Slowly Enlarging Black Nodule Over Back: Not All Black Lesions Are Moles

CLINICAL SCENARIO

A 42-year-old housewife without significant comorbidities reported with complaints of a slowly progressive, asymptomatic, black-coloured lesion on her back for 3 years. There was no history of bleeding, change in colour, or similar lesion over the body. Dermatological examination revealed a well-defined, firm, solitary, black-coloured nodule over the photoexposed area on the right side of the upper back, measuring 1 cm in diameter with a slight central depression [Figure 1]. Based on clinical findings, the diagnosis of acquired melanocytic naevus was considered. Since we were reasonably sure about the diagnosis, dermoscopy was not performed.

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Figure 1: Well-defined hyperpigmented firm nodule measuring approximately 1 cm in diameter over the back.

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As the lesion was aesthetically displeasing, the patient opted for surgical removal. Histopathologically, the lesion was well-defined with a central opening at the top, appearing as an epidermal outgrowth with a large, keratin-filled central cavity. The epidermis extended on both sides of the central opening, resembling lip buttresses [Figure 2a]. Irregular epidermal proliferation extended downward from the central lesion, poorly demarcated from the surrounding stroma. Multiple horn pearls showing complete keratinisation were observed [Figure 2b]. The lower limit of the lesion was well-defined and did not extend below the sweat glands. A dense inflammatory infiltrate was present at the base of the lesion. Atypical mitoses were noted in a few areas [Figure 2c].

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Figure 2: (a) Large keratin-filled lesion at the centre with epidermis arching above from both sides of the lesion like lip buttressing. The epidermal projections embedded in the surrounding stroma are extending downwards from the central lesion. Multiple horn pearls are seen. (H&E, 4x), (b) The medium power view shows atypical mitosis in the basal layer of the epidermis, along with completely keratinised horn pearls. The epidermal projections are surrounded by mononuclear infiltrate. (H&E, 10x), (c) The high-power view depicts the atypical mitosis of the basal layer of the epidermis. (H & E, 40x). (H&E: Haematoxylin and eosin.)

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WHAT IS YOUR DIAGNOSIS?/WHAT WOULD BE THE TREATMENT OF CHOICE?

DISCUSSION

KA, commonly referred to as molluscum sebaceum, is characterised as an abortive variant of squamous cell carcinoma (SCC). According to the latest World Health Organisation classification of tumours, KA is now categorised as a low-grade SCC, particularly in its non-regressing form, which has the potential to progress to invasive SCC.^[1] Clinically, KA typically manifests on sun-exposed areas of the skin as a well-defined, light-coloured nodule featuring a central keratin plug and an associated depression. Several clinical variants of KA have been identified, including the agglomerated form, giant form, centrifugum marginatum, eruptive forms described by Fergusson and Smith, Grzybowski-type, multiple familial KA of Witten and Zak, plate-shaped KA, distal digital KA, pseudorecidive KA, and reactive KA.^[2]

The dermoscopic features of KA include a central keratin plug along with peripheral hairpin vessels. Though in view of the clinical diagnosis of acquired melanocytic naevus (AMN), we didn’t perform dermoscopy of the lesion. Histopathological examination of KA reveals distinct stages of development, including early, proliferative, well-developed, regressing, and regressed phases.^[3] KA can be classified as follicular or non-follicular based on its anatomical location.^[4] Classic histopathological features of KA lesions include a central crater filled with keratin, with an overlying epidermis that arches above, creating a characteristic lip buttressing appearance. Microscopically, multiple keratin pearls are present, with the keratinisation process culminating in a homogeneous appearance at the centre of the lesion. Notably, the central lesion remains confined to the level of the sweat glands, which serves as a subtle marker for differentiating KA from SCC. In some cases, the epidermis may exhibit neutrophilic infiltration, manifesting as abscesses. Atypical mitotic figures can also be observed in the basal layer of KA lesions.^[5] Seborrhoeic keratosis is a histopathological differential diagnosis, characterised by numerous keratin pearls on histopathology; however, in seborrhoeic keratosis, the keratinisation process is more advanced, and the keratin pearls are dispersed throughout the epidermis, with interspersed basaloid cells. The immunohistochemical markers aid in differentiating between KA and invasive SCC. The Ki67 shows diffuse staining from the topmost layer of epidermis till the basal layer in the case of SCC, but it’s confined to the basal or suprabasal layer in KA. The differential expression of anti-P2X7, E-cadherin, cytokeratin 17 (CK17), and CD10 is also a useful marker for differentiation. BCL2 expression is retained in KA, whereas it is lost or weakly positive in SCC.^[6]

Verrucous carcinoma can be considered as another close differential on histopathology. But the lesions of verrucous carcinoma show prominent endophytic and exophytic growth. It lacks central crateriform architecture. It has bland cytologic features as compared to KA. Our patient had no history of previous skin malignancies or history of sun exposure. There was an absence of prolonged sun exposure, an absence of immunosuppression, radiation therapy, or exposure to chemical carcinogens, and the lesion closely resembled a typical acquired melanocytic naevus, which, on histopathological examination, revealed a distinct lack of a central crater, instead showing epidermal outgrowth with a large keratin filled cavity. Despite these atypical characteristics, key histopathological features— including epidermal arching, the presence of keratin pearls, and atypical mitotic activity in several layers—ultimately supported the diagnosis of KA. For aggressive lesions of KA, Mohs micrographic surgery is the gold standard, but in the case of clinically non-aggressive lesions, surgical excision is widely adopted. Other treatment modalities include intralesional injections of methotrexate and 5-fluorouracil, topical imiquimod and 5-fluorouracil, systemic retinoids for multiple KAs, and radiation therapy for the disseminated variant. This case highlights the importance of comprehensive histopathological evaluation in differentiating KA from other lesions.

In view of the recurrence rate of approximately 3%–8%, the patient was advised to follow up at 1 month, 3 months, 6 months, and then annually for 5 years to monitor for recurrence or development of new lesions. Also, she was advised to use sun protection on exposed sites.