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Background: Adult body size is related to ovarian cancer risks, but size in childhood may also influence risks. We investigated if childhood body mass index (kg/m2), height, and growth patterns were associated with ovarian cancer overall and by histologic subtypes, including effects of birthweight. Methods: A cohort of 155,958 girls from the Copenhagen School Health Records Register, born 1930 to 1989 with measured weights and heights from 7 to 13 years, were included. During follow-up, 1,041 ovarian cancers were recorded. Overweight was defined using International Obesity Task Force criteria. Cox regressions were performed. Results: Compared with non-overweight girls, at most ages girls with overweight had increased risks of ovarian cancer overall (HR range: 1.24–1.34), mucinous, endometrioid, and clear cell ovarian cancers, but not serous and other ovarian cancers. Childhood height had positive and significant associations with ovarian cancer overall (HR range: 1.07–1.10 per z-score) and the endometrioid subtype but not with the other subtypes. Adjusting for birthweight minimally altered the associations with childhood body size. In growth analyses, girls with overweight or who were tall at 7 and 13 years had increased risks of ovarian cancer overall compared with average-sized girls at both ages. Conclusions: Ovarian carcinogenesis is linked to childhood overweight, tallness, and growth, with variations across histological subtypes, suggesting that early life plays a role in the origins of this disease. Impact: These findings emphasize that healthy body size and growth during childhood are important as they may contribute to reducing ovarian cancer risks.

Background: Body size in adult life is likely associated with risks of endometriosis and adenomyosis, yet little is known about associations with body size earlier in life. Aim: To examine whether birth weight, childhood body mass index (BMI) and height are associated with risks of endometriosis and adenomyosis. Subjects and methods: From the Copenhagen School Health Records Register, 171,447 girls born 1930–1996, with measured weights and heights at ages 7–13 were included. Outcomes were obtained from health registers. Cox regressions were performed to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results: During follow-up, 2149 endometriosis cases and 1410 adenomyosis cases were diagnosed. Childhood BMI was inversely associated with endometriosis (HR = 0.92 [95% CI: 0.88–0.96] per z-score at age 7). In contrast, childhood height was positively associated with endometriosis (HR = 1.09 [95% CI: 1.05–1.14] per z-score at age 7). Associations with childhood body size did not differ by endometriosis location. Childhood BMI and height had limited associations with adenomyosis. Birth weight was not associated with endometriosis or adenomyosis. Conclusion: Lean and tall girls are more often diagnosed with endometriosis, but not adenomyosis. These findings suggest that indicators of endometriosis risk are already apparent at early ages.

Background Studies of birth weight associations with ovarian and endometrial cancer risks are limited with inconsistent results, and none has evaluated associations by histologic subtype. We utilized prospectively collected birth weight information to investigate the association with risk of ovarian and endometrial cancers overall and by histologic subtype. Methods 162,559 girls, born from 1930 to 1989, from the Copenhagen School Health Records Register (CSHRR) were followed prospectively via linkage with the Danish health registers. Ovarian (n=666) and endometrial (n=694) cancers were identified from 1978 to 2014. Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results Women with lower (2.0–3.25 vs. 3.26–3.75kg) and higher (3.75–5.5 vs. 3.26–3.75kg) birth weights had increased risks of ovarian cancer overall [HR (95% CI): 1.27 (1.06–1.52); 1.51 (1.21–1.87), respectively] and serous ovarian cancers [1.54 (1.19–1.98); 1.98 (1.47–2.67), respectively]. A decreased risk of Type II endometrial tumors was suggested per kilogram increase in birth weight [HR (95% CI): 0.63 (0.40–1.00)]. Conclusions Our results suggest that both lower and higher birth weights were associated with increased ovarian cancer risk and associations were particularly strong for serous ovarian cancer, the most common subtype. Birth weight was not associated with most types of endometrial cancer.

Item does not contain fulltext A growing number of premenopausal women are currently using antithrombotic and/or (dual) antiplatelet therapy for various cardiovascular indications. These may induce or exacerbate abnormal uterine bleeding and more awareness and knowledge among prescribers is required. Heavy and irregular menstrual bleeding is common in women in their forties and may have a variety of underlying causes that require different treatment options. Thus using anticoagulants in premenopausal women demands specific expertise and close collaboration between cardiovascular physicians and gynecologists. In this article we summarize the scope of the problem and provide practical recommendations for the care for young women taking anticoagulants and/or (dual) antiplatelet therapy. We also recommend that more safety data on uterine bleeding with novel anticoagulants in premenopausal women should be obtained.

Previously, we found that excess weight already in childhood has positive associations with endometrial cancer; however, associations with changes in body mass index (BMI) during childhood are not well understood. Therefore, we examined whether growth in childhood BMI is associated with endometrial cancer and its sub‐types. A cohort of 155,505 girls from the Copenhagen School Health Records Register with measured weights and heights at the ages of 6–14 years and born 1930–1989 formed the analytical population. BMI was transformed to age‐specific z scores. Using linear spline multilevel models, each girl's BMI growth trajectory was estimated as the deviance from the average trajectory for three different growth periods (6.25–7.99, 8.0–10.99, 11.0–14.0 years). Via a link to health registers, 1,020 endometrial cancer cases were identified, and Cox regressions were performed. A greater gain in BMI during childhood was positively associated with endometrial cancer but no differences between the different growth periods were detected in models adjusted for baseline BMI. The hazard ratios for the associations with overall growth during childhood per 0.1 z score increase were 1.15 (95% confidence interval [CI]: 1.07–1.24) for all endometrial cancers, 1.12 (95% CI: 1.04–1.21) for estrogen‐dependent cancers, 1.16 (95% CI: 1.06–1.26) for endometrioid adenocarcinomas and 1.46 (95% CI: 1.16–1.84) for non‐estrogen‐dependent cancers. Growth in BMI in early life is positively linked to later endometrial cancer risk. We did not identify any sensitive childhood growth period, which suggests that excess gain in BMI during the entire childhood period should be avoided., What's new? High body mass index (BMI) early in life is linked to an increased risk of endometrial cancer in adulthood. Potentially influencing that association are the amount by which BMI increases in childhood, as well as the timing of BMI increase. Here, analyses of data from the Copenhagen School Health Records Register for girls ages 6 to 14 shows that endometrial cancer risk is increased by greater BMI gain across ages, while the specific age at which BMI increases occurs has little impact. Excess BMI gain at any time during childhood could set the stage for endometrial carcinogenesis.

Introduction Invasive as well as non-invasive methods are available for assessment of the endometrium. Aims The purpose of this clinical guide is to provide evidence-based advice on endometrial assessment in peri and postmenopausal women. Material and methods Literature review and consensus of expert opinion. Results and conclusions Presuming speculum examination and cervical cytology are assessed, transvaginal ultrasound should be undertaken initially as it is non-invasive and will not only measure endometrial thickness, but will also detect other pelvic pathology such as leiomyomas and ovarian tumours. The main indication for invasive methods is to obtain endometrial tissue to diagnose or exclude the presence of endometrial cancer or pre-malignancies. Biopsy is mainly undertaken as an outpatient procedure, but sampling is ‘blind’. Hysteroscopy is used when focal lesions affecting the uterine cavity are suspected such as endometrial polyps or sub-mucous fibroids. None of the available methods are perfect. Ultrasound evaluation is dependent on the experience of the examiner, the equipment and the quality of visualization. Hysteroscopy too is dependent on the examiner and fibroids may obstruct visualization. Blind endometrial biopsy procedures often miss focal lesions. Thus re-examination is necessary when symptoms persist and no explanation for these has been identified. This clinical guide will evaluate the different methods of endometrial assessment, their indications and limitations. Guidance is also given about dealing with inconclusive investigations and persistent symptoms.

This is a review of currently available data on local vaginal estrogen treatment with critical comments and a view on future perspectives. Vaginal atrophy affects 25–50% of postmenopausal women, and 40–45% of sexually active women suffer from dyspareunia. Treatment with all available local estrogen preparations is effective, but studies on dose–response relationship are lacking as is noncompany-sponsored comparisons between different estrogens and formulations. Local estrogen is effective in the prevention of recurrent urinary tract infection, but data on incontinence are mixed. Epidemiological data, long-term clinical safety data and data in women with a history of breast and other cancers are lacking. Safety data beyond 1 year are needed to support actual use. The use of local therapy is still likely to increase.

To examine the prevalence of undiagnosed endometrial carcinoma (EC) among women with a preoperative diagnosis of atypical endometrial hyperplasia (AEH) in correlation to age, BMI and menopause.Data extracted from the Danish Gynecological Cancer Database (DGCD) covering women diagnosed with AEH between January 1, 2005 and November 1, 2010 undergoing surgery. DGCD is a multidisciplinary, nationwide, clinical database of all cases of gynecological cancer and AEH in Denmark diagnosed after January 1, 2005. Registration is mandatory. Primary outcome was preoperative- and postoperative diagnoses. Secondary outcomes were relationship to BMI, age and menopause.The preoperative diagnosis of AEH was retained in 41% of 773 cases and 59% had endometrial cancer. Of the cancer cases, 18% had more than Stage I disease and 3% were non-endometrioid. Cancer risk was significantly related to age (p0.0001) and menopause (p0.0001). The 80% who were postmenopausal had a significantly higher risk of a postoperative cancer diagnosis compared with the premenopausal group (OR 2.8). There was no significant difference regarding BMI (p=0.25).More than half of the 773 Danish women primarily diagnosed with AEH had undiagnosed cancer. Failure to diagnose endometrial carcinoma preoperatively can lead to inadequate staging and potentially suboptimal treatment. We recommend that atypical endometrial hyperplasia should be treated as carcinoma in specialized gynecological-oncology centers.

Background The natural course of untreated endometrial adenocarcinoma is difficult to describe because observation of an already diagnosed cancer is unethical. However, occasionally, patients refuse therapy for different reasons, thus providing the opportunity to observe the natural course of the malignant disease. These patients are for obvious reasons rare cases. We present such a case and a review of the literature.

Background: Among women, body mass index (BMI; kg/m2) and attained height are positively associated with ovarian cancer. Few studies have, however, investigated associations with childhood body size. As such, it remains largely unknown if it is body size development in early life or adult life that contributes to these associations. Therefore, we examined if childhood BMI and height at age 13 years were associated with ovarian cancer in adult life. Methods: Individuals were girls in the Copenhagen School Health Records Register who were born between 1930 and1989 and had available measures of height and weight at age 13 years. BMI and height z-scores were calculated from an internal age-specific reference. Via a personal identification number, individuals were followed up for ovarian cancer diagnosis by linkage to the Danish Cancer Registry. Cox proportional hazard regressions were performed and stratified by birth cohort. Results: Among the included 137,416 girls, 1048 cases of ovarian cancer occurred during 5.2 million person-years of follow-up with a median age of diagnosis of 57 years (range: 19-83 years). BMI tended to be non-linearly associated with ovarian cancer such that only the heaviest girls had positive associations with ovarian cancer. Compared with a 13-year-old girl of average-size (BMI z-score = 0, corresponding to a weight of 45 kg and a height of 157 cm), an equally tall girl who was at least 9 kg heavier (corresponding to a BMI z-score >1.28) had a hazard ratio (HR) for ovarian cancer of 1.33 (95% confidence interval [CI]: 1.08-1.63). In analyses adjusted for childhood height, the association was only marginally attenuated (HR = 1.30, 95% CI: 1.06-1.60). Childhood height was positively and statistically significantly associated with ovarian cancer. At age 13 years, per height z-score (corresponding to approximately 7 cm), the HR for ovarian cancer was 1.07 (95% CI: 1.01-1.14). Conclusion: Body size in early life was associated with ovarian malignancies later in life suggesting that childhood height and BMI might impact if women are later diagnosed with ovarian cancer. As ovarian cancers vary widely in their etiologies, associations with childhood body size may differ depending on the tumor type, which will be investigated. Citation Format: Julie Aarestrup, Michael Gamborg, Nicolas Wentzensen, Lian G. Ulrich, Thorkild IA Sørensen, Jennifer L. Baker. Childhood body size at age 13 years and associations with ovarian cancer in adult life. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr LB-375.

To evaluate the endometrial hyperplasia and carcinoma rate after 52-week treatment with ultra-low-dose 10-microgram 17β-estradiol vaginal tablets in postmenopausal women with vaginal atrophy.Endometrial biopsy data from individuals using active treatment (n=205) in a randomized, double-blind, placebo-controlled trial were pooled with the data from an open-label endometrial safety trial (n=336). Patients received 10-microgram estradiol vaginal tablets for 52 weeks. All endometrial biopsy samples were histologically analyzed at baseline and at end of trial by the same laboratory in both trials.A total of 541 women using estradiol were included in the combined analysis of endometrial safety. A total of 456 women completed the trials, and 443 women had a biopsy performed at week 52: 85.6% were categorized as "atrophic endometrium," 12.6% had nonevaluable biopsy samples, 1.1% had polyps, and 0.2% were categorized as "weakly proliferative." One case of complex hyperplasia without atypia was reported in an individual exposed to trial drug for only 9 days. One woman's biopsy sample demonstrated endometrioid adenocarcinoma, grade 2, but the lack of an evaluable screening biopsy sample makes it uncertain whether the carcinoma was preexisting. In total, two events of hyperplasia and carcinoma were reported in 386 evaluable biopsy samples (incidence rate 0.52% per year).The reported background incidence rate of endometrial hyperplasia and carcinoma in postmenopausal women is 0% to 1%. The results of this pooled analysis therefore support the endometrial safety of unopposed ultra-low-dose vaginal estrogen. There was no increased risk of endometrial hyperplasia and carcinoma in postmenopausal women undergoing treatment with 10-microgram estradiol vaginal tablets for 1 year under study conditions.ClinicalTrials.gov, www.clinicaltrials.gov, NCT00108849 (VAG-2195) and NCT00431132 (VAG 1748).II.

(2004). Current controversies about combined hormone therapy and the relative risks to the breast and endometrium. Climacteric: Vol. 7, No. 3, pp. 229-237.

Our purpose was to examine the effects of postmenopausal estrogen therapy supplemented with progestogen on plasma lipoprotein levels.One hundred thirteen women were randomized to receive either placebo or a combination of 17 beta-estradiol and norethindrone acetate administered continuously (Kliogest) or sequentially (Trisequens). Plasma lipoprotein levels were measured at baseline and after 2 years of treatment and compared by analysis of variance.Hormone therapy lowered plasma cholesterol levels (p0.001) and low-density lipoprotein cholesterol (Kiogest, p0.001; Trisequens, p0.01), whereas high-density lipoprotein cholesterol levels were unchanged (Trisequens) or reduced (Kliogest, p0.01), primarily because of a decrease in the high-density lipoprotein-2 subfraction (p0.05). Low-density lipoprotein/high-density lipoprotein cholesterol ratios remained unchanged.Although hormonal replacement therapy with estradiol combined with norethindrone acetate eliminated the increase in high-density lipoprotein cholesterol levels observed with estrogen monotherapy, the reductions in low-density lipoprotein cholesterol concentrations still suggest reduced cardiovascular risk, according to the National Cholesterol Education Program and to recent observations indicating that risk is not necessarily inversely proportional to high-density lipoprotein cholesterol levels.