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Background: Eruptive squamous atypia (ESA), which is an idiopathic, sometimes koebnerizing, proliferation of atypical but well-differentiated keratinocytes (also termed eruptive keratoacanthoma), is often misdiagnosed as cancer and managed by excisional surgery, provoking further koebnerization. A clear definition of this phenomenon and treatment outcome data are lacking., Objective: To define ESA and evaluate efficacy of intralesional (IL) 5-fluorouracil (5-FU) treatment., Methods: A retrospective cohort study examined patients with ESA that arose spontaneously or within a recent surgical scar and was treated with IL 5-FU at a tertiary academic center between January 2008 and December 2016. Complete clearance, partial clearance, and number of surgical excisions performed were tabulated., Results: Of 30 patients with 136 ESA lesions, 20 (67%) had resolution of ESA with IL 5-FU monotherapy. In all, 10 patients (33%) required additional therapy (topical 5-FU, steroids, cryotherapy, or acitretin). No IL 5-FU-treated ESA lesions required surgical excision. The number of excisional procedures decreased significantly (P = .006), with 27 patients (90%) needing fewer excisions 12 months after versus 12 months before initiation of IL 5-FU therapy. Dyspigmentation was the only adverse event., Limitations: Limitations include retrospective analysis and use of data from a single institution., Conclusion: With close clinical monitoring, IL 5-FU can be used to successfully treat ESA., (Copyright © 2018 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.)

It is not easy to reach a differential diagnosis between keratoacanthoma (KA) and squamous cell carcinoma (SCC) and furthermore there is still considerable discussion about the relationship of these 2 tumors with immunity. To facilitate such a diagnosis, we assessed the Glut-1 antibody, reported to be strongly and diffusely expressed in SCC but never assessed in KA. We studied 43 lesions of immunocompetent patients: 17 SCCs, 13 typical KAs (tKAs), and 13 atypical KAs (aKAs), with histologic features of SCC in less than 30% of the lesions. In tKA, Glut-1 stained only the basal layers of the squamous nests (basal pattern) whereas in SCC the squamous nests were randomly and diffusely stained (diffuse pattern). In aKA, a biphasic pattern was observed, with the typical KA areas showing the basal pattern and the SCC-like areas showing the diffuse pattern. Glut-1, therefore, helps to distinguish tKAs from SCCs and highlights the intermediate aKA group, supporting the hypothesis of a progression from KA to SCC. Finally, we used CD1a, CD57, CD4, CD8, CD3, and CD20 antibodies to assess whether or not the progression might be related to an in situ immunologic deficit. Significant differences were found both in CD1a+ cells, more numerous in tKA than in SCC and in CD57+ cells, more numerous in tKA than in aKA and in SCC. This suggests a local immunological failure in aKA and SCC, probably related to the action of UV rays, leading us to consider KA as a model for the study of the interaction of skin cancer and immunity.

A 45-year-old man presented with a rapidly enlarging keratotic lesion of the distal subungual right middle finger. An X-ray of the digit revealed a well-defined cup-shaped lytic lesion of the phalynx underlying the subungual nodule. The lesion resolved spontaneously with reossification of the underlying bony defect. The clinical history and X-ray is consistent with a diagnosis of spontaneously resolving subungual keratoacanthoma.

Background: Keratoacanthoma (KA) is an extraordinary entity. Once considered a benign neoplasm that resembled a highly malignant one (pseudomalignancy), it is now viewed in an opposite light as a cancer that resembles a benign neoplasm (pseudobenignity)., Objective: The goal was to delineate the malignant potential of this neoplasm based on the author's experience and a review of recent data and research and to emphasize the KA as a possible part of an autosomal dominant familial cancer syndrome, the Muir-Torre syndrome., Methods: This is a review of the literature., Results: In this work, the KA is reviewed with recent advances emphasized., Conclusion: KA is an abortive malignancy that rarely progresses into an invasive SCC. The KA may serve as a marker for the important autosomal dominant familial cancer syndrome, the Muir-Torre syndrome, as a result of a defective DNA mismatch repair gene.

We report a case of Grzybowski's generalized eruptive keratoacanthoma which demonstrates the characteristic features of this rare condition. The recurring nature of the eruption each summer supports the suggestion that UV irradiation may act as a precipitating factor in eruptive keratoacanthoma.

KA develops from a rapidly growing, firm, smooth nodule into a mature dome-shaped lesion with a central core filled with keratin that usually degenerates into an involuting keratinous mass. KAs must be differentiated from squamous cell carcinoma. Classically, KA is a benign tumor that is self-limiting. However, there is controversy concerning the aggressiveness of the tumor. Some authors believe there is no way to determine the aggressiveness of the tumors and they should be classified as low grade squamous cell carcinomas (3). Others feel that the risk of malignant transformation is not a serious consideration but misdiagnosis is, due to the histopathologic similarities (31, 33). Overall, the literature shows that solitary and giant lesions should be excised. Excisional biopsy yields a more cosmetic scar and increases the chance for an accurate biopsy diagnosis. Multiple and multinodular lesions should be excised if they have the potential for causing a mutilating deformity but are otherwise treated systematically. If a solitary or multiple lesion which is left to spontaneously resolve shows signs of aggressiveness, even with a biopsy indicating that it is a KA, it should be immediately excised. Solitary and giant KA are usually not considered to be located on the palms and soles. However, with the cases presented here, there are now a total of 4 cases in the literature. Therefore, KA should be included in the differential diagnosis when dealing with rapidly growing tumors on the plantar aspect of the foot.

Transplants of experimental keratoacanthomas induced in skin grafts which were in the growth phase of the hair follicle cycle (anagen phase) were carried out in immunocompetent and immunoincompetent receipients ("nude" mouse, nu/nu). No differences in gross graft observations were noticed. More than 80% of all keratoacanthomas disappeared postgrafting. This percentage was the same for both groups of recipients. These data are in keeping with a nonimmunological regression of experimental keratoacanthomas. A possible correlation with the hair follicle cycle is suggested.

Keratoacanthomas have many characteristics of squamous cell carcinoma and in the past were interpreted as squamous cell carcinomas. It is now known that these lesions spontaneously resolve if left untreated. In man the lesions occur on sunlight damaged areas or areas exposed to tar. Many of the experimental cancers of animals produced by topical carcinogens are keratoacanthomas. Ultraviolet light and tar are known to damage fibroblast and ground substance viscosity. It has recently been proposed that anything that decreases ground substance viscosity would encourage the spread of tumors, by weakening tissue resistance. The rapidly growing keratoacanthoma produces invasive pressure and moves into deeper, less damaged dermis. An inflammatory reaction occurs in the depth of the lesion and a very characteristic granulocytic response occurs. Granulocytes release connective tissue active peptides which stimulate fibroblast and ground substance formation. The fibroblast proliferation is followed by fibrosis and the shrinking and disappearance of the tumor. The characteristic pustule that spurts granulocytes into the depth of the tumor has been experimentally blocked by hyaluronidase and other substances that damage ground substance viscosity. Edema is essential to produce this inflammatory reaction. However, this inflammatory phenomenon occurs vigorously in keratoacanthoma. It is proposed that a keratoacanthoma is a tumor that does not produce hyaluronidase or other substances that decrease ground substance viscosity. It is a deviant cell that can only move through areas of decreased ground substance viscosity. When it reaches tissues of normal viscosity edema and an inflammatory reaction occurs.(ABSTRACT TRUNCATED AT 250 WORDS)