Spontaneous regression of a giant keratoacanthoma on the hand

Dear Editor,

Keratoacanthoma (KA) is a benign skin tumour characterised by rapid growth and spontaneous regression. The incidence, rate of regression, and persistence of KA are not accurately known because of misdiagnosis as squamous cell carcinoma (SCC), underreporting, or spontaneous regression before diagnosis.¹ Although the widely accepted view is that KAs can spontaneously regress, to the best of our knowledge, only four cases of spontaneous regression of giant keratoacanthoma (GKA) have been reported. Surgical excision is generally advocated because of the malignant potential. If not excised, careful follow-up is required, and surgery should be performed promptly if signs of malignancy appear. We present a 63-year-old male who developed a giant keratoacanthoma on the dorsal surface of his right hand after minor trauma. This lesion eventually experienced spontaneous regression.

A 63-year-old male presented with a 5-month history of a rapidly growing nodule on the dorsum of the right hand that first developed 1 month after an accidental cotton husk puncture injury. Physical examination revealed an 8 × 6 cm, firm crateriform nodule above the skin surface on the dorsum of the right hand with a yellowish-white central keratin plug. The surface showed uneven texture with ulceration and crusting. Lesion margins were well-circumscribed without tenderness or pruritus [Figure 1]. A diagnostic incisional biopsy (not punch biopsy) targeting the annular elevated area demonstrated characteristic histopathological features of keratoacanthoma: epithelial lipping at the periphery flanking the central keratin plug, papillomatous hyperplasia, focal mild basal layer cytologic atypia, and intact basement membrane [Figure 2]. With these findings, a diagnosis of keratoacanthoma was established. Although surgery was the most reasonable option, a lower limb deformity of the patient and the large tumour size posed a risk of impairing hand function and reducing quality of life (QOL) if excised. The histopathologic diagnosis was clear; there was no malignant transformation. It was decided to continue follow-up after communicating with the patient. After 6 months, the lesion had completely disappeared; 10 years later, the follow-up showed that the disease did not recur, leaving a pale yellow scar at the site of the original lesion [Figure 3].

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Figure 1:

An 8 × 6 cm firm, well defined, crateriform nodule with a yellowish-white central, ulcerated keratin plug on the dorsum of the right hand.

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Figure 2:

Incisional biopsy from the margin showing epithelial lipping at the periphery flanking the central keratin plug (black arrow), papillomatous hyperplasia, focal mild basal layer cytologic atypia, and an intact basement membrane (red arrow). (Haematoxylin & eosin, 200x)

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Figure 3:

Follow-up at 10 years after diagnosis, showing a pale yellow scar at the original site of the keratoacanthoma on the dorsum of the right hand, with no recurrence.

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Keratoacanthoma usually grows rapidly in 4 to 5 weeks and spontaneously regresses after 6 months.² The giant keratoacanthoma is a rare variant of KA that exceeds 20-30 mm in diameter.² Because of its size, destructive potential, and close resemblance to cSCC in both clinical and histological features, giant keratoacanthoma presents unique diagnostic and therapeutic challenges. Other differential diagnoses include basal cell carcinoma and rapidly enlarging cutaneous tumours. Various treatments for GKA have been reported.² Surgical excision is generally considered the gold standard. Nonsurgical approaches such as cryotherapy, radiotherapy, and intralesional or systemic agents have also been attempted with variable outcomes. Despite these options, spontaneous regression of GKA remains exceedingly rare. The mechanisms underlying regression in KA appear multifactorial. Evidence suggests that activated (IL-2R+) CD4⁺ T lymphocytes, adhesion molecules, and Wingless-related integration site and retinoic acid (Wnt/RA) pathways play pivotal roles in keratoacanthoma regression.³ Apoptosis, possibly through Bak and granzyme B, contributes to KA regression. The lower anti-apoptotic protein Bcl-xL expression may be consistent with apoptosis.^4,5 Savage et al. reviewed 445 KA cases with documented follow-up and found that 52 (11.7%) underwent spontaneous regression without treatment, while 393 (88.3%) regressed with medication or excision.⁶ Local recurrence occurred in 18 cases (4.0%). Importantly, none of the 52 cases showed recurrence, suggesting that careful observation may be a reasonable strategy in selected patients.

In our case, the patient presented with an unusually large lesion (8×6 cm) on the dorsum of the hand. Surgical excision would likely have required extensive reconstruction and carried a risk of functional impairment. After discussion of risks and benefits, the patient declined surgery. We treated this GKA conservatively, ensuring reliability through follow-up, and achieved a satisfying result with spontaneous regression. This case adds to the limited literature on GKA and highlights that although surgery remains the standard of care, observation may be considered in carefully chosen clinical scenarios.