- CDC
- Heart Failure
- Cardiovascular Clinical Consult
- Adult Immunization
- Hepatic Disease
- Rare Disorders
- Pediatric Immunization
- Implementing The Topcon Ocular Telehealth Platform
- Weight Management
- Monkeypox
- Guidelines
- Men's Health
- Psychiatry
- Allergy
- Nutrition
- Women's Health
- Cardiology
- Substance Use
- Pediatrics
- Kidney Disease
- Genetics
- Complimentary & Alternative Medicine
- Dermatology
- Endocrinology
- Oral Medicine
- Otorhinolaryngologic Diseases
- Pain
- Gastrointestinal Disorders
- Geriatrics
- Infection
- Musculoskeletal Disorders
- Obesity
- Rheumatology
- Technology
- Cancer
- Nephrology
- Anemia
- Neurology
- Pulmonology
Continued Cytological Monitoring for Cervical Cancer Despite Prior Vaccination
The human papilloma viruses (HPVs) are among the widespread sexually transmitted pathogens infecting women. Like HIV, HPV–s
The human papilloma viruses (HPVs) are among the widespread sexually transmitted pathogens infecting women. Like HIV, HPV’s importance resides in the potential long-term consequences of infection with selective types. HPV types 16 and 18 are deemed to be carcinogens and/or co-carcinogens for the female genital tract. HPV DNA has been found in all grades of cervical intraepithelial neoplasia (CIN) as well as in invasive cervical cancer. Types 16 and 18 are present in approximately 70% of cancers. Types 10, 11, 31, 33, 35, 46, 51, and 56 account for most of the remaining cancers for which DNA typing has been done.
Using the HPV major coat protein, L1, researchers have developed 2 HPV vaccines: a quadrivalent vaccine with HPV 6/11/16/18 and a bivalent vaccine with HPV 16/18. The antibodies induced by the vaccines persist for at least 5 years.1 The presumed protection from these vaccines does not lessen the importance of continued cytological monitoring of the cervix and vagina.
Beller and Abu-Rustum2 reported 2 cases of cervical cancer after HPV vaccination. One case involved a poorly differentiated adenocarcinoma for which HPV has not been implicated as a cause despite a high prevalence of HPV DNA. The second case was in a young vaccinated female with cervical cancer associated with HPV 31, a type not covered by the current vaccines. The value of Beller and Abu-Rustum’s report is not primarily in the data but rather in what the data infer: that lifelong screening by periodic cytological cervical smears for cervical cancer is not negated by prior vaccination.
As demonstrated in the second case, a number of HPV types not included in the vaccines have been linked to cervical precancerous and cancerous lesions. In some countries, types 16 and 18 are not the most endemic HPV types associated with cervical cancer. Over time, the elimination of HPV 16 and 18 will probably result in a shift in the prevalence of HPV types. Other oncogenic types will probably predominate as causes of precancerous and cancerous lesions.
A final concern, not expressed in the article by Beller and Abu-Rustum,2 centers on the duration of induced immunity. Compared with live vaccines, subparticle vaccines have a limited period of effectiveness.
The advent of the prophylactic effectiveness of the HPV vaccines in reducing CIN and preinvasive genital lesions is a wonderful achievement, but it does not lessen the need for lifelong cytological screening after vaccination.
References:
REFERENCES
1. Villa LL, Costa RL, Petta CA, et al. High sustained efficacy of a prophylactic quadrivalent human papilloma virus types 6/11/16/18 L1 virus-like particle vaccine through 5 years of follow-up. Br J Cancer. 2006;95:1459-1463.
2. Beller U, Abu-Rustum NR. Cervical cancers after human papillomavirus vaccination. Obstet Gynecol. 2009;113(2 pt 2):550-552.
