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\r\n \r\n <!-' + '- message, attachments, sig -' + '->\r\n\r\n \r\n\r\n \r\n <!-' + '- icon and title -' + '->\r\n \r\n \r\n\r\n\r\n\r\n Understanding HPV (Human Papillomavirus)\r\n \r\n \r\n <!-' + '- / icon and title -' + '->\r\n \r\n\r\n <!-' + '- message -' + '->\r\n \r\n \r\n Understanding Human Papillomavirus (HPV) \r\n <!-' + '- / message -' + '->\r\n\r\n \r\n\r\n \r\n \r\n\r\n \r\n <!-' + '- sig -' + '->\r\n \n \nHuman papillomavirus (HPV) is one of the most common causes of \nsexually transmitted diseases (STD) in the world. More than 100 \ndifferent types of HPV exist, most of which are harmless. About 30 \ntypes are spread through sexual contact. Some types of HPV cause \ngenital warts�single or multiple bumps that appear in the genital \nareas of men and women including the vagina, cervix, vulva (area \noutside of the vagina), penis, and rectum. Many people infected with \nHPV have no symptoms. (25). \n \nThere are high-risk and low-risk types of HPV. High-risk HPV may \ncause abnormal Pap smear results, and could lead to cancers of the \ncervix, vulva, vagina, anus, or penis. Low-risk HPV also may cause \nabnormal Pap results or genital warts. (26). \n \nHealth experts estimate there are more cases of genital HPV infection \nthan any other STI in the United States. According to the American \nSocial Health Association, approximately 5.5 million new cases of \nsexually transmitted HPV infections are reported every year. At least \n20 million people in this country are already infected. (25, 26). \n \nAll types of HPV can cause mild Pap test abnormalities which do not \nhave serious consequences. Approximately 10 of the 30 identified \ngenital HPV types can lead, in rare cases, to development of cervical \ncancer. Specifically, HPV 16 and HPV 18 have been found in 90% of \ncases of cervical cancer. Research has shown that for most women (90 \npercent), cervical HPV infection becomes undetectable within two \nyears. Although only a small proportion of women have persistent \ninfection, persistent infection with "high-risk" types of HPV is the \nmain risk factor for cervical cancer. \n \nCervical intraepithelial neoplasia is also called "CIN." Sometimes it \nmay be called cervical dysplasia. CIN means that there is a change in \nthe cells on the surface of the cervix. The cervix is the bottom part \nof the uterus. With CIN normal cells are replaced with cells that are \nnot normal (abnormal). Over time, it is possible for these abnormal \ncells to turn into cancer. (3,4). \n \nAny woman can have CIN. CIN itself is not cancer. But it can turn \ninto cancer of the cervix. Following are the 3 types of CIN: \n \n \nCIN I (1). This is also called mild dysplasia. \nCIN II (2). This is also called moderate dysplasia. \nCIN III (3). This is also called severe dysplasia. \n \n \nIt is not known for sure what causes CIN but it may be caused by a \nvirus that is spread during sex. The virus that causes venereal warts \n("HPV") is thought to play a role in many cases of CIN and cervical \ncancer. You may be more likely to get CIN if you have many sex \npartners or if your partner has many sex partners. \n \nThe following may put you at a higher risk of having CIN. \n \n \n*Less than 20 years of age at time of first sex. \n*Having a sexually transmitted disease (STD), like HPV, herpes, or \ncytomegalovirus (CMV). \n*A Pap smear test that is not normal. \n*Cigarette smoking. \n \n \nA Pap test can detect pre-cancerous and cancerous cells on the \ncervix. Regular Pap testing and careful medical follow-up, with \ntreatment if necessary, can help ensure that pre-cancerous changes in \nthe cervix caused by HPV infection do not develop into life \nthreatening cervical cancer. The Pap test used in U.S. cervical \ncancer screening programs is responsible for greatly reducing deaths \nfrom cervical cancer. For 2004, the American Cancer Society estimates \nthat about 10,520 women will develop invasive cervical cancer and \nabout 3,900 women will die from this disease. Most women who develop \ninvasive cervical cancer have not had regular cervical cancer \nscreening. (26-29) \n \nAlthough there is currently no medical cure for papillomavirus \ninfection, the lesions and warts these viruses cause can be treated. \nMethods commonly used to treat lesions include cryosurgery (freezing \nthat destroys tissue), LEEP (loop electrosurgical excision procedure, \nthe removal of tissue using a hot wire loop), and conventional \nsurgery. Similar treatments may be used for external genital warts. \nIn addition, some drugs may be used to treat external genital warts. \nMore information about treatment for genital warts can be found in \nthe Centers for Disease Control and Prevention\'s (CDC) Sexually \nTransmitted Diseases Treatment Guidelines 2002. Copies of the \nguidelines are available at https://www.cdc.gov/STD/treatment \n \n \nAlternative Medicine \n \nA study of the clinical efficacy of green tea extracts (polyphenon E; \npoly E and (-)-epigallocatechin-3-gallate [EGCG]) delivered in a form \nof ointment or capsule in patients with human papilloma virus (HPV) \ninfected cervical lesions. Fifty-one patients with cervical lesions \n(chronic cervicitis, mild dysplasia, moderate dysplasia and severe \ndysplasia) were divided into four groups, as compared with 39 \nuntreated patients as a control. Poly E ointment was applied locally \nto 27 patients twice a week. For oral delivery, a 200 mg of poly E or \nEGCG capsule was taken orally every day for eight to 12 weeks. In the \nstudy, 20 out of 27 patients (74%) under poly E ointment therapy \nshowed a response. Six out of eight patients under poly E ointment \nplus poly E capsule therapy (75%) showed a response, and three out of \nsix patients (50%) under poly E capsule therapy showed a response. \nSix out of 10 patients (60%) under EGCG capsule therapy showed a \nresponse. (34). \n \nOverall, a 69% response rate (35/ 51) was noted for treatment with \ngreen tea extracts, as compared with a 10% response rate (4/39) in \nuntreated controls (P<0.05). Thus, the data collected here \ndemonstrated that green tea extracts in a form of ointment and \ncapsule are effective for treating cervical lesions, suggesting that \ngreen tea extracts can be a potential therapy regimen for patients \nwith HPV infected cervical lesions. (34). \n \nWomen who consume low amounts of foods rich in vitamin C, beta \ncarotene and folic acid have a higher incidence of CIN and HPV (14). \nA diet rich in fruits, vegetables, whole grains and legumes (beans) \nwill provide generous amounts of these nutrients. \n \nAntioxidants seem to reduce the risk of CIN (8) and cancer (21). Low \nlevels of vitamin A (16), vitamin C (15,16) and vitamin E (2,13) are \nassociated with a greater risk of CIN and possibly cervical cancer. \nThe amount of antioxidants in a daily multivitamin are reasonable and \nsafe. \n \nCopper levels tend to be higher in women with CIN (9) or gynecologic \ntumors (3). It may be wise to avoid taking copper supplements if \ndealing with CIN. \n \nFolic acid levels tend to be lower in women with dysplasia (7,10) and \nHPV (4). Folic acid may help prevent CIN but does not appear to \neradicate existing CIN (24). Very high doses of folic acid have been \nused in treatment but the amounts present in a B-complex supplement \nor a daily multivitamin are reasonable for preventive purposes. \n \nPyridoxine (B6) levels tend to be low in cervical cancer (20). It is \ninteresting that birth control pills can lower B6 levels (1,17) and \nbirth control pills also seem to be a risk factor for CIN (4,5) which \ncan progress to cervical cancer if left untreated. Taking vitamin B6 \nin a daily multivitamin or B-complex supplement may be beneficial, \nparticularly if using birth control pills. \n \nRiboflavin (B2) levels tend to be low in women with CIN (16). \nRiboflavin vaginal suppositories have actually been shown to cause \nregression of CIN (6). \n \nSelenium levels tend to be lower in women with cervical cancer (2). \nSelenium has been shown to reduce the incidence of experimentally \ninduced cervical cancer in laboratory animals (12). A dose of 200 \nmicrograms daily of selenium is reasonable and safe (18). This amount \nof selenium is often available in a daily multivitamin. \n \nZinc levels tend to be lower in women with CIN (9) or gynecologic \ntumors (3). Taking 15 - 30 milligrams of zinc daily in a multivitamin \nis reasonable. \n \n \nSTD information and referrals to STD Clinics \nCDC-INFO \n1-800-CDC-INFO (800-232-4636) \nTTY: 1-888-232-6348 \n \n \nReferences \n \n1. Bermond P: Therapy of side effects of oral contraceptive agents \nwith vitamin B6. Acta Vitaminol Enzymol 1982;4(1-2):45-54. \n \n2. Bhuvarahamurthy V, Balasubramanian N & Govindasamy S: Effect of \nradiotherapy and chemoradiotherapy on circulating antioxidant system \nof human uterine cervical carcinoma. Mol Cell Biochem 1996 May 10;158 \n(1):17-23. \n \n3. Brandes JM, Lightman A, Drugan A et al: The diagnostic value of \nserum copper/zinc ratio in gynecological tumors. Acta Obstet Gynecol \nScand 1983;62(3):225-9. \n \n4. Butterworth CE: Folate deficiency and cervical dysplasia. JAMA \n1992;267:528-533. \n \n5. Castaneda-Iniguez MS, Toledo-Cisneros R & Aguilera-Delgadillo M: \n[Risk factors for cervico-uterine cancer in women in Zacatecas] Salud \nPublica Mex 1998 Jul-Aug;40(4):330-8. \n \n6. Chen RD: [Chemoprevention of cervical cancer-' + '-intervention study \nof cervical precancerous lesions by retinamide II and riboflavin] \nChung Hua Chung Liu Tsa Chih 1993 Jul;15(4):272-4. \n \n7. Fowler BM, Giuliano AR, Piyathilake C et al: Hypomethylation in \ncervical tissue: is there a correlation with folate status? Cancer \nEpidemiol Biomarkers Prev 1998 Oct;7(10):901-6. \n \n8. Goodman MT, Kiviat N, McDuffie K et al:,,The association of plasma \nmicronutrients with the risk of cervical dysplasia in Hawaii. Cancer \nEpidemiol Biomarkers Prev 1998 Jun;7(6):537-44. \n \n9. Grail A & Norval M: Copper and zinc levels in serum from patients \nwith abnormalities of the uterine cervix. Acta Obstet Gynecol Scand \n1986;65(5):443-7. \n \n10. Grio R, Piacentino R, Marchino GL et al: Antineoblastic activity \nof antioxidant vitamins: the role of folic acid in the prevention of \ncervical dysplasia. Panminerva Med 1993 Dec;35(4):193-6. \n \n11. Ho GY, Kadish AS, Burk RD, Basu J, Palan PR, Mikhail M, Romney \nSL: HPV 16 and cigarette smoking as risk factors for high-grade \ncervical intra-epithelial neoplasia. Int J Cancer 1998 Oct 29;78 \n(3):281-5. \n \n12. Hussain SP, Rao AR: Chemopreventive action of selenium on \nmethylcholanthrene-induced carcinogenesis in the uterine cervix of \nmouse. Oncology 1992;49(3):237-40. \n \n13. Kwasniewska A, Charzewska J, Tukendorf A, Semczuk M: Dietary \nfactors in women with dysplasia colli uteri associated with human \npapillomavirus infection. Nutr Cancer 1998;30(1):39-45. \n \n14. Kwasniewska A, Tukendorf A, Semczuk M: Content of alpha- \ntocopherol in blood serum of human Papillomavirus-infected women with \ncervical dysplasias. Nutr Cancer 1997;28(3):248-51. \n \n15. Liu T, Soong SJ, Alvarez RD et al: A longitudinal analysis of \nhuman papillomavirus 16 infection, nutritional status, and cervical \ndysplasia progression. Cancer Epidemiol Biomarkers Prev 1995 Jun;4 \n(4):373-80. \n \n16. Liu T, Soong SJ, Wilson NP et al: A case control study of \nnutritional factors and cervical dysplasia. Cancer Epidemiol \nBiomarkers Prev 1993 Nov-Dec;2(6):525-30. \n \n17. Masse PG, van den Berg H, Duguay C et al: Early effect of a low \ndose (30 micrograms) ethinyl estradiol-containing Triphasil on \nvitamin B6 status. A follow-up study on six menstrual cycles. Int J \nVitam Nutr Res 1996;66(1):46-54 \n \n18. Patterson BH & Levander OA: Naturally occurring selenium \ncompounds in cancer chemoprevention trials: a workshop summary. \nCancer Epidemiol Biomarkers Prev 1997 Jan;6(1):63-9. \n \n19. Potischman N: Nutritional epidemiology of cervical neoplasia. J \nNutr 1993 Feb;123(2 Suppl):424-9. \n \n20. Ramaswamy PG & Natarajan R: Vitamin B6 status in patients with \ncancer of the uterine cervix. Nutr Cancer 1984;6(3):176-80. \n \n21. Reddy BS: Micronutrients as chemopreventive agents. IARC Sci Publ \n1996;(139):221-35. \n \n22. Roteli-Martins CM, Panetta K, Alves VA et al: Cigarette smoking \nand high-risk HPV DNA as predisposing factors for high-grade cervical \nintraepithelial neoplasia (CIN) in young Brazilian women. Acta Obstet \nGynecol Scand 1998 Jul;77(6):678-82. \n \n23. Yoshikawa H, Nagata C, Noda K et al: Human papillomavirus \ninfection and other risk factors for cervical intraepithelial \nneoplasia in Japan. Br J Cancer 1999 May;80(3-4):621-4. \n \n24. Zarcone R, Bellini P, Carfora E, et al. Folic acid and cervix \ndysplasia. Minerva Ginecol 1996;48:397-400. alteration of glucose \ntolerance. \n \n25. Centers for Disease Control and Prevention, Division of STD \nPrevention. Prevention of genital HPV infection and sequelae: Report \nof an external consultants\' meeting. December 1999. \n \n26. Centers for Disease Control and Prevention. Sexually transmitted \ndiseases treatment guidelines 2002. Morbidity and Mortality Weekly \nReport 2002; 51(RR�6). \n \n27. Chu NR. Therapeutic vaccination for the treatment of mucosotropic \nhuman papillomavirus-associated disease. Expert Opinion on Biological \nTherapy 2003; 3(3):477�486. \n \n28. Ho GYF, Bierman R, Beardsley L, Chang CJ, Burk RD. Natural \nhistory of cervicovaginal papilloma virus infection in young women. N \nEngl J Med 1998;338:423-8. \n \n29. Koutsky LA, Kiviat NB. Genital human papillomavirus. In: K. \nHolmes, P. Sparling, P. Mardh et al (eds). Sexually Transmitted \nDiseases, 3rd edition. New York: McGraw-Hill, 1999, p. 347-359. \n \n30. Kiviat NB, Koutsky LA, Paavonen J. Cervical neoplasia and other \nSTD-related genital tract neoplasias. In: K. Holmes, P. Sparling, P. \nMardh et al (eds). Sexually Transmitted Diseases, 3rd edition. New \nYork: McGraw-Hill, 1999, p. 811-831. \n \n31. Myers ER, McCrory DC, Nanda K, Bastian L, Matchar DB. \nMathematical model for the natural history of human papillomavirus \ninfection and cervical carcinogenesis. American Journal of \nEpidemiology 2000; 151(12):1158-1171. \n \n32. Watts DH, Brunham RC. Sexually transmitted diseases, including \nHIV infection in pregnancy. In: K. Holmes, P. Sparling, P. Mardh et \nal (eds). Sexually Transmitted Diseases, 3rd edition. New York: \nMcGraw-Hill, 1999, 1089-1132. \n \n33. Weinstock H, Berman S, Cates W. Sexually transmitted disease \namong American youth: Incidence and prevalence estimates, 2000. \nPerspectives on Sexual and Reproductive Health 2004; 36: 6-10.. \n \n34. WS Ahn, J Yoo, SW Huh -Protective effects of green tea extracts \non human cervical lesions - polyphenon E and EGCG - Brief Article, \nAlternative Medicine Review, Nov, 2003 \n \nhttps://www.peacefulmind.com/ailments.htm\r\n \r\n __________________ \r\n <!-' + '- / sig -' + '->\r\n \r\n\r\n \r\n\r\n \r\n\r\n \r\n\r\n <!-' + '- message, attachments, sig -' + '->\r\n\r\n \r\n "We can judge the heart of a man by his treatment of animals." ~Immanual Kant~ \r\n \r\nNatMedTalk and Beyond\r\n | \r\n
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Understanding HPV (Human Papillomavirus)
Understanding Human Papillomavirus (HPV)
Human papillomavirus (HPV) is one of the most common causes of sexually transmitted diseases (STD) in the world. More than 100 different types of HPV exist, most of which are harmless. About 30 types are spread through sexual contact. Some types of HPV cause genital warts�single or multiple bumps that appear in the genital areas of men and women including the vagina, cervix, vulva (area outside of the vagina), penis, and rectum. Many people infected with HPV have no symptoms. (25). There are high-risk and low-risk types of HPV. High-risk HPV may cause abnormal Pap smear results, and could lead to cancers of the cervix, vulva, vagina, anus, or penis. Low-risk HPV also may cause abnormal Pap results or genital warts. (26). Health experts estimate there are more cases of genital HPV infection than any other STI in the United States. According to the American Social Health Association, approximately 5.5 million new cases of sexually transmitted HPV infections are reported every year. At least 20 million people in this country are already infected. (25, 26). All types of HPV can cause mild Pap test abnormalities which do not have serious consequences. Approximately 10 of the 30 identified genital HPV types can lead, in rare cases, to development of cervical cancer. Specifically, HPV 16 and HPV 18 have been found in 90% of cases of cervical cancer. Research has shown that for most women (90 percent), cervical HPV infection becomes undetectable within two years. Although only a small proportion of women have persistent infection, persistent infection with "high-risk" types of HPV is the main risk factor for cervical cancer. Cervical intraepithelial neoplasia is also called "CIN." Sometimes it may be called cervical dysplasia. CIN means that there is a change in the cells on the surface of the cervix. The cervix is the bottom part of the uterus. With CIN normal cells are replaced with cells that are not normal (abnormal). Over time, it is possible for these abnormal cells to turn into cancer. (3,4). Any woman can have CIN. CIN itself is not cancer. But it can turn into cancer of the cervix. Following are the 3 types of CIN: CIN I (1). This is also called mild dysplasia. CIN II (2). This is also called moderate dysplasia. CIN III (3). This is also called severe dysplasia. It is not known for sure what causes CIN but it may be caused by a virus that is spread during sex. The virus that causes venereal warts ("HPV") is thought to play a role in many cases of CIN and cervical cancer. You may be more likely to get CIN if you have many sex partners or if your partner has many sex partners. The following may put you at a higher risk of having CIN. *Less than 20 years of age at time of first sex. *Having a sexually transmitted disease (STD), like HPV, herpes, or cytomegalovirus (CMV). *A Pap smear test that is not normal. *Cigarette smoking. A Pap test can detect pre-cancerous and cancerous cells on the cervix. Regular Pap testing and careful medical follow-up, with treatment if necessary, can help ensure that pre-cancerous changes in the cervix caused by HPV infection do not develop into life threatening cervical cancer. The Pap test used in U.S. cervical cancer screening programs is responsible for greatly reducing deaths from cervical cancer. For 2004, the American Cancer Society estimates that about 10,520 women will develop invasive cervical cancer and about 3,900 women will die from this disease. Most women who develop invasive cervical cancer have not had regular cervical cancer screening. (26-29) Although there is currently no medical cure for papillomavirus infection, the lesions and warts these viruses cause can be treated. Methods commonly used to treat lesions include cryosurgery (freezing that destroys tissue), LEEP (loop electrosurgical excision procedure, the removal of tissue using a hot wire loop), and conventional surgery. Similar treatments may be used for external genital warts. In addition, some drugs may be used to treat external genital warts. More information about treatment for genital warts can be found in the Centers for Disease Control and Prevention's (CDC) Sexually Transmitted Diseases Treatment Guidelines 2002. Copies of the guidelines are available at https://www.cdc.gov/STD/treatment Alternative Medicine A study of the clinical efficacy of green tea extracts (polyphenon E; poly E and (-)-epigallocatechin-3-gallate [EGCG]) delivered in a form of ointment or capsule in patients with human papilloma virus (HPV) infected cervical lesions. Fifty-one patients with cervical lesions (chronic cervicitis, mild dysplasia, moderate dysplasia and severe dysplasia) were divided into four groups, as compared with 39 untreated patients as a control. Poly E ointment was applied locally to 27 patients twice a week. For oral delivery, a 200 mg of poly E or EGCG capsule was taken orally every day for eight to 12 weeks. In the study, 20 out of 27 patients (74%) under poly E ointment therapy showed a response. Six out of eight patients under poly E ointment plus poly E capsule therapy (75%) showed a response, and three out of six patients (50%) under poly E capsule therapy showed a response. Six out of 10 patients (60%) under EGCG capsule therapy showed a response. (34). Overall, a 69% response rate (35/ 51) was noted for treatment with green tea extracts, as compared with a 10% response rate (4/39) in untreated controls (P<0.05). Thus, the data collected here demonstrated that green tea extracts in a form of ointment and capsule are effective for treating cervical lesions, suggesting that green tea extracts can be a potential therapy regimen for patients with HPV infected cervical lesions. (34). Women who consume low amounts of foods rich in vitamin C, beta carotene and folic acid have a higher incidence of CIN and HPV (14). A diet rich in fruits, vegetables, whole grains and legumes (beans) will provide generous amounts of these nutrients. Antioxidants seem to reduce the risk of CIN (8) and cancer (21). Low levels of vitamin A (16), vitamin C (15,16) and vitamin E (2,13) are associated with a greater risk of CIN and possibly cervical cancer. The amount of antioxidants in a daily multivitamin are reasonable and safe. Copper levels tend to be higher in women with CIN (9) or gynecologic tumors (3). It may be wise to avoid taking copper supplements if dealing with CIN. Folic acid levels tend to be lower in women with dysplasia (7,10) and HPV (4). Folic acid may help prevent CIN but does not appear to eradicate existing CIN (24). Very high doses of folic acid have been used in treatment but the amounts present in a B-complex supplement or a daily multivitamin are reasonable for preventive purposes. Pyridoxine (B6) levels tend to be low in cervical cancer (20). It is interesting that birth control pills can lower B6 levels (1,17) and birth control pills also seem to be a risk factor for CIN (4,5) which can progress to cervical cancer if left untreated. Taking vitamin B6 in a daily multivitamin or B-complex supplement may be beneficial, particularly if using birth control pills. Riboflavin (B2) levels tend to be low in women with CIN (16). Riboflavin vaginal suppositories have actually been shown to cause regression of CIN (6). Selenium levels tend to be lower in women with cervical cancer (2). Selenium has been shown to reduce the incidence of experimentally induced cervical cancer in laboratory animals (12). A dose of 200 micrograms daily of selenium is reasonable and safe (18). This amount of selenium is often available in a daily multivitamin. Zinc levels tend to be lower in women with CIN (9) or gynecologic tumors (3). Taking 15 - 30 milligrams of zinc daily in a multivitamin is reasonable. STD information and referrals to STD Clinics CDC-INFO 1-800-CDC-INFO (800-232-4636) TTY: 1-888-232-6348 References 1. Bermond P: Therapy of side effects of oral contraceptive agents with vitamin B6. Acta Vitaminol Enzymol 1982;4(1-2):45-54. 2. Bhuvarahamurthy V, Balasubramanian N & Govindasamy S: Effect of radiotherapy and chemoradiotherapy on circulating antioxidant system of human uterine cervical carcinoma. Mol Cell Biochem 1996 May 10;158 (1):17-23. 3. Brandes JM, Lightman A, Drugan A et al: The diagnostic value of serum copper/zinc ratio in gynecological tumors. Acta Obstet Gynecol Scand 1983;62(3):225-9. 4. Butterworth CE: Folate deficiency and cervical dysplasia. JAMA 1992;267:528-533. 5. Castaneda-Iniguez MS, Toledo-Cisneros R & Aguilera-Delgadillo M: [Risk factors for cervico-uterine cancer in women in Zacatecas] Salud Publica Mex 1998 Jul-Aug;40(4):330-8. 6. Chen RD: [Chemoprevention of cervical cancer--intervention study of cervical precancerous lesions by retinamide II and riboflavin] Chung Hua Chung Liu Tsa Chih 1993 Jul;15(4):272-4. 7. Fowler BM, Giuliano AR, Piyathilake C et al: Hypomethylation in cervical tissue: is there a correlation with folate status? Cancer Epidemiol Biomarkers Prev 1998 Oct;7(10):901-6. 8. Goodman MT, Kiviat N, McDuffie K et al:,,The association of plasma micronutrients with the risk of cervical dysplasia in Hawaii. Cancer Epidemiol Biomarkers Prev 1998 Jun;7(6):537-44. 9. Grail A & Norval M: Copper and zinc levels in serum from patients with abnormalities of the uterine cervix. Acta Obstet Gynecol Scand 1986;65(5):443-7. 10. Grio R, Piacentino R, Marchino GL et al: Antineoblastic activity of antioxidant vitamins: the role of folic acid in the prevention of cervical dysplasia. Panminerva Med 1993 Dec;35(4):193-6. 11. Ho GY, Kadish AS, Burk RD, Basu J, Palan PR, Mikhail M, Romney SL: HPV 16 and cigarette smoking as risk factors for high-grade cervical intra-epithelial neoplasia. Int J Cancer 1998 Oct 29;78 (3):281-5. 12. Hussain SP, Rao AR: Chemopreventive action of selenium on methylcholanthrene-induced carcinogenesis in the uterine cervix of mouse. Oncology 1992;49(3):237-40. 13. Kwasniewska A, Charzewska J, Tukendorf A, Semczuk M: Dietary factors in women with dysplasia colli uteri associated with human papillomavirus infection. Nutr Cancer 1998;30(1):39-45. 14. Kwasniewska A, Tukendorf A, Semczuk M: Content of alpha- tocopherol in blood serum of human Papillomavirus-infected women with cervical dysplasias. Nutr Cancer 1997;28(3):248-51. 15. Liu T, Soong SJ, Alvarez RD et al: A longitudinal analysis of human papillomavirus 16 infection, nutritional status, and cervical dysplasia progression. Cancer Epidemiol Biomarkers Prev 1995 Jun;4 (4):373-80. 16. Liu T, Soong SJ, Wilson NP et al: A case control study of nutritional factors and cervical dysplasia. Cancer Epidemiol Biomarkers Prev 1993 Nov-Dec;2(6):525-30. 17. Masse PG, van den Berg H, Duguay C et al: Early effect of a low dose (30 micrograms) ethinyl estradiol-containing Triphasil on vitamin B6 status. A follow-up study on six menstrual cycles. Int J Vitam Nutr Res 1996;66(1):46-54 18. Patterson BH & Levander OA: Naturally occurring selenium compounds in cancer chemoprevention trials: a workshop summary. Cancer Epidemiol Biomarkers Prev 1997 Jan;6(1):63-9. 19. Potischman N: Nutritional epidemiology of cervical neoplasia. J Nutr 1993 Feb;123(2 Suppl):424-9. 20. Ramaswamy PG & Natarajan R: Vitamin B6 status in patients with cancer of the uterine cervix. Nutr Cancer 1984;6(3):176-80. 21. Reddy BS: Micronutrients as chemopreventive agents. IARC Sci Publ 1996;(139):221-35. 22. Roteli-Martins CM, Panetta K, Alves VA et al: Cigarette smoking and high-risk HPV DNA as predisposing factors for high-grade cervical intraepithelial neoplasia (CIN) in young Brazilian women. Acta Obstet Gynecol Scand 1998 Jul;77(6):678-82. 23. Yoshikawa H, Nagata C, Noda K et al: Human papillomavirus infection and other risk factors for cervical intraepithelial neoplasia in Japan. Br J Cancer 1999 May;80(3-4):621-4. 24. Zarcone R, Bellini P, Carfora E, et al. Folic acid and cervix dysplasia. Minerva Ginecol 1996;48:397-400. alteration of glucose tolerance. 25. Centers for Disease Control and Prevention, Division of STD Prevention. Prevention of genital HPV infection and sequelae: Report of an external consultants' meeting. December 1999. 26. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines 2002. Morbidity and Mortality Weekly Report 2002; 51(RR�6). 27. Chu NR. Therapeutic vaccination for the treatment of mucosotropic human papillomavirus-associated disease. Expert Opinion on Biological Therapy 2003; 3(3):477�486. 28. Ho GYF, Bierman R, Beardsley L, Chang CJ, Burk RD. Natural history of cervicovaginal papilloma virus infection in young women. N Engl J Med 1998;338:423-8. 29. Koutsky LA, Kiviat NB. Genital human papillomavirus. In: K. Holmes, P. Sparling, P. Mardh et al (eds). Sexually Transmitted Diseases, 3rd edition. New York: McGraw-Hill, 1999, p. 347-359. 30. Kiviat NB, Koutsky LA, Paavonen J. Cervical neoplasia and other STD-related genital tract neoplasias. In: K. Holmes, P. Sparling, P. Mardh et al (eds). Sexually Transmitted Diseases, 3rd edition. New York: McGraw-Hill, 1999, p. 811-831. 31. Myers ER, McCrory DC, Nanda K, Bastian L, Matchar DB. Mathematical model for the natural history of human papillomavirus infection and cervical carcinogenesis. 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