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Cervical Dysplasia


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Introduction
Cervical dysplasia may be defined as pre-invasive neoplastic epithelial changes in the transformation zone of the uterine cervix often associated with human papillomavirus infections.(1) It is also known as cervical intraepithelial neoplasia, (CIN) or noted in reference to pap smear as squamous intraepithelial lesion (SIL). It is classified into categories of mild, moderate, or severe.

Mild dysplasia (CIN I or SIL low grade) is limited to cellular changes in the lower one-third of the squamous epithelium. Moderate dysplasia (CIN II or SIL high grade) includes cellular changes in the lower two-thirds of the squamous epithelium, and severe dysplasia (CIN III or SIL high grade or carcinoma in situ) involves the full thickness of the squamous epithelium.

The risk of cervical dysplasia, and cervical neoplasia is higher for women with multiple partners, women who's sexual partners are more promiscuous, and women whose first sexual intercourse was at an early age.(2)

Many studies have linked the number of sexual partners as a strong risk factor for both pre-invasive and invasive lesions of the cervix. Several epidemiologic studies have provided evidence supporting an association between cigarette smoking and CIN and invasive cervical cancer.(3) Most studies have shown a two-fold increased risk for cervical neoplasia among smokers and a dose-response relationship with the duration and intensity of smoking.(4)

Nutritional factors have been implicated in 60% of cancers in women and 40% of cancers in men.(5) Several lines of evidence suggest that some nutrients may have a protective effect against cervical neoplasia, particularly Vitamin A, carotenoids, vitamin C, vitamin E, and folic acid.(6) Comparison of such studies is difficult, however, due to use of different methods of nutrient measurement (dietary intake by food frequencies, food records, or 24h recall diet; tissue, serum, or red blood cell levels), selection of comparison groups, methods of diagnosis, and control of confounding factors.

In recent years, the risk of cervical dysplasia has shown strong linkage to human papilloma viruses type 6,11,16,18,31,and 35.

HPV infection has been strongly associated with the development of dysplasia and cancer of the uterine cervix. More than 90% of cervical cancers contain DNA of oncogenic (high-risk) HPV types such as 16,18, and 31.(7) HPV DNA is also present in the precursor lesions of cervical cancer (CIN).(8)

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Footnotes
1 Shiu AT. Cervical dysplasia. In: Dambro MR ed. Griffith's 5-minute Clinical Consult. Philadelphia: Lippincott, Wlliams, & Wilkins; 1999:103.
2 Munoz N. Bosch FX: Epidemiology of cervical cancer. IARC Sci Publ. 1989;94:9.
3 Wilkenstein W. Smoking and cervical cancer--current status: A review. Am J Epidemiol. 1990;131:945.
4 Brinton LA. Epidemiology of cervical cancer—overview. IARC Sci Publ. 1992;119:3.
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5 Schneider A, Shah K. The role of vitamins in the etiology of cervical neoplasia: An Epidemiologic review. Arch Gynecol Obstet. 1989;246:1.
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6 Morris M, Tortolero-Luna G, Malpica A, et al. Cervical intraepithelial neoplasia and cervical cancer. Obstet Gynecol Clin North Am. Jun1996;Vol 23(2):347-410.
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7 American Cancer Society. Cervical cancer fact sheet. Revised. Feb2000.
8 Reichman RC. Human Papillomavirus Infections, In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine, 14th ed. New York: McGraw-Hill; 1998:1099.
 
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