Exophytic Lesion of the Tongue in a Patient with Undetectable HIV-RNA in the Past 3 Years

Oral and oropharyngeal squamous cell cancer risk factors include tobacco use, alcohol consumption, and oncogenic human papillomavirus (HPV). ¹ HIV and HPV infection share the same risk factors, ² moreover HIV-infected patients show an increased burden of HPV-induced dysplasia and HPV-related cancer because of weakened immune systems. A 55-year-old heterosexual male, with 17 years of HIV-1 infection, previous intravenous drug abuser, with a history of tobacco (15 cigarettes/day) and alcohol consumption, developed an exophytic lesion of the tongue (Fig. 1A). Extraoral examination revealed no cervical lymphadenopathy. The patient was on stable antiretroviral therapy with emtricitabine, tenofovir, and rilpivirine in a single tablet regimen. The CD4 cell count was 447 per mmc (13.1%) and CD4/CD8 cell ratio was 0.2%, with no detectable plasma HIV-RNA (<3 copies/ml) in the past 3 years.

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FIG. 1.

(A) Exophytic lesion of the left side of the tongue. (B) Microphotograph of the lesion shows a moderately differentiated, focally keratinizing squamous cell carcinoma. Foci of clear-cut stromal invasion are shown on the bottom right of the picture.

Subsequent head and neck magnetic resonance imaging showed a 20 × 12 × 15 mm mass infiltrating the genioglossus muscle without apparent lymphonodal involvement. A diagnosis of squamous cell carcinoma was formulated on biopsies of the lesion. Immunohistochemical expression of p16 antigen resulted positive for both cytoplasmatic and nuclear in neoplastic cells of the bioptic specimens, suggesting the presence of HPV infection. The patient underwent surgical excision of the neoplasia and the histological examination confirmed the presence of a low-intermediate grade, partially keratinizing, squamous cell carcinoma (Fig. 1B).

This case shows the clinical relevance of HPV-HIV coinfection, particularly in patients with other risk factors for oral squamous cell carcinoma, such as tobacco and alcohol consumption. The patient was on effective antiretroviral therapy with optimal control of HIV replication but with a low CD4/CD8 cell ratio; this scenario is known to be associated with an increased risk of serious non-AIDS events. ³

It is conceivable that although other risk factors may have contributed to initiation and progression of the neoplasm, HPV infection, given the immunohistochemical data, may be considered the prominent trigger.

Current data show the efficiency of HPV vaccination in preventing dysplasia and intraepithelial neoplasia even after HPV infection. ⁴ It is important to emphasize the relevance of correct sexual behaviors and communication about the risk of HPV infection along with HPV vaccination, especially for all HIV-infected patients, as a valuable tool to reduce HPV-related complications.