- Email: [email protected]
THE RISK OF STROKE IN POSTMENOPAUSAL WOMEN RECEIVING HORMONAL THERAPY
S12
8th European Congress on Menopause (EMAS) / Maturitas 63, Supplement 1 (2009) S1–S136
confirmed the increased VTE risk among women using oral oestrogens [2.1 (1.4-3.1)]. The combination of oral oestrogens use and either thrombogenic mutations or obesity further enhanced VTE risk, whereas transdermal oestrogens might not confer additional risk on women at high VTE risk. Alteration in hemostatic variables due to a hepatic first pass effect may explain at least in part the difference in VTE risk between oral and transdermal oestrogens. Oral but not transdermal oestrogens activate blood coagulation and can induce a resistance to activated protein C. Few data are currently available regarding the impact of progestogens on VTE risk, but norpregnane derivatives might be thrombogenic. In conclusion, VTE is a main adverse effect of oral oestrogens, especially among postmenopausal women receiving short-term hormone therapy. Reducing VTE risk by using transdermal oestrogens could substantially improve the benefit-risk profile of hormone therapy, especially among women at high risk for VTE. More data are needed to assess differences in VTE risk beween the different types of progestogens. Keywords: venous thromboembolism, transdermal estrogens, progestogens
40 INDIVIDUAL CARDIOVASCULAR RISK ASSESSMENT AND REDUCTION STRATEGIES A. Pines. Ichilov Medical Center, Department of Medicine ’T’, Tel-Aviv, Israel Menopause marks a turning point in women’s health since the incidence of major illnesses, primarily cardiovascular (CV) disease, becomes more prominent around midlife. As a result, individual assessment of the CV risk factor profile is very important and preventive strategies that reduce that risk should be implemented. The classical risk parameters in men and women are the same and include smoking, obesity, hypertension, hyperlipidemia, diabetes mellitus and sedentarism. However, the impact of each of these risk factors may vary and a scoring system which integrates them into a unified risk scale helps the clinician to decide on priorities and actions that could improve the risk and reduce the chance for future CV events.
41
Parallel Session: Sexual Health 42 IMPROVING IMMUNITY IN THE CLIMATERIC YEARS F. Al-Azzawi. Gynaecology Research Unit, University Hospitals of Leicester, Leicester, United Kingdom Immunity has evolved to protect the organism from noxious microenvironment. While mechanisms of defence are generally similar between sexes, sexual dimorphism in dealing with pathogens has been widely documented thus implicating gonadal steroids in modulating immune responses. A prime example of the role of oestrogen is the shift from cell destructive Th1 immune response to antibody-mediated Th2 in models of multiple sclerosis. In this presentation the focus is made on the lower generative tract (LGT). The cyclical changes in gonadal steroids influence key immunity-regulating molecules in the LGT, largely to spare an immune attack against spermatozoa. In the climacteric, the changes in LGT involves reduction in blood supply, raised vaginal pH, thinning of epithelial cells, altered composition of the extra-cellular matrix as well changes in tissue constituents of immune defences. This renders the atrophic vagina susceptible to pathogens, but the introduction of oestrogen will restore most of these changes. In treating women with intact uterus the addition of progestogens particularly as a continuous regimen with oestrogen may antagonise the protective effects of oestrogen and such mechanisms will be discussed. Progestagens bind the progesterone receptors but exhibit binding affinities to the glucocorticoid and androgen receptors as well. They also alter immunity to viruses such as HPV and HIV. In conclusion, vaginal immunity should be an important consideration in defining the HRT regimens for postmenopausal women.
Parallel Session: The Menopausal Uterus and Ovary
THE RISK OF STROKE IN POSTMENOPAUSAL WOMEN RECEIVING HORMONAL THERAPY
43 R.A. Lobo. Columbia University, New York, United States
PRACTICAL ASSESSMENT OF THE ENDOMETRIUM
Stroke affects one in five women and is the third leading cause of death in the US. The incidence increases with age, and the female to male ratio is similar, unlike that of coronary disease. There are multiple risk factors for stroke, but the most significant ones influencing the relationship between hormones and stroke are obesity, hypertension and smoking. There have been multiple studies looking at the relationship between hormones and stroke. Among observational studies, 21 have shown no effect, while 6 have shown a decreased risk and 4 studies, an increased risk. It is clear that the risk of stroke with hormones is only for ischemic, and not hemorrhagic stroke. Among randomized trials, the Women’s Health Initiative data, because of its size have provided the greatest weight in meta-analytic reviews. Overall, an increase of 20-40% has been found, and because of various confounding factors, it has been difficult to determine if this is statistically significant; although several studies have confirmed this for all postmenopausal women treated. However, in younger women, aged 50-59 years, there is little evidence that the risk is significantly increased, and the overall background prevalence is low: 6-8/10,000 women/year. Recent studies have suggested the risk is not increased significantly with transdermal therapy and with lower doses; although use of progestogen does not appear to influence the risk assessment. There is lack of consistent data on whether early age of initiation of therapy affects the risk. Because this risk may pertain to younger postmenopausal women, and there is a very small risk of stroke reported for young women taking oral contraceptives, it is suggested that the small risk in younger women is through an inflammatory/thrombosis mechanism in susceptible women, rather than one of atherosclerosis, as with coronary disease. Nevertheless, in younger postmenopausal women, with a lower baseline prevalence rate, even if there is a 40% increased risk, the attributable risk, would result in 1-2 additional cases/10,000 women/year, which would be considered a very rare event.
T. Van den Bosch. University Hospitals Leuven, Obstetrics & Gynaecology, Leuven, Belgium For many years, dilatation and curettage (D&C) has been the method of choice to assess the endometrium. However, D&C necessitates a general anaesthesia and, because it is a blind procedure, lesions may be missed. The endometrium can be evaluated in a non-invasive way by sonography. Endometrial cancer is associated with a thickening of the endometrium. Contrariwise, if a thin and regular endometrium is visualized, malignancy is most unlikely. Endometrial polyps are relatively prevalent in postmenopausal women; most polyps remain asymptomatic. To enhance the diagnostic accuracy for focal intracavity lesions a negative contrast agent such as saline or gel may be injected into the uterine cavity during ultrasound. Office endometrial sampling is accurate in the diagnosis of endometrial hyperplasia and endometrial malignancy. However, most focal lesions such as polyps will be missed. Office hysteroscopy is very reliable in the diagnosis of focal lesions such as endometrial polyps and intracavity myomas, but is less accurate for diagnosing endometrial hyperplasia and cancer. When investigating the patients’ preference, vaginal ultrasound was the best accepted procedure, followed by respectively hydrosonography, outpatient hysteroscopy and office endometrial sampling. An algorithm for the diagnosis of uterine pathology in a “one stop clinic” setting is suggested, based on ultrasound with color Doppler imaging as initial investigation. Hydrosonography and/or Pipelle® endometrial sampling to exclude respectively focal intracavity lesions and more diffuse may be performed at the same visit. In cases where ultrasound, hydrosonography or endometrial biopsy do not provide conclusive information a diagnostic office hysteroscopy is indicated. Keywords: Endometrium, sonohysterography.
8th European Congress on Menopause (EMAS) / Maturitas 63, Supplement 1 (2009) S1–S136
confirmed the increased VTE risk among women using oral oestrogens [2.1 (1.4-3.1)]. The combination of oral oestrogens use and either thrombogenic mutations or obesity further enhanced VTE risk, whereas transdermal oestrogens might not confer additional risk on women at high VTE risk. Alteration in hemostatic variables due to a hepatic first pass effect may explain at least in part the difference in VTE risk between oral and transdermal oestrogens. Oral but not transdermal oestrogens activate blood coagulation and can induce a resistance to activated protein C. Few data are currently available regarding the impact of progestogens on VTE risk, but norpregnane derivatives might be thrombogenic. In conclusion, VTE is a main adverse effect of oral oestrogens, especially among postmenopausal women receiving short-term hormone therapy. Reducing VTE risk by using transdermal oestrogens could substantially improve the benefit-risk profile of hormone therapy, especially among women at high risk for VTE. More data are needed to assess differences in VTE risk beween the different types of progestogens. Keywords: venous thromboembolism, transdermal estrogens, progestogens
40 INDIVIDUAL CARDIOVASCULAR RISK ASSESSMENT AND REDUCTION STRATEGIES A. Pines. Ichilov Medical Center, Department of Medicine ’T’, Tel-Aviv, Israel Menopause marks a turning point in women’s health since the incidence of major illnesses, primarily cardiovascular (CV) disease, becomes more prominent around midlife. As a result, individual assessment of the CV risk factor profile is very important and preventive strategies that reduce that risk should be implemented. The classical risk parameters in men and women are the same and include smoking, obesity, hypertension, hyperlipidemia, diabetes mellitus and sedentarism. However, the impact of each of these risk factors may vary and a scoring system which integrates them into a unified risk scale helps the clinician to decide on priorities and actions that could improve the risk and reduce the chance for future CV events.
41
Parallel Session: Sexual Health 42 IMPROVING IMMUNITY IN THE CLIMATERIC YEARS F. Al-Azzawi. Gynaecology Research Unit, University Hospitals of Leicester, Leicester, United Kingdom Immunity has evolved to protect the organism from noxious microenvironment. While mechanisms of defence are generally similar between sexes, sexual dimorphism in dealing with pathogens has been widely documented thus implicating gonadal steroids in modulating immune responses. A prime example of the role of oestrogen is the shift from cell destructive Th1 immune response to antibody-mediated Th2 in models of multiple sclerosis. In this presentation the focus is made on the lower generative tract (LGT). The cyclical changes in gonadal steroids influence key immunity-regulating molecules in the LGT, largely to spare an immune attack against spermatozoa. In the climacteric, the changes in LGT involves reduction in blood supply, raised vaginal pH, thinning of epithelial cells, altered composition of the extra-cellular matrix as well changes in tissue constituents of immune defences. This renders the atrophic vagina susceptible to pathogens, but the introduction of oestrogen will restore most of these changes. In treating women with intact uterus the addition of progestogens particularly as a continuous regimen with oestrogen may antagonise the protective effects of oestrogen and such mechanisms will be discussed. Progestagens bind the progesterone receptors but exhibit binding affinities to the glucocorticoid and androgen receptors as well. They also alter immunity to viruses such as HPV and HIV. In conclusion, vaginal immunity should be an important consideration in defining the HRT regimens for postmenopausal women.
Parallel Session: The Menopausal Uterus and Ovary
THE RISK OF STROKE IN POSTMENOPAUSAL WOMEN RECEIVING HORMONAL THERAPY
43 R.A. Lobo. Columbia University, New York, United States
PRACTICAL ASSESSMENT OF THE ENDOMETRIUM
Stroke affects one in five women and is the third leading cause of death in the US. The incidence increases with age, and the female to male ratio is similar, unlike that of coronary disease. There are multiple risk factors for stroke, but the most significant ones influencing the relationship between hormones and stroke are obesity, hypertension and smoking. There have been multiple studies looking at the relationship between hormones and stroke. Among observational studies, 21 have shown no effect, while 6 have shown a decreased risk and 4 studies, an increased risk. It is clear that the risk of stroke with hormones is only for ischemic, and not hemorrhagic stroke. Among randomized trials, the Women’s Health Initiative data, because of its size have provided the greatest weight in meta-analytic reviews. Overall, an increase of 20-40% has been found, and because of various confounding factors, it has been difficult to determine if this is statistically significant; although several studies have confirmed this for all postmenopausal women treated. However, in younger women, aged 50-59 years, there is little evidence that the risk is significantly increased, and the overall background prevalence is low: 6-8/10,000 women/year. Recent studies have suggested the risk is not increased significantly with transdermal therapy and with lower doses; although use of progestogen does not appear to influence the risk assessment. There is lack of consistent data on whether early age of initiation of therapy affects the risk. Because this risk may pertain to younger postmenopausal women, and there is a very small risk of stroke reported for young women taking oral contraceptives, it is suggested that the small risk in younger women is through an inflammatory/thrombosis mechanism in susceptible women, rather than one of atherosclerosis, as with coronary disease. Nevertheless, in younger postmenopausal women, with a lower baseline prevalence rate, even if there is a 40% increased risk, the attributable risk, would result in 1-2 additional cases/10,000 women/year, which would be considered a very rare event.
T. Van den Bosch. University Hospitals Leuven, Obstetrics & Gynaecology, Leuven, Belgium For many years, dilatation and curettage (D&C) has been the method of choice to assess the endometrium. However, D&C necessitates a general anaesthesia and, because it is a blind procedure, lesions may be missed. The endometrium can be evaluated in a non-invasive way by sonography. Endometrial cancer is associated with a thickening of the endometrium. Contrariwise, if a thin and regular endometrium is visualized, malignancy is most unlikely. Endometrial polyps are relatively prevalent in postmenopausal women; most polyps remain asymptomatic. To enhance the diagnostic accuracy for focal intracavity lesions a negative contrast agent such as saline or gel may be injected into the uterine cavity during ultrasound. Office endometrial sampling is accurate in the diagnosis of endometrial hyperplasia and endometrial malignancy. However, most focal lesions such as polyps will be missed. Office hysteroscopy is very reliable in the diagnosis of focal lesions such as endometrial polyps and intracavity myomas, but is less accurate for diagnosing endometrial hyperplasia and cancer. When investigating the patients’ preference, vaginal ultrasound was the best accepted procedure, followed by respectively hydrosonography, outpatient hysteroscopy and office endometrial sampling. An algorithm for the diagnosis of uterine pathology in a “one stop clinic” setting is suggested, based on ultrasound with color Doppler imaging as initial investigation. Hydrosonography and/or Pipelle® endometrial sampling to exclude respectively focal intracavity lesions and more diffuse may be performed at the same visit. In cases where ultrasound, hydrosonography or endometrial biopsy do not provide conclusive information a diagnostic office hysteroscopy is indicated. Keywords: Endometrium, sonohysterography.