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CASE REPORT
Year : 2006  |  Volume : 51  |  Issue : 4  |  Page : 289-291
Acetylcholine esterase levels in different clinical types of vitiligo in Baroda, Gujarat


1 Department of Biochemistry, Faculty of Science, Maharaja Sayajirao University of Baroda, Vadodara, India
2 Department of Skin and VD, Sir Sayajirao Gaikwad Medical College, Vadodara, Gujarat, India

Correspondence Address:
Rasheedunnisa Begum
Department of Biochemistry, Faculty of Science, Maharaja Sayajirao University of Baroda, Vadodara, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.30299

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   Abstract 

Vitiligo is an acquired depigmentary disorder involving a progressive loss of melanocytes from the epidermis and hair follicles. Gujarat has a high prevalence of vitiligo. One of the major hypotheses in the pathogenesis of vitiligo is the neurochemical hypothesis. According to the neural hypothesis neurochemical mediator/s such as acetylcholine secreted by the nerve endings cause the destruction of melanocytes. Acetylcholine esterase (AChE) activity has been found to be lowered in vitiligo patients during the process of depigmentation. We have earlier reported impairment of systemic antioxidant status in Baroda vitiligo patients, and we now show analysis of blood AChE activity in these patients. The study consisted of 121 vitiligo patients and 126 age and sex-matched healthy controls. Acetylcholine esterase activity showed significant decrease in vitiligo patients. However, there is no significant difference in AChE activity in segmental and non-segmental types as well as in active and stable types of vitiligo. The age group 16-25 showed a significant decrease in AChE activity. This study suggests that AChE may be inactivated due to high systemic oxidative stress in these patients. This is the first report showing that AChE may be playing a role in the pathogenesis of vitiligo in Baroda patients.


Keywords: Acetylcholine esterase, clinical types, neural hypothesis, vitiligo


How to cite this article:
Shajil E M, Marfatia Y S, Begum R. Acetylcholine esterase levels in different clinical types of vitiligo in Baroda, Gujarat. Indian J Dermatol 2006;51:289-91

How to cite this URL:
Shajil E M, Marfatia Y S, Begum R. Acetylcholine esterase levels in different clinical types of vitiligo in Baroda, Gujarat. Indian J Dermatol [serial online] 2006 [cited 2020 Apr 4];51:289-91. Available from: http://www.e-ijd.org/text.asp?2006/51/4/289/30299



   Introduction Top


Vitiligo is a depigmenting disorder resulting from the loss of melanocytes in the skin and affects 1-2% of the world population.[1] The incidence of vitiligo is found to be 0.5-2.5% in India.[2] Gujarat and Rajasthan states have the highest prevalence ~8.8%.[3] Vitiligo is classified into non-segmental and segmental clinical types.[4] Non-segmental type includes vulgaris, acrofacial, focal, and universal sub-types. In vulgaris the lesions are found in typical zones with symmetrical distribution. Acrofacial sub-type of non-segmental vitiligo affects face and distal extremities. In focal vitiligo one or more patches are found in one area but not in segmental pattern. In universal vitiligo the depigmentation involves more than 80% of the body.[5] In segmental vitiligo one or more macules are found in dermatomal unilateral distribution.

Though vitiligo has been extensively studied in the past five decades, its etiology is still being debated.[6],[7],[8] Several hypotheses are proposed about the pathogenesis of vitiligo and oxidative stress hypothesis considers a systemic involvement during the course of the disease.[9],[10],[11] According to Taieb[6] the origin of segmental and non-segmental vitiligo may be different. Local/systemic factors affect the homeostasis of the epidermal melanin unit in segmental vitiligo whereas an impaired redox status of the epidermal melanin unit acts as the primary defect further leading to inappropriate immune response in non-segmental vitiligo. The neural theory is more related to segmental vitiligo whereas the autoimmune theory is involved in non-segmental vitiligo.[6] There are no reports on systemic acetylcholine esterase (AChE) levels in vitiligo patients. Hence, we have made an attempt to explore whether there is any involvement of systemic AChE in precipitating vitiligo. In this study we show analysis of blood AChE activity in different age groups of vitiligo patients compared to controls; in segmental and non-segmental types; and in active and stable forms of vitiligo.


   Materials and Methods Top


For the estimation of blood AChE activity, 121 vitiligo patients were divided into different age groups (5-15, 16-25, 26-35, 36-45, and 46-55 years) and clinical types after written informed consent has been obtained. The patients had no other associated diseases. The study included 126 age and sex-matched healthy consenting volunteers as controls. Blood AChE activity was assayed according to the method of Reiner et al .[12] Briefly, AChE catalyses the hydrolysis of acetylcholine to thiocholine and thiocholine in turn reacts with 5,5-dithiobis (2-nitrobenzoic acid) (DTNB) to produce yellow color due to the formation of 5-thio-2-nitrobenzoic acid. Rate of formation of the yellow anion is measured at 412 nm and the activity of AChE is expressed as micromoles of acetylthiocholine hydrolyzed (ATCh) per gram hemoglobin per minute.

Statistical analysis

Results in vitiligo patients and controls were compared using the paired student's t -test. One way analysis of variance (anova) was used to determine significant differences in AChE enzyme activities between different age groups and different clinical types of vitiligo utilizing statistical software program, Prism and P0.05 was considered significant.


   Results Top


The present study is an attempt to analyze blood AChE activity in vitiligo patients compared to controls. Acetylcholine esterase showed significant decrease in vitiligo patients compared to controls [Table - 1]. Patients were also classified into different clinical types for our further analysis. However, there is no significant difference in the AChE activity among different clinical types [Table - 1], between segmental and non-segmental types [Table - 1] as well as between active and stable vitiligo [Table - 1]. We have also analyzed the role of AChE in genetic predisposition of vitiligo, by comparing its activity in patients with positive family history with those with negative family history. However no significant difference was observed in AChE activity of these two groups of patients [Table - 1]. Further, AChE activity in different age groups of vitiligo patients has been analyzed [Table - 2] and the age group 16-25 showed a significant decrease in AChE activity compared to controls. Other age groups have not shown any difference in the activity compared to controls [Table - 2]. Our analysis by anova in different age groups and different clinical types showed no significant difference in the AChE activity among the age groups and clinical types.


   Discussion Top


Melanocytes are neural crest derived cells with an embryological link to the nervous system.[13] According to neural hypothesis neurochemical mediators including acetylcholine secreted by the nerve endings are toxic to melanocytes leading to their destruction in vitiligo patients. Thus segmental vitiligo may be associated with the dysfunction of cholinergic sympathetic nerves.[6],[14] Acetylcholine esterase activity was found to be lowered in vitiliginous skin during depigmentation,[15] suggesting that acetylcholine may aggravate the process of depigmentation in vitiligo.[15] Further, a possible cholinergic involvement in vitiligo has been reinforced by Elwary et al. by demonstrating decreased sweating in the depigmented epidermis of these patients.[16] Schallreuter et al. studied H 2 O 2 regulation of AChE and showed H 2 O 2 mediated oxidation of AChE, thus emphasizing the role of oxidative stress in precipitating vitiligo.[17] It was proposed that inactivation of AChE is due to the oxidation of Trp 432sub , Trp 435sub and Met 436sub residues of the enzyme by H 2 O 2 .[17] It has also been shown that acetylcholine has an inhibitory effect on Dopa oxidase activity in the melanocytes and inhibits the pigment production.[15]

Our present study shows a significant decrease in the blood AChE activity in vitiligo patients compared to controls [Table - 1], nevertheless our earlier reports[9],[18],[19] showed significant increase in the lipid peroxidation levels[9],[18] in the same vitiligo patients which was an indicator of oxidative stress. This report in conjunction with our earlier studies[9],[18],[19] provides evidence that AChE may be inactivated due to high systemic oxidative stress in these patients. Acetylcholine thus accumulated may lead to the destruction of melanocytes resulting in the precipitation of vitiligo in these patients. However we could not find any significant change in the AChE activity in segmental vitiligo [Table - 1], which is attributed to be of neurochemical origin.[6] This is the first report showing that systemic AChE may be playing a role in the pathogenesis of Baroda vitiliginous patients.

 
   References Top

1.Mosher DB, Fitzpatrick TB, Ortonne JP, Hori TB, Hypomelnosis Y. In : Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Kats SI, Fitzpatrick TB. Dermatology in General Medicine . Mc Graw Hill: New York; 1999. p. 945-1017.   Back to cited text no. 1      
2. Handa S, Kaur I. Vitiligo: Clinical findings in 1436 patients. J Dermatol 1999;26:653-7.   Back to cited text no. 2      
3.Valia AK, Dutta PK. IADVL Text book and Atlas of Dermatology. Bhalani Publishing House: New York; 1996. p. 500-86.  Back to cited text no. 3      
4.Shajil EM, Chatterjee S, Agrawal D, Bagchi T, Begum R. Vitiligo: Pathomechanisms and genetic polymorphism of susceptible genes. Indian J Exp Biol 2006;44:526-39.  Back to cited text no. 4  [PUBMED]    
5.Hann SK, Nordlund JJ. Clinical features of generalized vitiligo. In : Hann SK, Nordlund JJ, editors. Vitiligo a monograph on the basic and clinical science. Blackwell Science: 2000. p. 35-48.  Back to cited text no. 5      
6.Taieb A. Intrinsic and extrinsic pathomechanisms in vitiligo. Pigment Cell Res 2000;13:41-7.  Back to cited text no. 6  [PUBMED]    
7.Ortonne JP, Bose SK. Vitiligo: Where do we stand? Pigment Cell Res 1993;6:61-72.  Back to cited text no. 7  [PUBMED]    
8.Agrawal D, Sahani MH, Gupta S, Begum R. Vitiligo etiopathogenesis and therapy - A Review. J Mah Sayajirao Univ Baroda 2001;48:97-106.  Back to cited text no. 8      
9.Agrawal D, Shajil EM, Marfatia YS, Begum R. Study on the antioxidant status of vitiligo patients of different age groups in Baroda. Pigment Cell Res 2004;17:289- 94.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Yildirim M, Baysal V, Inaloz HS, Kesici D, Delibas N. The role of oxidants and antioxidants in generalized vitiligo. J Dermatol 2003;2:104-8.  Back to cited text no. 10      
11.Boisseau-Garsaud P, Lejoly-Boissaeu H, Robert M, Quist D, Arveiler B. Increase in the total antioxidant status and selenium levels in the black patients with active vitiligo. Int J Dermatol 2002;10:640-2.  Back to cited text no. 11      
12.Reiner E, Sinko G, Skrinjaric-Spoljar M, Simeon-Rudolf V. Comparison of protocols for measuring activities of human blood cholinesterases by Ellman Mehotd. Arth Hig Rada Toksikol 2000;51:13-8.  Back to cited text no. 12  [PUBMED]    
13.Reedy MV, Parichy DM, Erickson CA, Mason KA, Frost-Mason SK. Regulation of melanoblasts migration and differentiation. In : Nordlund JJ, Boissey RE, Hearing VJ, King RA, Ortonne JP, editors. The Pigmentary system. Physiology and pathophysiology. Oxford University Press: New York; 1998. p. 75-95.   Back to cited text no. 13      
14.Koga M. Vitiligo: A new classification and therapy. Br J Dermatol 1997;97:255-61.  Back to cited text no. 14      
15.Iyengar B. Modulation of melanocytic activity by acetylcholine. Acta Anat (Basel) 1989;136:139-41.  Back to cited text no. 15  [PUBMED]    
16.Elwary SM, Headley K, Schallreuter KU. Calcium homeostasis influences epidermal sweating in patients with vitiligo. Br J Dermatol 1997;137:81-5.  Back to cited text no. 16  [PUBMED]    
17.Schallreuter KU, Elwary SM, Gibbons CJ, Rokos H, Wood JM. Activation/deactivation of acetylcholine esterase by H2O2: More evidence for oxidative stress in vitiligo. Biochem Biophys Res Commun 2004;315:502-8.  Back to cited text no. 17      
18.Agrawal D. Antioxidant status of vitiligo patients relative to controls , M. Phil Dissertation. M.S. University of Baroda: Vadodara; 2002.  Back to cited text no. 18      
19.Shajil EM, Begum R. Antioxidant status of segmental and nonsegmental vitiligo. Pigment Cell Res 2006;19:179-80.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]  



 
 
    Tables

  [Table - 1], [Table - 2]

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