Chapter 10 10.3 Anal Intraepithelial Neoplasia 10.4 Diagnostic Methods for AIN 10.5 Histologic Terminology and Classification The anus consists of the anal canal and the anal margin. The anal canal begins at the apex of the anal sphincter complex, where the rectum enters the puborectalis sling, and ends with the squamous mucosa blending with the perianal skin. This roughly coincides with the palpable intersphincteric groove. Immediately proximal to the dentate line, a narrow zone of transitional mucosa is variably present—the anal transformation zone (TZ). Distal to this, the mucosa consists of squamous epithelium devoid of hairs and glands. The anal margin extends distal to the anal verge (the junction of the hair-bearing skin) (Fig. 10.1). About 80% of anal cancers are of squamous cell origin, with the remainder being adenocarcinomas. More than 85% of anal cancers are associated with human papillomavirus (HPV) and develop via anal intraepithelial neoplasia (AIN). In HPV-associated anal cancer, HPV 16 predominates, followed by HPV 18, as well as HPV 33 and HPV 59. The entry of HPV is most likely by way of skin abrasions. Anal intercourse is a likely risk factor. The proximity of the vaginal introitus to the anus also facilitates nonsexual and autoinoculation in women via vaginal secretions, digital transfer, or transfer of fomites. Women with other HPV-related gynecologic neoplasms are at increased risk for developing anal cancer. A minority of squamous cell carcinomas of the anus develop independently of HPV in a background of lichen sclerosus or lichen planus (Fig. 10.2). The mechanism of HPV-independent carcinogenesis of the anus has not yet been elucidated but seems to parallel that of the vulva (Fig. 10.3). Topographically, anal cancers are located in the anal canal or, to a lesser extent, at the anal margin. Most anal cancers originate from the anal TZ (linea dentata) of the anal canal. The AIN lesions can be intra-anal or perianal. AIN can involve the anal canal by extending from the perianal skin inward or into the canal in isolation. Thus, evidence of perianal HPV infection must prompt the possibility of AIN within the anal canal. More than 75% of AIN lesions are located on the anal TZ. Risk factors are unprotected receptive anal intercourse, lifetime number of sexual partners, a history of genital warts, immunodeficiency, smoking, and a history of HPV-related gynecologic neoplasm including vulvar intraepithelial neoplasia (VIN) and cervical intraepithelial neoplasia (CIN). AIN can also present as part of a multifocal disease process involving any or all anogenital sites (Fig. 10.4). In a study of immunocompetent women with CIN, VIN, or vaginal intraepithelial neoplasia, 12% had AIN and 8% had high-grade (HG)-AIN. Another study of immunocompetent women found AIN in 17% of women with CIN, with 4% having HG-AIN. Interestingly, patients with multiple lesions in different areas of the female genital tract often show the same HPV type in all of the lesions. HPV 16, 18, 33, and 58 are the types most frequently detected in HG-AIN. The prevalence of multiple-type infections decreased from 54% in low-grade (LG)-AIN 1 to 7% in anal carcinoma. The rate of progression from LG-AIN to HG-AIN is reported to be 36 to 66% over 2 years; the rate of progression from HG-AIN to invasive anal cancer has been reported as 5 to 26% over 5 years. Patients with AIN report pruritus and burning sensations or are asymptomatic. Clinically, AIN can present as erythroplakia, leukoplakia, pigmentation, or verrucous lesions. The lesions are usually flat and solitary; 10 to 20% of patients have multiple foci (Fig. 10.5). Fig. 10.1 Anatomy of the anus. 1 Rectum; 2 anal transformation zone with columns of Morgagni; 3 dentate line; 4 anal canal; 5 anal margin.
Colposcopy of the Perianal Region
10 Colposcopy of the Perianal Region
10.1 Anatomy and Histology
10.2 Anal Carcinogenesis
10.3 Anal Intraepithelial Neoplasia
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