Week Two— My Story
My Story
How I found out
Family history
Timeline
As a health professional I understand the importance of preventive care, so I see my primary care provider annually. I have gotten pap smears since 2014 when I was 24 years old. Since then, I’ve never had any abnormalities. This was especially important for me because of my family history. My paternal grandfather passed after his battle with prostate cancer, and my father’s sister passed in 2013 from stage 4 cervical cancer. My aunt’s passing was especially difficult because I was the one who took her to her doctor’s appointments and learned about her prognosis-she had kept it a secret from our family. She constantly told me to “make sure you take care of yourself”.
In February 2019, I went to my primary care provider for my annual examination, with a pap smear. This was the first time in 5 years that I had an abnormal pap. At first it was scary and overwhelming. Imagine reading your lab results and seeing ‘Pathology’ and then I had to follow up with a gynecologist for a colposcopy, this made things even more serious. Over the course of one year I would go back and forth to the gynecologist and weigh my options on treatment vs. wait and see.
What is a colposcopy? If you recall from Week 1, a “colposcopy is the primary diagnostic method used to detect cervical cancer in women. It can identify and determine the severity of the lesion so that a biopsy of the highest level of abnormality detection can be taken, when necessary. Colposcopy includes a visual assessment of the system of the lower genital tract (cervical, vulva and vagina), primarily for the appearance of a metaplastic epithelium, consisting of a transformation zone on the cervix” [10].
At that point, a colposcopy was the most uncomfortable medical procedure that I’ve had. Thankfully my gynecologist and the nurse were so compassionate and they made me feel safe. After the colposcopy, I waited for the results of the biopsy. About one week later it was confirmed that I had CIN3. From that point I researched all that I could about the pathology present on my cervix.
At that point, a colposcopy was the most uncomfortable medical procedure that I’ve had. Thankfully my gynecologist and the nurse were so compassionate and they made me feel safe. After the colposcopy, I waited for the results of the biopsy. About one week later it was confirmed that I had CIN3. From that point I researched all that I could about the pathology present on my cervix.
What is CIN3?
Thus, observation is the preferred approach for most younger patients and those with CIN 1. Because some CIN 2 lesions will regress, observation is also an option for some CIN 2 patients, such as those who plan future childbearing and are concerned about the potential adverse obstetric outcomes (eg, preterm delivery) that have been associated with treatment of CIN. CIN 3, however, is a direct precursor to cervical cancer, and treatment is always recommended in these cases.
Although age and CIN grade are predictive of risk for progression to cancer, other factors also affect this risk. These factors include the patient's HPV and cytology results preceding the diagnosis of CIN. For this reason, the American Society for Colposcopy and Cervical Pathology's recommendations for management of CIN also take these factors into account in determining a patient's risk for progression and in formulating a plan for observation versus treatment [2,15,16]. These risk estimates were derived from a cohort study of over 1.5 million patients followed for more than a decade [16]. (https://www.uptodate.com/contents/cervical-intraepithelial-neoplasia-management/print)
Natural history of CIN 2,3 – Data on the natural history of untreated high-grade disease (CIN 2,3) are limited since most patients are treated.
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For CIN 3, the estimated spontaneous regression rate is 32 to 47 percent, with 12 to 40 percent progressing to invasive cancer if untreated [8-13]. The best data on the natural history of histologically confirmed CIN 3 are from an historic study that evaluated the incidence of invasive cancer over time in two groups of patients with CIN 3 (not all patients with CIN 3 received treatment): 143 patients received close follow-up but no treatment, and 593 patients received adequate or probably adequate treatment [13]. The cumulative incidence of invasive cancer of the cervix/vaginal vault was significantly higher in untreated patients at 10 years (20.0 versus 0.3 percent) and 30 years (31.0 versus 0.7 percent). Ninety-two of the 143 patients who were managed with close follow-up but no treatment had cytologic evidence of persistent disease 6 to 24 months after the initial diagnosis of CIN 3. In this subgroup, the cumulative incidence of invasive cancer of the cervix/vaginal vault at 10 and 30 years was 31 and 50 percent, respectively. Given the high rate of progression to invasive cancer, prolonged follow-up of persistent CIN is no longer recommended.
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For CIN 2, it appears that approximately one-half of patients will have regression if left untreated. In a meta-analysis of 36 studies (both randomized trials and observational studies) including 3160 patients with CIN 2, at 24 months, lesions regressed in 50 percent of patients, persisted in 32 percent, and progressed to CIN 3+ in 18 percent [14]. The rate of progression increased with time, from 5 percent at 3 months to 24 percent at 36 months; this result is expected as most patients regress and those remaining are likely at a higher risk of progression. Progression rates were lower in patients with negative HPV testing at baseline; however, this was based on few data since HPV status was not reported in most studies and most patients regressed at 24 months regardless of initial HPV status. There were 15 cases of adenocarcinoma in situ and 15 cases of invasive cervical cancer (2 of these were advanced-stage disease).
One explanation for the lower rate of progression of CIN 2 compared with CIN 3 is that CIN 2 is more likely to be caused by oncogenic HPV subtypes 31, 33, 35, 39, 45, 51, 52, and 58, which have a weaker association with development of cancer than the more highly oncogenic subtypes HPV 16 and 18, which are commonly found with CIN 3 [17].
