Anal squamous cell carcinoma (SCC) – caused by human papillomavirus (HPV) infection and arises from premalignant lesions termed squamous intraepithelial lesions (SILs) – is not a common disease in the general population, but its incidence is higher in people living with human immunodeficiency virus (PLHIV).
This is according to a study – “Anal Dysplasia Screening in People Living with HIV: Long-Term Follow-Up in a Large Cohort from Northwest Spain” by Alexandre Pérez-González, Silvia Rodríguez-Rivero, Pilar Fernández-Veiga, et al – that appeared in AIDS Patient Care and STDs.
In this study, the researchers performed a retrospective cohort study at the anal dysplasia unit of Álvaro-Cunqueiro Hospital (Spain). Epidemiological and clinical data were gathered from the Infectious Diseases Sample Collection (an open sample cohort including PLWH) from January 2011 to January 2022. A total of 493 PLWH were considered, 122 (24.7%) of whom were diagnosed with anal dysplasia at baseline, including two cases of anal SCC. Most of individuals were young men (median age, 38 years old) born in Spain (76%), whose vaccination rate before their inclusion in the program was scarce (<3%).
The study found:
- 81 (16.4%) cases were diagnosed with high-grade squamous-intraepithelial lesions (HSILs) and three with anal SCC
- at the baseline, severe immunosuppression (i.e. nadir CD4+ lymphocyte count below 200 cell/μL), and prior diagnosis of condyloma acuminata were more frequent within the group with SILs
- conversely, the baseline CD4+ lymphocyte count was similar among both groups
- HPV-16 was related to a higher risk of HSILs (odds ratio: 2.76)
At the end of the follow-up, 385 PLWH had been retained in care; one patient had died of anal cancer. Anal dysplasia was common (25% of cases), especially among patients infected by HPV-16, diagnosed with condyloma acuminata, and who were severely immunosuppressed. HPV-16 was the main risk factor for the presentation of HSILs.
The researchers concluded that “HPV infection and anal dysplasia, including HSIL, were common (among PLHIV). A poorer immune status (i.e. a nadir lymphocyte CD4+ count below 200 cells/μL) was related to an increased overall frequency of SILs, although this was not true for the HSIL subgroup. Condyloma acuminata and HPV-16 were both related to an increased prevalence of HSILs and so PLWH diagnosed with anogenital condylomas or HPV-16 infection should be screened and followed-up in more detail. Diagnosis of anal SSC was unusual in this cohort but was strongly related to the detection of HPV-16 in these patients.”
