Increased human papillomavirus type 31 DNA load in a verrucous high-grade intraepithelial neoplasia of a human immunodeficiency virus-infected patient with extensive bowenoid papulosis
Authors: A. Kreuter, N.H. Brockmeyer, H. Pfister, P. Altmeyer, U. Wieland
Journal: British Journal of Dermatology (2007)

Conflicts of interest: none declared. Sir, Bowenoid papulosis (BP) represents a multifocal intraepithelial neoplasia primarily located in the anogenital region of predominantly young adults.1 Although BP shows clinically benign‐looking papular lesions, histopathological findings reveal features of a squamous cell carcinoma (SCC) in situ, and high‐risk human papillomaviruses (HPVs), mainly HPV 16, are regularly found in the lesions. BP usually has a benign course and tends to regress spontaneously, in contrast to Bowen's disease (BD), which develops into SCC after a certain duration of time. Malignant transformation has so far only sporadically been reported in BP. Immunosuppression, especially human immunodeficiency virus (HIV) infection, greatly increases the risk for premalignant and invasive HPV‐related conditions.2 We report a 57‐year‐old HIV‐infected heterosexual man with extensive genital BP. He was diagnosed as HIV‐1 positive in May 2005, presenting with a severely compromised immunological and virological HIV status (CD4+ cells 67 μL−1; HIV RNA 244 000 copies mL−1). At first physical examination, he revealed widespread brownish papules with a scaly or smooth surface located on the mons pubis, genitals, inguinal folds, buttocks, and the inner aspects of the thighs (Fig. 1a). Concomitant Candida albicans infection of the intertriginous areas was present. Furthermore, a wart‐like, verrucous nodule at the perineal area, 8 × 8 mm in diameter, was detected that differed clinically from the other BP lesions (Fig. 1b). Histopathological examination of the nodule revealed acanthosis, parakeratosis, and atypical cells within the entire epidermis consistent with SCC in situ. Immunohistochemical staining of the nodule using anti‐p16 monoclonal antibody demonstrated strong and diffuse immunoreactivity in both the nuclei and the cytoplasm. p16 staining of the nodule reached the upper layers of the epidermis (Fig. 2) and exceeded that of the BP lesions (Table 1). HPV typing for 37 different low‐ and high‐risk HPVs from the two different types of lesions (the verrucous nodule shown in Fig. 1b and the widespread brownish papules shown in Fig. 1a) showed identical high‐risk HPV types in both types of lesions (HPV 31 and 52). The low‐risk HPV 84 was present only in the brownish papules (Table 1). Further genital low‐ or high‐risk HPV types were not detected. Interestingly, HPV 31 loads (quantitated by real‐time polymerase chain reaction with type‐specific primers and probes and expressed as HPV DNA copies per β‐globin gene copy3) significantly differed in the two types of lesions: HPV 31 load of the verrucous nodule was two orders of magnitude higher than that in the brownish papules (Table 1). Semiquantitative viral load determination for HPV 52 and HPV 84 revealed similar loads in the two brownish papules, and a lower HPV 52 load in the warty nodule compared with the brownish papules (Table 1). The nodule was surgically removed and all other lesions were treated with cautery fulguration. Imiquimod 5% cream therapy was offered to prevent recurrences, but was declined by the patient. He finally refrained from therapy and was lost to follow up.