Squamous Cell Carcinoma Occurring Over Discoid Lupus Erythematosus of the Scalp: A Rare Occurrence
Year: 2025
Type: article
Study design: Case Report
Abstract: Sir, Discoid lupus erythematosus (DLE) is a benign inflammatory disorder of the skin, most frequently involving the face and scalp, characterized by well‐defined red scaly patches of variable sizes, which heal with atrophy, scarring, and pigmentary changes.[1] Squamous cell carcinoma (SCC) is the most common form of nonmelanoma skin cancer, which presents with ulcerated lesions and can be patchy, papulonodular, papillomatous, or exophytic.[2] SCC occurring over preexisting dermatosis is uncommon and has been reported previously in inflammatory dermatoses such as oral lichen planus, lichen simplex chronicus, lupus vulgaris, and lichen sclerosus et atrophicus.[3] SCC occurring over preexisting DLE is extremely uncommon, with few cases reported previously.[1,4] We report a case of disseminated DLE who developed an ulcerated growth over the scalp, which on thorough evaluation was diagnosed as Stage II SCC and was managed successfully with radiotherapy. A 31-year-old female agricultural worker presented with a painful growth on the scalp for 2 months. The lesion initially started as a small, raised lesion, which later gradually progressed to attain its present size. The patient was a known case of disseminated DLE diagnosed 15 years back. She was treated with oral hydroxychloroquine, oral steroids, azathioprine, topical steroids, and sunscreen which she used intermittently. There was no history of trauma, prior drug intake, exposure to ionizing radiation, or arsenicals. Personal history revealed exposure to sunlight for more than 4 h per day on most days in the past 7 years. General examination and systemic examination were within normal limits. On dermatological examination, a large, depigmented plaque of size 20 cm × 15 cm was seen over the central scalp with loss of follicular orifices, cicatricial alopecia, atrophy, and scaling over the margins of the plaque [Figure 1]. An erythematous tender nodule of size 1.8 cm diameter with central ulceration and bleeding points was seen over the center of the scalp lesion [Figure 2]. Multiple hyperpigmented and hypopigmented atrophic plaques with scaling were seen over the retroauricular area, interscapular area, back, and left hand.Figure 1: A large depigmented plaque of size 20 cm × 15 cm seen over the central scalp with cicatricial alopecia and skin atrophyFigure 2: An erythematous tender nodule of size 1.8 cm diameter with central ulceration and bleeding points seen over the center of the scalp lesionBased on the above clinical features, a differential diagnosis of SCC, keratoacanthoma, and actinic keratosis was considered for the scalp growth. Hemogram, serum biochemistry, and collagen profile were normal. Dermoscopy of the atrophic plaques showed follicular plugging, perifollicular whitish halo, and linear blood vessels, suggesting the possibility of DLE, whereas the scalp growth showed keratin, white circles, and blood spots. Computed tomography scan of the head showed a heterogeneously attenuating lesion involving the scalp at the left parietal region without skull bone involvement, suggesting the possibility of neoplastic growth. Histopathological examination of the skin sample taken from the depigmented plaque showed follicular plugging, basal layer degeneration, dermal perivascular, and periadnexal lymphohistiocytic infiltration suggestive of DLE. Histopathology of the scalp nodule revealed hyperplastic, hyperkeratotic epidermis with moderate acanthosis; tumor proper consisting of nests and sheets of atypical squamous cells was arising from the epidermis [Figure 3a]. The squamous cells were large, polygonal, and showed abundant eosinophilic cytoplasm with pleomorphic, vesicular nucleus [Figure 3b]. Few keratin pearls were noted, and the adjacent dermis showed mild lymphocytic infiltrate.Figure 3: (a) Tumor proper arising from the epidermis and consists of nests and sheets of atypical, squamous cells. (b) Large, polygonal squamous cells with abundant eosinophilic cytoplasm and pleomorphic, vesicular nucleusBased on the clinical, dermoscopic, and histopathological features, a diagnosis of disseminated DLE with SCC was made. The patient was evaluated thoroughly and graded as Stage II as per the current American Joint Committee on Cancer staging system for cutaneous SCC based on T2 (tumor >2 cm in greatest dimension), N0 (no regional lymph node metastasis), and M0 (no distant metastasis). The patient was treated with oral hydroxychloroquine, topical steroids, and sunscreen for DLE, while for SCC, she was referred to a cancer institute where she was treated with brachytherapy. After 10 radiotherapy sessions, the growth resolved completely with superficial erosion over the surface [Figure 4].Figure 4: Posttreatment image showing resolution of the scalp growth with superficial erosion over the surface at the site of brachytherapySCC may develop as an end-stage complication in a wide array of inflammatory skin conditions such as long-standing oral ulcerative lichen planus, hypertrophic lichen planus, scarring conditions such as dystrophic epidermolysis bullosa, long-standing burn scars, and chronic draining osteomyelitic sinus tracts. There have been sporadic reports of neoplastic change in DLE, which range from SCC and basal cell carcinoma to malignant fibrous histiocytoma and atypical fibroxanthoma.[5] SCC usually arises in the skin damaged by actinic rays. Keratinocytes that have sustained long-term ultraviolet (UV) radiation-induced DNA damage develop mutations in p53 tumor suppressor gene which leads to defect in apoptosis, ultimately resulting in transformation to SCC.[6] Pathogenetic mechanisms responsible for the development of SCC within DLE include the chronic scarring in combination with constant local inflammatory stimuli and hypopigmented DLE plaques predisposing the lesions to actinic damage.[7] The most common site for the development of SCC in DLE is the scalp, followed by the lips. The interval between the onset of DLE and SCC has varied from 4 to 20 years. Precipitating factors for SCC are age more than 40 years, male sex, UV ray exposure, skin pigmentation, and chronic inflammatory processes.[8] In the present case, SCC developed secondary to long-standing disseminated DLE, and the important predisposing factor was frequent and prolonged exposure to sunlight in her occupation as an agriculture worker. The long-term intermittent use of immunosuppressive drugs, including systemic steroids and azathioprine, may have also acted as a trigger factor for neoplasia. Histological variants of SCC include classic/no special type, acantholytic, spindle cell, desmoplastic, basaloid, verrucous, pseudovascular, and follicular types. The classic/no special type is the most common variant. The cells of SCC vary from large, polygonal cells with vesicular nuclei, prominent nucleoli, an abundant cytoplasm, overt evidence of keratinization, and well‐developed intercellular bridges (well‐differentiated lesions) to pleomorphic cells which provide no clear cytological evidence of their origin (poorly differentiated lesions).[9] In our case, histopathology revealed features in favor of classic/no special type. Treatment modalities of SCC occurring over preexisting dermatosis include wide local excision with lymph node dissection, followed by radiotherapy to the tumor bed. Chemotherapy is indicated in cases with systemic spread.[10] In the present case, the patient was treated with brachytherapy alone in view of the localized involvement without systemic spread, which resulted in complete resolution of the lesion after 10 sessions. To conclude, patients with skin of color have been observed to have poorer outcomes from skin cancers, possibly because of delayed diagnosis. Hence, early intervention and treatment are especially important to reduce the risk of morbidity and mortality when SCC occurs in DLE lesions in patients with darker skin phototypes. Patients with DLE should be advised to have frequent follow-up examinations, use broad-spectrum sunscreen regularly, and avoid direct sun exposure to discoid lesions. This case is being presented to raise awareness of this potential complication in Indian patients. 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. Authors’ contributions Literature search: S.B.K, R.R.B; Data acquisition: B.B.S, K.V.T.G; Manuscript preparation: B.B.S, K.V.T.G; Manuscript editing: S.B.K, R.R.B; Manuscript review: B.B.S, K.V.T.G. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Source: Clinical Dermatology Review
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W4409185682