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E-IJD® - CORRESPONDENCE
Year : 2022  |  Volume : 67  |  Issue : 3  |  Page : 316
Acquired epidermodysplasia verruciformis during highly active antiretroviral therapy


Department of Dermatology, Venereology, and Leprosy, R. G. Kar Medical College, Kolkata, West Bengal, India

Date of Web Publication22-Sep-2022

Correspondence Address:
Dibyendu B Bhanja
Department of Dermatology, Venereology, and Leprosy, R. G. Kar Medical College, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijd.IJD_747_20

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How to cite this article:
Sil A, Bhanja DB, Panigrahi A, Biswas SK. Acquired epidermodysplasia verruciformis during highly active antiretroviral therapy. Indian J Dermatol 2022;67:316

How to cite this URL:
Sil A, Bhanja DB, Panigrahi A, Biswas SK. Acquired epidermodysplasia verruciformis during highly active antiretroviral therapy. Indian J Dermatol [serial online] 2022 [cited 2022 Sep 29];67:316. Available from: https://www.e-ijd.org/text.asp?2022/67/3/316/356754




Sir,

Epidermodysplasia verruciformis (EDV) is an inherited cutaneous disorder characterized by an increased susceptibility to specific human papilloma virus (HPV) genotypes, resulting in both benign and malignant lesions. This autosomal recessive condition, rarely X-linked recessive and autosomal dominant, was initially described by Lewandowski and Lutz in 1922 and typically features impaired immunity and viral oncogenesis.[1] The rarely described acquired form of EDV occurs in immunocompromised individuals especially in patients with human immunodeficiency virus (HIV) infection, systemic lupus erythematosus, lymphoma or those on some immunosuppressive therapy.[2] In this report, we describe a case of acquired EDV in an HIV infected patient on highly active antiretroviral therapy.

A 42-year-old HIV positive male laborer, on highly active anti-retroviral therapy (tenofovir, lamuvudine, and efavirenz) for preceding 2 years, presented with 6-month history of generalized asymptomatic pale skin eruptions. He denied any pre-existing cutaneous condition; there was no family history of such lesions. Examination revealed multiple hypopigmented discrete and coalescent plane-topped papules and plaques distributed over the face, trunk and upper extremities; koebner phenomenon could be appreciated in a few lesions [Figure 1]a and [Figure 1]b. Other mucocutaneous sites and systemic examination did not reveal anything unusual. Results of routine laboratory investigations, chest radiography, and abdominal ultrasound were normal; CD4 count was 722 cells/mL and viral load 94 copies/ml. Histopathological examination demonstrated hyperkeratosis, hypergranulosis, acanthosis with papillomatosis and nests of large cells having prominent perinuclear halo and blue-gray pallor [Figure 2]. Based on the clinicopathological features, a diagnosis of acquired epidermodysplasia verruciformis was established. Owing to widespread involvement, the patient was prescribed acitretin (25 mg) once daily; the lesions showed substantial reduction in 3 months. No recurrence was observed on 12-month follow-up.
Figure 1: (a) Discrete hypopigmented and coalescent plane-topped papules and plaques distributed over the face, chest and upper extremities; koebnerization of few lesions over forearms noted. (b): Discrete hypopigmented and coalescent plane-topped papules and plaques distributed over the back

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Figure 2: Histopathological examination demonstrating hyperkeratosis, hypergranulosis, acanthosis with papillomatosis and nests of large cells having prominent perinuclear halo and blue-gray pallor (H&E; ×100)

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EDV, a rare genodermatosis, classically presents as distinctive erythematous to skin-colored scaly macules (pityriasis versicolor-like), or flat-to-papillomatous, wart-like lesions (verruca plana and seborrheic keratosis-like) that often amalgamate to form reddish-brown pigmented plaques over the face, trunk, and extremities.[3] A few cases of acquired EDV have been described in patients infected with HIV.[2],[4] However, development of EDV lesions appears to be unrelated to the CD4 count and viral load. Acquired EDV in HIV infected patients has been thought to be a manifestation of immune restoration inflammatory syndrome following initiation of highly active antiretroviral therapy.[4] The rise in CD4 count and possibly, improvement in antigen recognition, increases the risk of patients developing HPV-associated disease.

EDV has been linked to the EV1 and EV2 loci on chromosomes 17 and 2 respectively; mutations in EVER 1 and EVER 2 genes, found on chromosome 17, increases the risk of HPV infection. The benign form of the condition may present with only flat warts associated with HPV 3 and 10, that are non-oncogenic and affect normal hosts.[5] Certain HPV subtypes like HPV-5,8, and 14 are highly oncogenic and strongly associated with cutaneous malignancy. In 30-50% of patients with EDV, initial cutaneous lesions undergo malignant transformation into actinic keratosis, Bowen's disease and squamous cell carcinoma over a period of two to three decades. These malignant lesions preferentially arise on sun-exposed areas of face, neck, trunk and extremities.[4],[5]

Therapeutic interventions like topical 5-fluorouracil, 5-aminolevulinic acid, photodynamic therapy, imiquimod, glycolic acid, cimetidine, and systemic retinoids with or without interferon alpha 2a have been used but with variable results. Photoprotection and broad-spectrum sunscreens are also recommended.

We highlight the importance of timely diagnosis and adequate treatment as these patients require long-term monitoring to detect malignant transformation.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Oliveira WRP, Neto CF, Tyring SK. Clinical aspects of epidermodysplasia verruciformis. An Bras Dermatol 2002;77:545-56.  Back to cited text no. 1
    
2.
Lowe SM, Katsidzira L, Meys R, Sterling JC, de Koning M, Quint W, et al. Acquired epidermodysplasia verruciformis due to multiple and unusual HPV infection among vertically-infected, HIV-positive adolescents in Zimbabwe. Clin Infect Dis 2012;54:e119-23.  Back to cited text no. 2
    
3.
Chakraborty S, Sil A. Visual Dermatology: Epidermodysplasia Verruciformis. J Cutan Med Surg 2020; 24:636.  Back to cited text no. 3
    
4.
Jacobelli S, Laude H, Carlotti A, Rozenberg F, Deleuze J, Morini JP, et al. Epidermodysplasia verruciformis in human immunodeficiency virus–infected patients: A marker of human papillomavirus–related disorders not affected by antiretroviral therapy. Arch Dermatol 2011;147:590-6.  Back to cited text no. 4
    
5.
Patel T, Morrison LK, Rady P, Tyring S. Epidermodysplasia verruciformis and susceptibility to HPV. Dis Markers 2010;29:199-206.  Back to cited text no. 5
    


    Figures

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