Figure 1. Presentation of the left shin prior to ED&C (A); follow-up 2 months after ED&C (B); 3 months after skin graft (C); and 2 months after Mohs surgery (D).
A 77-year-old man with a past medical history of hypertension presented to his initial dermatologist with a 3-cm pink, crusted, scaly plaque on the left shin consistent with a squamous cell carcinoma (SCC) with keratoacanthoma (KA) features (Figure 1A). An initial attempt of electrodesiccation and cautery (ED&C) was performed. At his 2-month followup he had continued clinical involvement (Figure 1B) and was referred to surgical oncology for definitive treatment where clear margins were achieved after wide local excision and split-thickness skin graft. Three months after treatment, he presented to our clinic with a new exophytic nodule at the inferior border of the skin graft site on his left shin (Figure 1C). Biopsy revealed SCC with KA features. Mohs micrographic surgery was performed, and margins were clear after one stage. At his Mohs surgery, a new, unrelated exophytic nodule was identified on his left posterior calf in a scar from an excision done 2 months prior for a KA-type SCC (Figure 2A). Biopsy again revealed a KA-type SCC, which cleared with Mohs surgery after two stages. Two months later, another exophytic nodule was identified at the inferior portion of the scar from the Mohs surgery performed on his left shin (Figure 1D). Biopsy was again consistent with SCC with KA features, and Mohs surgery was performed with clearance after two stages.
On three separate occurrences, our patient developed new KAs in prior surgical sites: one developed at the border of a skin graft recipient site, one appeared in an excision site, and one presented in a Mohs site. Two of these occurred on the left shin and one on the left posterior calf (Figure 2B). All KAs were noted between 2 to 3 months after the prior procedure. This patient did not have any known immunosuppression, no known family history of KAs, and no history of trauma to the initial lesions on the left shin or left posterior calf.
Figure 2. Presentation of the left posterior calf prior to initial excision (A) and at follow-up 2 months after excision (B).
KAs are usually solitary, rapidly growing, erythematous, crateriform nodules occurring on sun-exposed areas in middle-aged to elderly individuals with equal occurrence in men and women.1,2 They range from several millimeters to several centimeters in size, have well-demarcated borders, and appear as endoexophytic nodules with a central keratinous plug.1 Predisposing factors for KAs include sun exposure, immunosuppression, genetics, HIV infection, and trauma. Variants of solitary KAs include KA centrifugum marginatum and giant KA, while multiple KAs can be seen in the familial Ferguson-Smith type, Gryzbowski syndrome, Muir-Torre syndrome, and xeroderma pigmentosum.3,4
KAs are thought to progress through three stages from rapid proliferation to maturation and finally to involution.1,3 Although KAs may spontaneously resolve, their appearance, rapid growth, and the ability of KAs to behave like invasive SCCs can all present the clinician with a difficult therapeutic dilemma, especially since metastases of KAs have also been reported.1,5 Hodak et al5 presented 3 cases of metastatic KAs in 1993 and proposed that because of this life-threatening potential, KAs are, in fact, a variant of SCCs and should be treated as such. Savage and Maize2 performed a systematic review in 2013 and found that, in 445 confirmed cases of KAs (which did not include the three cases reported by Hodak et al), none resulted in distant metastases or death. Of these cases, 4% showed recurrence and 10% showed perineural or perivascular invasion.2
Given these findings, physicians must weigh the options of treatment for patients presenting with these KAs; however, solitary KAs are often treated as SCCs due to the difficulty in predicting their behavior. Some differentiating features have been reported on pathology that may assist in the diagnosis of KAs. In KAs, the base of the lesions tends to be well demarcated, unlike in SCCs, and usually does not extend below the level of the sweat gland.3 A thin, well-defined stroma is often found between the proliferating epidermis of the KA and the dermis, and the dermis is rarely invaded by proliferating cells.3 Finally, the keratinocytes seen in KAs are rarely atypical as is seen in SCCs. Despite these distinct features and further attempts to differentiate KAs from SCCs based on cellular markers, extensive controversy remains as to whether or not SCCs and KAs are separate entities.6 This is even further complicated by reports that SCCs can develop within KAs and the finding that 10% of KAs may demonstrate perineural or perivascular invasion.2