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Table of Content - Volume 11 Issue 2 - August 2018


 

Study of vitiligo at a tertiary care hospital

 

P Ravindra Kumar

 

Associate Professor, Department of Dermatology, Mahavir Institute of Medical Sciences, Vikarabad, Telangana, INDIA.

Email: smalkud@yahoo.com

 

Abstract              Background: Vitiligo is a common acquired, progressive, multifactorial, depigmenting disorder characterized by the appearance of circumscribed white macules varying patterns, varying from small macules with scalloping borders to near total depigmentation of body, supposed to be due to chronic, progressive loss of functional melanocytes in the epidermis. This study was aimed to study vitiligo in our tertiary care hospital. Material and Methods: This prospective, observational and descriptive study was conducted in OPD patients clinically diagnosed as vitiligo during study period. Results: A total of 300 patients were included in the study after applying inclusion and exclusion criteria. Among these 179 (59.67%) were females and 121 (40.33%) were males. The female to male ratio was 1.5:1. The age at onset was found to be in the 11-20 age group in 104 (34.5%) patients. Most common duration was noted as between 1 to 5 years, 169 (56.5%) patients. A positive family history was present in 62 (20.5 %) patients In 67 patients triggering factor was noted. Koebner’s phenomenon was noted in 62 (22.2%) patients while leucotrichia was seen in 33 (11 %) patients in our study. Most common site affected was lower limb in 204 patients (68.17%), followed by upper limb in 194 (64.67%) patients. Clinically most common morphological pattern was vitiligo vulgaris noted in 52.5% patients. Acrofacial, segmental, universal, mucosal patterns were noted in 23.83 %, 7.67 %, 5.67 %, 1 % patients respectively. Conclusion: Vitiligo has a multifactorial origin, unpredictable triggers and progress of disease. Early age of onset, family history, HLA antigen, presence of leucotrichia, other skin problems are predictors for poor prognosis.

Key Words: vitiligo, vulgaris, Koebner’s, leucotrichia, psoriasis

 

INTRODUCTION

Vitiligo is a common acquired, progressive, multifactorial, depigmenting disorder characterized by the appearance of circumscribed white macules of varying patterns, varying from small macules with scalloping borders to near total depigmentation of body, supposed to be due to chronic, progressive loss of functional melanocytes in the epidermis1. Incidence is nearly 1%–2% of the world population irrespective of race and ethnicity with highest numbers recorded in Indian subcontinent2,3. In India prevalence of vitiligo is found to be 0.46% to 8.8%4.Vitiligo is a multifactorial disease with a complex pathogenesis and several postulations for destruction of the melanocyte function such as autoimmune, cytotoxic, biochemical, oxidant– antioxidant, viral, and neural mechanisms in genetically predisposed patients.. Autoimmune etiology is considered strongly as presence of autoimmune diseases like autoimmune thyroiditis, Grave’s disease, Addison’s disease, diabetes mellitus, alopecia areata, and pernicious anemia is associated in patients with vitiligo5. While other study proposed strong family history as from 6% to 18% in general population6 and up to 40% in Indian population7. Clinically vitiligo can range from small macules to whole non-pigmentation of body. The progress of the disease is often unpredictable, Factors such as poor nutrition, emotional stress, autoimmunity, trauma, drugs, infections, sepsis, and exposure to the sun, chemicals, and toxins are often considered to trigger it8. Cosmetic disfigurement caused by vitiligo varies, but associated other conditions like psychosocial impact affects general quality of life. Females and young individuals have increased risk of psychiatric morbidity. Many communities still consider it as social stigma, contagious disease, punishment for sins of the previous birth, etc. Many patients take treatment from quacks and land up in more cosmetic disfigurement. This study was aimed to study vitiligo in our tertiary care hospital.

 

MATERIAL AND METHODS

This prospective, observational and descriptive study was conducted in department of Dermatology and Venereology, Mahavir medical college and general hospital. Study period was of 5 months from March 2019 to July 2019. Study approval was taken from institutional Ethical Committee for this study. Study was conducted in the Outpatient department (OPD) of the hospital. Patients visiting the OPD with idiopathic depigmented lesions and clinically diagnosed as vitiligo during study period were included in this study. Diagnosis was purely based on history and clinical examination. Before participation consent of the patient was taken. Patients with depigmented patches due to causes such as congenital patches or acquired depigmented lesions due to infections, physical trauma, chemical injury, burns, nutritional deficiency, inflammatory dermatosis, and drug reaction induced depigmentation were excluded from this study. Patients included in the study underwent detailed history taking with socio-demographic profile. mainly age of onset, duration of disease, precipitating factors, family history, and any other cutaneous or systemic illness. Clinical examination including site of onset, most common site, presence of leucotrichia, Koebner’s phenomenon, etc was taken. Routine blood and urine examination, blood sugar and thyroid function test were done where ever necessary. and according to area of body part involvement. Clinically lesions were classified into acrofacial (lesions noted over both face and acral regions), segmental (lesions distributed in a segmental/dermatomal pattern), vitiligo vulgaris (lesions affecting many parts of the body), mucosal (lesions confined only to mucous membranes) and universal. Data collected in pre-designed Microsoft excel sheet and analysed.

 

RESULTS AND DISCUSSION

Pathogenesis of vitiligo is still a mystery. Various theories of origin, genetic, toxic, neurogenic, and autoimmune have been proposed by different workers, yet none is definite8. The prevalence of vitiligo in India has been invariably reported between 0.25% and 4% of dermatology outpatients across in various studies9. The different ethnic background of the population, residing in different geographic regions with different environmental conditions may contribute to the wide variation in the prevalence of vitiligo in India. A total of 300 patients were included in the study after applying the inclusion and exclusion criteria. Among these 179 (59.67%) were female and 121 (40.33%) were male [table 1]. The female to male ratio was 1.5:1. We noted female predominance in our study. Similar reports with a predilection for women being affected are noted in other studies.2,11The increased number of female vitiligo patients can be explained as they notice the change in appearance and approach the doctors sooner than men and of the social stigma in the community, young females tend to report earlier due to matrimonial anxiety.

 

Table 1: Distribution of patients in male and female

Age(years)

Male (%)

Female (%)

Total (%)

1-10

5 (1.5)

7 (2.33)

12 (3.83)

11-20

26 (8.83)

38 (12.67)

64 (21.5)

21-30

31 (10.33)

56 (18.67)

87 (29)

31-40

28 (9.16)

38 (12.67)

66 (21.83)

41-50

14 (4.67)

19 (6.33)

33 (11)

51-60

11 (3.83)

11 (3.83)

22 (7.5)

61-70

5 (1.83)

6 (1.83)

11 (3.66)

71-80

1 (0.33)

4 (1.33)

5 (1.67)

Total

121 (40.33)

179 (59.67)

300

The age at onset was found to be in the 11-20 age group in 104 (34.5%) patients, followed by age group between 21- 30 years in 70 (23.5 %) patents [table 2]. These findings are consistent with the other reports12

 

Table 2: Age at onset of vitiligo in different age groups

Age(years)

Male (%)

Female (%)

Total (%)

1-10

16 (5.5)

30 (9.83)

46 (15.33)

11-20

43 (14.17)

61 (20.33)

104 (34.5)

21-30

28 (9.33)

42 (14.17)

70 (23.5)

31-40

12 (4.17)

26 (8.5)

38 (12.67)

>40

22 (7.17)

20 (6.83)

42 (14)

Total

121 (40.33)

179 (59.67)

300

Most common duration was noted as between 1 to 5 years 169 (56.5 %) patients [table 3]. Unpredictable disease progression, adjustment with cosmetic appearance at later stage may have reduced the number of patients with more than 5 years duration of disease.

Table 3: Duration of disease in different age group

Duration(years)

Male (%)

Female (%)

Total (%)

<1

14 (4.67)

33 (10.83)

47 (15.5)

1-5

70 (23.5)

99 (33)

169 (56.5)

6-10

7 (2.17)

19 (6.33)

26 (8.5)

11-15

14 (4.5)

11 (3.83)

25 (8.33)

16-20

10 (3.67)

11 (3.5)

21 (7.17)

>20

6 (2.17)

6 (2.17)

12 (4)

Total

121 (40.33)

179 (59.67)

300

A positive family history was present in 62 (20.5%) patients. Genetic factors play an important role in manifestation of vitiligo. Though various studies indicate different patterns of involvement of genetic factors and patterns appear to be polygenic. Other studies reported familial occurrence from 5 to 30% in different studies13. A study reported as human leucocyte antigen (HLA) type significantly related to family history and early onset of vitiligo14. Positive family history is considered to be a poor prognostic factor2 [table 4].

Table 4: Family history of vitiligo

Family history of vitiligo

Total

Percentage (%)

Father

11

3.5

Mother

27

9.17

Both father and mother

4

1.33

Sister

7

2.33

Brother

13

4.17

Total

62

20.5

In 67 of patients a triggering factor was noted for vitiligo. Physical trauma in 33 (49%) was the most common triggering factor noted, followed by surgery in 10 (14.9%), pregnancy, medical illness and psychological stress in 8 patients respectively [table 5]. Koebner’s phenomenon was noted in 62 (22.2%) patients while leucotrichia was seen in 33 (11 %) patients in our study. Shajil et al12, noted 9% patients with leucotrichia. Leucotrichia is considered to be a poor prognostic factor2. Some studies shows higher prevalence16.

 

Table 5: Triggering factors in vitiligo patients

Triggering factors

No. of patients

Physical trauma

33 (49%)

Pregnancy

8 (11.9%)

Medical illness

8(11.9%)

Psychological stress

8(11.9%)

Surgery

10 (14.9%)

Total

67

Most common site affected was lower limb in 204 patients (68.17%), followed by upper limb affection in 194 patients (64.67%). Other sites noted were face, trunk, scalp and genitals in 46 %, 40.67 %, 17 % and 5.5 % patients respectively [table 6]. Findings are consistent with other studies.12,13

Table 6: Site affected

Site

Total

Percentage (%)

Lower limb

204

68.17

Upper limb

194

64.67

Face

138

46

Trunk

122

40.67

Scalp

51

17

Genitals

16

5.5

Clinically the most common morphological pattern noted was vitiligo vulgaris in 52.5 % patients. Acrofacial, segmental, universal, mucosal patterns were noted in 23.83 %, 7.67 %, 5.67 %, 1 % of patients respectively. These findings are similar with other studies.12,16,17 This indicates that the process of depigmentation, either immune-mediated or toxic may occur simultaneously or subsequently at various unrelated distant sites.

 

Table 7: Types of vitiligo

Type

Total

(%)

Vitiligo vulgaris

158

52.5

Acrofacial

71

23.83

Segmental

23

7.67

Universal

17

5.67

Mucosal

3

1

CONCLUSION

Vitiligo has a multifactorial origin, unpredictable triggers and progress of disease. Early age of onset, family history, HLA antigen, presence of leucotrichia and other skin problems are predictors for poor prognosis.

 

REFERENCES

  1. Guerra L, Dellambra E, Brescia S, Raskovic D (2010) Vitiligo: pathogenetic hypotheses and targets for current therapies. Curr Drug Metab 11(5): 451-467.
  2. Alikhan A, Felsten LM, Daly M, Petronic‑Rosic V. Vitiligo: A comprehensive overview part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work‑up. J Am Acad Dermatol 2011;65:473‑91.
  3. Krüger C, Schallreuter KU. A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol 2012;51:1206‑12.
  4. Shah H, Mehta A, Astik B (2008) Clinical and sociodemographic study of vitiligo. Indian J Dermatol Venereol Leprol 74(6): 701.
  5. Kutlubay Z, Karakus O, Engin B, Serdaroglu S. Vitiligo as an autoimmune disease. J Turk Acad Dermatol 2012;6:1262.
  6. Kostovic K, Pasic A. New treatment modalities for vitiligo: Focus on topical immunomodulators. Drugs 2005;65:447‑59.
  7. Behl PN, Agarval A, Srivastava G. Etiopathogenesis of vitiligo: Are we dealing with an environmental disorder? Indian J Dermatol Venereol Leprol 1999;65:161‑7.
  8. Jeon IK, Park CJ, Lee MH, Lee DY, Kang HY, Hann SK, et al. A multicenter collaborative study by the Korean society of vitiligo about patients’ occupations and the provoking factors of vitiligo. Ann Dermatol 2014;26:349‑56.Kar PK. Vitiligo: A study of 120 cases. Indian J Dermatol Venereol Leprol 2001;67:302-4.
  9. Krüger C, Schallreuter KU. A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol 2012;51:1206‑12.
  10. Shah H, Mehta A, Astik B. Clinical and sociodemographic study of vitiligo. Indian J Dermatol Venereol Leprol 2008;74:701.
  11. Shajil EM, Agrawal D, Vagadia K, Marfatia YS, Begum R. Vitiligo: Clinical profiles in Vadodara, Gujarat. Indian J Dermatol 2006;51:100-4.
  12. Shankar DS, Shashikala K, Madala R. Clinical patterns of vitiligo and its associated co morbidities: A prospective controlled cross-sectional study in South India. Indian Dermatol Online J 2012;3:114-8.
  13. Misri R, Khopkar U, Shankarkumar U, Ghosh K. Comparative case control study of clinical features and human leukocyte antigen susceptibility between familial and nonfamilial vitiligo. Indian J Dermatol Venereol Leprol 2009;75:583-7.
  14. Alissa A, Al Eisa A, Huma R, Mulekar S. Vitiligo-epidemiological study of 4134 patients at the National Center for Vitiligo and Psoriasis in Central Saudi Arabia. Saudi Med J 2011;32:1291-6.
  15. Shankar DS, Shashikala K, Madala R. Clinical patterns of vitiligo and its associated co morbidities: A prospective controlled cross-sectional study in South India. Indian Dermatol Online J 2012;3:114-8.
  16. Pasricha JS, Khaitan BK, Dash S. Pigmentary disorders in India. Dermatol Clin 2007;25:343-52.

 


 

 








 





 


 

 



 





 


 

 

 



 




 











 









 


 









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