Indian Journal of Dermatology
ORIGINAL ARTICLE
Year
: 2006  |  Volume : 51  |  Issue : 2  |  Page : 100--104

Vitiligo: Clinical profiles in Vadodara, Gujarat


EM Shajil1, Deepali Agrawal1, Krishna Vagadia2, YS Marfatia2, Rasheedunnisa Begum1,  
1 Department of Biochemistry, Faculty of Science, Maharaja Sayajirao University of Baroda, India
2 Department of Skin and VD, Sir Sayajirao Gaikwad Medical College, Vadodara, Gujarat - 390002, India

Correspondence Address:
Rasheedunnisa Begum
Department of Biochemistry, Faculty of Science, Maharaja Sayajirao University of Baroda
India

Abstract

Purpose: Vitiligo is an acquired depigmentary condition involving a progressive loss of melanocytes from the epidermis and hair follicles We have earlier reported impairment of systemic antioxidant status of Baroda vitiligo patients ( Pigment Cell Res 2004; 17; 289-94) and we now show analysis of the clinical profiles of these patients. Procedure: The study comprised of 424 vitiligo patients. Clinical and demographic details of all the patients were obtained from the vitiligo clinical proformas. Lipid peroxidation levels (LPO) in erythrocytes of vitiligo patients and healthy controls were estimated. Result: Out of four hundred and twenty four outpatients, males constituted 38.44% and females were 61.56%. Mean age of the patients was 25.59 years. The sites of onset were the lower limb, face, trunk, upper limb, genital, hand, labia and scalp in the descending order of frequency. Koebner«SQ»s phenomenon was observed in 12.74%, diabetes mellitus in 1.18%, leukotrichia in 9.2% and premature graying of hair in 23.11% patients. A family history of vitiligo was present in 21.93% of the patients. Significant increase ( P <0.002) in the LPO levels of the vitiliginous patients was observed compared to the controls. Conclusion: Vitiligo vulgaris was the most common form of the disease which constituted 52.36% of the patients followed by focal vitiligo (28.54%), segmental vitiligo (6.84), acrofacial (7.55%), mucosal (2.83%) and universal vitiligo (1.89%). Systemic oxidative stress may have a pathophysiological role in precipitating all clinical types of vitiligo in Vadodara vitiliginous patients.



How to cite this article:
Shajil E M, Agrawal D, Vagadia K, Marfatia Y S, Begum R. Vitiligo: Clinical profiles in Vadodara, Gujarat.Indian J Dermatol 2006;51:100-104


How to cite this URL:
Shajil E M, Agrawal D, Vagadia K, Marfatia Y S, Begum R. Vitiligo: Clinical profiles in Vadodara, Gujarat. Indian J Dermatol [serial online] 2006 [cited 2020 Sep 23 ];51:100-104
Available from: http://www.e-ijd.org/text.asp?2006/51/2/100/26928


Full Text

 Introduction



Vitiligo is an idiopathic, acquired, circumscribed hypomelanotic skin disorder, characterized by milky white patches of different sizes and shapes and affects 1-2% of the world population.[1],[2] Based on a few dermatological outpatient records, the incidence of vitiligo is found to be 0.25-2.5% in India.[3],[4] Gujarat and Rajasthan states have the highest prevalence ~ 8.8%.[5] There is a stigma attached to vitiligo and affected persons and family, particularly girls are socially ostracized for marital purpose.[6] Since Gujarat shows high prevalence of vitiligo in India, we have undertaken a systematic study to understand the etiopathogenesis of vitiligo. In this context we have reported the age-dependent antioxidant parameters of vitiligo patients in Vadodara, and found impairment in the systemic antioxidant status of the patients suggesting that melanocyte damage in vitiligo may be linked with generalized oxidative stress.[7],[8],[9]

The present report is an effort to learn more about its precipitating factors and clinical features of Vadodara vitiligo patients.

 Materials and Methods



The study consisted of 424 vitiligo patients who visited the Sir Sayajirao Gaikwad Medical College hospital Skin and Venereal OPD and a service hospital in Vadodara. The diagnosis was essentially clinical and demographic details of all the patients including the age of onset, initial site of onset, duration of the disease, precipitating factors, and presence of leukotrichia, Koebner's phenomenon, halo nevi, other associated diseases and family history were obtained from the vitiligo clinical proformas. Lesions confined to one or a few patches localized in a particular area were grouped as focal vitiligo; lesions distributed in a segmental/dermatomal pattern as segmental vitiligo; lesions noted over both face and acral regions as acrofacial vitiligo; lesions affecting many parts of the body as vitiligo vulgaris and lesions confined only to mucous membranes as mucosal vitiligo.[4]

Blood samples were collected from one hundred and twenty three vitiligo patients without any other associated disaeses and also from one hundred and six age matched healthy consenting volunteers for the estimation of Lipid peroxidation (LPO) levels. Written consent had been obtained from the vitiligo patients. LPO levels in erythrocytes were estimated according to the procedure of Beuge and Aust.[10] Malonaldehyde produced during peroxidation of lipids served as an index of LPO. Methylenedioxyamphetamine (MDA) reacts with thiobarbituric acid to generate a colored product, which was measured at 532 nm and the results were expressed as nmoles MDA formed/g Hb/ min.

 Results



Among the patients 61.56% (261) were women and 38.44% (163) were men. The female to male ratio was 1.6:1. Duration of the disease varied from 15 days to 60 years and the average disease duration at the time of hospital visit was 3.3 years. Age and sex distribution of the patients along with various clinical types of vitiligo is shown in [Table 1]. One hundred and fifty two women (58.23%) reported the disease in the second (35.63%) and third (22.60%) decades as compared to 29.45 and 22.70% of men respectively. Out of 163 men 85 (52.15%) were in their second and third decades. The mean age of the disease was 25.59 years.

A detailed clinico-demographic profile of the patients is given in [Table 2]. Vitiligo vulgaris was the most common form of the disease in 222 (52.36%) patients. The sites of onset were the lower limb (45.52%), face (20.04%), trunk (12.03%), upper limb (8.96%), genital (5.19%), hand (3.54%), labial (2.83%) and scalp (1.87%) in the descending order.

Around 61 (21.93%) patients had a positive family history of vitiligo. The first-degree relatives (parent/brother/sister/son/daughter) were affected in 58 (13.68%), second-degree relatives (grandparent/maternal and/or paternal uncle or aunt) in 24 (5.66%) and third degree relatives in 11 (2.59%) patients, [Table 3].

Leukotrichia was seen in 39 (9.20%) patients, of these 23 (5.42%) were males and 17 (4.00%) females. Koebner phenomenon was observed in 54 (12.75%) patients, out of which 31 (7.31%) were males and 23 (5.42%) females. Premature graying of hair was observed in 98 (23.11%) patients. Of the various diseases associated with vitiligo, diabetes mellitus was found in 5 (1.18%), thyroidism in 4 (0.94%), tuberculosis in 4 (0.94%) hypertension in 3 (0.71%), psoriasis in 1 (0.24%), bronchial asthma in 3 (0.71%) and halo nevus in 2 (0.47%) patients [Table 4]. Major precipitating factor was found to be physical injury (15.33%), others included emotional tension, plastic footwear, etc. [Table 5]. Association of Koebner phenomenon and leukotrichia was observed in 12.74 and 9.2% of the patients respectively, [Table 6]. A significant increase in lipid peroxidation levels was observed in vitiligo patients compared to controls ( P P P P P P et al[11] and Sarin et al .[12] Thus, most of the reports showed that males and females were affected with almost equal frequency.[3],[6],[13],[14],[15],[16] The number of female vitiligo patients reported at the hospitals in Baroda was found to be higher than males and females predominate presumably because women notice the change in appearance and approach the doctors sooner than men. In 55.90% of the patients, the age of onset was in the second or third decade, consistent with the most reports from India[11],[12],[17] and the west.[13],[16],[18] This shows that the disease starts at a younger age in the Indian population. However, Howtiz et al[15] showed the age of onset to be between 40-60 years.

The duration of the disease varied widely from 2 weeks to 60 years, with the mean duration of 3.3 years in this study. The slow progression in the rate of disease may be the underlying reason for showing long duration of vitiligo in this study.

In our study vitiligo vulgaris was the most common type observed followed by focal, acrofacial, segmental, mucosal and universal. The frequency of distribution of clinical types of vitiligo varies in different studies.[11],[12],[18],[19] According to the reports of Koranne et al[11] and Sarin et al[12] generalized vitiligo was found to be more common. Thus our results suggest that Indians not only have an increased incidence of the disease but also have more widespread disease.

Lower limbs were the most common site of onset in 45.52% of the out patients in this study irrespective of the clinical type of vitiligo. This is in concordance with the studies by Behl and Bhatia,[17] Dutta and Mandal[14] and Lerner,[20] however, it is at variance with Handa and Kaur[4] and Sehgal,[19] in which the face was found to be most common site of onset. In Western studies also extremities were the most commonly involved sites of onset.[18],[20]

Leucotrichia was seen in 9.2% of the patients in this study. Leucotrichia was reported in 9.45% of patients with vitiligo.[14],[19] Leucotrichia is considered to be a poor prognostic factor. Koebner phenomenon was seen in 12.74% of Baroda patients. Koebner phenomenon was reported to occur in as many as 33% of vitiligo patients[13],[16] which is a common feature found in active vitiligo.

The association of vitiligo with thyroid disease was 0.94% in our study, which was reported to be 7.8% by Schallreuter et al .[21] Diabetes mellitus was found to be 1.18% in our study, whereas the reported value was 0.6%.[21] Premature graying and hypertension were found to be 23.11 and 0.70% in our study, but premature graying was reported to be 2.8%.[21] Tuberculosis and psoriasis were found to be 0.94 and 0.24%, and the incidence of bronchial asthma was found to be 0.71% in our study. We observed halo nevi in 0.47% of our patients. Halo nevi in vitiligo have been reported to occur commonly and to be single or multiple.[11],[16],[17]

There was a family history of vitiligo in 21.93% of Vadodara patients and 20 patients had more than one family member with the disease. Vitiligo has a polygenic or autosomal dominant inheritance pattern with incomplete penetrance and variable expression.[13],[16],[18] Familial occurrence has been reported to vary from 6.25- 30%.[11],[12],[14],[17],[19],[20],[22] Positive family history is considered to be a poor prognostic factor.

A significant increase in lipid peroxidation levels was observed in vitiligo patients compared to controls ( P et al.[23] Systemic oxidative stress may have a pathophysiological role in precipitating all clinical types of vitiligo in Vadodara vitiliginous patients.

 Acknowledgement



Physical facilities provided by M.S. University are gratefully acknowledged. This work was supported by a grant to RB [F-12-138/2001 (SR-1)] from the University Grants Commission, New Delhi. Sincere help of Dr. Salil Acharya, Param Hospital, Sakarda during this study is gratefully acknowledged.

References

1Agrawal D, Sahani MH, Gupta S, Begum R. Vitiligo etipathogenesis and therapy - A Review. J Maharaja Sayajirao University of Baroda 2001;48:97-106.
2Moscher DB, Fitzpatrick TB, Ortonne JP, Hori Y. Hypomelnosis and hypermelanosis. In : Dermatology in General Medicine, Eisen AZ, Wolff K, Austen, KF, Goldsmith LA, Kats SI, Fitzpatrick TB, editors. MC Graw Hill: New York; 1999. p. 945-1017.
3Das SK, Majumder PP, Chakraborty R, Majumdar TK, Haldar B. Studies on vitiligo: Epidemiological profile in Calcutta, India. Genet Epidemiol 1985;2:71-8.
4Handa S, Kaur I. Vitiligo: Clinical findings in 1436 patients. J Dermatol 1999;26:653-7.
5Valia AK, Dutta PK. IADVL Text book and Atlas of Dermatology. Bhalani Publishing House: Mumbai; 1996. p. 500-86.
6Mehta NR, Shaha KC, Theodore C, Vyas V, Patel A. Epidemiological study of vitiligo in Surat area, South Gujarat. Indian J Med Res 1973;61:145-54.
7Agrawal D, Sahani MH, Gupta S, Begum R. Antioxidant status of vitiligo patients. Poster presentation at the "Second International Symposium on Molecular Medicine with special reference to the molecular and pharmacological aspects of allergy and related diseases" held at Baroda from; 20th to 23rd January 2002.
8Agrawal D. Antioxidant status of vitiligo patients relative to controls. M. Phil dissertation submitted to Biochemistry department. MS University of Baroda 2002.
9Agrawal D, Shajil EM, Marfatia YS, Begum R. Study of the antioxidant status of vitiligo patients of different age groups in Baroda. Pigment Cell Res 2004;17:289-94.
10Begue JA, Aust SD. Microsomal lipid peroxidation. Met Enzymol 1978;52:302-10.
11Koranne RV, Sehgal VN, Sachdeva KG. Clinical profile of vitiligo in North India. Indian J Dermatol Venereol Leprol 1986;52:81-2.
12Sarin RC, Kumar AS. A clinical study of vitiligo. Indian J Dermatol Venereol Leprol 1977;43:300-14.
13Bleehen SS, Ebling FJ, Champion RH. Disorders or skin colour. In : Text book of Dermatology, Champion RH, Burton JL and Ebling FJ, editors. Blackwell Scientific Publications: London; 1992. p. 1561-622.
14Dutta AK, Mandal SB. A clinical study of 650 cases of vitiligo and their classification. Indian J Dermatol 1969;14:103-5.
15Howits J, Brodthagen H, Schwarts M, Thomsen K. Prevalence of vitiligo. Epidemiological survey the Isle of Bornholm, Denmark. Arch Dermatol 1977;113:47-52.
16Moscher DB, Fitzpatrick TB, Hori Y, Ortonne JP. Disorders of pigmentation. In : Dermatology in general medicine, Fitzpatick TB, Isen AZ, Wolff K, Freedberg, IM, Austen, KF, editors. McGraw Hill: New York; 1993. p. 903.
17Behl PN, Bhatia RK. 400 cases of vitiligo. A clinico-therapeutic analysis. Indian J Dermatol 1972;17:51-5.
18Bolognia JL, Pawelek JM. Biology of hypopigmentation. J Am Acad Dermatol 1988;19:217-55.
19Sehgal VN. A clinical evaluation of 202 cases of vitiligo. Cutis 1974;14:439-45.
20Lerner AB. Vitiligo. J Invest Dermatol 1959;32:285-310.
21Schallreuter KU, Lemke R, Brandt O, Schwartz R, Westhofen M, Montz R, et al . Vitiligo and other diseases: Coexistence or true association? Hamburg study on 321 patients. Dermatology 1994;188:267-75.
22Hafez M, Sharaf L, Abd El-Nabi SM. The genetics of vitiligo. Acta Derm Venereol (Stokh) 1983;63:249-51.
23Picardo M, Passi S, Morrone A, Grandinetti M. Antioxidant status in the blood of patients with vitiligo. Pigment Cell Res 1994;2:110-5.