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Year : 2001  |  Volume : 67  |  Issue : 6  |  Page : 302-304

Vitiligo: A study of 120 cases

Department of Dermatology in 167 Military Hospital C/o 56, APO, India

Correspondence Address:
167 Military Hospital, C/o 56 APO, India


Vitiligo is a common pignientary disorder and of major social and cosmetic concern in India. Purpose of the study was to find out age at onset and sex incidence in vitiligo, role of hereditary factors and associations with other diseases. 120 self reporting vitiligo patients attending out patient department of a service hospital were selected for the study and this data was analysed. In the present series out of 120 cases 62 (51.6%) were males and 58(48.35%)were females. There was practically no difference in sex incidence. The lowest age of onset was two years and the oldest was 65 years. In the majority of patients,52(43.2%), disease started before twenty years of age.8 (6.6%) cases gave definite family history of vitiligo. Exposed areas of the body were commonly affected in majority (66.6%) of cases. The legs were commonest site of involvement in 60(50%) cases. Circunicript type of vitiligo (46.6%) was heading the list. Majority of patients (56.6%) had multiple lesions. Diabetes mellitus was found in 2 (2.6%) patients. Cause of vitiligo is still idiopathic. Hereditary factors hardly play any role in manifestation of vitiligo

How to cite this article:
Kar P K. Vitiligo: A study of 120 cases. Indian J Dermatol Venereol Leprol 2001;67:302-4

How to cite this URL:
Kar P K. Vitiligo: A study of 120 cases. Indian J Dermatol Venereol Leprol [serial online] 2001 [cited 2020 Sep 26];67:302-4. Available from:

   Introduction Top

Vitiligo is a common pigmentary disorder seen in our country. It is an acquired idiopathic depigmentary condition. It is characterised by completely depigmented milky white macules of varying sizes and shapes. Besides loss of colour there is no other structural changes. This disorder does not result in restriction of capacity to work or expectancy of life, but it causes cosmetic disfigurement leading to psychological trauma to the patients. The reported incidence of vitiligo in various dermatological clinics now in India varies from 0.5% to 1%.[1] An OPD based study of analysis of basic data like, age, sex, occurrence in family and associations of vitiligo was undertaken to know various aspects of vitiligo.

   Materials and Methods Top

Our study was conducted among the patients attending out patient department of Dermatology of a service hospital. A total number of 120 cases showing definite clinical evidence of vitiligo were taken up for this study. A clinical diagnosis of vitiligo was made only when there was unequivocal evidence of depigmented patches of milky white colour. The cases showing white patches due to secondary causes were excluded from this study. Details of dietary habit and family history was taken in each case. History of associated disease notably diabetes mellitus, thyroid disorder, pernicious anaemia, and alopecia areata were noted. History of precipitating/ initiating factors especially physical trauma, sun exposure, acute mental/ emotional stress, contact with chemicals/ synthetic foot wears etc were noted. Routine laboratory investigation of urine and stool, blood cell counts, hemoglobin, fasting and post prandial (PP) blood sugar estimations were carried out in all cases.

   Results Top

The youngest patient in this series was a 2 year- old girl and oldest patient was 65 year of old male [Table - 1]. In 52 (43.2%) patients disease started before the age of 20. The duration of disease varied from 2 months to ten years. Eight cases gave the family history of vitiligo [Table - 2]. In one occasion, both mother and her two daughters had vitiligo. Twenty six (28.3%) were married, but there was no divorcees. Exposed areas of body were most commonly affected in 80 (66.6%) cases [Table - 3]. Bilaterally symmetrical lesions were present in 8 (6.6%) cases. The legs were the commonest site in 60 (50%) cases [Table - 4]. Circumscript type of vitiligo was seen in 56 (46.6%) cases [Table - 5]. Ninety- six (79.9%) patients had multiple lesions. All routine laboratory investigations were within normal limits, except for the presence of Giardia lambiia in the stool of 14 (12%) cases and Ascaris Lumbricoides in 12 (10%) cases. Raised blood sugar with fasting blood sugar, 130-160 mg% and PP 220-240 mg% was found in two (2.6%) cases.

   Discussion Top

The untiring efforts of the scientists, over a period of many years, have failed to lift up the curtain of ignorance till today and as we know, the aetiology of vitiligo is still an enigma. Various theories of origin, genetic,[2] toxic,[3] neurogenic,[4] and auto-immune[5] have been proposed by different workers, yet none is definite.
The male:female ratio in vitiligo was observed in our study to be nearly equal, meaning there by that this disease has no predilection for any sex. Similar observations were also noted by various workers.[6],[7] Further, the incidence of vitiligo was 43.2% cases in 0-20 year of age as compared to a low incidence of only 9.9% in individuals over 40 years of age [Table - 1] which means more and more younger people are getting afflicted with this disorder. Because of social stigma in the community young females tend to report earlier due to matrimonial anxiety.
In our study, out of 8 (6.6%) patients who gave the family history of vitiligo, only in one occasion both mother and her two daughters had vitiligo. In the rest seven patients only one relative was suffering from vitiligo. Universal vitiligo was found in 2 (1.6%) cases and both of them had a positive family history. A positive family history has been reported in 10% of cases by Sarin et al and 6.25% of cases by Behl et al.[7] The mode of transmission seems to be by autosomal dominant gene with variable penetrance.[8]
In our study the lesions were typically milky white and border was not hyperpigmented. Hairs in the involved patches were of black colour in younger patients but in 13% of older patients the hairs were white. Besides loss of pigment no other abnormality was detected in the vitiliginous patches. The legs seems to be most frequently affected in majority (50%) of cases. Hands, face and bony prominence were the next commonest site followed by feet, trunk and neck.
Exposed areas of the body were most frequently affected in majority of patients (66%) in our study [Table - 4]. The lesions were present mostly on the front of the legs in 60 (50%) cases, hands in 44 (36.6%), feet in 22(18.3%) and bony prominence in 28 (23.3%) patients. The development of vitiligo at the site of physical trauma is a koebner phenomenon. This may be explained as due to release of antigens of injured melanocytes into the blood and production of antibodies against them resulting in further loss of melanocytes.[9]
Among the various types, vitiligo vulgaris showing circumscript, scattrered macular variety was found to be the commonest. This indicates that the process of depigmentation (either immune mediated or toxic) may occur simultaneously or subsequently at unrelated sites.[9]
Our study also revealed association of diabetes mellitus in 2 (2.6%) cases. Other conditions with proposed auto-immune mechanisms like thyroid disease, alopecia areata, and pernicious anaemia were not found in any of our cases. Diet[10] did not play an important role in the causation of the disease. However, it is interesting to note that about 90% of the cases were not on a purely vegetarian diet in our study. They were on mixed diet. More intensive comparative study is required to establish the role of the non vegetarian diet as an exciting factor in the aetiology of vitiligo.
Higher incidence of association of conditions like giardiasis, ascariasis and worm infestations is difficult to correlate and just reflect their higher incidence in tropical population.
The non occurrence of vitiligo in other family members throughout their life, strengthen our assumption that genetic tendency is far from significant, unless and until there is repeated insult on the melanocytes, either by nutritional aberrations, recurrent infections/their toxins, repeated antibiotic therapy, taking of fast ready food that has an alarming high concentration of lethal preservatives, additives, colorants, drinking of polluted, chemical laden water and eating of vegetables grown in fields using water contaminated with industrial wastes.[10],[11] 

   References Top

1.Das SK, Mazumdar PP, Chakraborty R, et al. Studies on vitiligo, I : Epidemiological profile in Calcutta. India Genet Epid 1985;2: 7178.  Back to cited text no. 1    
2.Majumdar PP, Nordlund JJ, Nath SK. Pattern of familial aggregation of vitiligo, Arch Dermatol 1993;129: 994-998.  Back to cited text no. 2    
3.Graham DG, Tiffany SM, Vogel RS. The toxicity of melanin precursors. J Invest Dermatol 1978;70:113-116.  Back to cited text no. 3    
4.Morrone A, Picardo M, de-Luca C, et al. Catecholamines and Vitiligo. Pigment Cell Res 1992;5:65-69.  Back to cited text no. 4    
5.Naughton GK, Eisinger M, Bystryn JC. Antibodies to normal human melanocytes in vitiligo. J Exp Med 1983; 158: 246-251.  Back to cited text no. 5    
6.Sarin RC, Kumar AS. A clinical study of vitiligo. Indian J Dermatol Venereol Lepr 1977;83:190-194.  Back to cited text no. 6    
7.Behl PN, Agarwal RS, Singh G. Aetiological studies in vitiligo and therapeutic response to standard treatment. Indian J Dermatol 1961;6:101.  Back to cited text no. 7    
8.Ando-I, Chi-HI, Nakagawa H, et al. Differences in clinical features and HLA antigens between familial and non familial vitiligo of non segmental type. Br J Dermatol 1993; 123:408-410.  Back to cited text no. 8    
9.Ramaiah A, Puri N, Mojamdar M. Etiology of vitilgo. A new hypothesis. Acta Dermatol Venereol (Stockh) 1989;69: 323-326.  Back to cited text no. 9    
10.Behl PN, Kotia A, Sawal P. Vitiligo: Age group related trigger factor and morphological variants. Indian J Dermatol Venereol Lepr 1994;60:275-279.  Back to cited text no. 10    
11.Tawade YV, Parakh AP, Bharatia PR, et al. Vitiligo: A study of 998 cases attending KEM hospital in Pune. Indian J Dermatol Venereol Lepr 1997;63: 95-98.  Back to cited text no. 11    


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