> The tumor of the neck of the uterus. Prevention of cervical neoplasia

In particular, the fraction of squamous cell carcinoma attributed to HPV infection is equal to 96% and that of adenocarcinomas is equal to 93% [2].

In the world, the HPV infection è the più frequent among those sexually transmitted diseases: over 75% of sexually active women become infected in the course of life. The infection può as in a way that is completely asymptomatic.

The peak prevalence of infection occurs in young people under 25 years; in fact, it seems that the risk of contracting the infection is highest in the first years following the onset of the activitiesà sexual, and is reduced over time as a result of a spontaneous clearance of the virus and a very low risk of reinfettarsi in the following periods [3,4].

This pattern is found in women of European and North Americans do not seem to be valid for the rest of the World. A multicenter study that involved more than 18 thousand women of age between 15 and 74 years from 11 different countries among Europe, South America, Asia, sub-saharan Africa, has shown that the curves of prevalence for età differ markedly between rich and poor countries [5]. the

While in the women coming from rich areas to confirm the peak of prevalence in young ageà, in women of South America there are two peaks of prevalence of HPV: one before the age of 25 years and one after age 55.

In the women of the areas più the poor of Asia and in Nigeria, however, the prevalence of HPV is stably high in all of the età and è in these countries the prevalence of cervicocarcinoma è, however, più high.

on The contrary, in women who live in rural areas of Vietnam and Thailand, the incidence is consistently low [5].

it is difficult to draw any conclusions from these data, but it is possible to hypothesize that different sexual behaviors, different exposure to prevention interventions and different capacity of the organism to defend itself against the infection can account for these variations.

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The risk factor più significant for acquiring the infection by HPV is the have recently entered a new sexual relationship, così as is the case for the majority of sexually transmitted infections. The risk of having the HPV infection is multiplied by a factor from two to five when the woman has two or more partners in the last year (OR 1.8 95%CI 1.1, 3.0; OR 2.74 95%CI 1.52, 4.94; OR 5.33 95%CI 2.14, 13.0;) [6-8].

The habit of smoking appears to increase the risk of infection of two times (OR 1.87 95%CI 1.15, 3.06) [8], even though the association is not è confirmed in another study (OR 1.6 95%CI 0.6, 5.0) [9].

The history of or susceptibility to infection by herpes simplex genital, similarly to other sexually transmitted diseases, increases of about four times the risk of becoming infected with HPV (OR 3.54 95%CI 1.37, 9.1) [10]. With regard to the use of oral contraceptives, the data are conflicting, with studies that argue for a protective role (OR 0.49 95%CI 0.28, 0.86) [10] and others, who conclude for the role of risk (OR 3.36 95%CI 1.30, 8.68) [8].

A cohort study, multicenter trial that has analyzed the relationship between intake of oral contraceptives, the prevalence of HPV infection and progression to precancerous lesions and invasive carcinoma, has compared: (a) women not taking any contraceptive; (b) women who were using contraceptives other than those oral; c) women who used only oral contraceptives [11].

The study demonstrated that the use of oral contraceptives is not; the real risk factor but only an epiphenomenon of sexual behavior, which is the real cause of the increased risk of infection, and then the progression of the disease [11].

it is likely that the different weight that the risk factors for the infection have in the various studies and the results are sometimes conflicting, depend just by the weight that each of these has in different settings as a marker of sexual behaviour to a greater or lesser risk.

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About 75% of infections from HPV resolve spontaneously, but some give rise to persistent infections, and possibly precancerous lesions, which if not identified and treated properly may progress over 20 to 30 years in cervical cancer [3,4].

You should, however, remember that over 70% of lesions of low-grade regresses spontaneously within three years from diagnosis, with the exception of the women immunocompromesse [4].

For more information:

the Pap Test is unnecessary after a hysterectomy


1. World Health Organization. Preparing for the introduction of HPV vaccines. Policy and programme guidance for countries. UNFPA & World Health Organization, Geneva. 2006

2. Castellsague X, Diaz M, de Sanjose S, Munoz N, Herrero R, Franceschi S, Peeling RW, Ashley R, Smith JS, Snijders PJ, Meijer CJ, Bosch FX; International Agency for Research on Cancer Multicenter Cervical Cancer Study Group. Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. J Natl Cancer Inst. 2006;98:303-15 [Medline]

3. Schiffman M, Castle PE. The promise of global cervical-cancer prevention. N Engl J Med. 2005;353:2101-4 [Medline]

4. Frazer IH, Cox JT, Mayeaux EJ Jr, Franco EL, Moscicki AB, Palefsky JM, Ferris DG, Ferenczy AS, Villa LL. Advances in prevention of cervical cancer and other human papillomavirus-related diseases. Pediatr Infect Dis J. 2006;25:S65-81 [Medline]

5. Franceschi S, Herrero R, Clifford GM, Snijders PJ, Arslan A, Anh PT, Bosch FX, Ferreccio C, Hieu NT, Lazcano-Ponce E, Matos E, Molano M, Qiao YL, Rajkumar R, Ronco G, de Sanjose S, Shin HR, Sukvirach S, Thomas JO, Meijer CJ, Munoz N. Variations in the age-specific curves of human papillomavirus prevalence in women worldwide. Int J Cancer. 2006;119:2677-84 [Medline]

6. Li LK, Dai M, Clifford GM, Yao WQ, Arslan A, Li N, Shi JF, Snijders PJ, Meijer CJ, Qiao YL, Franceschi S. Human papillomavirus infection in Shenyang City, People’s Republic of China: A population-based study. Br J Cancer. 2006;95:1593-7[Medline]

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7. Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, Markowitz LE. Prevalence of HPV infection among females in the United States. JAMA. 2007;297:813-9 [Medline]

8. Rousseau MC, Franco EL, Villa LL, Sobrinho JP, Termini L, Prado JM, Rohan TE. A cumulative case-control study of risk factor profiles for oncogenic and nononcogenic cervical human papillomavirus infections. Cancer Epidemiol Biomarkers Prev. 2000;9:469-76 [Medline]

9. Hernandez-Giron C, Smith JS, Lorincz A, Arreola Chaidez E, Lazcano E, Hernandez-Avila M, Salmeron J. [The prevalence of high-risk HPV infection in pregnant women from Morelos, Mexico] Salud Publica Mex. 2005;47:423-9 [Medline]

10. Moscicki AB, Hills N, Shiboski S, Powell K, Jay N, Hanson E, Miller S, Clayton L, Farhat S, Broering J, Darragh T, Palefsky J. Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females. JAMA. 2001;285(23):2995-3002 [Medline]

11. Syrjanen K, Shabalova I, Petrovichev N, Kozachenko V, Zakharova T, Pajanidi J, Podistov J, Chemeris G, Sozaeva L, Lipova E, Tsidaeva I, Ivanchenko O, Pshepurko A, Zakharenko S, Nerovjna R, Kljukina L, Erokhina O, Branovskaja M, Nikitina M, Grunberga V, Grunberg A, Juschenko A, Santopietro R, Cintorino M, Tosi P, Syrjanen S. Oral contraceptives are not an independent risk factor for cervical intraepithelial neoplasia or high-risk human papillomavirus infections. Anticancer Res. 2006;26(6C):4729-40 [Medline]

edited SaPeRiDoc – www.saperidoc.it


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Page updated on April 1, 2007