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Anal cancer is a squamous cell cancer associated with human papillomavirus (HPV), the same virus that is associated with cervical cancer. In the United States, the current incidence of anal cancer in the general population is approximately 1:100,000 per year, and rising. The incidence of anal cancer is significantly higher in HIV-infected women and men than in the general population. Before the HIV epidemic, the anal cancer incidence in men who have sex with men population was 35:100,000. Current rates in an HIV-infected MSM population are as high as 70-80:100,000. Thus, the incidence of anal cancer in this population is greater than the incidence of cervical cancer in women before the introduction of cervical cytology screening.
Anal squamous cell cancer shares many similarities with cervical cancer in anatomy and histology as well as its association with HPV infection. Somewhat less is known about anal cancer to date. Two recent studies that conducted HPV typing of anal cancer specimens reported HPV positivity rates 83 & 81% (all men), 95% & 88% (all women), and 98% (MSM). Most of these HPV infections were with "high oncogenic risk" (HR) HPV types such as HPV 16, 18, 31, 33, 35, etc. However, "low oncogenic risk" HPV types such as HPV 6, 11, can be detected alone in a small minority (~2.5%) of anal cancers.*
*Frisch M, Fenger C, van den Bruke AJ, et al. Variants of squamous cell carcinoma of the anal canal and perianal skin and their relation to human papilloma viruses. Cancer Res 1999; 59: 753-757
Daling JR, Madeleine M, Johnson LG, et al. Human papillomavirus, smoking, and sexual practices in the etilogy of anal cancer. Cancer 2004; 101: 270-280
Tests for Detection of Anal Pre-Cancer
WCPL uses sensitive PCR methodology to detect HPV in anal cytology specimens as well as in swabs of the anal epithelium. Anal cytology provides sampling of the anal cells that may demonstrate nuclear changes that identify premalignant changes. HPV testing identifies the presence of HPV viruses that are associated with anal carcinoma in situ and anal carcinoma. Frequently, anal dysplasia (premalignant changes) are accompanied by anal warts, the latter being markers for exposure to the HPV virus.
Collection swabs and transport media are provided free of charge by WCPL if anal HPV testing and/or cytology are desired. Anal evaluation is desirable in all patients, male or female, who have unprotected anal intercourse as well as women who have high grade dysplasia of the cervix or vulva. These patients are at greatest risk of dysplastic changes in the anal epithelium. Smoking is associated with an increased risk of anal dysplasia in those patients exposed to high risk HPV viruses.
Anal warts are frequently encountered in clinical practice, and can be problematic to treat. Ano-genital warts can be caused by HPV 6 and HPV 11. Recent studies using sensitive PCR methodology have detected either HPV 6 or HPV 11 in ~100% of genital wart lesion, but have also shown that genital wart lesions are frequently co-infected with high risk HPV types, especially in HIV infected individuals, where co-infection rates of up to 100% are seen.* Thus when anal warts are present anal intra-epithelial neoplasia (AIN) can be frequently detected concomitantly.
AIN affecting the peri-anal skin, perineum, or natal cleft can produce symptoms of itching and soreness. It also often produces recognizable clinical signs of pigmentation, white lesions, fissuring, etc. If there is ulceration, tests for HSV should be carried out. Diagnostic punch biopsies should be carried out if there are physical signs suggestive of AIN, or persistent ulceration.
However, when AIN alone affects the anal canal there are usually no symptoms and often no overt clinical signs. Occasionally AIN can be suspected on naked eye inspection, manifesting as white plaques, or red lesions. When invasive cancer is present there may be symptoms of soreness and bleeding, and there are signs of ulceration or induration.
*Brown DR, Schroeder JM, Bryan JT, et al. Detection of multiple human papillomavirus types in condyloma acuminata lesions from otherwise healthy and immunosuppresed patients. J Clin Micro 1999; 37: 3316-3322
The current definitive treatment for Cervical Intraepithelial Neoplasia III (3) is excision of the cervical transformation zone. Unfortunately the anatomy and complex physiology of the anal canal precludes any similar such approach in anal dysplasia or premalignancy. The anal mucosa also surmounts only a narrow bandwidth of sub-mucosa before deeper fundamental structures are encountered, and thus excision or ablative surgical therapies performed on the mucosa have to be restricted to the superficial layers, and excision of too extensive an area can result in the serious consequence of anal stenosis. Perhaps because of these difficulties a variety of treatments of AIN have been described. These include treatments that are evidence-based for genital warts, including podophyllotoxin, trichloracetic acid, imiquimod, and electrosurgery, although the evidence base for using these treatments for genital warts in HIV infected subjects is much smaller. However, the number of published trials at present that have actually systematically examined treatments for AIN is minute.
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