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Giant verrucous porokeratosis of Mibelli mimicking psoriasis in a patient with psoriasis
DERMATOPATHOLOGY
Giant verrucous porokeratosis of Mibelli mimicking psoriasis in a patient with psoriasis Clara De Simone, MD,a Andrea Paradisi, MD,a Guido Massi, MD,b Ilaria Proietti, MD,a Angela Capponi, MD,a Pier Luigi Amerio, MD,a and Rodolfo Capizzi, MDa Rome, Italy Porokeratosis of Mibelli is a disorder of epidermal keratinization characterized by annular plaques with an atrophic center surrounded by a keratotic wall. We report a case of a giant verrucous porokeratosis of Mibelli mimicking psoriasis that developed in a patient with psoriasis and therefore went unrecognized for a long time. Histologically the lesion combined features of porokeratosis at the periphery and of psoriasis at its center, a picture recently described as ‘‘psoriasis encircled by porokeratosis.’’ The possible pathogenetic relationship between psoriasis and the development of porokeratosis is also discussed. ( J Am Acad Dermatol 2007;57:665-8.)
O
riginally described independently by Mibelli1 and Respighi2 in 1893, porokeratosis (PK) is a heterogeneous group of disorders of epidermal keratinization of uncertain etiology, characterized by annular plaques with an atrophic center surrounded by a raised keratotic wall. It may develop as a result of genetic predisposition,3 sporadically,4 or induced by local immunosuppression.5 Several clinical variants are recognized: classic PK of Mibelli, giant PK, disseminated superficial (actinic) PK, PK palmaris et plantaris disseminata, linear PK, and punctuate PK. Giant PK is a very rare form of porokeratosis. Several reports classify it as a morphologic variant of PK of Mibelli,6 but others consider it to be a distinct clinical form.7 Additional rare variants have been described, including a form affecting the buttocks with verrucous lesions that clinically mimics psoriasis.8 Whatever the variant, the disorder is always associated with aberrant keratinocyte differentiation that manifests histologically as a stack of parakeratin termed the ‘‘cornoid lamella.’’ PK is also considered a premalignant condition, with reports of malignant transformation into skin tumors ranging from 7.5%9 to 11.6%.10 An association with other conditions, especially immunosuppression, has also been described.11 Our patient presented
From the Departments of Dermatology and Venereologya and of Anatomic Pathology,b Universita` Cattolica del Sacro Cuore. Funding sources: None. Conflicts of interest: None declared. Reprints not available from the authors. Correspondence to: Andrea Paradisi, MD, Department of Dermatology, Policlinico A. Gemelli, Universita` Cattolica del Sacro Cuore, Largo Gemelli 8 - 00168 Rome, Italy. E-mail: [email protected]. 0190-9622/$32.00 ª 2007 by the American Academy of Dermatology, Inc. doi:10.1016/j.jaad.2007.03.020
with giant verrucous PK of Mibelli, which clinically resembled plaque psoriasis. This condition was not recognized until the plaque persisted after widespread plaques of psoriasis had resolved after aggressive therapy.
CASE REPORT A 73-year-old Caucasian woman presented with a 55-year history of generalized plaque-type psoriasis (Fig 1). She had a family history of psoriasis and suffered from essential hypercholesterolemia. Her general health was otherwise unremarkable. The patient had received several treatments for psoriasis including topical (clobetasol propionate, coal tar, calcipotriene, tazarotene) and systemic therapies (cyclosporine, acitretin, efalizumab, and etanercept). Psoralens and ultraviolet A therapy had never been performed. The treatments cleared all lesions except for a large pruritic plaque in the lumbar region (Fig 2). The lesion was a well-demarcated, scaly, redbrown, verrucous plaque (12 3 7 cm in diameter) with hyperpigmented raised borders. Two 4-mm punch biopsy specimens were collected, one in the middle of the plaque and one from the edge. During histology examination, prominent cornoid lamellae were detected (Fig 3) on the border of the surgical specimen, at the level of the clinically apparent keratotic ring. Dyskeratotic keratinocytes in the spinous layer were observed close to the cornoid lamella; the basal layer was vacuolated. The granular layer was absent or disrupted. All these findings are typical of PK of Mibelli. The histologic features in the center of the lesion were more intriguing. Fairly uniform epidermal hyperplasia was associated with elongated rete ridges forming a comb-like pattern (Figs 4 and 5). The 665
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Fig 1. Generalized plaque-type psoriasis. Note large verrucous keratotic plaque at right side of photograph.
Fig 2. Well-demarcated, scaly, red-brown, verrucous plaque (11 3 6 cm in diameter) with hyperpigmented raised borders resistant to therapy.
Fig 3. Characteristic cornoid lamella arising from the epidermis and leaning toward center of the lesion. On the right of the lamella, note basketweave appearance of the horny layer of normal epidermis. Vacuolar alteration and dyskeratotic cells are seen in the epidermis beneath the cornoid lamella. (Hematoxylin-eosin stain; original magnification 333.)
suprapapillary plate was focally thinned. The epidermal granular layer was absent and the massive horny layer was parakeratotic. The PK was in fine, discrete, delicate scales, desquamating from the
Fig 4. Epidermal psoriasiform hyperplasia with elongated rete ridges and thinned suprapapillary plates in center of lesion. Horny layer is thickened and parakeratotic. (Hematoxylin-eosin stain; original magnification: 366.)
Fig 5. Parakeratotic scales are discrete and appear as thin flakes, as in psoriasis. (Hematoxylin-eosin stain; original magnifications: 333.)
skin. Remarkable alterations were also found in the dermis, in particular, club-shaped dermal papillae containing tortuous capillary vessels engulfed with erythrocytes. Histopathologic examination confirmed classic cornoid lamellae at the periphery of the entire lesion and psoriasiform hyperplasia at the center of the plaque. All these findings, although not specific, are consistent with psoriasis. Because the lesion caused discomfort and enlarged over time, the patient accepted a radical surgical procedure. No clinical evidence of PK was apparent in the area of excision at 9 months. The lesion could be designated as PK of Mibelli combined with features of psoriasis (in a psoriatic patient). This unique picture was recently described by other authors as ‘‘psoriasis encircled by porokeratosis.’’12
DISCUSSION Development of PK in association with psoriasis, although rare, is not wholly surprising. Indeed, Hivnor et al13 recently demonstrated that gene
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expression profiling of the cornoid lamella in PK had similarities with psoriasis. In that study of porokeratosis messenger RNA of the hyperproliferative keratins (keratins 16, 6A, 6B, and 17), specific members of S-100 calcium-binding proteins (A7: psoriasin 1, A8: calgranulin A, A9: calgranulin B, and A11: calgizarin), and gap junction proteins (connexin 26 and 30) were significantly up-regulated similar to the pattern seen in psoriasis. These findings were confirmed by K16, anti-S-100 A8 and A9, and connexin 26 immunohistochemistry. Nonetheless, a combination of giant verrucous PK with psoriatic histologic features in the same lesion has never, to our knowledge, been reported in the English-language literature. Yazkan et al12 recently proposed a classification of PK associated with psoriasis into 3 groups. The first includes cases of PK that mimic psoriasis, where verrucous porokeratotic plaques are usually localized to the natal cleft; this appears to be a distinct clinical entity, hence the name ‘‘porokeratosis ptychotropica.’’14 The second group includes patients with PK who also have plaque psoriasis. The psoriasiform changes at the center of the plaque of PK may be a reflection of the isomorphic response phenomenon (Koebner). Not surprisingly, correct diagnosis can be difficult in these patients.15 The third group consists of patients with psoriasis and disseminated superficial actinic porokeratosis induced by therapeutic phototherapy or photochemotherapy.5,16 The small, multiple lesions attenuate or become less prominent after discontinuation of the therapy. Our patient had a single large lesion, with features of a gigantic Mibelli variant of PK and had never been treated with phototherapy. Porokeratotic lesions interspersed among and mimicking psoriatic lesions may go undetected, as indeed happened to our patient, whose giant PK became clinically apparent only after treatment cleared the psoriatic lesions. The porokeratotic lesion of our patient might conceivably have evolved from local immunosuppression caused by prolonged application of topical corticosteroids.12 Over the past two decades several cases of PK have been reported during immunodeficiency associated with organ transplantation, hematopoietic malignancies, lymphoma, HIV infection, use of immunosuppressive drugs, or chemotherapy,17 high doses of corticosteroids,18 and also occurring during local immunosuppression caused by ultraviolet light.5 Many therapies have been applied to treat solitary giant PK lesions, including surgical resection, cryosurgery,19 electrocautery, carbon dioxide laser ablation,20 keratolytics, oral retinoids,21 topical
5-fluorouracil,22 corticosteroids, and, recently, topical imiquimod.23 Treatment selection depends on lesion size and location, functional and aesthetic requirements, and patient condition. Our patient was treated by surgical excision of the lesion, and no recurrence was detected after 9 months. To sum up, the large lumbar lesion of our patient combined features of PK at the periphery (cornoid lamella and corresponding focal vacuolar changes and dyskeratosis) and of psoriasis at its center (regular psoriasiform epidermal hyperplasia and fine parakeratotic scaling). The latter, peculiar feature is probably the result of a sort of Koebner phenomenon (ie, a psoriasis-like alteration induced by PK of Mibelli) in a psoriatic patient. It is worth noting that a biopsy specimen from the center of the lesion would have given a misleading result consistent with psoriasis, whereas Mibelli’s variant of PK is a precancerous process and requires specific therapy. REFERENCES 1. Mibelli V. Contributo allo studio della ipercheratosi dei canali sudoriferi (porokeratosis). G Ital Mal Veneree Pelle 1893;28: 313-35. 2. Respighi E. Di una ipercheratosi non ancora descritta. G Ital Mal Veneree Pelle 1893;28:356-86. 3. Anderson DE, Chernosky ME. Disseminated superficial actinic porokeratosis. Genetic aspects. Arch Dermatol 1969;99:408-12. 4. Schamroth JM, Zlotogorsky A, Gilead L. Porokeratosis of Mibelli: overview and review of the literature. Acta Derm Venereol Suppl (Stockh) 1997;77:207-13. 5. Cockerell CJ. Induction of disseminated superficial actinic porokeratosis by phototherapy for psoriasis. J Am Acad Dermatol 1991;24:301-2. 6. Gotz A, Kopera D, Wach F, Hohenleutner U, Landthaler M. [Porokeratosis Mibelli gigantea: case report and literature review.] Hautarzt 1999;50:435-8. German. 7. Lucker GP, Steijlen PM. The coexistence of linear and giant porokeratosis associated with Bowen’s disease. Dermatology 1994;189:78-80. 8. Wallner J, Fitzpatrick J, Brice S. Verrucous porokeratosis of Mibelli on the buttock mimicking psoriasis. Cutis 2003;72: 391-3. 9. Otsuka F, Someya T, Ishibashi Y. Porokeratosis and malignant skin tumors. Cancer Res Clin Oncol 1991;117:55-60. 10. Sasson M, Krain AD. Porokeratosis and cutaneous malignancy. A review. Dermatol Surg 1996;22:339-42. 11. Bencini PL, Tarantino A, Grimalt R, Ponticelli C, Caputo R. Porokeratosis and immunosuppression. Br J Dermatol 1995; 132:74-8. 12. Yazkan F, Turk BG, Dereli T, Kazandi AC. Porokeratosis of Mibelli induced by topical corticosteroid. J Cutan Pathol 2006;33:516-8. 13. Hivnor C, Williams N, Singh F, VanVoorhees A, Dzubow L, Baldwin D, Seykora J. Gene expression profiling of porokeratosis demonstrates similarities with psoriasis. J Cutan Pathol 2004;31:657-64. 14. Lucker GP, Happle R, Steijlen PM. An unusual case of porokeratosis involving the natal cleft: porokeratosis ptychotropica? Br J Dermatol 1995;132:150.
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15. Beer WE, Smith NP. Hyperkeratotic porokeratosis (Mibelli) with psoriasis: response to an aromatic retinoid. Clin Exp Dermatol 1984;9:509. 16. Hazen PG, Carney JF, Walker AE, Stewart JJ, Engstrom CW. Disseminated superficial actinic porokeratosis: appearance associated with photochemotherapy for psoriasis. J Am Acad Dermatol 1985;12:1077-8. 17. Wilkinson SM, Cartwright PH, English JS. Porokeratosis of Mibelli and immunosuppression. Clin Exp Dermatol 1991;16:61. 18. Feuerman EJ, Sandbank M. Disseminated superficial porokeratosis in patients with pemphigus vulgaris treated with steroids. Acta Derm Venereol Suppl (Stockh) 1979;59:59.
19. Dereli T, Ozyurt S, Ozturk G. Porokeratosis of Mibelli: successful treatment with cryosurgery. J Dermatol 2004;31:223-7. 20. Barnett JH. Linear porokeratosis: treatment with carbon dioxide laser. J Am Acad Dermatol 1986;14:902-4. 21. Scott OLS. Porokeratosis of Mibelli with squamous cell carcinoma. Br J Dermatol 1983;109:74. 22. McDonald SG, Peterka ES. Porokeratosis (Mibelli): treatment with topical 5-fluorouracil. J Am Acad Dermatol 1983;8: 107-10. 23. Agarwal S, Berth-Jones J. Porokeratosis of Mibelli: successful treatment with 5% imiquimod cream. Br J Dermatol 2002; 146:331-4.
Giant verrucous porokeratosis of Mibelli mimicking psoriasis in a patient with psoriasis Clara De Simone, MD,a Andrea Paradisi, MD,a Guido Massi, MD,b Ilaria Proietti, MD,a Angela Capponi, MD,a Pier Luigi Amerio, MD,a and Rodolfo Capizzi, MDa Rome, Italy Porokeratosis of Mibelli is a disorder of epidermal keratinization characterized by annular plaques with an atrophic center surrounded by a keratotic wall. We report a case of a giant verrucous porokeratosis of Mibelli mimicking psoriasis that developed in a patient with psoriasis and therefore went unrecognized for a long time. Histologically the lesion combined features of porokeratosis at the periphery and of psoriasis at its center, a picture recently described as ‘‘psoriasis encircled by porokeratosis.’’ The possible pathogenetic relationship between psoriasis and the development of porokeratosis is also discussed. ( J Am Acad Dermatol 2007;57:665-8.)
O
riginally described independently by Mibelli1 and Respighi2 in 1893, porokeratosis (PK) is a heterogeneous group of disorders of epidermal keratinization of uncertain etiology, characterized by annular plaques with an atrophic center surrounded by a raised keratotic wall. It may develop as a result of genetic predisposition,3 sporadically,4 or induced by local immunosuppression.5 Several clinical variants are recognized: classic PK of Mibelli, giant PK, disseminated superficial (actinic) PK, PK palmaris et plantaris disseminata, linear PK, and punctuate PK. Giant PK is a very rare form of porokeratosis. Several reports classify it as a morphologic variant of PK of Mibelli,6 but others consider it to be a distinct clinical form.7 Additional rare variants have been described, including a form affecting the buttocks with verrucous lesions that clinically mimics psoriasis.8 Whatever the variant, the disorder is always associated with aberrant keratinocyte differentiation that manifests histologically as a stack of parakeratin termed the ‘‘cornoid lamella.’’ PK is also considered a premalignant condition, with reports of malignant transformation into skin tumors ranging from 7.5%9 to 11.6%.10 An association with other conditions, especially immunosuppression, has also been described.11 Our patient presented
From the Departments of Dermatology and Venereologya and of Anatomic Pathology,b Universita` Cattolica del Sacro Cuore. Funding sources: None. Conflicts of interest: None declared. Reprints not available from the authors. Correspondence to: Andrea Paradisi, MD, Department of Dermatology, Policlinico A. Gemelli, Universita` Cattolica del Sacro Cuore, Largo Gemelli 8 - 00168 Rome, Italy. E-mail: [email protected]. 0190-9622/$32.00 ª 2007 by the American Academy of Dermatology, Inc. doi:10.1016/j.jaad.2007.03.020
with giant verrucous PK of Mibelli, which clinically resembled plaque psoriasis. This condition was not recognized until the plaque persisted after widespread plaques of psoriasis had resolved after aggressive therapy.
CASE REPORT A 73-year-old Caucasian woman presented with a 55-year history of generalized plaque-type psoriasis (Fig 1). She had a family history of psoriasis and suffered from essential hypercholesterolemia. Her general health was otherwise unremarkable. The patient had received several treatments for psoriasis including topical (clobetasol propionate, coal tar, calcipotriene, tazarotene) and systemic therapies (cyclosporine, acitretin, efalizumab, and etanercept). Psoralens and ultraviolet A therapy had never been performed. The treatments cleared all lesions except for a large pruritic plaque in the lumbar region (Fig 2). The lesion was a well-demarcated, scaly, redbrown, verrucous plaque (12 3 7 cm in diameter) with hyperpigmented raised borders. Two 4-mm punch biopsy specimens were collected, one in the middle of the plaque and one from the edge. During histology examination, prominent cornoid lamellae were detected (Fig 3) on the border of the surgical specimen, at the level of the clinically apparent keratotic ring. Dyskeratotic keratinocytes in the spinous layer were observed close to the cornoid lamella; the basal layer was vacuolated. The granular layer was absent or disrupted. All these findings are typical of PK of Mibelli. The histologic features in the center of the lesion were more intriguing. Fairly uniform epidermal hyperplasia was associated with elongated rete ridges forming a comb-like pattern (Figs 4 and 5). The 665
666 De Simone et al
J AM ACAD DERMATOL OCTOBER 2007
Fig 1. Generalized plaque-type psoriasis. Note large verrucous keratotic plaque at right side of photograph.
Fig 2. Well-demarcated, scaly, red-brown, verrucous plaque (11 3 6 cm in diameter) with hyperpigmented raised borders resistant to therapy.
Fig 3. Characteristic cornoid lamella arising from the epidermis and leaning toward center of the lesion. On the right of the lamella, note basketweave appearance of the horny layer of normal epidermis. Vacuolar alteration and dyskeratotic cells are seen in the epidermis beneath the cornoid lamella. (Hematoxylin-eosin stain; original magnification 333.)
suprapapillary plate was focally thinned. The epidermal granular layer was absent and the massive horny layer was parakeratotic. The PK was in fine, discrete, delicate scales, desquamating from the
Fig 4. Epidermal psoriasiform hyperplasia with elongated rete ridges and thinned suprapapillary plates in center of lesion. Horny layer is thickened and parakeratotic. (Hematoxylin-eosin stain; original magnification: 366.)
Fig 5. Parakeratotic scales are discrete and appear as thin flakes, as in psoriasis. (Hematoxylin-eosin stain; original magnifications: 333.)
skin. Remarkable alterations were also found in the dermis, in particular, club-shaped dermal papillae containing tortuous capillary vessels engulfed with erythrocytes. Histopathologic examination confirmed classic cornoid lamellae at the periphery of the entire lesion and psoriasiform hyperplasia at the center of the plaque. All these findings, although not specific, are consistent with psoriasis. Because the lesion caused discomfort and enlarged over time, the patient accepted a radical surgical procedure. No clinical evidence of PK was apparent in the area of excision at 9 months. The lesion could be designated as PK of Mibelli combined with features of psoriasis (in a psoriatic patient). This unique picture was recently described by other authors as ‘‘psoriasis encircled by porokeratosis.’’12
DISCUSSION Development of PK in association with psoriasis, although rare, is not wholly surprising. Indeed, Hivnor et al13 recently demonstrated that gene
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expression profiling of the cornoid lamella in PK had similarities with psoriasis. In that study of porokeratosis messenger RNA of the hyperproliferative keratins (keratins 16, 6A, 6B, and 17), specific members of S-100 calcium-binding proteins (A7: psoriasin 1, A8: calgranulin A, A9: calgranulin B, and A11: calgizarin), and gap junction proteins (connexin 26 and 30) were significantly up-regulated similar to the pattern seen in psoriasis. These findings were confirmed by K16, anti-S-100 A8 and A9, and connexin 26 immunohistochemistry. Nonetheless, a combination of giant verrucous PK with psoriatic histologic features in the same lesion has never, to our knowledge, been reported in the English-language literature. Yazkan et al12 recently proposed a classification of PK associated with psoriasis into 3 groups. The first includes cases of PK that mimic psoriasis, where verrucous porokeratotic plaques are usually localized to the natal cleft; this appears to be a distinct clinical entity, hence the name ‘‘porokeratosis ptychotropica.’’14 The second group includes patients with PK who also have plaque psoriasis. The psoriasiform changes at the center of the plaque of PK may be a reflection of the isomorphic response phenomenon (Koebner). Not surprisingly, correct diagnosis can be difficult in these patients.15 The third group consists of patients with psoriasis and disseminated superficial actinic porokeratosis induced by therapeutic phototherapy or photochemotherapy.5,16 The small, multiple lesions attenuate or become less prominent after discontinuation of the therapy. Our patient had a single large lesion, with features of a gigantic Mibelli variant of PK and had never been treated with phototherapy. Porokeratotic lesions interspersed among and mimicking psoriatic lesions may go undetected, as indeed happened to our patient, whose giant PK became clinically apparent only after treatment cleared the psoriatic lesions. The porokeratotic lesion of our patient might conceivably have evolved from local immunosuppression caused by prolonged application of topical corticosteroids.12 Over the past two decades several cases of PK have been reported during immunodeficiency associated with organ transplantation, hematopoietic malignancies, lymphoma, HIV infection, use of immunosuppressive drugs, or chemotherapy,17 high doses of corticosteroids,18 and also occurring during local immunosuppression caused by ultraviolet light.5 Many therapies have been applied to treat solitary giant PK lesions, including surgical resection, cryosurgery,19 electrocautery, carbon dioxide laser ablation,20 keratolytics, oral retinoids,21 topical
5-fluorouracil,22 corticosteroids, and, recently, topical imiquimod.23 Treatment selection depends on lesion size and location, functional and aesthetic requirements, and patient condition. Our patient was treated by surgical excision of the lesion, and no recurrence was detected after 9 months. To sum up, the large lumbar lesion of our patient combined features of PK at the periphery (cornoid lamella and corresponding focal vacuolar changes and dyskeratosis) and of psoriasis at its center (regular psoriasiform epidermal hyperplasia and fine parakeratotic scaling). The latter, peculiar feature is probably the result of a sort of Koebner phenomenon (ie, a psoriasis-like alteration induced by PK of Mibelli) in a psoriatic patient. It is worth noting that a biopsy specimen from the center of the lesion would have given a misleading result consistent with psoriasis, whereas Mibelli’s variant of PK is a precancerous process and requires specific therapy. REFERENCES 1. Mibelli V. Contributo allo studio della ipercheratosi dei canali sudoriferi (porokeratosis). G Ital Mal Veneree Pelle 1893;28: 313-35. 2. Respighi E. Di una ipercheratosi non ancora descritta. G Ital Mal Veneree Pelle 1893;28:356-86. 3. Anderson DE, Chernosky ME. Disseminated superficial actinic porokeratosis. Genetic aspects. Arch Dermatol 1969;99:408-12. 4. Schamroth JM, Zlotogorsky A, Gilead L. Porokeratosis of Mibelli: overview and review of the literature. Acta Derm Venereol Suppl (Stockh) 1997;77:207-13. 5. Cockerell CJ. Induction of disseminated superficial actinic porokeratosis by phototherapy for psoriasis. J Am Acad Dermatol 1991;24:301-2. 6. Gotz A, Kopera D, Wach F, Hohenleutner U, Landthaler M. [Porokeratosis Mibelli gigantea: case report and literature review.] Hautarzt 1999;50:435-8. German. 7. Lucker GP, Steijlen PM. The coexistence of linear and giant porokeratosis associated with Bowen’s disease. Dermatology 1994;189:78-80. 8. Wallner J, Fitzpatrick J, Brice S. Verrucous porokeratosis of Mibelli on the buttock mimicking psoriasis. Cutis 2003;72: 391-3. 9. Otsuka F, Someya T, Ishibashi Y. Porokeratosis and malignant skin tumors. Cancer Res Clin Oncol 1991;117:55-60. 10. Sasson M, Krain AD. Porokeratosis and cutaneous malignancy. A review. Dermatol Surg 1996;22:339-42. 11. Bencini PL, Tarantino A, Grimalt R, Ponticelli C, Caputo R. Porokeratosis and immunosuppression. Br J Dermatol 1995; 132:74-8. 12. Yazkan F, Turk BG, Dereli T, Kazandi AC. Porokeratosis of Mibelli induced by topical corticosteroid. J Cutan Pathol 2006;33:516-8. 13. Hivnor C, Williams N, Singh F, VanVoorhees A, Dzubow L, Baldwin D, Seykora J. Gene expression profiling of porokeratosis demonstrates similarities with psoriasis. J Cutan Pathol 2004;31:657-64. 14. Lucker GP, Happle R, Steijlen PM. An unusual case of porokeratosis involving the natal cleft: porokeratosis ptychotropica? Br J Dermatol 1995;132:150.
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15. Beer WE, Smith NP. Hyperkeratotic porokeratosis (Mibelli) with psoriasis: response to an aromatic retinoid. Clin Exp Dermatol 1984;9:509. 16. Hazen PG, Carney JF, Walker AE, Stewart JJ, Engstrom CW. Disseminated superficial actinic porokeratosis: appearance associated with photochemotherapy for psoriasis. J Am Acad Dermatol 1985;12:1077-8. 17. Wilkinson SM, Cartwright PH, English JS. Porokeratosis of Mibelli and immunosuppression. Clin Exp Dermatol 1991;16:61. 18. Feuerman EJ, Sandbank M. Disseminated superficial porokeratosis in patients with pemphigus vulgaris treated with steroids. Acta Derm Venereol Suppl (Stockh) 1979;59:59.
19. Dereli T, Ozyurt S, Ozturk G. Porokeratosis of Mibelli: successful treatment with cryosurgery. J Dermatol 2004;31:223-7. 20. Barnett JH. Linear porokeratosis: treatment with carbon dioxide laser. J Am Acad Dermatol 1986;14:902-4. 21. Scott OLS. Porokeratosis of Mibelli with squamous cell carcinoma. Br J Dermatol 1983;109:74. 22. McDonald SG, Peterka ES. Porokeratosis (Mibelli): treatment with topical 5-fluorouracil. J Am Acad Dermatol 1983;8: 107-10. 23. Agarwal S, Berth-Jones J. Porokeratosis of Mibelli: successful treatment with 5% imiquimod cream. Br J Dermatol 2002; 146:331-4.