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Year : 2013  |  Volume : 4  |  Issue : 3  |  Page : 254-255  

Radiotherapy induced keobernisation of vitiligo

Department of Dermatology, Assistant Professor, L. T. M. Medical College and General Hospital, Sion, Mumbai, Maharashtra, India

Date of Web Publication24-Jul-2013

Correspondence Address:
Meghana Phiske
Department of Dermatology, Assistant Professor, L. T. M. Medical College and General Hospital, Sion, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-5178.115542

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How to cite this article:
Phiske M. Radiotherapy induced keobernisation of vitiligo. Indian Dermatol Online J 2013;4:254-5

How to cite this URL:
Phiske M. Radiotherapy induced keobernisation of vitiligo. Indian Dermatol Online J [serial online] 2013 [cited 2020 Aug 11];4:254-5. Available from: http://www.idoj.in/text.asp?2013/4/3/254/115542

I write with reference to the article titled 'Koebnerization and generalized spread of vitiligo following radiotherapy'. [1] by Sanghavi SA et al published in the Indian Dermatol Online J 2013. I wish to share points about spread of vitiligo following radiotherapy.'

Koebner phenomenon, also known as isomorphic phenomenon (iso=same, morphic = form) was first described by Heinrich Koebner in 1878. It refers to development of isomorphic/new lesions of the disease at sites of local trauma in traumatized but otherwise normal skin(uninvolved skin). The response should be reproducible and not limited to one type of trauma. [2] It is seen in psoriasis, vitiligo, lichen planus etc. Many forms of mechanical/physical/chemical/allergic trauma, incision and laceration, skin tests, burns, freezing, UV light and ionizing radiation have been implicated. [2],[3],[4] Koebnerization occurs commonly in vitiligo, developing on sites of mild friction, cuts burns and abrasion. [5]

Irradiation is associated with early and late toxicity to the skin and subcutaneous tissues, common being fibrosis and/or necrosis. [6] Tissues with a slow rate of cell division, such as subcutaneous fat, fibrous tissue and small blood vessels, show radiation effects months or years after treatment, which is the late reaction. The irradiated skin may show pallor and a degree of atrophy [7] (differentiating it from vitiligo which is depigmented and does not show atrophy). Patients with collagen vascular diseases have an increased radiation sensitivity of normal tissues to radiation damage, but there is no evidence for increased severity of acute or chronic reactions in patients with vitiligo. [8]

Depigmentation is rarely associated with irradiation, being documented in few vitiligo patients, few patients with breast carcinoma and a single case of metastatic melanoma and nasopharngeal carcinoma respectively. [8],[9],[10],[11] Vitiligo following radiotherapy is reported in patients with a history of vitiligo, being considered as Koebner's phenomenon. [8] Depigmentation develops in the area irradiated by oblique or tangential portals with sparing with a direct incident portal. Tangential portals cause increased electron build-up and consequently increase the dose delivered to the skin. [6]

The suggested mechanism for hypopigmentation is radiation- induced apoptosis of susceptible melanocytes. Loss of melanocytes in the irradiated skin has been demonstrated by Pajonk et al and correlated with dose-dependent decrease in red/green and yellow/blue saturation and overall increase in brightness on colorimetry. Free radical-mediated damage, induced by radiotherapy, may be the initial pathogenic event in melanocyte degeneration in the irradiated skin. Vitiligo is caused by melanocyte depletion, and there is an increased radiosensitivity of melanocyte in vitiligo. [8] The early cell death of melanocytes in vitiligo is related to their increased sensitivity to oxidative stress caused by irradiation, which may arise from complex processes of abnormal synthesis and processing of tyrosinase related protein-1 and its interaction with calnexin. Thus, oxidative stress can occur in irradiated human cells and may play a direct role in radiation induced apoptosis. [6],[8]

Keratinocyte apoptosis can cause lower expression of keratinocyte derived factors, including stem cell factors and basic fibroblast growth factor. These factors might be responsible for passive melanocyte death, leading to their detachment and transepidermal elimination, and may explain the Koebner's phenomenon in the vitiligo patients. Auto cytotoxic mechanism may occur through inhibition of thioredoxin reductase by high extracellular calcium levels observed in keratinocytes of vitiligo patients. High levels of thioredoxin and thioredoxin reductases have been shown to protect from ionizing radiation induced cell death. Thus, inhibition of thioredoxin reductase in vitiligo might account for the increased radiosensitivity of melanocytes in this disorder. [8]

In patients with preexisting vitiligo, the risks and benefits of radiation therapy should be carefully weighed in order to prevent undesired cosmetic results. Preserving the skin by using megavoltage beams and low dose per fraction might improve the cosmetic results of radiation therapy in patients with a history of vitiligo. [8]

Thus, prior to therapy, the possibility of development of vitiligo should be taken into account for patients who are candidates for radiotherapy, even if they have no history of vitiligo. [11]

   References Top

1.Sanghavi SA, Dongre AM, Khopkar US. Koebnerization and generalized spread of vitiligo following radiotherapy. Indian Dermatol Online J 2013;4:147-8  Back to cited text no. 1
2.Kennedy CT Burd DR, Creamer D. Mechanical and thermal injury. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology 8 th ed, Vol. 3. UK: Wiley Black-Well; 201p 28.1.94.  Back to cited text no. 2
3.Pavithran K, Karunakaran M, Palit A, et al. Disorders of keratinization. In: Valia RG, Valia AR, editors. IADVL textbook of Dermatology. 3 rd ed, Vol. 2. India: Bhalani Publishing House 2008. p. 995-1069.  Back to cited text no. 3
4.Bedi BM. Principles of clinical diagnosis. In: Valia RG, Ameet R Valia AR, editors. IADVL textbook of Dermatology. 3 rd ed, Vol. 2. India: Bhalani publishing house 2008. p. 94-111.  Back to cited text no. 4
5.Halder RM, Taliaferro SJ. In Fitzpatricks Dermatology in General Medicine. In: Wolff K, Goldsmith LA, Katz SI et al. 7 th ed, Vol. 2. New York: McGraw Hill Medical 2008. p. 616-22.  Back to cited text no. 5
6.Weitzen R, Pfeffer R, Mandel M. Vitiligo after Radiotherapy for Breast Cancer in a woman with depigmentation disorder. J Clin Oncol 2005;23:644.  Back to cited text no. 6
7.Kelly CG, Peat I. Radiotherapy and Reactions to Ionizing Radiation. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed, Vol. 3. UK: Wiley Black-Well;2010. p. 79.1-.19.  Back to cited text no. 7
8.Munshi A, Jain S, Budrukkar A, Jalali R, Sarin R. Radiotherapy- induced depigmentation in a patient with breast cancer. Indian J Cancer 2007;44:157-8.  Back to cited text no. 8
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9.Levine EL, Ribeiro GG. Vitiligo and radio therapy: The koebnerphenomenon demonstrated in patients with vitiligo undergoing radiotherapy for carcinoma of the breast. Clin Oncol (R Coll Radiol) 1994;6:133-4.  Back to cited text no. 9
10.Kopacz A, Kucharski A, Kruszewski W. Vitiligo following radiotherapy for carcinoma of the breast. Br J Dermatol 1989;135:852-3.  Back to cited text no. 10
11.Polat M, Yalçin B, Alli N. Vitiligo at the site of radiotherapy for nasopharyngeal carcinoma. Am J Clin Dermatol 2007;8:247-9.  Back to cited text no. 11


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