ASCCP - Practice Recommendations - Practice Management Materials

PRACTICE RECOMMENDATIONS: Practice Management Materials

• Vulva • Vagina • Cervix • Anus

THE CERVIX: Premalignant Lesions of the Cervix: Definition

• I.	Introduction	• V.	Invasive Cancer of the Cervix
• II.	Anatomy of the Uterine Cervix	• VI.	Colposcopy
• III.	Histology of the Normal Cervix	• VII:	Cervical Cancer Screening and Colposcopy During Pregnancy
• IV.	Premalignant Lesions of the Cervix		Cervical Cancer Screening and Colposcopy During Pregnancy

The incidence and mortality of invasive cervical cancer in the United States and other developed countries has decreased over 70% over the past 50 years due cervical cancer screening programs. The Pap test, despite its limitations, is the most effective screening test of modern medicine. In this country, the numbers of cases of cervical cancer diagnosed each year has been stable for over a decade at approximately 13,000; the numbers of deaths each year number just under 4,000. These numbers remain stable despite the rapid rise in the incidence of pre-invasive disease since the 1960s, coincident with the increase in number of sexual partners and earlier age of onset of sexual relations in the general population. It is important to note that over half of the women diagnosed with and dying from cervical cancer have never undergone cytologic screening, or have been inadequately screened. Older women, socio-economically disadvantaged women, and recent immigrants to the United States from underdeveloped countries are at highest risk for lack of adequate screening.

Over the past two decades, we have come to understand that human papillomviruses (HPVs) are present in nearly all cervical neoplasia, explaining the epidemiology of the disease. Of the more than 100 types of HPVs approximately 40 may involve the anogenital tract. Approximately 15 HPV types are considered oncogenic, causing virtually all cases of cervical cancer. HPV 16 alone accounts for over 50% of cancers and HPV 18 is responsible for an additional 10%. Identified risk factors for cervical cancer such as early age at first intercourse and multiple sexual partners are proxies for risk of HPV infection. However, HPV infection is very common and cervical cancer is not. Co-factors such as smoking, high parity, and host immune responses also play a role.

Serologic measurements of antibodies against HPV capsid antigens, indicative of past infection, provide evidence that a majority of sexually active individuals have been infected with HPV at some point. Prevalence studies show that between 5% and 20% of the general population has HPV DNA detectable in cervical samples; prevalence is higher in younger women (< age 30), compared to those over age 30. In most cases, infection with HPV is transient and may or may not be associated with cervical abnormalities of LSIL or CIN 1. Typically, viral DNA is no longer detected in cervical samples after 1 to 2 years. It is persistent infection with an oncogenic HPV that dramatically increases the risk for developing CIN 3 or cancer.

Potentially cancerous precursor lesions found on the uterine cervix are referred to as cervical intraepithelial neoplasia, or CIN. Traditionally, high-grade CIN is thought to arise as a small focus within a larger area of low-grade CIN that expands and eventually replaces much of the low-grade lesion. This "monoclonal" theory is supported by the fact that there is a 5-year difference between the peak prevalence of CIN 1 and CIN2/3, and detection of a LGSIL Pap greatly increases the risk that a high-grade CIN will be found on subsequent smears. It has been difficult to document the rate of progression because most studies use cervical biopsy to establish an accurate diagnosis, which influences the rate of disease progression.

With the discovery that most CIN 1 lesions regress or persist, the question has been raised as to whether high-grade CIN might be a process that develops concurrently with low-grade CIN. This theory is supported by the fact that CIN 3 can develop without a detectable preceding low-grade CIN lesion, and high-grade CIN is almost always found closer to the squamo-columnar junction (SCJ) than concomitant low-grade lesions. It has also been found that women who turned HPV 16/18 positive had a 39% rate of high-grade CIN at 2 years compared to HPV negative women. Schiffman, et al. reported that both CIN 1 and CIN 2/3 lesions developed within the same time frame in a large group of women who turned HPV positive and were followed for 4 years. This isuue continues to be studied.

Search: