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Keratoacanthoma

Keratoacanthoma is a rapidly appearing "self-healing" variety of squamous cell carcinoma. To be safe, they are usually treated by dermasurgeons with an excisional biopsy.

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Keratoacanthoma arising from an excisional surgery scar
From Journal of Drugs in Dermatology, 3/1/04 by Arash Kimyai-Asadi

Abstract

A causal relationship between keratoacanthomas and a variety of preceding traumatic events has been postulated in the literature. We report a patient who developed a keratoacanthoma at the site of a recent cutaneous excision site, demonstrating that surgical trauma can precede the development of keratoacanthomas.

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Introduction

Keratoacanthomas (KAs) are considered low-grade cutaneous malignancies believed to arise from the epithelium of the pilose-baceous unit. Clinically, KAs are characterized by rapid growth over several weeks or months, followed by spontaneous resolution over 4-6 months. Histopathologically, KAs resemble squamous cell carcinomas (SCC), and invasive or metastatic lesions have rarely been reported. A causal relationship between KAs and a variety of preceding traumatic events has been postulated in a number of reported cases (1,2). We describe a patient who developed a rapidly-growing KA at the site of a recent surgical scar. To our knowledge, this is the first reported case of an iatrogenic KA resulting from excisional cutaneous surgery.

Report of a Case

A 76-year-old man with a history of multiple basal cell carcinomas and actinic keratoses presented for evaluation of a lesion on the right dorsal hand. A shave biopsy was performed and a diagnosis of actinic keratosis with a focus of squamous cell carcinoma in situ was made. The lesion was excised as a disc with 4 mm margins, the margins of which were histologically clear of carcinoma. Dog-ear repairs were performed at the proximal and distal flanks of the defect to create a flat surgical scar. At two-week follow-up, there were no clinical signs of infection or residual or recurrent neoplasm. The sutures were removed at that time.

The patient returned 2 months post-operatively for evaluation of a rapidly-developing nodule on the dorsum of the right wrist that the patient first noted a few days after suture removal. Physical examination revealed a 1.5 cm erythematous hyperkeratotic nodule at the superior margin of the scar in an area corresponding to the proximal tip of the excised dog-ear (Figure 1). A biopsy was performed which revealed an epidermal invagination filled with highly keratinized, eosinophilic keratinocytes. The underlying and adjacent dermis demonstrated a loose fibrous stroma with bundles of collagen arranged parallel to the epidermal surface. Both the clinical and histologic findings were consistent with a diagnosis of a KA arising from a surgical scar. The KA was surgically excised with no recurrence over a one-year period.

[FIGURE 1 OMITTED]

Discussion

KAs are relatively common cutaneous neoplasms that are difficult to distinguish from well-differentiated SCCs (4). They are characterized by a rapid proliferative phase resulting in an endo-exophytic ulcerative nodule that subsequently flattens and resolves over a course of several months, leaving a fibrous scar (4,5). Histologically, KAs are characterized by a cup-shaped epidermal invagination with a keratin-filled crater and an underlying atypical squamous cell proliferation (5). The epidermal proliferation around the tumor has extension to, but not beyond, the eccrine glands (4). Architectural features such as lack of invasion, minimal anaplasia, and lack of pleomorphism distinguish this neoplasm from a SCC (4).

One theory hypothesizes that KAs and SCCs are different presentations of the same neoplastic entity (4). Both occur in sunexposed areas of light-skinned individuals, and have similar proliferative capacities and cytological appearances (3-5). The presence of the p53 protein in both SCCs and KAs also supports the view that KA is a type of malignancy (4).

An alternative hypothesis is that KAs are rapidly-forming tumors resulting from the proliferation of the infundibular portion of hair follicles (1,5). This may represent a stereotypical reaction pattern to various stimuli in view of the range of associated etiological factors (5). Several case reports have postulated inflammatory factors as contributing to the formation of KAs. Okuyama et al. reported a case in which repeated cryotherapy and mechanical trauma to one nodule of prurigo nodularis resulted in the development of a KA (1). KAs have also been reported to arise from a skin graft donor site and from a scar resulting from a previous traumatic injury (2,6). KAs have been found to be associated with mechanical trauma, contact with carcinogenic agents, and with a variety of inflammatory skin lesions such as chronic eczema, seborrheic dermatitis, and psoriasis (1). These cases support the notion that preceding traumatic events or cutaneous inflammation are the underlying cause of KAs (1). It has been found that these causes are capable of stimulating epithelial mitotic activity, which might result in the development of KAs (1).

The development of a KA in this patient appears to be related to epidermal regeneration at the surgical site. Since the KA did not occur at the site of the original tumor (squamous cell carcinoma in situ) and did not have a histologically similar pattern, it is highly unlikely that the KA represented a recurrence of the original tumor. Indeed, this case lends credence to traumatic injuries of the skin causing KAs in at least some cases. It is likely that increased mitotic activity of epidermal stem cells during the epidermal healing process results in the rapid proliferation of either a benign yet abnormal or a frankly neoplastic clone of cells that form the KA.

References

1. Okuyama R. Takahashi K. Ohi T. Tagami H. Keratoacanthoma developing in prurigo nodularis treated with cryotherapy. Dermatology 1997; 194:290-292.

2. Tamir G. Morgenstern S. Ben-Amitay D. Okon E. Hauben D. Synchronous appearance of keratoacanthomas in burn scar and skin graft donor site shortly after injury. J Am Acad Dermatol 1999; 40:870-1.

3. Manstein C. Frauenhoffer C. Besden J. Keratoacanthoma: Is it a real entity? Annals of Plastic Surgery 1998; 40:469-72.

4. Hamilton S. Dickson W. O'Brien C. Keratoacanthoma developing in a split skin graft donor site. Annals of Plastic Surgery 1997; 50:560-1.

5. LeBoit P. Can we understand keratoacanthoma? Am J Dermatopathol 2002; 24:166-8.

6. Watanabe D. Tachi N. Tomita Y. Keratoacanthoma Centrifugum Marginatum Arising from a Scar after Skin Injury. The Journal of Dermatology 1999; 26:541-543.

ARASH KIMYAI-ASADI MD, CHRISTY SHAFFER MD, VICKI J LEVINE MD, MING H JIH MD PHD

THE RONALD O. PERELMAN DEPARTMENT OF DERMATOLOGY, NEW YORK UNIVERSITY SCHOOL OF MEDICINE, NEW YORK, NEW YORK

ADDRESS FOR CORRESPONDENCE:

Christy Shaffer MD

Roger Williams Medical Center

Department of Dermatology

825 Chalkstone Avenue

Providence, RI 02908

Phone: 401-456-2104

E-mail: ksderml@yahoo.com

COPYRIGHT 2004 Journal of Drugs in Dermatology
COPYRIGHT 2004 Gale Group

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