• 2019-10
  • 2020-07
  • 2020-08
  • br Conclusions br Our findings suggest that among women


    4. Conclusions
    Our findings suggest that, among women CCK8 aged 50 or younger who underwent oophorectomy as part of surgical treatment for endometrial cancer, BMI is inversely related to complaints of menopausal symptoms. We identified a precipitous decline in the frequency of symptoms rang-ing from 45.5% in women with BMI of b30 to only 14.7% in women with BMI N50, but quality of menopausal symptoms did not vary by BMI. Pre-viously reported data is limited to patients undergoing natural meno-pause and those women without an underlying malignancy, but have suggested patients with a high BMI have significantly more vasomotor symptoms than women with a lower BMI [13]. An Australian study identified patients with BMI N35 have lower estradiol and estrone than those with BMI b25 [14]. Our study cohort is unique as compared to the women included in prior studies for three reasons. First, our co-hort underwent surgical menopause instead of natural menopause. Sec-ond, the mean BMI of our cohort was 40, which is substantially higher than that reported in previous studies. Third, our cohort is composed of women with endometrial cancer. Thus, by focusing on premeno-pausal women with endometrial cancer, we may have selected for obese women with increased peripheral conversion of androgen to estrogen.
    Menopausal symptoms cause a significant decrease in overall quality of life by limiting work productivity, impairing daily activities, substan-tially increasing healthcare utilization [15], and potentially negatively affecting personal relationships by impairing sexual function [16]. Addi-tionally, menopausal symptoms may portend adverse cardiovascular outcomes, reduced bone health, memory loss, and increased risk of stroke and colorectal cancers [7,17–20]. Vasomotor symptoms alone are associated with elevated systolic blood pressure and increased total cholesterol [21]. Age at menopause is critically important, as each
    Table 2
    Multivariate analysis: factors associated with menopausal symptoms.
    Relative risk 95% confidence interval
    year's delay in menopause is associated with a 2% decrease in overall mortality [22]. Our data suggest that the prevalence of menopausal symptoms decreases with increasing BMI. However, a lack of meno-pausal symptoms may not translate to the absence of adverse cardiovas-cular outcomes, especially given the known detrimental cardiac effects of obesity. Additionally, women with morbid obesity, who have a suspected increase in peripheral estrogen, may not be affected by oophorectomy.
    The gold standard treatment for menopausal symptoms is CCK8 replacement therapy. This can help women with vasomotor symptoms, who have significantly lower levels of estradiol than those without symptoms [23]. However, although estrogen effectively manages symp-toms, it has not been shown to change the long-term cardiovascular im-pact of menopause. Additionally, in endometrial cancer patients, the effect of estrogen therapy on cancer recurrence is a concern. The Gyne-cologic Oncology Group opened protocol 137, a randomized controlled trial of estrogen vs. placebo in patients with stage I and II endometrial cancer. A total of 1236 patients were enrolled with a median follow up of 35.7 months. This study had a preponderance of low risk endometrial cancers with a median age of 57 years and 88% of these were stage IA. Deeply invasive tumors or grade 3 lesions accounted for only 8% and 7% respectively. Thus, the rate of recurrence was low (2.1%), this study was closed early secondary to the concerns raised in the Women's Health Initiative study that estrogen therapy increases the risk of breast cancer and heart disease. The insufficient enrollment and premature closure prevented the author's ability to conclusively refute or support the safety of exogenous estrogen with regard to risk of endometrial can-cer recurrence [24,25]. Lastly, local estrogen may be safely administered to low risk endometrial cancer survivors, however this may only effect vulvo-vaginal symptoms [26].
    The decision to proceed with oophorectomy is complicated and im-pacted by the patient's malignancy as well as BMI. Given the concerns raised in the Women's Health initiative, as well as findings that ovarian conservation does not reduce overall survival in premenopausal endo-metrial cancer patients [5–7,25], it may be prudent to conserve ovaries instead of prescribing estrogen therapy after oophorectomy. However, this is with the caveat that patients have had genetic predispositions such as Lynch syndrome excluded. Conversely, oophorectomy may be supported by the suboptimal imaging that radiologists face regarding the monitoring of these patient's ovarian pathology. Radiology depart-ments are having increasing difficulties transporting, accommodating, and obtaining adequate image quality in obese patients [27]. This is compounded by the fact that 50% of patients with polycystic ovarian syndrome are obese, necessitating further imaging [28]. Careful consid-eration of the risks and benefits is necessary and should take the pa-tients social and medical into account.