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| CASE REPORT |
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| Year : 2017 | Volume
: 4
| Issue : 2 | Page : 115-117 |
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Squamous cell carcinoma on vitiligo patch: A rare association
Anita Vijay, Suresh K Jain, Ramesh Kumar
Department of Dermatology, Venereology and Leprology, Government Medical College, Kota, Rajasthan, India
| Date of Web Publication | 1-Dec-2017 |
Correspondence Address:
Suresh K Jain
Department of Dermatology, Venereology and Leprology, Government Medical College, Kota, Rajasthan 324 005
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-5847.219682
Vitiligo is an immune-mediated disease characterized by idiopathic destruction of melanocyte. The loss of pigment melanin predisposes vitiligo patients to photosensitivity and early photodamage. Despite this, the incidence of squamous cell carcinoma (SCC) is not found to be increased in vitiligo. SCC is a common malignancy of keratinocytes that arises in sites of exposure to excessive ultraviolet radiation. Various theories have been proposed for lower incidence of SCC in vitiligo. These include decrease in cytokines, such as transforming growth factor-β and IL-10, along with increase in IL-1, TNF-α, p53, superoxide dismutase, and glutathione peroxidase. We hereby report a rare case of SCC arising in a patient with longstanding vitiligo of photoprotected skin with no history of phototherapy.
Keywords: Squamous cell carcinoma, ultraviolet radiation, vitiligo
How to cite this article:
Vijay A, Jain SK, Kumar R. Squamous cell carcinoma on vitiligo patch: A rare association. Pigment Int 2017;4:115-7 |
| Introduction | |  |
Squamous cell carcinoma (SCC) is a common malignancy of keratinocytes that arises in sites of exposure to excessive ultraviolet radiation (UVR). The pigment melanin present in the skin is believed to be protective against the harmful effects of UVR, thereby decreasing the risk of malignancy in dark skin individuals. Accordingly, the loss of melanin in patients with vitiligo predisposes them to early photodamage, and therefore, a higher incidence of cutaneous malignancy is congruously expected. However, studies have failed to show a linear association between nonmelanoma skin cancer (NMSC) and vitiligo.[1],[2],[3] Though occasional cases of NMSC arising in vitiligo have been documented,[2],[4] it is now commonly believed that patients with vitiligo do not have an increased risk and perhaps have even a lower incidence of skin cancer than the general population.[4] Herein we report a case of SCC arising in a patient with longstanding vitiligo of photoprotected skin.
| Case report | | |
A 55-year-old man presented to us with an asymptomatic ulceroproliferative mass over left leg for last 4 months. He had multiple focal vitiligo patches over both legs for last 15 years. As vitiligo was present on the covered sites, patient did not seek treatment for the same. He noticed a small lemon-sized nodular lesion over vitiligo patch of the left leg 4 months back. The lesion ulcerated and progressed in size and extent to attain the present size. He had no history of significant sun exposure, cough, dyspnea, bone pain, or weight loss. Family history for vitiligo was negative.
Local cutaneous examination revealed a large noduloulcerative exophytic mass of around 18 × 10 cm in size present over the anterior and lateral aspect of upper one-third of left leg and extending up to the lower one-third of lateral aspect of thigh [Figure 1]. The margins were elevated and rolled out, and base covered by dirty yellow-white slough with foul smelling discharge. On palpation, the lesion was nontender, not fixed to the underlying tissue and bled on touch. There was no regional lymphadenopathy. Rest of the cutaneous examination and systemic examination was normal. | Figure 1: (a) Noduloulcerative exophytic mass arising over vitiligo patch on left leg, (b) extending up to lower one third of lateral aspect of thigh
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Investigations, including hemogram, liver function tests, renal function tests, serum thyroid stimulating hormone, X-ray chest, X-ray left leg, X-ray lumbar spine, and ultrasound abdomen, were normal. Swab taken from the surface showed Staphylococcus aureus on culture and gram stain.
Incisional biopsy was taken from the margin and revealed hyperplastic epidermis with irregular masses of anaplastic cells with nuclear atypia, high nuclear-to-cytoplasmic ratio, hyperchromasia and pleomorphism of nuclei invading the dermis. Also many well-defined horny pearls surrounded by keratinocytes were seen [Figure 2]. | Figure 2: (a) Hyperplastic epidermis with irregular masses of anaplastic cells invading the dermis (H&E, 100×), (b) anaplastic cells with high nucleo-cytoplasmic ratio and well-defined horny pearls surrounded by keratinocytes (H&E, 400×)
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The diagnosis of well-differentiated SCC was made and the patient was referred to surgery department for further management.
| Discussion | | |
SCC is a cutaneous NMSC arising from keratinocytes. There are number of factors, acquired and genetic, predisposing to SCC. Most importantly, a linear correlation has been shown between SCC and UVR exposure. UV rays incident on human skin causes oxidative damage, which is generally taken care by several endogenous antioxidant pathways, including glutathione peroxidise and superoxide dismutase. Therefore, any defect or inactivation of these antioxidant mechanisms may act as an initiating event in UV induced SCC formation. Moreover, Toll-like receptors (TLRs), especially TLR4, play a significant role in the cellular response to UV exposure and contribute to UV-induced transforming growth factor-β (TGF-β) and IL-10 secretion.[5] There is convincing evidence that UV-induced expression of IL-10 contributes to the development of photocarcinogenesis by suppressing protective cellular immune responses. In addition, in the tumor microenvironment of SCC, increased TGF-β can be observed, and it is known to drive tumor progression in epithelial tumors.[6] Eventual explanations for this procarcinogenic effect of TGF-β may be loss of adhesion molecules, increased angiogenesis, protease activation, and immune suppression. Melanin, an endogenous brown-black pigment, is located in the supranuclear area of keratinocytes and absorbs the UV rays reaching the skin surface, thereby protecting against its ill effects.
Vitiligo, characterized by idiopathic destruction of melanocytes, is an immune-mediated disease, resulting in depigmented macules and patches. Although loss of the protective pigment is expected to increase the risks associated with sun exposure, interestingly, vitiligo is not associated with higher incidence of NMSC. Decreased photodamage and low incidence of NMSC in 136 sun-exposed Caucasian patients with vitiligo.[1] In a study conducted by Hexsel et al.,[2] only six vitiligo patients out of a total of 477 developed NMSC. Markedly reduced incidence of melanoma and NMSC in nonconcurrent cohort of 10,040 patients with vitiligo.[3] There are various proposed mechanisms for lower incidence of SCC in vitiligo [Table 1]. Vitiligo is associated with overproduction of protective factors against carcinogenesis, such as IL-1, TNF-α, p53, superoxide dismutase, and glutathione peroxidase. Moreover, the procarcinogenic factors, such as TGF-β and IL-10, are significantly decreased in vitiligo.[7] All these factors combined may explain the negative association between vitiligo and skin cancer. Despite vitiligo patients being more prone to photosensitivity, they rarely develop SCC. | Table 1: Possible explanations for lower incidence of squamous cell carcinoma in vitiligo
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Though SCC developing in vitiligo patients after PUVA has been observed, the de novo occurrence has been rarely reported.[8] Moreover, most cases have developed SCC on the photoexposed parts of the body.[4] The case presented here is of an Indian man presenting with SCC arising on a vitiligo patch on the photoprotected site with no history of phototherapy. The case is reported due to its rarity and scarcity of reports from Indian subcontinent.[9],[10],[11],[12]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Schallreuter KU, Tobin DJ, Panske A. Decreased photodamage and low incidence of non-melanoma skin cancer in 136 sun-exposed Caucasian patients with vitiligo. Dermatology 2002;204:194-201.  [ PUBMED] |
| 2. | Hexsel CL, Eide MJ, Johnson CC, Krajenta R, Jacobsen G, Hamzavi I et al. Incidence of nonmelanoma skin cancer in a cohort of patients with vitiligo. J Am Acad Dermatol 2009;60:929-33. |
| 3. | Paradisi A, Tabolli S, Didona B, Sobrino L, Russo N, Abeni D. Markedly reduced incidence of melanoma and nonmelanoma skin cancer in a nonconcurrent cohort of 10,040 patients with vitiligo. J Am Acad Dermatol 2014;71:1110-6. [ PUBMED] |
| 4. | Saarinen K, Lestringant GG, Masouye I, Frossard PM. Actinic damage and squamous cell carcinoma in sun-exposed skin affected by vitiligo. Br J Dermatol 2000;143:219-21. [ PUBMED] |
| 5. | Lewis W, Simanyi E, Li H, Thompson CA, Nasti TH, Jaleel T et al. Regulation of ultraviolet radiation induced cutaneous photo immune suppression by Toll-like receptor-4. Arch Biochem Biophys 2011;508:171-7. |
| 6. | Rahimi RA, Leof EB. TGF-beta signaling: a tale of two responses. J Cell Biochem 2007;102:593-608. [ PUBMED] |
| 7. | Basak PY, Adiloglu AK, Ceyhan AM, Tas T, Akkaya VB. The role of helper and regulatory T cells in the pathogenesis of vitiligo. J Am Acad Dermatol 2009;60:256-60. [ PUBMED] |
| 8. | Seo SL, Kim IH. Squamous cell carcinoma in a patient with generalized vitiligo. J Am Acad Dermatol 2001;45:227-9. [ PUBMED] |
| 9. | Gangopadhyay A, Das JK, Agarwal AK. Squamous cell carcinoma in a patient with vitiligo of photo-covered skin. Indian J Dermatol 2014;59:193-4. [ PUBMED] [Full text] |
| 10. | Dhawan AK, Verma P, Singal A, Sharma S. Squamous cell carcinoma complicating vitiligo in an Indian man. J Cutan Aesthet Surg 2012;5:36-7. [Full text] |
| 11. | Seo SL, Kim IH. Squamous cell carcinoma in a patient with generalized vitiligo. J Am Acad Dermatol 2001;45:S227-9. [ PUBMED] |
| 12. | Hexsel CL, Mahmoud BH, Mitchell D, Rivard J, Owen M, Strickland FM et al. A clinical trial and molecular study of photoadaptation in vitiligo. Br J Dermatol 2009;160:534-9. |
[Figure 1], [Figure 2]
[Table 1]
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