> Genital Warts
> Cause of cervical dysplasia and warts
Cause of cervical dysplasia and warts
Cervical dysplasia is believed to be caused by HPV (human papillomavirus) in over 95% of the cases, but it is probably the cause in 100%. Moreover, HPV is the ONLY PROVEN CAUSE of cervical dysplasia, genital warts, and plantar warts. HPV may not be detected at certain times even when it is the cause, due to the state of the immune system at the time of testing or due to false negative test results.
Clin Lab Med 2000 Jun;20(2):257-70:
Human papillomavirus in cervical neoplasia. Role, risk factors, and implications.
McLachlin CM Department of Pathology, London Health Sciences Centre, University of Western Ontario, Canada.
“A rapidly increasing body of evidence links human papillomavirus (HPV) to cervical neoplasia through epidemiologic associations, pathologic features, molecular detection, and mechanisms of oncogenesis. HPV is now accepted as the primary cause of cervical neoplasia and accounts for most of the risk factors traditionally associated with this disease. The role that HPV plays in the induction and progression of cervical neoplasia is becoming clearer; however, the challenge now is to find other factors that may play a role in the outcome of cervical cancer and that might serve as targets for novel treatments.”
Even as early as 1993, it was clearly established that HPV caused most cervical dysplasia. J Natl Cancer Inst 1993 Jun 16;85(12):958-64:
Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia.
Schiffman MH, Bauer HM, Hoover RN, Glass AG, Cadell DM, Rush BB, Scott DR, Sherman ME, Kurman RJ, Wacholder S, et al Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
“Background: Experimental studies have provided strong evidence that human papillomavirus (HPV) is the long-sought venereal cause of cervical neoplasia, but the epidemiologic evidence has been inconsistent.
Purpose: Given improvements in HPV testing that have revealed a strong link between sexual activity history and cervical HPV infection, we conducted a large case-control study of HPV and cervical intraepithelial neoplasia (CIN) to evaluate whether sexual behavior and the other established risk factors for CIN influence risk primarily via HPV infection.
Methods: We studied 500 women with CIN and 500 control subjects receiving cytologic screening at Kaiser Permanente, a large prepaid health plan, in Portland, Ore. The established epidemiologic risk factors for CIN were assessed by telephone interview. We performed HPV testing of cervicovaginal lavage specimens by gene amplification using polymerase chain reaction with a consensus primer to target the L1 gene region of HPV. Unconditional logistic regression analysis was used to estimate relative risk of CIN and to adjust the epidemiologic associations for HPV test results to demonstrate whether the associations were mediated by HPV.
Results: The case subjects demonstrated the typical epidemiologic profile of CIN: They had more sex partners, more cigarette smoking, earlier ages at first sexual intercourse, and lower socioeconomic status. Statistical adjustment for HPV infection substantially reduced the size of each of these case-control differences. Seventy-six percent of cases could be attributed to HPV infection; the results of cytologic review suggested that the true percentage was even higher. Once HPV infection was taken into account, an association of parity with risk of CIN was observed in both HPV-negative and HPV-positive women.
Conclusion: The data show that the great majority of all grades of CIN can be attributed to HPV infection, particularly with the cancer-associated types of HPV. Implications: In light of this conclusion, the investigation of the natural history of HPV has preventive as well as etiologic importance.”