Bowenoid Papulosis at the Site of Prior Herpes Progenitalis

Eleonora Ruocco, MD; Francesco Tripodi Cutrì, MD; Adone Baroni, MD


Skinmed. 2004;3(6) 

A 35-year-old dentist came to the authors' attention for papular and vegetating lesions that had appeared on his penile shaft over the last 2 months. The lesions differed in their features: pink and vegetating on the left side, brown and papular on the right side (Figure 1). The obvious clinical diagnoses of genital warts on the left and Bowenoid papulosis on the right were confirmed by punch biopsies, which showed epithelial hyperplasia with diffuse cell vacuolization (koilocytes) in the left biopsy and moderate nuclear dysplasia in the right one (Figure 2). Human papillomavirus phenotyping was not performed. Interestingly, the patient reported a clear medical history of herpes progenitalis (only one episode) that had involved the right side of his glans and prepuce 4 years ago. An immunomodulating treatment with imiquimod was started in the attempt to cure both the genital warts and Bowenoid papulosis lesions (imiquimod was applied three times a week for 8 weeks). At the end of the treatment, the genital warts had disappeared, whereas many Bowenoid papulosis lesions were still present on the right side of the penis (Figure 3). Treated with liquid nitrogen as well, the Bowenoid papulosis lesions disappeared.

Genital warts on the left, Bowenoid papulosis on the right.

Histological patterns of epithelial cell vacuolization (koilocytes) on the left and of moderate epithelial dysplasia on the right (hematoxylin-eosin stain, x400).

Treatment with imiquimod cured the genital warts (left) but had little affect on Bowenoid papulosis (right).

A great number of cutaneous disorders have been reported to occur at the site of a previously healed herpes varicella-zoster virus (VZV) or herpes simplex virus (HSV) infection. Table I lists 146 cases that encompass granulomatous reactions (mainly of the granuloma annulare type), malignancies (single tumors, leukemic or lymphomatous infiltrations), dysimmune reactions (e.g., lichen planus), infections (viral, bacterial, fungal), and others (e.g., acneiform lesions, reactive perforating collagenosis). The occurrence of one of these disorders at exactly the site of a prior herpetic infection is a well-known phenomenon named Wolf's post-her-petic isotopic response.[1,2,3] The pathogenesis may depend on a subtle local damage of the sensory nerve fibers, induced by the virus (varicella-zoster virus or HSV), and involving the network of neuropeptides secreted from these fibers. The imbalance of neuropeptide functions would lead to a local neuroimmune dysregulation responsible for the onset of the postherpetic isotopic response.

The patient the authors' have presented demonstrates a case of the genital human papillomavirus infection, which showed two different clinical patterns, i.e., typical genital warts and Bowenoid papulosis. Noteworthy is the observation that the Bowenoid papulosis lesions appeared at exactly the site of a previously suffered herpes progenitalis, so featuring a sort of unilateral postherpetic isotopic response. In fact, the authors' cannot consider it coincidental that the different distribution of the lesions, i.e., simple genital warts on an area never affected by the herpes infection, Bowenoid papulosis appeared on the area that had been a site of a HSV infection 4 years before. Moreover, the local treatment with imiquimod, an immunomodulating drug, worked well on the genital warts located on the left side, whereas it proved to be almost ineffective on the Bowenoid papulosis lesions located on the area previously affected by the HSV infection. In this patient, the prior herpes progenitalis may have locally conditioned both the clinical aspect (Bowenoid papulosis) and the unresponsiveness to the treatment of the supervened human papilloma-virus infection. The authors' think that the local neuroimmune dysregulation connected with herpesvirus-induced lesions of sensory nerve fibers may have had a pivotal role in this peculiar (unilateral) postherpetic isotopic response presented.