Guest Columnist: Stephanie Veit. Stephanie is from Chesterfield, Missouri and will graduate with her MD degree from The Commonwealth Medical College in May 2016. She will begin her OB/GYN residency in July at Aurora Health Care in Milwaukee. Stephanie is dedicated to promoting women’s health and awareness.
Cervical cancer was once one of the leading causes of death in woman until the regular use of Pap smears became widespread practice according to the National Institutes of Health. The majority of cervical cancers are caused by high risk strains of sexually transmitted human papillomavirus (HPV). As a result, HPV testing has become part of the guidelines set out by The American College of Obstetricians and Gynecologists (ACOG) in screening for cervical cancer.
While several strains exist, HPV16 and HPV18 are the two strains of virus which cause the majority of all cervical cancers. The development of cervical cancer is step-wise in fashion and so pre-cancerous changes can be observed with Pap smears and further cervical changes can be predicted.
Women who have infections with high risk HPV strains have greater risk of developing pre-cancerous and cancerous lesions than those who do not have HPV infections. Guidelines now include testing for these high risk HPV strains as well as looking at the cells under the microscope with a Pap smear. The results of these two tests guide healthcare providers in the management of patients. Those women who test positive for high risk strains of HPV can go on to have more testing to see if they have any concerning lesions that could be pre-cancerous or cancerous. Women who are negative for the high risk strains but still test positive for HPV can be retested the following year to see if the infection has resolved.
Not every HPV infection leads to cervical cancer. In fact, many HPV infections are cleared spontaneously by the immune system, especially in younger women. 71% of women who were HPV positive but had normal Pap smears, tested negative for that specific HPV type at the following visit. The HPV infections which persist carry the increased risk of developing cervical cancer. Women who test positive for HPV at one visit and retest positive for HPV at a follow-up visit are at greater risk for precancerous and cancerous lesions then women who retested negative at a follow-up visit. Women who test positive for the same high risk strain of HPV at two visits in a row are at even greater risk, according to the National Cancer Institute. With this in mind, ACOG recommends repeat co-testing in one year if co-testing shows a negative Pap smear and positive HPV unless the patient tests positive for a high risk strain of HPV, thus allowing women time to clear the HPV infection spontaneously while also retaining the ability to treat those women who test HPV positive on repeat co-testing.
HPV testing is a good screening test on its own when compared to Pap smears alone. However, combining the two tests gives even better results. Women who test positive with co-testing consisting of both HPV testing and a Pap smear are more likely to have a true positive result. This allows for more women who have changes in their cervix to be identified and then treated. For example, if a woman tests negative for HPV, but has a borderline abnormal Pap smear, it is recommended that she receive repeat co-testing in three years. Should she test positive for HPV, especially a high risk type, and have an abnormal Pap smear, it is recommended that she receive a colposcopy (instrument assisted examination of the cervix) which allows healthcare providers to further visualize the cervix to determine if there is a lesion requiring further testing.
In summary, guidelines have been recommended for the screening of cervical cancer and management when screening comes back positive. Women who have not been infected with HPV have a very small chance of developing cervical cancer. One way to reduce the risk of being infected with HPV in the first place is with the HPV vaccine. The first HPV vaccine was introduced for use in 2006 and protects women against the most common strains causing genital warts and cervical cancer. The vaccine is targeted to girls and boys aged 11-12, and catch-up is offered to women up to age 26. Research shows that vaccinated women had a decrease of 88% in infection by HPV strains covered by the vaccine with a predicted 82% effectiveness of one dose of the vaccine. This essentially means that the vaccine is effective in preventing HPV infection and thus cervical cancer.
Cervical cancer has a yearly incidence for women under the age of 25 of 1.4 per 100,000 women. This number has fallen, on average, 1% per year for the past 10 years the HPV vaccine has been in use. In vaccinated women in this age group, this number should be reduced by at least 50% for an incidence of 0.7 per 100,000 women. This means that only 7 out of every 1,000,000 women who have been vaccinated against HPV will develop cervical cancer.
The HPV vaccine can help prevent cervical cancer while the introduction of HPV testing to Pap smears has enabled more women to receive treatment of pre-cancerous lesions. Co-testing has also enabled women to receive fewer unnecessary tests without increasing their risk. Cervical cancer is a preventable and treatable condition, and these measures will help decrease the number of women who develop cervical cancer.
Medical Reviewer: Michael Ferraro, MD, is an associate dean for TCMC’s South (Wilkes-Barre) Regional Campus and a practicing gynecologist.
Sources: Centers for Disease Control, Journal of Infectious Diseases, National Cancer Institute.
Read Dr. Mackarey’s Health & Exercise Forum – every Monday in the Scranton Times-Tribune. This article is not intended as a substitute for medical treatment. If you have questions related to your medical condition, please contact your family physician. For further inquires related to this topic email: email@example.com
Paul J. Mackarey PT, DHSc, OCS is a Doctor in Health Sciences specializing in orthopaedic and sports physical therapy. Dr. Mackarey is in private practice and is an associate professor of clinical medicine at The Commonwealth Medical College.