Hypertrophic Lichen Planus Like Reactions

OBSERVATION Hypertrophic Lichen Planus–Like Reactions Combined With Infundibulocystic Hyperplasia Pathway to Neoplasia

Steven Kossard, FACD; Carol Thompson, PhD; Gary M. Duncan, FRACS

Background: Retinoids have the capacity to accelerate cystic squamous cell carcinoma. Polymerase chain reac- the involution of multiple keratoacanthomas, including tion analysis of biopsy material from 2 patients failed to unusual variants such as keratoacanthoma marginatum detect human papillomavirus. All 3 presentations pro- centrifugum and keratoacanthoma en plaque that may vided a therapeutic dilemma, but responded rapidly to persist and be associated with progressive growth and pro- acitretin treatment at a dosage of 10 to 25 mg daily, which vide difficulties in diagnosis and management. was continued for 15 to 24 months.

Observations: We describe 3 patients who had un- Conclusions: These cases illustrate an unusual reac- usual infiltrated and keratotic plaques affecting the lower tion pattern that is hypertrophic lichen planus–like but, legs or nasolabial area that persisted or recurred that may instead of evolving to classic lichen planus, progresses be related to this group of unusual keratoacanthomas. to infundibulocystic hyperplasia and the development of The 3 patients had differing clinical lesions that did not multiple keratoacanthomas or infundibulocystic squa- resemble classic keratoacanthomas, but were linked by mous cell carcinomas. Retinoids represent a therapeutic their biopsy findings of hypertrophic lichen planus–like option for this difficult clinical problem and may obvi- reaction and pseudoepitheliomatous hyperplasia with a ate repeated and extensive surgery. prominent infundibulocystic component that progressed to multiple keratoacanthomas or infundibulo- Arch Dermatol. 2004;140:1262-1267

ERATOACANTHOMAS USU- The 3 patients had differing clinical pre- ally arise as solitary lesions sentations that did not resemble classic but may occasionally pre- keratoacanthoma but were linked by their sent as multiple lesions1,2 or biopsy findings, which showed pseudoepi- as unusual variants such as theliomatous hyperplasia combined with keratoacanthoma marginatum centrifu- hypertrophic lichen planus–like areas and K 3-7 gum or keratoacanthoma en plaque. These infundibulocystic follicular hyperplasia unusual variants may persist and can be as- merging with keratoacanthoma or infun- sociated with progressive growth and pro- dibulocystic squamous cell carcinoma. In- vide difficulties in classification, particu- fundibulocystic squamous cell carcinoma may larly in reference to squamous cell be a more appropriate term for tumors that carcinomas and their treatment. Retinoids fail to fulfill the clinical and histologic fea- have been used successfully to treat all vari- tures of keratoacanthoma but share a com- ants of keratoacanthoma1-8 and appear to ac- mon path of initial follicular infundibulo- celerate their involution, possibly by pro- cystic hyperplasia. The atypical clinical From the Skin & Cancer moting differentiation. The relationship of appearance, lack of spontaneous involu- Foundation Australia, keratoacanthoma and squamous cell carci- tion, and deeply infiltrative growth of cords Darlinghurst (Dr Kossard), and noma has been a subject of debate, and even of atypical keratinocytes on biopsy are key Department of Infectious the use of newer probes capable of quanti- clues to the diagnosis of infundibulocystic Diseases, University of Sydney, tating proliferation markers and detecting squamous cell carcinoma. These infun- Sydney, New South Wales, abnormalities in tumor suppressor genes dibulocystic follicular tumors share the ca- Australia, (Dr Thompson) and and upgraded cellular oncogenes has not pacity, in some cases, to respond to acitre- Wellington Regional Plastic, 9 Maxillofacial and Burns Unit, provided an answer. tin treatment, but their identification may Hutt Hospital, Lower Hutt, We describe 3 patients who had un- be delayed because of the unusual reac- New Zealand (Dr Duncan). usual infiltrated keratotic plaques that were tion pattern dominated by hypertrophic li- The authors have no relevant progressive and may be related to this group chen planus–like lesions with infundibu- financial interest in this article. of unusual persistent keratoacanthomas. locystic hyperplasia.

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PATIENT 1 An 86-year-old woman developed a keratotic papule on the lower left pretibial area. The papule grew gradually during 6 months into a large plaque measuring 5.5ϫ4.0 cm in diameter (Figure 1A). The plaque had a violaceous color and an elevated keratotic rim. The patient had been referred to a plastic surgeon, who was reluc- tant to excise the plaque because of her poor general health. Her medications included enalapril maleate, aten- olol, diltiazem hydrochloride, and frusemide for hyper- tension and cardiac failure. The patient had previous skin cancers that had been removed from her nose and lip. General skin examination revealed evidence of long- term solar damage but no other lesions resembling lichen planus. A skin biopsy specimen from the keratotic C D rim revealed an irregularly acanthotic epidermis with prominent infundibulocystic hyperplasia outlined by lymphocytes. Hypertrophic lobules of keratinocytes demonstrating premature keratinization and focal atypia projected into the mid dermis (Figure 1B). These findings were reported as squamous cell carcinoma arising in a background of infundibulocystic pseudoepitheliomatous hyperplasia with lichenoid inflammation. Acitretin was prescribed at a dosage of 10 mg daily and was increased to 20 mg after 2 weeks. The patient was unable to tolerate this dosage, and the acitretin was reduced to 10 mg again. After 3 months at this dosage, the plaque had flattened and was no longer infiltrated. At 6 months’ follow-up, the patient had a series of lichenoid plaques resembling lichen planus on the right Figure 1. Patient 1. A, Violaceous plaque with keratotic rim on the left leg. leg (Figure 1C) corresponding to keratoses that had been B, Skin biopsy specimen demonstrating infundibulocystic hyperplasia with lichenoid inflammation and irregular lobules of keratinocytes penetrating into treated with cryotherapy by her local referring physi- the mid dermis (hematoxylin-eosin, original magnification ϫ40). cian. The plaque on the left leg had completely re- C, Violaceous lichen planus–like reaction on the right leg at sites of solved. Therapy with acitretin, 10 mg daily, was contin- cryotherapy. D, Appearance of the left leg 1 year after commencing ued, and at the 1-year follow-up, all the lichenoid lesions treatment. had cleared, with no recurrence of the plaque on the left leg (Figure 1D). mens were obtained from the left and right alae, above the upper lip, and left nasal floor. All biopsy specimens PATIENT 2 were dominated by marked pseudoepitheliomatous hyperplasia with a prominent infundibulocystic follicular A 73-year-old man, after trekking in Kathmandu (Nepal), component outlined by lichenoid inflammation. The in- developed rhinorrhea and a vegetative nodule over the fundibulocystic cavities showed buds of epithelium that left side of the columella of his nose. During the follow- projected into the surrounding tissue and showed a dis- ing month, the lesion became ulcerated and an indu- organized architecture and keratinocyte atypia. In some rated erythematous plaque developed below the nose ex- areas, the keratinocytes were associated with extensive tending to his upper lip (Figure 2A). An initial biopsy terminal keratinization, and the keratin spilled into the specimen from the nasal nodule showed pseudoepithe- dermis and was surrounded by granulomatous tissue re- liomatous hyperplasia. Cultures grew proteus organ- action. The inflammatory infiltrate included eosino- isms of doubtful significance. A subsequent biopsy speci- phils, neutrophils, plasma cells, and lymphocytes, but men from the infiltrated plaque below the nose showed there were no abscesses or suppurative granulomas. These a prominent lymphocytic infiltrate producing a lichen- changes extended to the full depth of the biopsies, which oid reaction around dilated follicular canals that were hy- measured up to 5 to 7 mm (Figure 2C). The histopatho- perplastic but lacked atypia (Figure 2B). The pathologic logic findings were reported as squamous cell carci- findings resembled lichen planopilaris, but the patient noma arising in the background of lichenoid pseudoepi- had no other lesions or history of lichen planus. The pa- theliomatous and infundibulocystic follicular hyperplasia. tient returned home to New Zealand and was examined The patient began taking acitretin, 25 mg daily, and by a plastic surgeon, who found an infiltrated plaque mea- during the next 2 months, the infiltrated nasal nodule suring 2 cm in diameter extending from the columella and adjacent plaque resolved. After 4 months of treat- to both alae and to the upper lip. Separate biopsy speci- ment, only biopsy scars were present (Figure 2D). The

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C D C D

Figure 2. Patient 2. A, Ulcerated nasal columella with infiltrated violaceous plaque extending to the upper lip. B, Skin biopsy specimen of plaque Figure 3. Patient 3. A, Hypertrophic verrucous nodules covering a skin graft revealed multiple dilated follicles outlined by prominent lymphocytic infiltrate on the left leg. B, Biopsy specimen from the left leg demonstrating marked resembling lichen planopilaris. C, Skin biopsy specimen from right nasal ala infundibulocystic hyperplasia, with irregular buds of epithelium extending to showing marked infundibulocystic hyperplasia, irregular cords, and lobules base of the specimen with lymphocytic reaction. C, Biopsy specimen from of keratinocytes penetrating through the full depth of the biopsy nodule in graft on the right leg with a central cavity and series of irregular (hematoxylin-eosin, original magnification ϫ40 [B and C]). D, Appearance lobules of keratinocytes penetrating the mid dermis with lymphocytic ϫ after 4 months of taking acitretin. inflammation (hematoxylin-eosin, original magnification 40 [B and C]). D, Appearance of the left graft site 10 months after commencing treatment with acitretin. acitretin was continued for 20 months, and the area re- mained clear of recurrent tumor a year after stopping the drug. matous hyperplasia with lichenoid inflammation. Two months later, 2 keratotic and infiltrated papules on the PATIENT 3 right calf were removed, with skin grafting. The pathologic findings were reported as representing keratoac- A 76-year-old man recalled that 30 years before consul- anthomas. During the subsequent 6 months, both grafts tation he had sustained a hot water burn to both lower developed recurrent nodules. At the time of his initial legs, which had resulted in extensive blisters that had consultation at our center, there were 2 violaceous hy- taken 5 weeks to heal. Two years before consultation, 2 perkeratotic nodules measuring 2 cm in diameter within small keratotic papules had developed on his right lower the graft on the right calf and a violaceous papule within leg that were excised by his local physician. The patho- a scar below the graft. The left skin graft was totally re- logic findings had been reported as well-differentiated placed by confluent keratotic and verrucous nodules that squamous cell carcinoma with lichenoid inflammation. were separated by fissures (Figure 3A). The skin graft Seven months later, the papules recurred, were reex- donor site was unaffected. There was no associated lymph- cised, and were reported as showing only pseudoepithe- adenopathy, and the rest of the clinical examination liomatous hyperplasia with lichenoid inflammation. One showed no evidence of lichen planus or other skin can- year before consultation, 2 infiltrated nodules devel- cers. The patient was taking prazosin hydrochloride, di- oped on his other leg. A punch biopsy specimen was re- pyridamole, and temazepam, as well as perindopril er- ported as squamous cell carcinoma with lichenoid in- bumine, which had been substituted for amlodipine flammation. He was referred to a plastic surgeon, who besylate 1 month before consultation. A biopsy speci- excised both lesions on the left calf and performed skin men taken from the verrucous keratotic plaque from the grafts. The surgical specimen showed pseudoepithelio- left graft showed multiple infundibulocystic cavities par-

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©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 tially outlined by lichenoid inflammation. These ex- sponse to skin malignancies, including nonmelanocytic tended into the deep dermis. Under the base of the cys- tumors, actinic keratoses, keratoacanthomas, and squa- tic cavities, there were irregular cords of keratinocytes mous cell carcinomas. These reactions present as lichen- that showed premature keratinization and focal nuclear oid keratoses and may resemble solitary lichen planus. atypia (Figure 3B). A biopsy specimen from the nodule In our patients, pseudoepitheliomatous hyperplasia with on the right calf showed a central cavity, under which lichenoid reactions in association with follicular infun- there were lobular clusters of keratinocytes extending into dibulocystic hyperplasia presented as hyperplastic li- the mid dermis (Figure 3C). In areas, there was an in- chen planus–like nodules or plaques. Such lesions may fundibulocystic component, and the lobules were asso- provide a pitfall in diagnosis and require multiple bi- ciated with focal lichenoid inflammation. There was opsy samples that extend into the deep tissue. In 2 of our focal nuclear atypia and a disorganized pattern of matu- patients, infiltrating cords of atypical keratinocytes were ration. The biopsy specimen of the papule below the graft present in the deep dermis and were masked by overly- and within a scar showed changes that were identical to ing lichenoid infundibulocystic follicular hyperplasia. Al- those seen with hypertrophic lichen planus. These find- though squamous cell carcinoma may develop in the set- ings were equated with squamous cell carcinoma aris- ting of classic hypertrophic lichen planus, this usually ing in the background of lichenoid pseudoepithelioma- emerges in the background of long-standing lichen pla- tous infundibulocystic hyperplasia and hypertrophic nus,12,13 in contrast to the short history and early lichen- lichen planus–like reaction. Acitretin was prescribed at oid reactions seen in our patients. a dosage of 25 mg daily, and within a month, the nod- The distinction between pseudoepitheliomatous hy- ules over both grafts were disintegrating and the infil- perplasia and squamous cell carcinoma can be problem- trative areas were resolving. The violaceous plaque be- atic. Pseudoepitheliomatous hyperplasia may merge with low the graft on the right leg had resolved. The dosage squamous cell carcinoma. The histopathologic findings of acitretin was reduced to 10 mg daily, but 4 months of pseudoepitheliomatous hyperplasia usually reveal bul- later, 2 further nodules emerged over the left graft and bous acanthotic down-growth of the epidermis and usu- the treatment regimen acitretin was again increased to ally involve the follicular infundibular canals and sweat 20 mg daily, with clearance. At the 10-month follow- ducts. The phenomenon of pseudoepitheliomatous hy- up, all areas were free of tumor, including the left graft perplasia may occur, particularly in the wake of injury (Figure 3D). The acitretin regimen was continued for 2 or surgery and as a response to different infections. These years and then discontinued, without recurrence after 6 factors were present in our patients, one of whom de- months of stopping the drug. veloped the reaction in his skin grafts and the other as a vegetative nasal nodule after trekking in Kathmandu. The POLYMERASE CHAIN REACTION ANALYSIS shin is particularly prone to injury and appears to be a FOR HUMAN PAPILLOMAVIRUS common site associated with infundibulocystic follicular reactions that can be difficult to classify. Multiple bi- Paraffin-embedded tissue was used for polymerase chain opsy specimens of the vegetative nodule failed to reveal reaction analysis for human papillomavirus (HPV) in bi- suppurative granulomas or abscesses typical of an infec- opsy specimens taken from patients 2 and 3. Sets of con- tive process, and the biopsy findings were a key to diag- sensus primers designed to amplify a wide range of nosis and management. The presence of lichenoid in- mucosal and cutaneous HPV types were applied. Ampli- flammation in addition to pseudoepitheliomatous fication of a sequence of the human ␤-globulin gene served hyperplasia was an important clue in recognizing our as a control for amplifiable DNA. The primers and am- cases. plification protocols for the detection of HPVs in this study The clinical presentations and histologic findings in have been previously described.10,11 All specimens were our patients also raised the issue of whether the tumors positive for ␤-globulin, but, despite repeated testing, none represented unusual variants of keratoacanthoma. Kera- produced positive signals with any of the HPV consen- toacanthomas have been observed in the setting of li- sus primer sets used. chen planus14,15 and have developed within skin grafts or their donor site16,17 and at sites of trauma.18 There ap- COMMENT pears to be a close relationship of some keratoacanthomas to the infundibular portion of follicles.19,20 Kerato- Despite the differing clinical presentations, these cases acanthomas often are associated with infundibular are linked by their histologic findings and response to hyperplasia and can result in squamous metaplasia of the acitretin treatment. The histopathologic findings were sweat duct apparatus. The clinical presentation of the characterized by epidermal and follicular hyperplasia pro- plaque in patient 1 shares features with keratoacan- ducing pseudoepitheliomatous features with a promi- thoma marginatum centrifugum,21,22 and in patient 3, the nent infundibulocystic component. A prominent lichen- confluent verrucous keratotic plaque over the graft may oid reaction was also a common feature and resembled be compared with keratoacanthoma en plaque.23,24 These hypertrophic lichen planus or lichen planopilaris. The are unusual keratoacanthomas, often associated with a large violaceous plaques and lichenoid patches that fol- progressive history, and they may not readily involute. lowed cryotherapy in patient 1 and the violaceous pap- This pattern differs from that of classic keratoacan- ule in the scar in patient 3 resembled lichen planus, but thoma. We prefer to classify our cases as examples of there was no evidence of lichen planus at other sites. Li- pseudoepitheliomatous hyperplasia with a prominent in- chenoid reactions are commonly seen as a host re- fundibulocystic component outlined by lichenoid

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©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 inflammation, and the emerging tumors as infundibulo- tracted course with tumor progression before the intro- cystic squamous cell carcinoma rather than keratoacan- duction of retinoid therapy. thomas. In contrast to previous cases of keratoacan- Our observations suggest that there is a subgroup thoma marginatum and keratoacanthoma en plaque,3-7 of patients who develop hypertrophic lichen planus– our patients’ initial lesions were dominated by changes like reactions with infundibulocystic follicular hyper- that resembled hypertrophic lichen planus rather than plasia that may progress to follicular-based squamous cell discrete keratoacanthomas. The term infundibulocystic carcinomas. These tumors may be related to keratoac- squamous cell carcinoma may be more appropriate for tu- anthomas, but may be more appropriately classified as mors that may not resemble keratoacanthoma clini- infundibulocystic squamous cell carcinoma. The iden- cally, have a prominent infundibulocystic component, and tification of this subset of squamous cell carcinoma in do not follow the biological course of keratoacanthoma. the setting of hypertrophic lichen planus–like reactions The frequency of detecting HPV in keratoacantho- may be important, as acitretin offers a potential alterna- mas in previous studies25-28 has varied. We were unable tive to difficult surgery and, at least in some cases, can to demonstrate the presence of HPV by polymerase chain induce tumor regression and settle the lichenoid epider- reaction analysis using several consensus HPV primer sets mal hyperplasia. on tissue extracts from 2 of our patients. There were no papilloma-related viral cytopathic changes in the bi- Accepted for publication April 27, 2004. opsy material, but these findings do not exclude the pos- Correspondence: Steven Kossard, FACD, Skin & Can- sible presence of HPV as a cofactor. cer Foundation Australia, 277 Bourke St, Darlinghurst, New All 3 of our patients provided a therapeutic di- South Wales, Australia 2010 ([email protected]). lemma, as the tumors were difficult to treat surgically. The presence of infiltrative cords or lobules of atypical REFERENCES keratinocytes in the deep dermis under the infundibulocystic pseudoepitheliomatous hyperplasia was a fea- 1. Benoldi D, Alinovi A. Multiple persistent keratoacanthomas: treatment with oral ture that made us favor the diagnosis of squamous cell etretinate. J Am Acad Dermatol. 1984;10:1035-1038. carcinoma. Even in the absence of proven squamous cell 2. Street ML, White JW Jr, Gibson LE. Multiple keratoacanthomas treated with oral carcinoma, these marked hyperplastic reactions repre- retinoids. J Am Acad Dermatol. 1990;23(pt 1):862-866. 3. Schaller M, Korting HC, Wolff H, et al. Multiple keratoacanthomas, giant kerato- sent a therapeutic challenge. Retinoids have been used acanthoma and keratoma centrifugum marginatum: development in a single pa- successfully to slow the development and reduce the num- tient and treatment with oral isotretinoin. Acta Derm Venereol. 1996;76:40-42. ber of solar keratoses and squamous cell carcinomas, par- 4. Lo Schiavo A, Pinto F, Degener AM, Bucci M, Ruocco V. Keratoacanthoma cen- ticularly in transplant patients receiving immunosup- trifugum marginatum: possible etiological role of papillomavirus and therapeutic pressive therapy.29 Retinoids have also been shown to response to etretinate [in French]. Ann Dermatol Venereol. 1996;123:660-663. 5. Cherif F, Mebezaa A, Kort R, et al. Multiple keratoacanthoma centrifugum mar- accelerate the involution of keratoacanthomas and have ginatum. Ann Dermatol Venereol. 2002;129:413-415. been useful in the management of unusual variants of 6. Ogasawara Y, Kinoshita E, Ishida T, Hamamoto Y, Fujiyama J, Muto M. A case keratoacanthoma, including keratoacanthoma margi- of multiple keratoacanthoma centrifugum marginatum: response of oral etreti- natum centrifugum and keratoacanthoma en plaque. We nate. J Am Acad Dermatol. 2003;48:282-285. 7. Kato N, Ito K, Kimura K, Shibata M. Ferguson Smith type multiple keratoacan- had previously used acitretin to successfully treat a pa- thomas and keratoacanthoma marginatum in a woman from Japan. J Am Acad tient who had hypertrophic lichen planus–like reaction Dermatol. 2003;49:741-746. in a burn scar and biopsy specimens that showed pseu- 8. Watson AB. Etretinate therapy of solar-related keratoacanthoma. Australas J Der- doepitheliomatous hyperplasia and early squamous cell matol. 1993;34:9-11. carcinoma.30 Because of the age of our patients, we chose 9. Le Boit PE. Can we understand keratoacanthoma? Am J Dermatopathol. 2002; 24:166-168. a conservative dosage of 25 mg daily of acitretin to mini- 10. de Roda Husman SM, Walboomers JMM, van den Brule AJC, Meijer CJ, Snij- mize adverse effects. We did not need to increase the dos- ders PJ. The use of general primers GP5 and GP6 elongated at their 3Ј ends with age higher than 25 mg daily, as there was response to treat- adjacent highly conserved sequences improves human papillomavirus detec- ment in the first month. One of our patients only tolerated tion by PCR. J Gen Virol. 1995;76(pt 4):1057-1062. 11. Forslund O, Antonsson A, Norden P, Stenquist B, Hansson BG. A broad range of 10 mg of acitretin daily, but even this dosage resulted in human papillomavirus types detected with a general PCR method suitable for a halt of the progression of her tumors and gradual in- analysis of cutaneous tumours and normal skin. J Gen Virol. 1999;80(pt 9): volution of all lesions. We monitored all patients care- 2437-2443. fully, as we were concerned that these tumors may have 12. Gawkrodger DJ, Stephenson TJ, Thomas SE. Squamous cell carcinoma com- progressed. Previous experience has indicated that skin plicating lichen planus: a clinico-pathological study of three cases. Dermatol- ogy. 1994;188:36-39. malignancies and keratoses may rebound if retinoids are 13. Castano E, Lopez-Rios F, Alverez-Fernandez JG, et al. Verrucous carcinoma in ceased, particularly in immunosuppressed patients. Low- association with hypertrophic lichen planus. Clin Exp Dermatol. 1997;22:23-25. ering the dosage of acitretin in one of our patients re- 14. Allen JV, Callen JP. Keratoacanthomas arising in hypertrophic lichen planus: a sulted in the reappearance of nodules in the skin graft, case report. Arch Dermatol. 1981;117:519-521. 15. Badell A, Marcoval J, Gallego I, et al. Keratoacanthoma arising in hypertrophic but these resolved again by elevating the dosage. The main lichen planus. Br J Dermatol. 2000;142:380-382. adverse effects observed in all 3 patients were those re- 16. Hamilton SA, Dickson WA, O’Brien CJ. Keratoacanthoma developing in a split lated to retinoids, namely, dry skin and hair loss. The 3 skin graft donor site. Br J Plast Surg. 1997;50:560-561. patients did not have a strong history of skin cancers and 17. Tamir G, Morgenstern S, Ben-Amitay D, Okon E, Hauben DJ. Synchronous ap- were not immunosuppressed, and the acitretin was dis- pearance of keratoacanthomas in burn scar and skin graft donor site shortly after injury. J Am Acad Dermatol. 1999;40(pt 2):870-871. continued after 15 to 24 months. Although we cannot 18. Pattee SF, Silvis NG. Keratoacanthoma developing in sites of previous trauma: a exclude the possibility that the results of therapy were report of two cases and review of the literature. J Am Acad Dermatol. 2003;48 due to spontaneous involution, each patient had a pro- (suppl):S35-S38.

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©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 19. Choonhakarn C, Ackerman AB. Keratoacanthomas: a new classification based sequences of both genital and cutaneous HPV types in a small number of kera- on morphologic findings and on anatomic site. Dermatopathol Pract Concept. toacanthomas of nonimmunosuppressed patients. Dermatology. 1999;198:122- 2001;7:7-16. 125. 20. Weedon D. Keratoacanthoma: a personal perspective. Curr Diagn Pathol. 2003; 27. Viviano E, Sorce M, Mantegna M. Solitary keratoacanthomas in immunocom- 9:259-265. petent patients: no detection of papillomavirus DNA by polymerase chain reac- 21. Peteiro MC, Caeiro JL, Toribio J. Keratoacanthoma centrifugum marginatum vs tion. New Microbiol. 2001;24:295-297. low-grade squamous cell carcinoma. Dermatologica. 1985;170:221-224. 28. Forslund O, DeAngelis PM, Beigi M, Schjolberg AR, Clausen OP. Identification 22. Chaffai M, Houman MH, Haouet S, Ben Osman A. Keratoacanthoma centrifu- of human papillomavirus in keratoacanthomas. J Cutan Pathol. 2003;30:423- gum marginatum [in French]. Ann Dermatol Venereol. 1994;121:731-733. 429. 23. Schwartz RA. Multiple persistent keratoacanthomas. Oncology. 1979;36:281-285. 29. Bravinck JN, Tieben LM, Van der Woude FJ, et al. Prevention of skin cancer and 24. Washington CV, Mikhail GR. Eruptive keratoacanthoma en plaque in an immu- reduction of keratotic skin lesions during acitretin therapy in renal transplant re- nosuppressed patient. J Dermatol Surg Oncol. 1987;13:1357-1360. cipients: a double-blind, placebo-controlled study. J Clin Oncol. 1995;13:1933- 25. Gassenmaier A, Pfister H, Hornstein OP. Human papillomavirus 25–related DNA 1938. in solitary keratoacanthoma. Arch Dermatol Res. 1986;279:73-76. 30. Kossard S, Artemi P. Acitretin for hypertrophic lichen planus–like reaction in a 26. Stockfleth E, Meinke B, Arndt R, Christophers E, Meyer T. Identification of DNA burn scar. Arch Dermatol. 2000;136:591-594.

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