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Framingham Score Predicts Raloxifene's Stroke Risk
ORLANDO — The Framingham stroke risk score can predict a high-risk postmenopausal woman's likelihood of a future cerebrovascular event with raloxifene use, according to new analysis of data from the Raloxifene Use for the Heart (RUTH)study.
Investigators in 26 countries enrolled 10,101 women at risk for a major coronary event in RUTH. A total of 5,031 women had documented coronary heart disease and the remaining 5,070 had multiple coronary heart disease risk factors (Am. J. Cardiol. 2002;90:1204–10). Although overall stroke risk was not significantly different between women randomized to raloxifene versus placebo, a higher number of fatal stroke events occurred in the treatment group, 59, compared with 39 in the placebo group during a mean of 5.6 years follow-up (N. Engl. J. Med. 2006:355:125–37).
Investigators launched a second study to see how this increased risk associated with raloxifene (hazard ratio, 1.49; absolute risk increase, 0.7 per 1,000 woman-years) would apply to women stratified by baseline Framingham stroke scale score.
David Cox, Ph.D., and his associates retrospectively calculated 10-year cumulative risk. He presented findings at the annual meeting of the North American Menopause Society. Eli Lilly & Co. supported the study, and Dr. Cox is a clinical research scientist for the company.
Not surprisingly, risks appeared to congregate in the third and fourth highest quartiles of Framingham score risk. However, there were no significant differences between treatment groups in either all strokes or nonfatal strokes, regardless of baseline Framingham score.
Regarding fatal stroke, Dr. Cox said, “after 2 years, you start to see a split between placebo and raloxifene for risk of fatal stroke by Framingham stroke risk score in RUTH. We think the pattern and data would suggest most of the excess risk was among those in the upper half of risk.” Specifically, women who scored a 13 or greater on the Framingham tool at baseline (the median) were at increased risk of stroke death, compared with women who scored lower.
A meeting attendee asked at what age raloxifene should no longer be considered, offering 70 years as an example. “Even at age 70, she might not have enough risk factors,” Dr. Cox said. “But it depends on the risk factor.” For example, he said, “atrial fibrillation would put her over the 13 score.”
Dr. Cox and his colleagues also retrospectively assessed application of the Framingham risk score to 7,705 postmenopausal women with osteoporosis randomized to raloxifene or placebo in the Multiple Outcomes of Raloxifene Evaluation (MORE) study (JAMA 2002;287:847–57). In this study, raloxifene was not associated with an increase in rate of all strokes (hazard ratio, 0.71) or stroke death (HR, 0.57). He noted that the MORE population was generally lower risk than women in RUTH, with baseline Framingham scores of less than 13 in 80%.
Raloxifene's effect on the stroke death rate might differ by baseline stroke risk, Dr. Cox said. Assessing cumulative stroke risk may help target raloxifene treatment to postmenopausal women with the most favorable risk-benefit profile.
ORLANDO — The Framingham stroke risk score can predict a high-risk postmenopausal woman's likelihood of a future cerebrovascular event with raloxifene use, according to new analysis of data from the Raloxifene Use for the Heart (RUTH)study.
Investigators in 26 countries enrolled 10,101 women at risk for a major coronary event in RUTH. A total of 5,031 women had documented coronary heart disease and the remaining 5,070 had multiple coronary heart disease risk factors (Am. J. Cardiol. 2002;90:1204–10). Although overall stroke risk was not significantly different between women randomized to raloxifene versus placebo, a higher number of fatal stroke events occurred in the treatment group, 59, compared with 39 in the placebo group during a mean of 5.6 years follow-up (N. Engl. J. Med. 2006:355:125–37).
Investigators launched a second study to see how this increased risk associated with raloxifene (hazard ratio, 1.49; absolute risk increase, 0.7 per 1,000 woman-years) would apply to women stratified by baseline Framingham stroke scale score.
David Cox, Ph.D., and his associates retrospectively calculated 10-year cumulative risk. He presented findings at the annual meeting of the North American Menopause Society. Eli Lilly & Co. supported the study, and Dr. Cox is a clinical research scientist for the company.
Not surprisingly, risks appeared to congregate in the third and fourth highest quartiles of Framingham score risk. However, there were no significant differences between treatment groups in either all strokes or nonfatal strokes, regardless of baseline Framingham score.
Regarding fatal stroke, Dr. Cox said, “after 2 years, you start to see a split between placebo and raloxifene for risk of fatal stroke by Framingham stroke risk score in RUTH. We think the pattern and data would suggest most of the excess risk was among those in the upper half of risk.” Specifically, women who scored a 13 or greater on the Framingham tool at baseline (the median) were at increased risk of stroke death, compared with women who scored lower.
A meeting attendee asked at what age raloxifene should no longer be considered, offering 70 years as an example. “Even at age 70, she might not have enough risk factors,” Dr. Cox said. “But it depends on the risk factor.” For example, he said, “atrial fibrillation would put her over the 13 score.”
Dr. Cox and his colleagues also retrospectively assessed application of the Framingham risk score to 7,705 postmenopausal women with osteoporosis randomized to raloxifene or placebo in the Multiple Outcomes of Raloxifene Evaluation (MORE) study (JAMA 2002;287:847–57). In this study, raloxifene was not associated with an increase in rate of all strokes (hazard ratio, 0.71) or stroke death (HR, 0.57). He noted that the MORE population was generally lower risk than women in RUTH, with baseline Framingham scores of less than 13 in 80%.
Raloxifene's effect on the stroke death rate might differ by baseline stroke risk, Dr. Cox said. Assessing cumulative stroke risk may help target raloxifene treatment to postmenopausal women with the most favorable risk-benefit profile.
ORLANDO — The Framingham stroke risk score can predict a high-risk postmenopausal woman's likelihood of a future cerebrovascular event with raloxifene use, according to new analysis of data from the Raloxifene Use for the Heart (RUTH)study.
Investigators in 26 countries enrolled 10,101 women at risk for a major coronary event in RUTH. A total of 5,031 women had documented coronary heart disease and the remaining 5,070 had multiple coronary heart disease risk factors (Am. J. Cardiol. 2002;90:1204–10). Although overall stroke risk was not significantly different between women randomized to raloxifene versus placebo, a higher number of fatal stroke events occurred in the treatment group, 59, compared with 39 in the placebo group during a mean of 5.6 years follow-up (N. Engl. J. Med. 2006:355:125–37).
Investigators launched a second study to see how this increased risk associated with raloxifene (hazard ratio, 1.49; absolute risk increase, 0.7 per 1,000 woman-years) would apply to women stratified by baseline Framingham stroke scale score.
David Cox, Ph.D., and his associates retrospectively calculated 10-year cumulative risk. He presented findings at the annual meeting of the North American Menopause Society. Eli Lilly & Co. supported the study, and Dr. Cox is a clinical research scientist for the company.
Not surprisingly, risks appeared to congregate in the third and fourth highest quartiles of Framingham score risk. However, there were no significant differences between treatment groups in either all strokes or nonfatal strokes, regardless of baseline Framingham score.
Regarding fatal stroke, Dr. Cox said, “after 2 years, you start to see a split between placebo and raloxifene for risk of fatal stroke by Framingham stroke risk score in RUTH. We think the pattern and data would suggest most of the excess risk was among those in the upper half of risk.” Specifically, women who scored a 13 or greater on the Framingham tool at baseline (the median) were at increased risk of stroke death, compared with women who scored lower.
A meeting attendee asked at what age raloxifene should no longer be considered, offering 70 years as an example. “Even at age 70, she might not have enough risk factors,” Dr. Cox said. “But it depends on the risk factor.” For example, he said, “atrial fibrillation would put her over the 13 score.”
Dr. Cox and his colleagues also retrospectively assessed application of the Framingham risk score to 7,705 postmenopausal women with osteoporosis randomized to raloxifene or placebo in the Multiple Outcomes of Raloxifene Evaluation (MORE) study (JAMA 2002;287:847–57). In this study, raloxifene was not associated with an increase in rate of all strokes (hazard ratio, 0.71) or stroke death (HR, 0.57). He noted that the MORE population was generally lower risk than women in RUTH, with baseline Framingham scores of less than 13 in 80%.
Raloxifene's effect on the stroke death rate might differ by baseline stroke risk, Dr. Cox said. Assessing cumulative stroke risk may help target raloxifene treatment to postmenopausal women with the most favorable risk-benefit profile.
Testosterone Patch Improves Sexual Function in Postmenopausal Women
The testosterone patch improves sexual function and decreases emotional distress in postmenopausal women who have hypoactive sexual desire disorder, but the patch's long-term safety needs to be assessed, according to an international study of more than 800 women.
“The increase in the frequency of satisfying sexual episodes was modest but appeared to be clinically meaningful,” said Dr. Susan R. Davis of Monash University, Prahran, Victoria, Australia, and her associates.
This is the first large-scale, phase III clinical trial of testosterone therapy that involved postmenopausal women who were not taking concomitant estrogen. The results “indicate that exogenous estrogen or combined estrogen plus progestin are not required for testosterone to be effective in the treatment of hypoactive sexual disorder,” the authors wrote.
However, “additional data are needed to assess the long-term safety of testosterone use in women with estrogen depletion,” they added.
Of particular concern is the possibility that testosterone without concomitant estrogen may have adverse effects on the breast and endometrium. In this study, four cases of breast cancer occurred in women on active treatment, compared with no cases in women taking placebo, and vaginal bleeding also was significantly more common with active treatment.
The study involved women aged 20–70 years who had surgically induced menopause of at least 1 year's duration, and women aged 40–70 years who had natural menopause of at least 2 years' duration. These subjects all had hypoactive sexual desire and were treated at 65 medical centers throughout the United States, Canada, Australia, the United Kingdom, and Sweden between 2004 and 2006.
The study was sponsored by Procter & Gamble Pharmaceuticals Inc., which also was involved in study design and data collection, and conducted the data analysis. Procter & Gamble makes Intrinsa, a testosterone patch that has been approved by the European Medicines Agency for treatment of hypoactive sexual desire. A Food and Drug Administration advisory committee recommended against approval of the drug for the U.S. market in 2004.
In the study, 814 women were randomly assigned to use a 150-mcg testosterone patch, a 300-mcg testosterone patch, or a placebo patch every day for 1 year. The efficacy analysis was performed at 24 weeks, after which the effect of testosterone tends to plateau; the safety analysis was performed at 1 year. A total of 71% of the study subjects completed 24 weeks, and only 57% completed the full year.
Compared with the placebo group, both groups on active treatment reported significant increases in sexual desire and frequency of satisfying sexual episodes, as well as decreases in personal distress related to sexual function.
The improvement in frequency of satisfying sexual episodes was “numerically modest,” at only 1.4 more such episodes per month. However, this amount has been shown to be clinically meaningful in previous studies, Dr. Davis and her associates said (N. Engl. J. Med. 2008;359:2005–17).
Treatment effects did not differ between women who had undergone surgical menopause and those who had undergone natural menopause.
The overall incidence of adverse effects was similar among the three groups. The most common reasons for withdrawal from the study were patch-site reactions and androgenic events, principally the growth of facial hair.
Four women receiving active treatment developed breast cancer, compared with none receiving placebo. The size of the study groups was too small to allow for analysis, and this excess could be the result of chance. But “the possibility of a causal relationship must be considered,” the researchers noted.
Nearly 11% of women with an intact uterus who used the higher dose patch reported vaginal bleeding, compared with fewer than 3% of the other two groups. All women with vaginal bleeding had ultrasonography and/or endometrial biopsy. There were no cases of endometrial hyperplasia or carcinoma.
In an accompanying editorial comment, Julia R. Heiman, Ph.D., of the Kinsey Institute for Sex, Gender, and Reproduction at Indiana University, Bloomington, said that it is reasonable to wonder whether an absolute increase in satisfying sexual episodes of only 1.4 per month is worthwhile.
“Although the report does not indicate whether the women were asked whether this change was meaningful for them, a review of the baseline data suggests it probably was, since the mean number of such episodes almost doubled for the high-dose group,” she said (N. Engl. J. Med. 2008;359:2047–9).
The “potentially worrisome” excess of breast cancer cases “cannot be ignored,” Dr. Heiman added.
They “suggest the need for caution in using testosterone until we understand more about its possible link with breast cancer and are better able to predict which patients are more likely to be subject to negative effects.”
Dr. Davis reports receiving consulting or lecture fees from Acrux Ltd., AstraZeneca Oncology Australia, Organon, and Procter & Gamble Pharmaceuticals, as well as grant support from AstraZeneca Pharmaceuticals, Novartis Oncology Australia, and Procter & Gamble Pharmaceuticals. Dr. Heiman reports receiving grant support from Pfizer, Bayer HealthCare, and Zestra Laboratories Inc.
The testosterone patch improves sexual function and decreases emotional distress in postmenopausal women who have hypoactive sexual desire disorder, but the patch's long-term safety needs to be assessed, according to an international study of more than 800 women.
“The increase in the frequency of satisfying sexual episodes was modest but appeared to be clinically meaningful,” said Dr. Susan R. Davis of Monash University, Prahran, Victoria, Australia, and her associates.
This is the first large-scale, phase III clinical trial of testosterone therapy that involved postmenopausal women who were not taking concomitant estrogen. The results “indicate that exogenous estrogen or combined estrogen plus progestin are not required for testosterone to be effective in the treatment of hypoactive sexual disorder,” the authors wrote.
However, “additional data are needed to assess the long-term safety of testosterone use in women with estrogen depletion,” they added.
Of particular concern is the possibility that testosterone without concomitant estrogen may have adverse effects on the breast and endometrium. In this study, four cases of breast cancer occurred in women on active treatment, compared with no cases in women taking placebo, and vaginal bleeding also was significantly more common with active treatment.
The study involved women aged 20–70 years who had surgically induced menopause of at least 1 year's duration, and women aged 40–70 years who had natural menopause of at least 2 years' duration. These subjects all had hypoactive sexual desire and were treated at 65 medical centers throughout the United States, Canada, Australia, the United Kingdom, and Sweden between 2004 and 2006.
The study was sponsored by Procter & Gamble Pharmaceuticals Inc., which also was involved in study design and data collection, and conducted the data analysis. Procter & Gamble makes Intrinsa, a testosterone patch that has been approved by the European Medicines Agency for treatment of hypoactive sexual desire. A Food and Drug Administration advisory committee recommended against approval of the drug for the U.S. market in 2004.
In the study, 814 women were randomly assigned to use a 150-mcg testosterone patch, a 300-mcg testosterone patch, or a placebo patch every day for 1 year. The efficacy analysis was performed at 24 weeks, after which the effect of testosterone tends to plateau; the safety analysis was performed at 1 year. A total of 71% of the study subjects completed 24 weeks, and only 57% completed the full year.
Compared with the placebo group, both groups on active treatment reported significant increases in sexual desire and frequency of satisfying sexual episodes, as well as decreases in personal distress related to sexual function.
The improvement in frequency of satisfying sexual episodes was “numerically modest,” at only 1.4 more such episodes per month. However, this amount has been shown to be clinically meaningful in previous studies, Dr. Davis and her associates said (N. Engl. J. Med. 2008;359:2005–17).
Treatment effects did not differ between women who had undergone surgical menopause and those who had undergone natural menopause.
The overall incidence of adverse effects was similar among the three groups. The most common reasons for withdrawal from the study were patch-site reactions and androgenic events, principally the growth of facial hair.
Four women receiving active treatment developed breast cancer, compared with none receiving placebo. The size of the study groups was too small to allow for analysis, and this excess could be the result of chance. But “the possibility of a causal relationship must be considered,” the researchers noted.
Nearly 11% of women with an intact uterus who used the higher dose patch reported vaginal bleeding, compared with fewer than 3% of the other two groups. All women with vaginal bleeding had ultrasonography and/or endometrial biopsy. There were no cases of endometrial hyperplasia or carcinoma.
In an accompanying editorial comment, Julia R. Heiman, Ph.D., of the Kinsey Institute for Sex, Gender, and Reproduction at Indiana University, Bloomington, said that it is reasonable to wonder whether an absolute increase in satisfying sexual episodes of only 1.4 per month is worthwhile.
“Although the report does not indicate whether the women were asked whether this change was meaningful for them, a review of the baseline data suggests it probably was, since the mean number of such episodes almost doubled for the high-dose group,” she said (N. Engl. J. Med. 2008;359:2047–9).
The “potentially worrisome” excess of breast cancer cases “cannot be ignored,” Dr. Heiman added.
They “suggest the need for caution in using testosterone until we understand more about its possible link with breast cancer and are better able to predict which patients are more likely to be subject to negative effects.”
Dr. Davis reports receiving consulting or lecture fees from Acrux Ltd., AstraZeneca Oncology Australia, Organon, and Procter & Gamble Pharmaceuticals, as well as grant support from AstraZeneca Pharmaceuticals, Novartis Oncology Australia, and Procter & Gamble Pharmaceuticals. Dr. Heiman reports receiving grant support from Pfizer, Bayer HealthCare, and Zestra Laboratories Inc.
The testosterone patch improves sexual function and decreases emotional distress in postmenopausal women who have hypoactive sexual desire disorder, but the patch's long-term safety needs to be assessed, according to an international study of more than 800 women.
“The increase in the frequency of satisfying sexual episodes was modest but appeared to be clinically meaningful,” said Dr. Susan R. Davis of Monash University, Prahran, Victoria, Australia, and her associates.
This is the first large-scale, phase III clinical trial of testosterone therapy that involved postmenopausal women who were not taking concomitant estrogen. The results “indicate that exogenous estrogen or combined estrogen plus progestin are not required for testosterone to be effective in the treatment of hypoactive sexual disorder,” the authors wrote.
However, “additional data are needed to assess the long-term safety of testosterone use in women with estrogen depletion,” they added.
Of particular concern is the possibility that testosterone without concomitant estrogen may have adverse effects on the breast and endometrium. In this study, four cases of breast cancer occurred in women on active treatment, compared with no cases in women taking placebo, and vaginal bleeding also was significantly more common with active treatment.
The study involved women aged 20–70 years who had surgically induced menopause of at least 1 year's duration, and women aged 40–70 years who had natural menopause of at least 2 years' duration. These subjects all had hypoactive sexual desire and were treated at 65 medical centers throughout the United States, Canada, Australia, the United Kingdom, and Sweden between 2004 and 2006.
The study was sponsored by Procter & Gamble Pharmaceuticals Inc., which also was involved in study design and data collection, and conducted the data analysis. Procter & Gamble makes Intrinsa, a testosterone patch that has been approved by the European Medicines Agency for treatment of hypoactive sexual desire. A Food and Drug Administration advisory committee recommended against approval of the drug for the U.S. market in 2004.
In the study, 814 women were randomly assigned to use a 150-mcg testosterone patch, a 300-mcg testosterone patch, or a placebo patch every day for 1 year. The efficacy analysis was performed at 24 weeks, after which the effect of testosterone tends to plateau; the safety analysis was performed at 1 year. A total of 71% of the study subjects completed 24 weeks, and only 57% completed the full year.
Compared with the placebo group, both groups on active treatment reported significant increases in sexual desire and frequency of satisfying sexual episodes, as well as decreases in personal distress related to sexual function.
The improvement in frequency of satisfying sexual episodes was “numerically modest,” at only 1.4 more such episodes per month. However, this amount has been shown to be clinically meaningful in previous studies, Dr. Davis and her associates said (N. Engl. J. Med. 2008;359:2005–17).
Treatment effects did not differ between women who had undergone surgical menopause and those who had undergone natural menopause.
The overall incidence of adverse effects was similar among the three groups. The most common reasons for withdrawal from the study were patch-site reactions and androgenic events, principally the growth of facial hair.
Four women receiving active treatment developed breast cancer, compared with none receiving placebo. The size of the study groups was too small to allow for analysis, and this excess could be the result of chance. But “the possibility of a causal relationship must be considered,” the researchers noted.
Nearly 11% of women with an intact uterus who used the higher dose patch reported vaginal bleeding, compared with fewer than 3% of the other two groups. All women with vaginal bleeding had ultrasonography and/or endometrial biopsy. There were no cases of endometrial hyperplasia or carcinoma.
In an accompanying editorial comment, Julia R. Heiman, Ph.D., of the Kinsey Institute for Sex, Gender, and Reproduction at Indiana University, Bloomington, said that it is reasonable to wonder whether an absolute increase in satisfying sexual episodes of only 1.4 per month is worthwhile.
“Although the report does not indicate whether the women were asked whether this change was meaningful for them, a review of the baseline data suggests it probably was, since the mean number of such episodes almost doubled for the high-dose group,” she said (N. Engl. J. Med. 2008;359:2047–9).
The “potentially worrisome” excess of breast cancer cases “cannot be ignored,” Dr. Heiman added.
They “suggest the need for caution in using testosterone until we understand more about its possible link with breast cancer and are better able to predict which patients are more likely to be subject to negative effects.”
Dr. Davis reports receiving consulting or lecture fees from Acrux Ltd., AstraZeneca Oncology Australia, Organon, and Procter & Gamble Pharmaceuticals, as well as grant support from AstraZeneca Pharmaceuticals, Novartis Oncology Australia, and Procter & Gamble Pharmaceuticals. Dr. Heiman reports receiving grant support from Pfizer, Bayer HealthCare, and Zestra Laboratories Inc.
Recommendations on hormone therapy in peri- and postmenopause
Unresolved issues
The Expert Panel found that data were insufficient to answer these questions:
- Should women who are doing well on long-term hormone therapy (HT) discontinue?
- Is there a best way to discontinue HT?
- Does a continuous-combined EPT regimen have an effect different from continuous estrogen with sequential progestogen?
- Is HT associated with early risk of coronary heart disease?
New recommendations
Duration
- ET/EPT can be used for a time consistent with treatment goals and provided the patient is monitored regularly; there was no stipulation on when to reduce or stop therapy.
- So-called “bioidentical hormones” should be considered to have the same safety issues as traditional postmenopausal hormone therapy until clinical trials can specify their safety and effectiveness. (The statement refers to custommade alternatives to FDA-approved estrogen and progestogen formulations.)
- The risk of breast cancer probably increases with EPT use but not with ET use.
- The role of both ET and EPT in primary prevention of coronary heart disease remains unclear, especially in younger women starting therapy early and continuing for a number of years; however, until that evidence is forthcoming, ET or EPT should not be used for primary or secondary prevention of coronary heart disease.
Renewed recommendations
Hormones for hot flashes
- Strong endorsement to use ET/EPT for menopause-related symptoms such as hot flashes.
- ET or EPT should be limited to the lowest effective dose.
The complete report is in the NAMS official journal, Menopause (2004;11:589–600) and can be accessed at www.menopause.org
Unresolved issues
The Expert Panel found that data were insufficient to answer these questions:
- Should women who are doing well on long-term hormone therapy (HT) discontinue?
- Is there a best way to discontinue HT?
- Does a continuous-combined EPT regimen have an effect different from continuous estrogen with sequential progestogen?
- Is HT associated with early risk of coronary heart disease?
New recommendations
Duration
- ET/EPT can be used for a time consistent with treatment goals and provided the patient is monitored regularly; there was no stipulation on when to reduce or stop therapy.
- So-called “bioidentical hormones” should be considered to have the same safety issues as traditional postmenopausal hormone therapy until clinical trials can specify their safety and effectiveness. (The statement refers to custommade alternatives to FDA-approved estrogen and progestogen formulations.)
- The risk of breast cancer probably increases with EPT use but not with ET use.
- The role of both ET and EPT in primary prevention of coronary heart disease remains unclear, especially in younger women starting therapy early and continuing for a number of years; however, until that evidence is forthcoming, ET or EPT should not be used for primary or secondary prevention of coronary heart disease.
Renewed recommendations
Hormones for hot flashes
- Strong endorsement to use ET/EPT for menopause-related symptoms such as hot flashes.
- ET or EPT should be limited to the lowest effective dose.
The complete report is in the NAMS official journal, Menopause (2004;11:589–600) and can be accessed at www.menopause.org
Unresolved issues
The Expert Panel found that data were insufficient to answer these questions:
- Should women who are doing well on long-term hormone therapy (HT) discontinue?
- Is there a best way to discontinue HT?
- Does a continuous-combined EPT regimen have an effect different from continuous estrogen with sequential progestogen?
- Is HT associated with early risk of coronary heart disease?
New recommendations
Duration
- ET/EPT can be used for a time consistent with treatment goals and provided the patient is monitored regularly; there was no stipulation on when to reduce or stop therapy.
- So-called “bioidentical hormones” should be considered to have the same safety issues as traditional postmenopausal hormone therapy until clinical trials can specify their safety and effectiveness. (The statement refers to custommade alternatives to FDA-approved estrogen and progestogen formulations.)
- The risk of breast cancer probably increases with EPT use but not with ET use.
- The role of both ET and EPT in primary prevention of coronary heart disease remains unclear, especially in younger women starting therapy early and continuing for a number of years; however, until that evidence is forthcoming, ET or EPT should not be used for primary or secondary prevention of coronary heart disease.
Renewed recommendations
Hormones for hot flashes
- Strong endorsement to use ET/EPT for menopause-related symptoms such as hot flashes.
- ET or EPT should be limited to the lowest effective dose.
The complete report is in the NAMS official journal, Menopause (2004;11:589–600) and can be accessed at www.menopause.org