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Hypertrophic Lichen Planus Like Reactions

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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 pro- gressed 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. (REPRINTED) ARCH DERMATOL / VOL 140, OCT 2004 WWW.ARCHDERMATOL.COM 1262 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 REPORT OF CASES A B 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 viola- ceous 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 li- chen planus. A skin biopsy specimen from the keratotic C D rim revealed an irregularly acanthotic epidermis with prominent infundibulocystic hyperplasia outlined by lym- phocytes. Hypertrophic lobules of keratinocytes dem- onstrating premature keratinization and focal atypia pro- jected into the mid dermis (Figure 1B). These findings were reported as squamous cell carcinoma arising in a background of infundibulocystic pseudoepithelioma- tous 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 li- chenoid 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 hy- perplasia 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 (REPRINTED) ARCH DERMATOL / VOL 140, OCT 2004 WWW.ARCHDERMATOL.COM 1263 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 A B A B C D C D Figure 2. Patient 2. A, Ulcerated nasal columella with infiltrated violaceous plaque extending to the
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