HPV 16 and cigarette smoking as risk factors for high-grade cervical intra-epithelial neoplasia
Autor: | Robert D. Burk, Anna S. Kadish, Prabhudas R. Palan, Jayasri Basu, Magdy Mikhail, Seymour L. Romney, Gloria Y.F. Ho |
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Rok vydání: | 1998 |
Předmět: |
Gynecology
Cancer Research medicine.medical_specialty business.industry viruses Carcinoma in situ virus diseases Cancer medicine.disease Ascorbic acid Cervical intraepithelial neoplasia Gastroenterology female genital diseases and pregnancy complications Oncology Dysplasia Internal medicine medicine Sex organ Risk factor business Viral load |
Zdroj: | International Journal of Cancer. 78:281-285 |
ISSN: | 1097-0215 0020-7136 |
Popis: | Although genital human papillomavirus (HPV) infection is well established as the etiologic agent for cervical intraepithelial neoplasia (CIN), little is known about the cofactors involved in the development of high-grade lesions or the progression of low-grade to high-grade lesions. In our study of HPV-infected women with CIN (163 CIN I, 51 CIN II and 44 CIN III), women with CIN II or III were compared with those with CIN I for risk factors associated with high-grade lesions. After controlling for age, education, ethnicity and frequency of Pap smear screening, infection with HPV 16, but not high viral load or infection with multiple types, was associated with high-grade lesions (OR for CIN II 5 11.96, OR for CIN III 5 23.74). Risk of CIN III, but not CIN II, increased with number of cigarettes smoked per day (ORs 5 1.49 and 3.35 for I10 and G10 cigarettes per day, respectively) and decreased with frequency of condom use during sex (ORs 5 0.60 and 0.32 for women who used condoms occasionally/sometimes and most/ all of the time, respectively). There were no associations between high-grade lesions and plasma levels of micronutrients (retinol, b-carotene, a-tocopherol and reduced ascorbic acid). Our results indicate that infection with HPV 16 is associated with high-grade lesions. Additional cofactors, such as cigarette smoking, may be required as a carcinogen to advance HPV-infected cells toward neoplastic progression. Int. J. Cancer 78:281‐285, 1998. r 1998 Wiley-Liss, Inc. |
Databáze: | OpenAIRE |
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