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Year : 2019  |  Volume : 3  |  Issue : 2  |  Page : 142-144

Verruca vulgaris over seborrheic keratosis: A locoregional immune default!!

Department of Dermatology, ESI PGIMSR and Model Hospital, New Delhi, India

Date of Web Publication15-Jul-2019

Correspondence Address:
Tapankumar Dhali
Department of Dermatology, ESI PGIMSR and Model Hospital, New Delhi - 110 015
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CDR.CDR_10_19

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Immunocompromised cutaneous district (ICD) or locus minoris resistentiae is an old concept in dermatology, which represents vulnerability of a particular cutaneous site to the development of secondary dermatosis due to prior insults. Seborrheic keratosis (SK) is an asymptomatic benign epidermal keratinocytic tumor, commonly seen in elderly patients. It may also act as an acquired cutaneous lesion offering lesser resistance for the development of other dermatosis. A 65-year-old female patient having SK over cheek developed a new lesion of verruca vulgaris over it. So far as published literature is concerned, this is the first report of verruca vulgaris superimposed over SK; thus, the latter is acting as an example of immunocompromised cutaneous district (ICD).

Keywords: Immunocompromised cutaneous district, locus minoris resistentiae, seborrheic keratosis, verruca vulgaris

How to cite this article:
Lokhane AJ, Soni R, Sheoran P, Yadav MK, Dhali T. Verruca vulgaris over seborrheic keratosis: A locoregional immune default!!. Clin Dermatol Rev 2019;3:142-4

How to cite this URL:
Lokhane AJ, Soni R, Sheoran P, Yadav MK, Dhali T. Verruca vulgaris over seborrheic keratosis: A locoregional immune default!!. Clin Dermatol Rev [serial online] 2019 [cited 2023 Feb 5];3:142-4. Available from: https://www.cdriadvlkn.org/text.asp?2019/3/2/142/262766

  Introduction Top

The immunocompromised cutaneous district (ICD) represents a region of the skin which is vulnerable for the onset of opportunistic infections, tumors, or dysimmune reactions strictly confined to that particular site or sometimes even selectively sparing the site. It may present either in the form of locus minoris resistentiae (LMR) or locus maioris resistentiae.[1]

Recently, we observed an example of this unique dermatological phenomenon in a patient who developed verruca vulgaris over a preexisting seborrheic keratosis (SK).

  Case Report Top

A 65-year-old female patient presented with an asymptomatic raised pigmented lesion with “stuck on” appearance [Figure 1] red arrow] over the right cheek for 10 years. She developed a single new flower-like warty growth [Figure 1], green arrow] on the right corner of this preexisting lesion over a period of 2 months. There was no evidence of similar kind of lesions over any other body part.
Figure 1: Red arrow-pigmented lesion with stuck on appearance over the right cheek, green arrow flower-like warty growth

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Dermoscopy of the basal pigmented lesion showed comedo-like openings, ridges, and moth-eaten border suggestive of SK whereas the warty growth showed multiple finger-like longer projections, with the absence of thrombosed vessels suggestive of filiform verruca vulgaris [Figure 2]. Histopathological examination of basal hyper pigmented lesion showed hyperkeratosis, irregular acanthosis, and horn pseudocyst which confirmed the diagnosis of SK [Figure 3]. Biopsy from new onset warty lesion showed papillomatosis, acanthosis, and hyperkeratosis along with the presence of koilocytes in upper epidermis [Figure 4]. On the basis of clinical, dermoscopic, and histopathological examination, a final diagnosis of filiform wart over SK was made. The wart was removed by electrofulguration. The lesion of SK was left untreated as the patient did not want to get it removed.
Figure 2: Dermoscopy of comedo-like openings (red), ridges, and moth-eaten border (blue) suggestive of seborrheic keratosis whereas the warty growth showed multiple thread/finger-like long projections, with the absence of thrombosed vessels but slight pinkish hue at the base of projections suggestive of filiform verruca vulgaris (yellow). (Handheld contact dermoscope: Derm Lite DL3 gen. Polarized view with magnification, ×20)

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Figure 3: Histopathology H and E-hyperkeratosis, irregular acanthosis, horn pseudocyst, which confirmed the diagnosis of seborrheic keratosis (×10 and ×4)

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Figure 4: Histopathology H and E papillomatosis, acanthosis, and hyperkeratosis along with koilocytes verruca vulgaris, ×40

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  Case Discussion Top

LMR or Immunocompromised cutaneous district (ICD) is defined as a vulnerable area of the skin that offers lesser resistance (or hindrance) to the development of new dermatosis than the rest of the body. Few authors consider Köebner's phenomenon[1] as a part of LMR whereas others regard this as a separate entity.[2] Koebner's phenomenon is an isomorphic response in which a traumatized uninvolved skin of the body develops clinically and histopathologically identical dermatoses; thus, it may be considered as a prototype example of ICD, more specifically LMR like several other phenomena (e.g., Wolf's isotopic response). In LMR immunological dysregulated site foster development of secondary dermatosis.[2]

Several factors can be responsible for this localized immune dysregulation including chronic lymph stasis, local infections, ionizing or ultraviolet radiation, burns, any kind of trauma, tattooing, intradermal vaccinations, and others.[1] All these predisposing factors result in hampered trafficking of immunocompetent cells and impaired innate ability of the skin to counteract other dermatosis.[2]

Various examples of congenital as well as acquired LMR are described in the literature.[1],[2],[3],[4],[5]

The ideal example of this is Wolf's isotopic phenomenon. These immunologically compromised cutaneous regions may be present since birth or develop later in life.[5]

In this, a new skin disorder develops at the nidus of previously healed and unrelated dermatosis. This phenomenon is most commonly described in healed lesions of herpes zoster.[3]

Recently, Dalla Costa et al. reported a case of minocycline-induced fixed drug eruption at the sites of healed burn and zoster scar. The case is an example of acquired LMR and Wolf's isotopic response, respectively, where the drug minocycline acted as a triggering factor.[4]

Various infective as well as inflammatory skin disorders such as lupus vulgaris, Churg Strauss syndrome, granuloma annulare, and dermatophytosis have occurred over healed scar or posthealed herpes zoster scar.[5] Betti et al. has described a case of SK with compound nevus, junctional nevus, and basal cell carcinoma in the same lesion.[6]

All of these are examples of acquired LMR.

Ranugha et al. reported three cases of verruca over linear verrucous epidermal nevi.[5]

In a retrospective study of 596 cases of excised nevus sebaceous, authors found occurrence of benign tumors in 13.6%. Only 4 benign tumors and 2 warts along with nevus sebaceous were observed in patients younger than 16 years.[7]

Nevi (epidermal or sebaceous) are cutaneous hamartomas; thus, these genetically predisposed mosaic cells sometimes favors development of several secondarily acquired skin disorders superimposed on them.[5],[7] These examples delineate the fact that nevi being areas of cutaneous mosaicism acts as an example of congenital LMR.

SK is an asymptomatic benign epidermal keratinocytic tumor, commonly found in individuals aging more than 50 years. Sunlight has got predisposing role in its causation. They are more commonly seen on face and upper back.[8]

The lesions of SK show slow evolution; thus, patients with SK are generally keen for treatment for cosmetic purposes. However, in our case, the patient sought dermatological opinion for concern about the newer onset growth on the preexisting SK.

Dermoscopic examination of SK shows characteristic features such as cerebriform pattern, comedo-like openings, fingerprint structure, moth-eaten border, milia-like cysts, and hairpin vessels, among which the first three findings were present in our case.[8],[9] The newer verrucous growth showed the presence of multiple papillae on dermoscopy.[9] The characteristic clinical, dermoscopical, and histopathological findings helped to confirm different origin and diagnosis of the two distinct cutaneous lesions.

Lesions of SK display histological and etiopathological homology to benign epidermal nevi.[8],[10] Oncogenic mutations of FGFR3 and PIK3CA are seen as an underlying genetic defects in the cases of epidermal nevi as well as SK.[8] Activating FGFR3 mutations and antiapoptotic (through expression of bcl-2) signals for the keratinocytes hastens proliferation in SK.[8],[10] Such kind of genetic expression may have made the lesion of SK as ICD due to immune dysregulation and thus favored development of verruca superimposed over SK.

D'Souza et al. had reported a case of lepromatous leprosy wherein extensive truncal SK and acral verruca vulgaris occurred simultaneously but on different body parts, though in our case both dermatoses shared same locus.[11]

The probable hypothesis for cooccurrence of these two dermatoses could be lesion of SK is acting as a LMR or Immunocompromised cutaneous district (ICD), thus preferring simultaneous occurrence of verruca.

  Conclusion Top

On extensive web search we failed to find out similar case in English literature. To the best of our knowledge, this is the first case report of verruca vulgaris superimposed over SK, which exemplify the unique dermatological phenomenon of LMR or Immunocompromised cutaneous district (ICD).

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Caccavale S, Kannangara AP, Ruocco E. The immunocompromised cutaneous district and the necessity of a new classification of its disparate causes. Indian J Dermatol Venereol Leprol 2016;82:227-9.  Back to cited text no. 1
[PUBMED]  [Full text]  
Raghukumar S, Ravikumar BC. Immunosuppressed cutaneous district: The finale of the fascinating farrago of confounding responses? Clin Dermatol Rev 2017;1:78-81.  Back to cited text no. 2
  [Full text]  
Wolf R, Brenner S, Ruocco V, Filioli FG. Isotopic response. Int J Dermatol 1995;34:341-8.  Back to cited text no. 3
Dalla Costa R, Yang CY, Stout M, Kroshinsky D, Kourosh AS. Multiple fixed drug eruption to minocycline at sites of healed burn and zoster: An interesting case of locus minoris resistentiae. JAAD Case Rep 2017;3:392-4.  Back to cited text no. 4
Ranugha PS, Betkerur JB, Veeranna S, Basavaraj V. Appearance of verruca over linear verrucous epidermal nevus – An example of locus minoris resistentiae: A report of three cases. Indian Dermatol Online J 2018;9:334-7.  Back to cited text no. 5
[PUBMED]  [Full text]  
Betti R, Menni S, Cerri A, Vergani R, Crosti C. Seborrheic keratosis with compound nevus, junctional nevus and basal cell carcinoma in the same lesion. Dermatology 2001;203:265-7.  Back to cited text no. 6
Cribier B, Scrivener Y, Grosshans E. Tumors arising in nevus sebaceus: A study of 596 cases. J Am Acad Dermatol 2000;42:26s3-8.  Back to cited text no. 7
Madan V, Lear JT. Seborrhoeic keratosis. In: Griffiths C, Barker J, Bleiker T, Chalmers R, Creamer D, editors. Rook's Textbook of Dermatology. 9th ed. Chichester, West Sussex (UK): Wiley Blackwell; 2016. p. 3669-72.  Back to cited text no. 8
Zalaudek I, Argenziano G, Di Stefani A, Ferrara G, Marghoob AA, Hofmann-Wellenhof R, et al. Dermoscopy in general dermatology. Dermatology 2006;212:7-18.  Back to cited text no. 9
Hafner C, Hafner H, Groesser L. Genetic basis of seborrheic keratosis and epidermal nevi. Pathologe 2014;35:413-23.  Back to cited text no. 10
D'Souza M, Garg BR, Reddy BS, Ratnakar C. Lepromatous leprosy with extensive truncal seborrheic keratoses and acral verruca vulgaris. Int J Dermatol 1994;33:498-500.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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