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Porokeratosis is a clonal disorder of keratinization characterized by one or more atrophic patches surrounded by a clinically and histologically distinctive hyperkeratotic ridgelike border called the cornoid lamella. Historically, porokeratosis is a misnomer that was erroneously coined on the assumptions that cornoid lamellae emerged from pores of the sweat glands. [1] Multiple clinical variants of porokeratosis are recognized. Malignancies, typically squamous cell carcinomas, may develop within lesions of porokeratosis.

The most common forms of porokeratosis are as follows:

A patient may develop more than one type of porokeratosis simultaneously or consecutively. [2]

Less commonly reported clinical entities that share the histopathologic characteristic of cornoid lamellation include the following:

Clonal proliferation of atypical keratinocytes showing abnormal terminal keratinocyte differentiation leads to the formation of the cornoid lamella. Cornoid lamellation is typically seen in porokeratosis, where it corresponds to the threadlike scale present at the lesional border. [1] This expands peripherally and forms the raised boundary between abnormal and normal keratinocytes. The atypical keratinocytes show abnormal differentiation but do not show an increased rate of proliferation. [11, 12]

It is not known what triggers this process, and more than one causative factor may be involved. Several risk factors for the development of porokeratosis have been identified, including genetic inheritance, ultraviolet radiation, and immunosuppression.

Inherited or sporadic genetic defects, possibly creating a change in immune function and/or keratinocyte function, are thought to be responsible for several forms of porokeratosis. Familial cases of all forms of porokeratosis have been reported and appear to have an autosomal dominant inheritance pattern with incomplete penetrance. Several chromosomal loci have been identified for disseminated superficial actinic porokeratosis (DSAP), disseminated superficial porokeratosis (DSP), and porokeratosis palmaris et plantaris disseminata (PPPD). [13, 14, 15, 16, 17, 18, 19] The focal variants of porokeratosis (porokeratosis of Mibelli [PM] and linear porokeratosis) may occur through mosaicism, in which somatic mutations cause focal loss of heterozygosity. [20] Genetic mutations in the SART3 and MVK genes have been found in DSAP pedigrees.

A somatic mutation in the GJB2 mutation associated with keratosis-ichthyosis-deafness syndrome was found to cause porokeratotic eccrine ostial and dermal duct nevus. [21]

Natural or artificial ultraviolet radiation, electron beam therapy, and extensive radiation therapy are well-established trigger factors for DSAP and PM. Sun exposure in genetically susceptible individuals is thought to cause DSAP, although the sparing of facial skin in most patients is unexplained.

Immunosuppression associated with porokeratosis may be secondary to a disease process or medications. Diseases reported in association with porokeratosis include HIV infection, [22] diabetes mellitus, [23] liver disease, [24] and hematologic or solid organ malignancy. [25, 26] Immunomodulating drugs used to treat autoimmune diseases or to prevent organ transplant rejection may also trigger porokeratosis. [27, 28, 29, 30, 31, 32, 33, 34, 35] Localized cutaneous immunosuppression due to long-term application of a potent topical steroid was reported to induce PM. [36] The incidence of porokeratosis in organ transplant recipients has been reported to be anywhere from 1-11%. [28, 31]

Immunosuppression may induce new lesions or cause preexisting lesions to flare. New lesions of porokeratosis have occurred as quickly as 4 months after initiation of immunosuppressive therapy, or as long as 14 years [31, 33] and may resolve following cessation of immunosuppressive therapy. [34, 35]

Trauma, such as a burn, may also trigger porokeratosis. [37]

Risk factors for porokeratosis include genetic inheritance, ultraviolet light exposure, and immunosuppression. One study found that approximately 10% of patients who had undergone renal transplantation developed porokeratosis. [28]

Autosomal dominant inheritance and immunosuppression are the usual causes. Porokeratosis of Mibelli (PM) has been seen following radiation therapy, at burn wounds, and at hemodialysis sites.

Sun exposure and/or artificial ultraviolet radiation exposure in a patient who is genetically predisposed causes disseminated superficial actinic porokeratosis (DSAP). Exacerbations have been reported following prolonged sun exposure, repeated tanning bed exposure, electron beam radiation therapy, and therapeutic phototherapy or photochemotherapy for psoriasis. Drug-induced photosensitivity may play a role. Protection from ultraviolet radiation may lead to spontaneous resolution. Additionally, immunosuppression predisposes patients to both DSAP and nonactinic disseminated superficial porokeratosis (DSP).

No definite inheritance pattern has been established. Loss of heterozygosity has been proposed as a genetic mechanism and may explain the higher risk of malignant degeneration seen in linear porokeratosis in comparison to other forms of porokeratosis.

Familial porokeratosis palmaris et plantaris disseminata (PPPD) is transmitted in an autosomal dominant mode with variable penetrance. Acquired PPPD may be caused by immunosuppression, or it may be a cutaneous marker of internal malignancy.

This condition has no unique inheritance pattern and is usually associated with other forms of porokeratosis.

A case report on hyperkeratotic porokeratosis describes hepatitis C virus (HCV) infection as a link between the immunosuppressed state and development of acquired porokeratosis. A rare case of a hyperkeratotic variant has been described in a patient with known HIV and HCV infections and a coexisting therapy-related immunosuppressed state. [38]

Disseminated superficial actinic porokeratosis (DSAP) and porokeratosis of Mibelli (PM) are the most commonly seen variants. The other forms of porokeratosis are rare.

Porokeratosis most commonly occurs in fair-skinned individuals. Porokeratosis is rare in darker-skinned populations.

PM and porokeratosis palmaris et plantaris disseminata (PPPD) affect men twice as often as women.

DSAP is twice as likely to develop in women compared with men. [33]

Linear porokeratosis is seen with equal incidence in men and women.

PPPD and linear porokeratosis may be seen at any age, from birth to adulthood.

PM usually develops in childhood.

Disseminated superficial porokeratosis (DSP) generally develops in the third or fourth decade of life.

The prognosis is generally excellent. This is especially true for disseminated superficial porokeratosis (DSP).

Large lesions of porokeratosis, linear porokeratosis, or porokeratosis in an immunocompromised patients should be monitored carefully for the development of cutaneous malignancies within the porokeratosis lesions. Malignant transformation can occur in about 7.5% of patients. [39, 40, 41] Lesions that are large, long-standing, or linear have the greatest risk of developing an associated malignancy. [42] Chromosomal instability and reduced immune surveillance with overexpression of p53 are hypothesized to play a role in the development of cutaneous malignancies within porokeratosis. [43, 44, 45, 46, 47]

Porokeratosis of Mibelli (PM) circumferentially involving the digits may induce pseudoainhum. Most lesions are asymptomatic. Ulcerative lesions have been described. Giant PM in a facial or acral location may cause destruction of underlying soft tissue or pseudoainhum with amputation. [48]

Very rarely, porokeratosis-associated squamous cell carcinomas may metastasize and cause death. [49, 50]

Patients must practice strict sun precautions. These measures include wearing protective clothing; applying sunblock; avoiding exposure to midday sunlight; and discontinuing exposure to artificial ultraviolet light, such as tanning beds and therapeutic phototherapy.

Consideration for vitamin D3 supplementation should be made given the need for careful sun avoidance and protection.

Patients must periodically examine their skin for lesions suggestive of malignancy. A qualified physician should promptly evaluate any change in a porokeratosis lesion.

Family members should be examined for porokeratosis if familial porokeratosis is suspected.

Biswas A. Cornoid lamellation revisited: apropos of porokeratosis with emphasis on unusual clinicopathological variants. Am J Dermatopathol. 2015 Feb. 37 (2):145-55. [Medline].

Ma Y, Li C, Wu J, Cui P, Lin L, Feng S. Coexistence of porokeratosis ptychotropica with porokeratosis of Mibelli in a Chinese man. Postepy Dermatol Alergol. 2015 Aug. 32 (4):307-9. [Medline].

Lanka P, Lanka LR, Manivachagam D. Punctate Porokeratosis Palmaris et Plantaris. Indian J Dermatol. 2015 May-Jun. 60 (3):284-6. [Medline].

Wallner JS, Fitzpatrick JE, Brice SL. Verrucous porokeratosis of Mibelli on the buttocks mimicking psoriasis. Cutis. 2003 Nov. 72(5):391-3. [Medline].

Walsh SN, Hurt MA, Santa Cruz DJ. Porokeratoma. Am J Surg Pathol. 2007 Dec. 31(12):1897-901. [Medline].

Goddard DS, Rogers M, Frieden IJ, et al. Widespread porokeratotic adnexal ostial nevus: clinical features and proposal of a new name unifying porokeratotic eccrine ostial and dermal duct nevus and porokeratotic eccrine and hair follicle nevus. J Am Acad Dermatol. 2009 Dec. 61(6):1060.e1-14. [Medline].

Kanzaki T, Miwa N, Kobayashi T, Ogawa S. Eruptive pruritic papular porokeratosis. J Dermatol. 1992 Feb. 19(2):109-12. [Medline].

Kanekura T, Yoshii N. Eruptive pruritic papular porokeratosis: a pruritic variant of porokeratosis. J Dermatol. 2006 Nov. 33(11):813-6. [Medline].

Tan TS, Tallon B. Pigmented Porokeratosis. A Further Variant?. Am J Dermatopathol. 2016 Mar. 38 (3):218-21. [Medline].

Trikha R, Wile A, King J, Ward KH, Brodell RT. Punctate follicular porokeratosis: clinical and pathologic features. Am J Dermatopathol. 2015 Nov. 37 (11):e134-6. [Medline].

Fernandez-Flores A. Small lesions of porokeratosis show a normal proliferation rate with MIB-1. Acta Dermatovenerol Alp Panonica Adriat. 2008 Mar. 17(1):22-5. [Medline].

Kamata Y, Maejima H, Watarai A, Saito N, Katsuoka K, Takeda A. Expression of bleomycin hydrolase in keratinization disorders. Arch Dermatol Res. 2012 Jan. 304(1):31-8. [Medline].

Murase J, Gilliam AC. Disseminated superficial actinic porokeratosis co-existing with linear and verrucous porokeratosis in an elderly woman: Update on the genetics and clinical expression of porokeratosis. J Am Acad Dermatol. 2010 Nov. 63(5):886-91. [Medline].

Xia JH, Yang YF, Deng H, Tang BS, Tang DS, He YG. Identification of a locus for disseminated superficial actinic porokeratosis at chromosome 12q23.2-24.1. J Invest Dermatol. 2000 Jun. 114(6):1071-4. [Medline].

Xia K, Deng H, Xia JH, Zheng D, Zhang HL, Lu CY. A novel locus (DSAP2) for disseminated superficial actinic porokeratosis maps to chromosome 15q25.1-26.1. Br J Dermatol. 2002 Oct. 147(4):650-4. [Medline].

Liu P, Zhang S, Yao Q, Liu X, Wang X, Huang C. Identification of a genetic locus for autosomal dominant disseminated superficial actinic porokeratosis on chromosome 1p31.3-p31.1. Hum Genet. 2008 Jun. 123(5):507-13. [Medline].

Luan J, Niu Z, Zhang J, Crosby ME, Zhang Z, Chu X. A novel locus for disseminated superficial actinic porokeratosis maps to chromosome 16q24.1-24.3. Hum Genet. 2011 Mar. 129(3):329-34. [Medline].

Wei S, Yang S, Lin D, Li M, Zhang X, Bu L. A novel locus for disseminated superficial porokeratosis maps to chromosome 18p11.3. J Invest Dermatol. 2004 Nov. 123(5):872-5. [Medline].

Wei SC, Yang S, Li M, Song YX, Zhang XQ, Bu L. Identification of a locus for porokeratosis palmaris et plantaris disseminata to a 6.9-cM region at chromosome 12q24.1-24.2. Br J Dermatol. 2003 Aug. 149(2):261-7. [Medline].

Happle R. Mibelli revisited: a case of type 2 segmental porokeratosis from 1893. J Am Acad Dermatol. 2010 Jan. 62(1):136-8. [Medline].

Levinsohn JL, McNiff JM, Antaya RJ, Choate KA. A Somatic p.G45E GJB2 Mutation Causing Porokeratotic Eccrine Ostial and Dermal Duct Nevus. JAMA Dermatol. 2015 Jun. 151 (6):638-41. [Medline].

Rodriguez EA, Jakubowicz S, Chinchilla DA, Carril A, Viglioglia PA. Porokeratosis of Mibelli and HIV-infection. Int J Dermatol. 1996 Jun. 35(6):402-4. [Medline].

Nakamura M, Fukamachi S, Tokura Y. Acute onset disseminated superficial porokeratosis associated with exacerbation of diabetes mellitus due to development of anti-insulin antibodies. Dermatoendocrinol. 2010 Jan. 2(1):17-8. [Medline].

Hunt SJ, Sharra WG, Abell E. Linear and punctate porokeratosis associated with end-stage liver disease. J Am Acad Dermatol. 1991 Nov. 25(5 Pt 2):937-9. [Medline].

Cannavo SP, Borgia F, Adamo B, Guarneri B. Simultaneous development and parallel course of disseminated superficial porokeratosis and ovarian cancer: Coincidental association or true paraneoplastic syndrome?. J Am Acad Dermatol. 2008 Apr. 58(4):657-60. [Medline].

Kono T, Kobayashi H, Ishii M, Nishiguchi S, Taniguchi S. Synchronous development of disseminated superficial porokeratosis and hepatitis C virus-related hepatocellular carcinoma. J Am Acad Dermatol. 2000 Nov. 43(5 Pt 2):966-8. [Medline].

Raychaudhuri SP, Smoller BR. Porokeratosis in immunosuppressed and nonimmunosuppressed patients. Int J Dermatol. 1992 Nov. 31(11):781-2. [Medline].

Herranz P, Pizarro A, De Lucas R, Robayna MG, Rubio FA, Sanz A. High incidence of porokeratosis in renal transplant recipients. Br J Dermatol. 1997 Feb. 136(2):176-9. [Medline].

Alexis AF, Busam K, Myskowski PL. Porokeratosis of Mibelli following bone marrow transplantation. Int J Dermatol. 2006 Apr. 45(4):361-5. [Medline].

Komorowski RA, Clowry LJ. Porokeratosis of mibelli in transplant recipients. Am J Clin Pathol. 1989 Jan. 91(1):71-4. [Medline].

Kanitakis J, Euvrard S, Faure M, Claudy A. Porokeratosis and immunosuppression. Eur J Dermatol. 1998 Oct-Nov. 8(7):459-65. [Medline].

Rothman IL, Wirth PB, Klaus MV. Porokeratosis of Mibelli following heart transplant. Int J Dermatol. 1992 Jan. 31(1):52-4. [Medline].

Sertznig P, von Felbert V, Megahed M. Porokeratosis: present concepts. J Eur Acad Dermatol Venereol. 2012 Apr. 26(4):404-12. [Medline].

Gilead L, Guberman D, Zlotogorski A, et al. Immunosuppression-induced porokeratosis of Mibelli: Complete regression of lesions upon cessation of immunosuppressive therapy. J EurAcad Dermatol Venereol. 1995. 5:170.

Tsambaos D, Spiliopoulos T. Disseminated superficial porokeratosis: complete remission subsequent to discontinuation of immunosuppression. J Am Acad Dermatol. 1993 Apr. 28(4):651-2. [Medline].

Yazkan F, Turk BG, Dereli T, Kazandi AC. Porokeratosis of Mibelli induced by topical corticosteroid. J Cutan Pathol. 2006 Jul. 33(7):516-8. [Medline].

Nova MP, Goldberg LJ, Mattison T, Halperin A. Porokeratosis arising in a burn scar. J Am Acad Dermatol. 1991 Aug. 25(2 Pt 2):354-6. [Medline].

Parekh V, Kabihting FD, Junkins-Hopkins JM. Hyperkeratotic variant of porokeratosis in a patient with Hepatitis C virus infection and a concomitant immunosuppressed state. Dermatol Online J. 2015 Nov 18. 21 (11):[Medline].

James WD, Rodman OG. Squamous cell carcinoma arising in porokeratosis of mibelli. Int J Dermatol. 1986 Jul-Aug. 25(6):389-91. [Medline].

Sasson M, Krain AD. Porokeratosis and cutaneous malignancy. A review. Dermatol Surg. 1996 Apr. 22(4):339-42. [Medline].

Seishima M, Izumi T, Oyama Z, Maeda M. Squamous cell carcinoma arising from lesions of porokeratosis palmaris et plantaris disseminata. Eur J Dermatol. 2000 Aug. 10(6):478-80. [Medline].

Otsuka F, Umebayashi Y, Watanabe S, Kawashima M, Hamanaka S. Porokeratosis large skin lesions are susceptible to skin cancer development: histological and cytological explanation for the susceptibility. J Cancer Res Clin Oncol. 1993. 119(7):395-400. [Medline].

Magee JW, McCalmont TH, LeBoit PE. Overexpression of p53 tumor suppressor protein in porokeratosis. Arch Dermatol. 1994 Feb. 130(2):187-90. [Medline].

Ninomiya Y, Urano Y, Yoshimoto K, Iwahana H, Sasaki S, Arase S. p53 gene mutation analysis in porokeratosis and porokeratosis-associated squamous cell carcinoma. J Dermatol Sci. 1997 Mar. 14(3):173-8. [Medline].

Sasaki S, Urano Y, Nakagawa K, Nagae H, Nakanishi H, Arase S. Linear porokeratosis with multiple squamous cell carcinomas: study of p53 expression in porokeratosis and squamous cell carcinoma. Br J Dermatol. 1996 Jun. 134(6):1151-3. [Medline].

Urano Y, Sasaki S, Ninomiya Y, Oura H, Arase S. Immunohistochemical detection of p53 tumor suppressor protein in porokeratosis. J Dermatol. 1996 May. 23(5):365-8. [Medline].

Arranz-Salas I, Sanz-Trelles A, Ojeda DB. p53 alterations in porokeratosis. J Cutan Pathol. 2003 Aug. 30(7):455-8. [Medline].

Ramesh V, Misra RS, Mahaur BS. Pseudoainhum in porokeratosis of Mibelli. Cutis. 1992 Feb. 49(2):129-30. [Medline].

Silver SG, Crawford RI. Fatal squamous cell carcinoma arising from transplant-associated porokeratosis. J Am Acad Dermatol. 2003 Nov. 49(5):931-3. [Medline].

Sawai T, Hayakawa H, Danno K, Miyauchi H, Uehara M. Squamous cell carcinoma arising from giant porokeratosis: a case with extensive metastasis and hypercalcemia. J Am Acad Dermatol. 1996 Mar. 34(3):507-9. [Medline].

Leow YH, Soon YH, Tham SN. A report of 31 cases of porokeratosis at the National Skin Centre. Ann Acad Med Singapore. 1996 Nov. 25(6):837-41. [Medline].

Raychaudhury T, Valsamma DP. Indian J Dermatol VenereolLeprol. Giant porokeratosis. 2011. 77:601.

Robinson JB, Im DD, Jockle G, Rosenshein NB. Vulvar porokeratosis: case report and review of the literature. Int J Gynecol Pathol. 1999 Apr. 18(2):169-73. [Medline].

Neri I, Marzaduri S, Passarini B, Patrizi A. Genital porokeratosis of Mibelli. Genitourin Med. 1995 Dec. 71(6):410-1. [Medline].

Koley S, Sarkar J, Choudhary S, Dhara S, Choudhury M, Bhattacharya S. Different morphological variants of hypertrophic porokeratosis and disseminated lesions of porokeratosis of Mibelli: a rare co-existence. Indian J Dermatol Venereol Leprol. 2011 Mar-Apr. 77(2):199-202. [Medline].

Thomas C, Ogboli MI, Carr RA, Charles-Holmes R. Hypertrophic perianal porokeratosis in association with superficial actinic porokeratosis of the leg. Clin Exp Dermatol. 2003 Nov. 28(6):676-7. [Medline].

Jang KA, Choi JH, Sung KJ, Moon KC, Koh JK. The hyperkeratotic variant of disseminated superficial actinic porokeratosis (DSAP). Int J Dermatol. 1999 Mar. 38(3):204-6. [Medline].

BENCINI, PL, TARANTINO, A, GRIMALT, R., et al. Undefined. British Journal of Dermatology,. 1995. 132:74–78.

Murase J, Gilliam AC. Disseminated superficial actinic porokeratosis co-existing with linear and verrucous porokeratosis in an elderly woman: Update on the genetics and clinical expression of porokeratosis. J Am Acad Dermatol. 2010 Nov. 63(5):886-91. [Medline].

Patrizi A, Passarini B, Minghetti G, Masina M. Porokeratosis palmaris et plantaris disseminata: an unusual clinical presentation. J Am Acad Dermatol. 1989 Aug. 21(2 Pt 2):415-8. [Medline].

Marschalkó M, SomlaiB.Porokeratosis plantaris, palmaris, et. disseminata. Arch Dermatol. 1986 Aug. 122(8):890-1.

Tallon B, Blumental G, Bhawan J. Porokeratosis ptychotropica: a lesser-known variant. Clin Exp Dermatol. 2009 Dec. 34(8):e895-7. [Medline].

McGuigan K, Shurman D, Campanelli C, Lee JB. Porokeratosis ptychotropica: a clinically distinct variant of porokeratosis. J Am Acad Dermatol. 2009 Mar. 60(3):501-3. [Medline].

Flanagan N, Boyadjiev SA, Harper J, Kyne L, Earley M, Watson R. Familial craniosynostosis, anal anomalies, and porokeratosis: CAP syndrome. J Med Genet. 1998 Sep. 35(9):763-6. [Medline].

Hartman R, Rizzo C, Patel R, Kamino H, Shupack JL. Porokeratosis palmaris et plantaris disseminata or a disseminated late-onset variant of porokeratotic eccrine ostial and dermal ductal nevus (PEODDN) with follicular involvement. Dermatol Online J. 2009. 15(8):8. [Medline].

Zaballos P, Puig S, Malvehy J. Dermoscopy of disseminated superficial actinic porokeratosis. Arch Dermatol. 2004 Nov. 140(11):1410. [Medline].

Uhara H, Kamijo F, Okuyama R, Saida T. Open pores with plugs in porokeratosis clearly visualized with the dermoscopic furrow ink test: report of 3 cases. Arch Dermatol. 2011 Jul. 147(7):866-8. [Medline].

Reed C, Reddy R, Brodell RT. Diagnosing porokeratosis of Mibelli every time: a novel biopsy technique to maximize histopathologic confirmation. Cutis. 2016 Mar. 97 (3):188-90. [Medline].

Sander CA, Pfeiffer C, Kligman AM, Plewig G. Chemotherapy for disseminated actinic keratoses with 5-fluorouracil and isotretinoin. J Am Acad Dermatol. 1997 Feb. 36(2 Pt 1):236-8. [Medline].

Shelley WB, Shelley ED. Disseminated superficial porokeratosis: rapid therapeutic response to 5-fluorouracil. Cutis. 1983 Aug. 32(2):139-40. [Medline].

Danby W. Treatment of porokeratosis with fluorouracil and salicylic acid under occlusion. Dermatol Online J. 2003 Dec. 9(5):33. [Medline].

Böhm M, Luger TA, Bonsmann G. Disseminated superficial actinic porokeratosis: treatment with topical tacalcitol. J Am Acad Dermatol. 1999 Mar. 40(3):479-80. [Medline].

Thiers BH. The use of topical calcipotriene/calcipotriol in conditions other than plaque-type psoriasis. J Am Acad Dermatol. 1997 Sep. 37(3 Pt 2):S69-71. [Medline].

Bakardzhiev I, Kavaklieva S, Pehlivanov G. Successful treatment of disseminated superficial actinic porokeratosis with calcipotriol. Int J Dermatol. 2011 Jul 5. [Medline].

Harrison S, Sinclair R. Porokeratosis of Mibelli: successful treatment with topical 5% imiquimod cream. Australas J Dermatol. 2003 Nov. 44(4):281-3. [Medline].

Gracia-Cazaña T, Vera-Álvarez J, García-Patos V, Gilaberte Y. Imiquimod and Photodynamic Therapy Are Useful in the Treatment of Porokeratosis in Children with Bone Marrow Transplantation. Pediatr Dermatol. 2015 Jul 29. [Medline].

Kindem S, Serra-Guillén C, Sorní G, Guillén C, Sanmartín O. Treatment of porokeratosis of Mibelli with ingenol mebutate: a possible new therapeutic option. JAMA Dermatol. 2015 Jan. 151 (1):85-6. [Medline].

Parks AC, Conner KJ, Armstrong CA. Long-term clearance of linear porokeratosis with tacrolimus, 0.1%, ointment. JAMA Dermatol. 2014 Feb. 150 (2):194-6. [Medline].

Marks S, Varma R, Cantrell W, Chen SC, Gold M, Muellenhoff M. Diclofenac sodium 3% gel as a potential treatment for disseminated superficial actinic porokeratosis. J Eur Acad Dermatol Venereol. 2009 Jan. 23(1):42-5. [Medline].

Knobler RM, Neumann RA. Exacerbation of porokeratosis during etretinate therapy. Acta Derm Venereol. 1990. 70(4):319-22. [Medline].

Carmichael AJ, Tan CY. Digitate keratoses–a complication of etretinate used in the treatment of disseminated superficial actinic porokeratosis. Clin Exp Dermatol. 1990 Sep. 15(5):370-1. [Medline].

Hong JB, Hsiao CH, Chu CY. Systematized linear porokeratosis: a rare variant of diffuse porokeratosis with good response to systemic acitretin. J Am Acad Dermatol. 2009 Apr. 60(4):713-5. [Medline].

Garg T, Ramchander, Varghese B, Barara M, Nangia A. Generalized linear porokeratosis: a rare entity with excellent response to acitretin. Dermatol Online J. 2011. 17(5):3. [Medline].

Cohen PR, Held JL, Katz BE. Linear porokeratosis: successful treatment with diamond fraise dermabrasion. J Am Acad Dermatol. 1990 Nov. 23(5 Pt 2):975-7. [Medline].

Ross NA, Rosenbaum LE, Saedi N, Arndt KA, Dover JS. Disseminated superficial actinic porokeratosis improved with fractional 1927-nm laser treatments. J Cosmet Laser Ther. 2016 Feb. 18 (1):53-5. [Medline].

Itoh M, Nakagawa H. Successful treatment of disseminated superficial actinic porokeratosis with Q-switched ruby laser. J Dermatol. 2007 Dec. 34(12):816-20. [Medline].

Liu HT. Treatment of lichen amyloidosis (LA) and disseminated superficial porokeratosis (DSP) with frequency-doubled Q-switched Nd:YAG laser. Dermatol Surg. 2000 Oct. 26(10):958-62. [Medline].

Cavicchini S, Tourlaki A. Successful treatment of disseminated superficial actinic porokeratosis with methyl aminolevulinate-photodynamic therapy. J Dermatolog Treat. 2006. 17(3):190-1. [Medline].

Amarateedha Prak LeCourt, MD Naval Flight Surgeon, Marine Aircraft Group 39, MCAS Camp Pendleton

Amarateedha Prak LeCourt, MD is a member of the following medical societies: Aerospace Medical Association, Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Kristina Marie Dela Rosa, MD Dermatologist, Insight Dermatology, San Diego, CA

Kristina Marie Dela Rosa, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: Lilly; Amgen <br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.

Linda V Spencer, MD Spencer Dermatology Associates, LLC

Linda V Spencer, MD is a member of the following medical societies: American Academy of Dermatology, Dermatology Foundation, American Medical Association, Indiana State Medical Association

Disclosure: Nothing to disclose.

Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Andrea Leigh Zaenglein, MD is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting.

The view(s) expressed herein are those of the authors and do not reflect the official policy or position of the U.S. Navy Medical Department, the U.S. Navy Office of the Surgeon General, the Department of the Navy, Department of Defense, or the U.S. Government.


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