The Role of Human Papilloma Virus Testing in Cervical Cancer Prevention

Molly C. Fey, FNP, MSN; Margaret W. Beal, CNM, PhD


J Midwifery Womens Health. 2004;49(1) 

In This Article

Cervical Cancer

Worldwide, approximately 500,000 new cases of cervical cancer are diagnosed annually, with nearly 13,000 of these cases occurring in the United States. Incidence and mortality have dropped dramatically during the 20th century in developed nations due to high rates of Papanicolaou (Pap) screening and treatment of cervical cancer precursors, but recent trends indicate a slow resurgence over the last decade, particularly in women under the age of 50. Only one fifth of all HPV-associated lesions will ultimately cause cervical cancer if no intervention occurs.[3,5,28]

The small incidence of women with HPV who develop cervical dysplasia suggests that other factors may play a role in the carcinogenic process. Some women carry HPV for years with minimal sequelae, whereas others develop quickly progressing, severe cervical neoplasia.[8] Research supports that the malignant transformation is also influenced by independent, sexual, and non-sexual factors.

Both active and passive cigarette smoking are significantly and independently associated with cervical lesions. Metabolites of nicotine become concentrated in the cervical tissue of women who smoke, and women with HPV are at higher risk for high-grade cervical intraepithelial lesions if they are active smokers. Smoking also lowers the immune response, increasing the chances of persistent infection. Smokers have a two-fold higher risk of cervical cancer. In fact, the number of cigarettes per day is positively correlated to disease severity, and women who smoke more than 10 cigarettes per day are at higher risk for high-grade cervical intraepithelial lesions.[2,7,36]

Oral contraceptive (OC) use has also been considered a potential cofactor in cervical cancer development. A recent metanalysis examined the increased risk of carcinoma in situ and invasive cervical carcinoma in women with HPV who used hormonal contraception for varying duration. No increased risk was conferred with OC use of 4 years or less, whereas use for 5 years or more was associated with an increase in both invasive cervical cancer and carcinoma in situ. In this study, cervical cancer risk was more highly linked to duration of use, as opposed to age at first use. Results suggest that OC use may promote some step in the natural history of HPV infection, encouraging the likelihood of carcinogenesis, but that risk for initial HPV infection or persistence is not influenced.[37,38] Other studies have investigated the link between cervical cancer and OC use, but the relative risks have varied significantly and continue to remain unclear. The metanalysis has been criticized on several methodological grounds, including significant variation in the types of hormonal contraceptive between data subsets. Combined and progestin-only oral and injectable contraceptives of varying dosages were used, and the medication data were collected retrospectively. OC users are also less likely to use barrier protection, thus increasing the risk of contracting HPV. Findings to date do not warrant discontinuing OC use in the case of an abnormal Pap test.[37,38]

Parity is another independent risk factor for cervical disease among HPV-positive women. A direct association exists between a higher number of full-term pregnancies and the increased risk of squamous cell malignancy. After adjustment for age at first intercourse, one study found that women with one or two full-term pregnancies had a 2.3 times greater risk of developing cervical cancer, whereas those with a history of seven or more full-term pregnancies had a 3.8 times greater risk. It is hypothesized that high parity is related to progression of HPV infection because cervical ectopy is higher in parous women, increasing with the number of full-term pregnancies and thus maintaining the transformation zone on the exocervix. Parous women are not more likely to be infected with HPV, indicating that this factor, similar to OC use, may act by promoting the progression of neoplasia to cancer, and not through enhanced acquisition or persistence of HPV.[39]

Immune status is also a principal factor in the clearance or suppression of HPV infection. Immunocompromised women, such as those with HIV, are at increased risk.[8,29]


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