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IMS Menopause Live

Commentaries from the IMS on recently published scientific papers that may be of interest. The latest articles from September 2018 onward are available to Members only when logged in. Selected articles are open to public.

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Information and misinformation on hormone therapy and meningiomas

12 August, 2013

Meningiomas, which arise from tissues that cover the brain and spinal cord, represent about a fifth of all brain tumors, and they affect women more often than men [1]. The reason for a female predominance is not known, although most meningiomas express receptors for progesterone and some also express estrogen or androgen receptors [2]. Most arise from the arachnoid villi in association with the dura mater or intracranial venous sinuses. Meningiomas are typically slow growing and may compress the brain, but they usually do not invade neural tissues or metastasize to distant sites. Many meningiomas are asymptomatic, discovered only as incidental findings at autopsy or on brain imaging studies performed for some other reason (e.g. ordered because of headache or light-headedness) [3].

In a nationwide case-control study, Danish investigators recently reported associations between menopausal hormone therapy (HT) and meningioma [4]. Their findings, which are largely consistent with other observational research, are also notable from the perspectives of interpretation, perception, and validity.

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Should we be satisfied with the available anti-fracture therapies?

29 July, 2013

Although oral bisphosphonates are highly effective in preventing fractures, some patients will still suffer a fracture while on treatment. In fact, it is important to explain to the patient that any anti-fracture treatment is indeed capable of reducing, but not aborting the risk for fractures. The following study from Spain quantified the remaining risk of fracture while on bisphosphonate therapy [1].

The SIDIAP database was searched to identify new users of oral bisphosphonates in 2006–2007. SIDIAP includes pharmacy invoice data and primary-care electronic medical records for a representative 5 million people in Catalonia (Spain). Exclusion criteria were: Paget disease, < 40 years of age, and any anti-osteoporosis treatment in the previous year. A priori defined risk factors included age, gender, body mass index, vitamin D deficiency, smoking, alcohol drinking, pre-existing co-morbidities, and medications. Fractures were considered if they appeared after at least 6 months after treatment initiation. Fractures while on treatment were defined as those occurring among participants persisting for at least 6 months and with an overall high compliance (medication possession ratio ≥ 80%). Only 7449/21,385 (34.8%) participants completed > 6 months of therapy. Incidence of 'fracture while on treatment' was 3.4/100 person-years (95% confidence interval (CI) 3.1–3.7). Predictors of these among patients persisting and adhering to treatment included: older age (sub-hazard ratio (SHR) for 60 to < 80 years 2.18; 95% CI 1.70–2.80; for ≥ 80 years, SHR 2.5; 95% CI 1.82–3.43), previous fracture (SHR 1.75; 95% CI 1.39–2.20 and SHR 2.49; 95% CI 1.98–3.13 in the last 6 months and longer, respectively), underweight (SHR 2.11; 95% CI 1.14–3.92), inflammatory arthritis (SHR 1.46; 95% CI 1.02–2.10), use of proton pump inhibitors (SHR 1.22; 95% CI 1.02–1.46), and vitamin D deficiency (SHR 2.69; 95% CI 1.27–5.72). Thus, even among high compliers, 3.4% of oral bisphosphonate users will fracture every year. Older age, underweight, vitamin D deficiency, proton pump inhibitor use, previous fracture and inflammatory arthritides are associated with increased fracture risk.

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Mortality toll due to avoiding estrogen therapy in hysterectomized women: estimates for 2002–2011

22 July, 2013

Sarrel and colleagues [1] calculated the mortality toll due to avoiding estrogen in hysterectomized women aged 50–59 between 2002 and 2011. The calculation was motivated by the Women's Health Initiative (WHI) estrogen-only trial report in 2011 [2] which indicated an excess mortality in women in this age group who did not take estrogen, i.e.. received placebo. The excess mortality was 13/10,000 women/year. Twelve of the 13 deaths were due to cardiovascular disease. An increase in deaths from invasive breast cancer was also seen in the women who received placebo [3]. The Yale research team calculated the best point estimates for the total excess mortality for hysterectomized women aged 50–59 in the United States from 2002 through 2011 to be between 40,292 and 48,835.

A calculation was made for each of the years using the excess mortality rate of 13/10,000/year, annual US Census population estimates, hysterectomy rates as reported in the peer-reviewed literature, and percent decline in estrogen use each year compared to 2001, as reported in the WHI paper [2]. Adjustment was made for different pre-2002 rates of estrogen use depending on whether or not ovaries had been retained at the time of hysterectomy. The best point estimates represent the aggregate of all the years taking into account all the assumptions.

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Measuring vulvovaginal symptoms in postmenopausal women

8 July, 2013

Erekson and colleagues recently published in the journal Menopause on their development of a Vulvovaginal Symptoms Questionnaire (VSQ) to determine the symptoms, emotions, life impact, and sexual impact of vulvovaginal symptoms on postmenopausal women [1]. They performed a number of validation tests which confirmed the utility of the questionnaire. Postmenopausal vulvovaginal symptoms include dryness, burning, pruritus, and dyspareunia. Vulvovaginal symptoms are common and have been reported by 9.6–44.4% of postmenopausal women. The authors found the VSQ to be a reliable and internally consistent instrument for measuring vulvovaginal symptoms in postmenopausal women. The authors demonstrated a reasonable validity of the VSQ, particularly in the absence of a gold standard for measuring vulvovaginal symptoms.

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Sugary foods and gynecological cancer risk

17 June, 2013

Once in 5 years, the American Cancer Society publishes its updated guidelines on nutrition and physical activity in the context of cancer prevention [1]. Among the detailed advice is the following quote: 'Limit consumption of sugar-sweetened beverages such as soft drinks, sports drinks, and fruit-flavored drinks.' How this general phrasing relates to specific cancer types is discussed below, and a recent study serves as a good starting point [2]. The investigators evaluated the impact of dietary intake of sugary foods and beverages, as well as added sugar and total sugar on endometrial cancer risk in a population-based, case-control study, including 424 cases and 398 controls. Participants completed an interview and food frequency questionnaire and provided self-recorded waist and hip measurements. Women in the highest quartile of added sugar intake had significantly increased endometrial cancer risk (OR 1.84, 95% CI 1.16–2.92). Among women with waist-to-hip ratio ≥ 0.85, risk was significantly higher for the highest versus lowest tertile of added sugar intakes (OR 2.50, 95% CI 1.38–4.52). The association with added sugar also became stronger when analyses were restricted to never users of hormone replacement therapy (OR 2.03, 95% CI 1.27–3.26, for highest versus lowest tertile). There was little evidence of effect modification by body mass index or physical activity.

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Vitamins and bone health in women

27 May, 2013

Have you heard of a potential interaction between vitamin E and bone health? A recent study from Spain evaluated the relationship between vitamin E status and osteoporosis in early postmenopausal women [1]. Anthropometric data, osteoporosis risk factors, vitamin E serum levels, bone mineral density (BMD) and other serum parameters that may influence bone mineral density in postmenopausal women were analyzed in a cross-sectional study. The associations between osteoporosis and age, age of menopause, body mass index, osteocalcin, calcium, vitamin D, vitamin E (measured as 25-hydroxyvitamin D and as the α-tocopherol : lipid ratio, respectively), bone alkaline phosphatase, smoking status, leisure physical activity and alcohol intake were modeled by a multivariate logistic regression and multi-linear regression analysis in 232 early postmenopausal women. A lower vitamin E : lipid ratio was associated with osteoporosis in multivariate logistic regression. In a multivariate linear model with BMD of the lumbar spine as a dependent variable, the vitamin E : lipid ratio was clearly related with BMD of the lumbar spine (Fratio = 6.30,p= 0.002). BMD of the lumbar spine was significantly higher in the highest tertile of the vitamin E : lipid ratio than in the lowest tertile. The mean vitamin E : lipid ratio was significantly lower in osteoporotic postmenopausal women (Tscore ≤ -2.5) (3.0 ± 0.6 μmol/mmol) than normal postmenopausal women (Tscore > -1) (3.5 ± 0.7 μmol/mmol) using multivariable-adjusted BMD. These findings highlight that vitamin E may increase BMD in healthy postmenopausal women.

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Menopausal women with symptoms do cost more

20 May, 2013:

Kleinman and colleagues have attempted to quantify the economic burden of employees who are diagnosed with menopause symptoms [1]. Their regression-based study analyzed the 2001–2010 medical, pharmacy, sick leave, disability, workers' compensation, and productivity data of large US employers. A cohort of employed women with diagnosed menopause symptoms (DMS), aged more than 40 years, was identified using medical claims. Control employees were propensity-matched on age, employer, plan enrollment length, and enrollment end date. The study included 17,322 women in each cohort. Employees with DMS had significantly higher medical costs ($4315 vs. $2972, p< 0.001), pharmacy costs ($1366 vs. $908, p < 0.001), sick leave costs ($647 vs. $599, p < 0.001), and sick leave days (3.57 vs. 3.30, p < 0.001). Employees with DMS had 12.2% (p = 0.007) lower hourly productivity and 10.9% (p = 0.014) lower annual productivity than controls.

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Endogenous androgen and body fat in the menopause

13 May 2013

Menopause is associated with dramatic changes in a woman's hormonal and metabolic profile. Whereas menopause per se does not seem to affect body weight, the estrogen decline around menopause is associated with a body fat redistribution favoring an android pattern [1]. Furthermore, although incapable of producing estrogens, the postmenopausal ovary remains an active endocrine organ, contributing substantially to the circulating androgen pool [2]. Cao and colleagues [3] in their recent paper conducted a cross-sectional study in early (≤ 5 years) and late (≥ 10 years) postmenopausal women to investigate the association of these two parameters, namely body fat distribution and circulating serum androgens. Late postmenopausal women had a higher percentage of body fat, compared to their younger counterparts, although body mass index (BMI) did not differ between groups. Both early and late obese postmenopausal women had higher androgen levels and more abdominal fat compared to women with normal weight. Serum androgens (free testosterone in early and DHEAS in late postmenopausal women) showed an independent and significant positive association with abdominal adiposity.

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Peripheral arterial disease and menopause

29 April, 2013: 

Looking at the cardiovascular system, it is clear that the heart has been extensively investigated and discussed in regard to the effects of menopause on the one hand, and hormone therapy (HT) on the other hand. But the area of peripheral arterial disease (PAD) in this respect has received much less attention. In a new cross-sectional study on 887 women aged 52–81 years, reproductive parameters were obtained by standardized interviews, and PAD was assessed by measuring non-invasively the ankle-brachial index (using a cut-off value of 0.9) and by assessing the presence of claudication using the Edinburgh questionnaire [1]. The only significant associations with the presence of PAD were later age at menarche (> 15 years) compared to age at menarche between 12 and 15 years (odds ratio (OR) 0.48; 95% confidence interval (CI) 0.24–0.98), and the presence of hot flushes (OR 2.09; 95% CI 1.11–3.92). Other reproductive parameters, such as parity, age at menopause, time since menopause, duration of fertility, ever use or current use of HT, ever use of oral contraceptives, history of hysterectomy, bilateral oophorectomy and depressive mood in relation to menopausal transition showed no significant association with PAD.

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WHI and breast cancer risk: the same old story

15 April, 2013:

WHI investigators keep hammering the issue of hormone therapy (HT) and related increased risk of breast cancer. Their 'money' is actually on what they call the estrogen + progestin (E+P) users, since they cannot claim a real risk in the estrogen-alone users. So now they bring new data from the WHI observational study [1]. Here is the Abstract:

In the WHI randomized trial, estrogen plus progestin increased both breast cancer incidence and mortality. In contrast, most observational studies associate estrogen plus progestin with favorable prognosis for breast cancers. To address differences, a cohort of WHI observational study participants with characteristics similar to the WHI clinical trial was studied. We identified 41,449 postmenopausal women with no prior hysterectomy and mammogram-negative within 2 years who were either not hormone users (n = 25,328) or estrogen and progestin users (n = 16,121). After a mean of 11.3 (SD = 3.1) years, with 2236 breast cancers, incidence was higher in estrogen plus progestin users than in non-users (0.60% vs. 0.42%, annualized rate, respectively; hazard ratio (HR) 1.55, 95% confidence interval (CI) 1.41–1.70, p < 0.001). Women initiating hormone therapy closer to menopause had higher breast cancer risk with linear diminishing influence as time from menopause increased (p < 0.001). Survival after breast cancer, measured from diagnosis, was similar in combined hormone therapy users and non-users (HR 1.03, 95% CI 0.79–1.35). On a population basis, there were somewhat more deaths from breast cancer, measured from cohort entry (HR 1.32, 95% CI 0.90–1.93, p = 0.15), and more all-cause deaths after breast cancer (HR 1.65, 95% CI 1.29–2.12, p < 0.001) in estrogen plus progestin users than in non-users.

Thus the investigators concluded that, consistent with WHI randomized trial findings, estrogen plus progestin use is associated with increased breast cancer incidence. Because prognosis after diagnosis on combined hormone therapy is similar to that of non-users, increased breast cancer mortality can be expected.

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