Squamous Intraepithelial Lesion of the Anus in a Man With HIV Infection

Susan C. Ball, MD, MPH

Disclosures

AIDS Read. 2004;14(9) 

In This Article

Similarities to Cervical Cancer, Role of HPV

Many biologic parallels have been drawn between anal and cervical cancer. While cervical cancer occurs at a rate that is nearly 10 times that of anal cancer in the general population, anal cancer has much in common with cervical cancer in terms of its risk factors, epidemiology, cytology, and natural history.

Both cervical cancer and anal cancer are now considered sexually transmitted cancers through their causative link with HPV.[6] Nearly 90% of anal squamous cell carcinomas contain HPV DNA, as do more than 99% of cervical cancers.[7] The presence of HPV in the anogenital tract is considered a risk factor for malignancy.[8]

HPV was isolated as the etiologic agent for warts in 1949.[9] A DNA papovavirus, HPV consists of more than 100 genotypes. Thirty of these genotypes cause warts in the anogenital tract, but only a few are implicated in oncogenesis. Types 16, 18, 31, and 45 account for 80% of cervical cancers. Other HPV subtypes make up the remaining 20%.[10] HPV 16 and 18 are most frequently associated with anogenital cancer. The potential of certain HPV types to become tumorigenic has to do with specific proteins encoded by their genes. All HPV types infect squamous epithelial cells. Whether this infection yields a plantar's wart, a common wart, or a more ominous anogenital dysplasia or neoplasia depends on multiple viral and host factors.

HPV in the anogenital region can be entirely asymptomatic, or it can present in a variety of forms ranging from flat, barely discernible patches to bulky, bleeding masses. Lesions associated with dysplasia or neoplasia may not be visible to the naked eye. Most cutaneous warts are self-limited and even SILs induced by high-risk HPV subtypes resolve spontaneously in the majority of cases. The specific mechanism for oncogenic transformation of these lesions is being sought. The risk for this transformation appears to be low but is undefined. In one study of untreated patients with cervical carcinoma in situ in New Zealand, 20% to 30% of lesions progressed to invasive carcinoma in 5 to 10 years.[11] High-grade cervical lesions are no longer monitored but are treated routinely. Malignant transformation of anal lesions likely reflects the cervical rates.

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