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LETTER TO EDITOR
Year : 1996  |  Volume : 62  |  Issue : 3  |  Page : 200-201

Genesis of cutaneous depigmentation



Correspondence Address:
S S Sawhney


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Source of Support: None, Conflict of Interest: None


PMID: 20948047

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How to cite this article:
Sawhney S S. Genesis of cutaneous depigmentation. Indian J Dermatol Venereol Leprol 1996;62:200-1

How to cite this URL:
Sawhney S S. Genesis of cutaneous depigmentation. Indian J Dermatol Venereol Leprol [serial online] 1996 [cited 2019 Dec 13];62:200-1. Available from: http://www.ijdvl.com/text.asp?1996/62/3/200/4384



  To the Editor, Top


Theories[1] on the aetiology of leucoderma abound but data about its initiation, progression or recession is extremely sparse. This report seeks to understand the causes and progress of cutaneous depigmentation.

Each chemical (2% w/v or v/v in Et. OH): hydroquinone (OH. C6 H4. OH), p (benzyloxy)phenol (C6 H5. CH2O. C6 H4. OH) p-hydroxypropiophenone (OH.C6H4.CO.CH2.CH3) butylphenol (C4H9.C6H4.OH) and amylphenol (C5H11.C6H4.OH) having a common hydrogen donor group (-OH), when appllied topically for 20 days on the vitiligo patients (6 in active stage and 4 in steady stage) and 10 controls without any skin disease, caused pigment dilution on the spots involved, progessing slowly with the repeat application of the chemical. In both groups depigmentation may be the consequence of a reaction between the colour determinant and the chemical in epidermis. The response after the cessation of the chemical application was different; original status of the test spots was restored in control groups after 20 to 30 days, but the acquired transition persisted in the patients with vitiligo. These observations clearly indicate the loss of a mechanism in the vitiligo patients. Further except cosmetic defect, the vitiligo patients show soundness in clinical status like those of healthy individuals. Also both these groups respond alike to the chemical structures with antigenic determinants and are capable to rid off these non-self structures through complement fixation, suggesting that the biomechanisms to neutralise the toxins with and without antigenic determinant(s) are active in the control groups whereas the mechanism to deal effectively with the candidate chemical structures, which fail to elicit antibodies, is lost in the vitiligo patients. Further in controls, skin colour is conditional upon the molecular viability of the colour determining melanolipoprotein as envisaged by Sawhney,[2] and sustainment of the threshold limits of toxin concentration in skin matrix. The bioactive inherent disposition mechanism armed with a neutralising protein does this job through conjugation of the intruders. However the skin faculty is not endowed with the ability to perform protein synthesis, its demand is met through the likely events which include the hepatic synthesis of such neutralising protein and its subsequent transfer via plasma to the skin faculty. This specific reaction may get stalled in vitiligo patients as their ability to sweat off excess toxin concentration is lost. In acquired hostile environment the colour determinant may undergo structural modification through conjugation with the available toxins with complementary surfaces at the vacant spaces as predicted by Sawhney,[2] losing its property to impart natural shade to epidermis. The resultant structural crisis sets in the trigger mechanism of the pigment dilution in the stratum corneum with slow progression with the percutaneous diffusion of these toxins in skin matrix.



 
  References Top

1.El Mofty AM. In: Vitiligo and psoralens. London: Pergamon, 1968:147-95.  Back to cited text no. 1    
2.Sawhney SS. Thermal stability of melanin. Thermochim Acta 1994;247:377-80.  Back to cited text no. 2    




 

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