggering factors-recurrent infections and/or antibiotic therapy, malnutrition and consumption of junk food having high contents of preservatives, colorants and anti-oxidants. Lerner,[4] observed that nearly 50 per cent of vitiligo developed below 20 years of age, while it was much higher (61.9%) in our series.

Vitiligo is believed to be a hereditary disorder probably inherited through an autosomal dominant gene of variable penetrance. The incidence of positive family history has variously been reported from 5% to 40% in different studies. In our study it was 21.7 per cent. In studies in two small communities in India, family history was documented as high as 78.29%, and 90.38% respectively.[10][11] Vitiligo has been observed in monozygotic twins.[12]

The elucidation of precipitating factors in as many as 68.45 per cent patients in our study is quite significant. These were largely preventable, and require elimination for an effective cure. Although genetic, autoimmune, neurogenic and melanocyte self-destruction hypothesis have time and again been described[8][13] in the etiopathogenesis of vitiligo, the preceding factors have seldom been stressed. The occurrence of vitiligo after major illness, severe emotional stress, pregnancy, surgical operation and physical trauma has been recorded.[2][4][8] Some noxious, melanocyte-destroying chemical entering the body through diet, consumption of ready made preserved stale food/medicines/contaminated water (through industrial waste) or the air might be an important factor in precipitation of vitiligo in a susceptible host. The occurrence of vitiligo following repeated drug intake in as many as 535 (26.75 per cent) patients is far more than just a co-incidence, and warrants serious thought prior to prescribing antibiotic therapy in patients who have a family history of vitiligo. A high prevalence of vitiligo was noticed by the authors in the population near a textile industry. It did not have an effective waste disposal system and discharged the effluents in the nearby canal. These people used this contaminated water for drinking and irrigation purposes.

All these precipitating factors might have contributed to disturb the immunological balance of the body, thus causing an autoimmune or other process to paralyse the affected patient's melanocyte system to produce the lesions of vitiligo. Our presumption is further supported by the work of Puri et al[14] which suggests that in vitiligo whole of the melanocyte system is defective. It was also found that the cultured melanocytes were defective, stunted and slow growing. Further studies at the Skin Institute in histopathological sections of margins of active vitiligo, showed the presence of mononuclear infiltrate hugging the basal layer of epidermis suggesting some type of auto-immune reaction.[25][26]

Management of the disease appeared to vary with the activity of the disease. Active or galloping vitiligo cases (VI-stage) required a different approach compared to the static and healing vitiligo (V2 and V3-stages). Every effort was made to eliminate the suspected precipitating factors and improve the general health of the patient. The patients invariably had psychosomatic stress, and we preferred to administer a herbal preparation.[15] The only indication of oral/topical corticosteroid in vitiligo should be galloping VI-stage. Adrenocorticotropic hormone (ACTH) injections (20-40 I.U.im) weekly should be preferred as a short course.[16] We strictly resist giving psoralens in VI-stage, as initially the whole body requires restorative measures. And only after all the system is toned up, there is logic in stimulating melanocytes. Placental extract either topically,[17] or by intramuscular route (biweekly) can also be given in VI-stage. Oral or topical L-phenylalanine cream can be alternatively used. [18, 19] With such a conservative regimen, Vl-stage is likely to enter a stable V2 stage in 2 to 4 months.

Once the control of the disease is achieved (V2-stage), and the borders are hyperpigmented, psoralen or Ammi majus, therapy can be started. It can be given by oral or topical route on alternate days followed by sun or UVA exposure. Pigmentation gradually enhances to the whole patches in the next 2-3 months (V3 stage).

In late V3 stages, when no further pigmentation can be anticipated, Thin Thiersch's grafts[21], can be undertaken to achieve a Cure. It will also prevent the ugly tanning and ageing of the remainder of the skin by prolonged injudicious use of psoralens.

 
  References Top

1.Behl PN. Vitiligo update-etiology and management. Paper read at Chungking University, China, 1987.  Back to cited text no. 1    
2.Mosher DB, Fitzpatrick TB Ortonne JP, et al. Abnormalities of pigmentation. In Dermatology in General Medicine Fitzpatrick TB, Eisen A Z, Wolff K, et al. 3rd Ed. M c Graw-Hill, New York 1986, 794-876.  Back to cited text no. 2    
3.Bleechen SS, Ebling FJG. Disorders of skin colour. Vitiligo. In: Textbook of Dermatology Eds. Rook A. Wilkinson DS, et al. Vol. 2,4th Ed. Black-well scientific Publication, London, 1986;1594.  Back to cited text no. 3    
4.Lerner AE. Vitiligo. J Invest Dermatol 1959;32:285-310.  Back to cited text no. 4    
5.Dutta AK, Mandal SB. A clinical study of 650 cases of vitiligo. Indian J Dermatol 1969;14:103-111.  Back to cited text no. 5    
6.Behl PN, Bhatia RK. 400 cases of vitiligo-A clinico therapeutic analysis. Indian J Dermatol 1971;17:51-54.  Back to cited text no. 6    
7.Sehgal VN. A clinical evaluation of 202 cases of vitiligo cutis 1974;14:299-323.  Back to cited text no. 7    
8.Koranne RV, Sachdeva KG. Vitiligo. Indian J Dermatol 1988;27:676-681.  Back to cited text no. 8    
9.Behl PN, Aggarwal RS, Singh R. Etiological studies in vitiligo and therapeutic response to standard treatment. Indian J Dermatol 1961;6:101-109.  Back to cited text no. 9    
10.Mehta NR, Shah KC. Theodore C, et al., Epidemiological study of vitiligo in Surat area. South Gujarat. Indian J Med Res 1973;61:145-154.  Back to cited text no. 10    
11.Ramaiah A, Majumdar M, Amar Nath NM. Vitiligo in the SIS K. community of Bangalore. Indian J Dermatol Vener Leprol 1988;54:251-254.  Back to cited text no. 11    
12.Mohr JL. Vitiligo in a pair of monovular twins. Acta Genet 1951;2:252-255.  Back to cited text no. 12    
13.Ortonne JP, Mosher DB, Fitzpatrick TB. Vitiligo and other hypomelanoses of hair and skin. New York, Plenum Medical Book Co. New York, 1983;129-310.  Back to cited text no. 13    
14.Puri N, Majumdar M, Ramaiah A. In vitro growth characteristics of melanocytes from adult normal and vitiligo subjects. J Invest Dermatol 1987;58:434-438.  Back to cited text no. 14    
15.Behl PN, Arora RB, Srivastava G. The role of psychosomatic factors in dermatological disorders. In: Traditional Indian Dermatology Ist Ed. SISD Publication, 1992;33-35.  Back to cited text no. 15    
16.Gokhale BB. ACTH in vitiligo. The Schoch Letter 1975;25:3.  Back to cited text no. 16    
17.Behl PN, Aggarwal A, Majumdar M. Aqueous placental extract lotion therapy in vitiligo. Derm Times 1989;4:3-4.  Back to cited text no. 17    
18.Cormane RH, Siddiqui AH, Westerhof W, et al. Phenylalanine and UVA light for the treatment of vitiligo. Arch Dermatol Res 1985;277:126-130.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Antonio C, Schulpis H, Michas T, et al. Vitiligo therapy with oral and topical phenylalanine with UVA exposure. Int J Dermatol 1989;28:545-547.  Back to cited text no. 19    
20.Behl P N, Arora R B, Srivastava G. In: Herbs useful in Dermatological Therapy. 1 st Ed. CBS Publishers and Distributors, New Delhi, India, 1992.  Back to cited text no. 20    
21.Behl P N, Bhatia R K. Treatment of vitiligo with autologous thin Thiersch's grafts. Int J Dermatol 1973;12:329-331.  Back to cited text no. 21    
22.Falabella R, Escobar C, Borrero I. Transplantation of in-vitro cultured epidermis bearing melanocytes for repigmenting vitiligo. J Am Acad Dermatol 1989;21:257-264.  Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Halder L.R.M, Pham HN, Breadon JY, et al. Micropigmentation for the treatment of vitiligo. J Dermatol Surg. Onco, 1989;15:1092-1098.  Back to cited text no. 23    
24.Srivastava G. Vitiligo: Introduction. Asian Clin Dermatol 1994;1:1-4.  Back to cited text no. 24    
25.Behl P N. Etiology of vitiligo. Asian Clin Dermatol 1994;1:11-15.  Back to cited text no. 25    
26.Behl P N, Pradhan B K. Feature of mononuclear hugging in vitiligo. Ind J Dermatol Venereol Leprol 1978;44:66-73.  Back to cited text no. 26    


    Figures

[Figure - 1]

    Tables

[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7]



 

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