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Categories available are: Androgens; Estrogens; Progesterone; Bone: Brain; Breast; Cardiovascular; Formulations; Menopausal Symptoms; Premenopause; Progestin; Safety; Uterus.
1. - The Bioidentical Hormone Debate: Are Bioidentical Hormones (Estradiol, Estriol, and Progesterone) Safer or More Efficacious than Commonly Used Synthetic Versions in Hormone Replacement Therapy? Holtorf K.
Postgrad Med 2009;121(1):1-13.
This literature review presents the substantial evidence for the safety and efficacy of bioidentical hormone therapy, including estradiol, estriol, and progesterone, which shows that it presents lower risks for breast cancer and cardiovascular disease than synthetic or animal-derived hormones. Studies show that Progestins have a number of negative effects on the cardiovascular system and an association with breast cancer risk that can be avoided by using bioidentical progesterone.
Not available on Pubmed
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2. - Progesterone receptor A-regulated gene expression in mammary organoid cultures. Santos SJ, Aupperlee MD, Xie J, Durairaj S, Miksicek R, Conrad SE, Leipprandt JR, Tan YS, Schwartz RC, Haslam SZ.
J Steroid Biochem Mol Biol. 2009;115(3-5):161-72.
This experimental study used breast cells from mice, cultured in vitro. First, the behavior of the cells was compared after exposure to either progesterone or the synthetic Progestin, promogestone. After seeing similar proliferation with both progestogens, they then went on to conduct gene expression studies (again in the mouse mammary cells) using only the promogestone. They found that certain genes were activated by the promogestone, and these were regulated by progesterone receptor A, which is increased relative to progesterone receptor B in more aggressive breast cancers in humans. The researchers imply that the expression of these genes in the cultured mouse breast cells may translate to growth-promoting actions of progesterone in the breast tissue in humans. However, human tissue was not studied here, and the mouse cells under investigation were in an environment very different to that under which they would be growing in the intact mouse. Any conclusions regarding the possibility that progesterone in itself could promote breast cancer in a living human can, therefore, not be inferred from this study. In addition, synthetic progestins are already known to have very different actions to those of progesterone itself in clinical studies. Progesterone has not been shown to cause or exacerbate breast cancer in women; on the contrary, it has been found in clinical studies to be associated with a lower breast cancer risk.
Article on Pubmed
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3. - Cardiovascular effects of medroxyprogesterone acetate and progesterone: a case of mistaken identity? Hermsmeyer RK, Thompson TL, Pohost GM, Kaski JC.
Nat Clin Pract Cardiovasc Med 2008;5(7):387-95.
The authors present the current state of knowledge about the cardiovascular effects of progesterone compared to medroxyprogesterone acetate (MPA). They caution that the beneficial effects of natural progesterone on cardiovascular risk have been obscured by the negative results of large trials involving hormone therapy that included MPA, in which cardiac risk was seen to increase. The review covers the evidence that natural progesterone actually improves cardiovascular function, and compares oral and transdermal delivery.
Article on Pubmed
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4. - Could transdermal estradiol + progesterone be a safer postmenopausal HRT? A review. L'Hermite M, Simoncini T, Fuller S, Genazzani AR.
Maturitas 2008;60(3-4):185-201.
This detailed review examines the way different types of hormone replacement therapy (HRT) affect the cardiovascular system, the brain, and the risk of breast cancer. It discusses the research that shows that non-oral estrogens have more favorable cardiovascular effects, such as improved blood pressure control and lower risk of thrombosis. It discusses the benefits of using natural progesterone rather than synthetic Progestins in association with estrogens in HRT. Natural progesterone has a beneficial effect on blood vessels and the brain, and confers less or even no risk of breast cancer, compared with synthetic progestins.
Article on Pubmed
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5. - Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study. Fournier A, Berrino F, Clavel-Chapelon F.
Breast Cancer Res Treat 2008;107(1):103-11.
This large multicenter study in France followed 80,377 postmenopausal women for up to 12 years, and looked in particular at whether the type of progestogen used in combination with estrogen made a difference to the risk of developing breast cancer in those women who used hormone replacement therapy (HRT). The estrogen in HRT is primarily transdermal estradiol in France. Compared with those women who did not use HRT at all, women using estrogen alone had a 1.29-fold increased risk of developing breast cancer; women using estrogen plus natural progesterone had the same risk as women using no HRT. In women using synthetic Progestins in combination with estrogen, the particular progestin used made a difference to breast cancer risk; women using dydrogesterone had a 1.16-fold increased risk of breast cancer, but those using other progestins had a 1.69-fold increased risk of breast cancer, compared to women not using HRT. The authors note that dydrogesterone is the progestin most similar to natural progesterone in its chemical structure and pharmacological effects.
Article on Pubmed
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6. - Correcting misconceptions about compounding bioidentical hormones: a review of the literature. Paoletti J.
Int J Pharm Compounding 2007;11(4):269-272.
The author proposes that any physician prescribing compounded bioidentical hormones should be aware of current information published in the scientific literature. There is much published evidence for the safety of bioidentical progesterone and estrogens, compared to their synthetic alternatives. Unfortunately, some expert advisory groups ignore the published evidence and state opinion rather than fact.
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7. - Is Bio-Identical Hormone Replacement Therapy Safer than Traditional Hormone Replacement Therapy? A Critical Appraisal of Cardiovascular Risks in Menopausal Women. Curcio JJ, Wollner DA, Schmidt JW, Kim LS.
Treat Endocrinol. 2006;5(6):367-374.
This review examines currently used bioidentical hormones used as alternatives to conventional hormone replacement therapy. The authors acknowledge that the clinical evidence shows natural progesterone to be superior to synthetic Progestins, because of its more beneficial effects on lipids, the nervous system, and overall quality of life. Oral estriol has been associated with similar adverse effects to oral synthetic estrogens with respect to cardiovascular risks, but there is evidence that transdermal application of estrogens offers a safer alternative that "should be explored". The authors recommend longer term clinical trials of topical estriol to confirm its cardiovascular safety.
Article on Pubmed
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8. - A comprehensive review of the safety and efficacy of bioidentical hormones for the management of menopause and related health risks. Moskowitz D.
Altern Med Rev. 2006 Sep;11(3):208-23.
This review describes the various synthetic estrogens and Progestins used in hormone replacement therapy and discusses their safety in relation to natural alternatives. Natural estrogens and progesterone are being increasingly used in clinical practice and have demonstrated effectiveness in treating menopausal symptoms. They also have improved safety profiles with respect to breast cancer risk and cardiovascular effects.
Article on Pubmed
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9. - Progestins and progesterone in hormone replacement therapy and the risk of breast cancer. Campagnoli C, Clavel-Chapelon F, Kaaks R, Peris C, Berrino F.
J Steroid Biochem Mol Biol 2005; 96(2):95-108.
The authors discuss the non-progesterone-like effects of synthetic Progestins, which can contribute to the increased risk of breast cancer when these are used as part of a combined hormone therapy regimen. In contrast, bioidentical progesterone does not increase the risk of breast cancer, consistent with experimental in vivo data that shows progesterone has no adverse effect on breast tissue.
Article on Pubmed
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10. - Transdermal progesterone cream as an alternative Progestin in hormone therapy. Leonetti HB, Landes J, Steinberg D, Anasti JN.
Altern Ther Health Med 2005; 11(6):36-38.
This study evaluated the endometrial effects and determined patients' acceptance of transdermal progesterone cream (PC) compared to standard hormone therapy. Healthy menopausal women were recruited and received a pretreatment endometrial biopsy (EMB). They were randomized to 0.625 mg conjugated equine estrogen (CEE) daily and 2.5 mg medroxyprogesterone acetate (MPA) (PremproTM) or daily 0.625 mg CEE and twice daily 20 mg transdermal PC (Pro-gest®). At the end of 6 months, a repeat EMB was obtained, and the women were crossed over to other treatment. A final EMB was performed after the final 6 months. Twenty-six women completed both arms of the study. Seventy-seven percent of women preferred the CEE/PC to the CEE/MPA (P<.001). Of the 52 post-treatment endometrial biopsies: 40 revealed atrophic endometrium and 12 proliferative endometrium (7 in the oral Progestin group and 5 in the PC group). There was no evidence of endometrial hyperplasia in any of the specimens. The incidence of vaginal spotting was similar in both groups. Conclusion: Patients preferred transdermal PC over oral MPA. These preliminary data indicate that CEE/PC has a similar effect on the endometrium as standard (CEE/MPA) oral HT over a 6-month period.
Article on Pubmed
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11. - Pregnancy, progesterone and Progestins in relation to breast cancer risk. Campagnoli C, Abba C, Ambroggio S, Peris C.
J Steroid Biochem Mol Biol 2005; 97(5):441-50.
The authors review recent findings that show that the production of progesterone during pregnancy and the use of bioidentical progesterone in hormone therapy do not increase breast cancer risk, and can even protect against the development of breast cancer.
Article on Pubmed
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12. - Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort. Fournier A, Berrino F, Riboli E, Avenel V, Clavel-Chapelon F.
Int J Cancer 2005; 114(3):448-54.
Combined HRT with estrogen (either oral or transdermal) and synthetic Progestins was found to carry a significantly increased risk of breast cancer compared with estrogens plus oral micronized progesterone. In fact, no increase in breast cancer risk was seen in the estrogen plus oral micronized progesterone group compared with estrogen alone. This large multicenter study therefore suggests that there is a dramatic difference between the effects of bioidentical progesterone versus synthetic progestins on breast cancer risk.
Article on Pubmed
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13. - Chronic treatment with progesterone but not medroxyprogesterone acetate restores the endothelial control of vascular tone in the mesenteric artery of ovariectomized rats. Chataigneau T, Zerr M, Chataigneau M, Hudlett F, Hirn C, Pernot F, Schini-Kerth VB.
Menopause 2004;11(3):255-63.
This study helps explain the more beneficial effects on the cardiovascular system of progesterone compared with MPA because of its enhancement of the protective effects of endothelial cells on the arterial walls.
Article on Pubmed
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14. - A perspective on HRT for women: picking up the pieces after the Women's Health Initiative trial - Part 1. Gillson GR, Zava DT.
Int J Pharm Compounding 2003;7(4):250-6.
This article discusses some fundamental aspects of safer hormone replacement therapy that may have been overlooked in the debate surrounding bioidentical versus synthetic hormones: Oral delivery of hormones is not optimal; application of hormones to the skin (transdermal application) has many important advantages; and synthetic Progestins are not acceptable as a substitute for natural progesterone. The evidence for and principles behind these factors are presented.
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15. - Postmenopausal hormone therapy and change in mammographic density. Greendale GA, Reboussin BA, Slone S, Wasilauskas C, Pike MC, Ursin G.
J Natl Cancer Inst 2003; 95(1):30-7.
Breast cancer risk independently increases with mammographic density. Use of hormone replacement therapy (HRT) postmenopausally is associated with an increase in mammographic density, but the extent of the density increase is unknown. This study evaluated mammograms from 571 of the 875 women enrolled in the PEPI trial at baseline and after 12 months HRT. The women had been randomized to receive placebo, conjugated equine estrogens (CEE) + medroxyprogesterone acetate (MPA) in a continuous or cyclic fashion, or CEE + micronized progesterone (MP). Mammograms were analyzed digitally and a linear regression analysis was utilized to quantify breast density change in all four treatment arms. The adjusted absolute mean changes in mammographic percent density over 12 months were 4.76% (95% confidence interval [CI] = 3.29% to 6.23%), 4.58% (95% CI = 3.19% to 5.97%), and 3.08% (95% CI = 1.65% to 4.51%) for women in the CEE+MPA-cyclic, CEE+MPA-continuous, and CEE-MP groups, respectively. Each of those absolute mean changes was statistically significantly different from the adjusted absolute mean change in mammographic percent density for women in the placebo group, which was -0.07% (95% CI = -1.50% to 1.38%). Greater mammographic density was associated with the use of estrogen/Progestin combination therapy, although the micronized progesterone containing arm appeared to induce a smaller increase that that with MPA.
Article on Pubmed
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16. - All Progestins are not created equal. Stanczyk FZ.
Steroids 2003; 68:879-90.
This paper describes the molecular and pharmacokinetic differences between various Progestins and progesterone. Orally administered progestins require relatively high doses for therapeutic use because of extensive first pass metabolism in the liver. Also, the various molecules show profound differences in progestational activity between human and animal tissues, particularly with respect to androgenicity, which has led to erroneous conclusions being drawn from animal studies regarding androgenicity in humans. The author classifies the various molecules by chemical structure and concludes that they differ widely in metabolism, pharmacokinetics, and potency.
Article on Pubmed
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17. - Progestogens in hormonal replacement therapy: new molecules, risks, and benefits. Sitruk-Ware R.
Menopause 2002;9(1):6-15.
The classifications of various progestogens (natural and synthetic) are reviewed in terms of their risks and benefits. This review clearly elucidates the differences in the mode of action of various synthetic Progestins as well as progesterone.
Article on Pubmed
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18. - Part 3 - The science behind bioidentical hormone replacement therapy. Wepfer ST.
Int J Pharm Compounding 2002;6(2):142-6
Differences between synthetic Progestins and bioidentical progesterone in terms of their effects on breast cancer risk, estrogen dominance, and vasomotor symptoms are discussed. The review also covers the use of testosterone for postmenopausal women who have androgen deficiency because of surgically induced menopause. Androgen deficiency is also seen in women receiving estrogen replacement therapy, which reduces bioavailable testosterone because it increases levels of sex hormone binding globulin in the blood. The author concludes that bioidentical hormones are more effective and safer than the synthetic alternatives, but hopes that large trials will soon be conducted to confirm their promising effects.
Link to Abstract
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19. - Part 2 - The science behind bioidentical hormone replacement therapy. Wepfer ST.
Int J Pharm Compounding 2002;6(1):50-54
The author describes the differences between natural progesterone and the synthetic Progestin medroxyprogesterone acetate (MPA), saying that the number 1 problem in women's health care today is a lack of understanding about progesterone and a belief that it is the same thing as MPA. The benefits of progesterone on the heart and bone are discussed.
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20. - Effects of progestogens on the postmenopausal breast. De Lignieres B.
Climacteric 2002; 5(3):229-35.
In this review, the author highlights the differences between progesterone and synthetic Progestins in the breast and cautions that progestogens not be “all put in the same bag” with respect to safety and risk of breast cancer. A strong case is made for the protective effect of progesterone on the breast.
Article on Pubmed
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21. - Vaginal micronized progesterone in continuous hormone replacement therapy. A prospective randomized study. Ferrero S, Gerbaldo D, Fulcheri E, Cristoforoni P.
Minerva Ginecol 2002; 54(6):519-30.
Transvaginal micronized progesterone (100 mg/day for 12 days/month) effectively promoted a functional, secretory endometrium, while cyclic oral medroxyprogesterone acetate or transdermal norethisterone acetate more often produced endometrial atrophy, in women receiving continuous transdermal estradiol.
Article on Pubmed
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22. - The effects of short-term medroxyprogesterone acetate and micronized progesterone on glucose metabolism and lipid profiles in patients with polycystic ovary syndrome: a prospective randomized study. Bagis T, Gokcel A, Zeyneloglu HB, Tarim E, Kilicdag EB, Haydardedeoglu B.
J Clin Endocrinol Metab 2002;87(10):4536-40.
This randomized prospective study evaluated and compared the effects of ten days treatment with oral and vaginal micronized progesterone (MP) and medroxyprogesterone acetate (MPA) on glucose metabolism, lipid profiles, and hormonal parameters in 28 patients with polycystic ovary syndrome (PCOS). Oral MPA and oral MP decreased luteinizing hormone (P = 0.028, P = 0.009, respectively) and total testosterone (P = 0.013, P = 0.037, respectively) levels. There was no change in hormonal parameters with vaginal MP. Basal insulin decreased (P = 0.021) and insulin sensitivity increased significantly in the oral MPA group. Low density lipoprotein cholesterol (LDL) and lipoprotein (a) levels decreased only in the MPA group. This study concluded that MPA and oral MP may reduce insulin sensitivity in patients with PCOS. Vaginal MP had no effect on glucose metabolism and lipid profiles.
Article on Pubmed
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23. - Efficacy of progesterone and progestogens in management of premenstrual syndrome: systematic review. Wyatt K, Dimmock P, Jones P, Obhrai M, O'Brien S.
BMJ 2001;323(7316):776-80.
This systematic review of published studies of progesterone or progestogens for treatment of PMS found a small positive effect of oral micronized progesterone over placebo in the 3 trials that studied this. No published studies of progesterone cream were found. A statistically, but not clinically, significant improvement was seen with progestogen treatment.
Article on Pubmed
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24. - Progesterone, but not medroxyprogesterone, inhibits vascular cell adhesion molecule-1 expression in human vascular endothelial cells. Otsuki M, Saito H, Xu X, Sumitani S, Kouhara H, Kishimoto T, Kasayama S.
Arterioscler Thromb Vasc Biol 2001 Feb;21(2):243-8.
This study utilizing human umbilical vein endothelial cells (HUVEC’s) demonstrated that progesterone, but not medroxyprogesterone acetate (MPA) inhibited expression of vascular cell adhesion molecule-1 (VCAM-1), demonstrating a role for progesterone in the prevention of atherosclerosis. The differing effects of progesterone and MPA are clinically important, as MPA is widely used in hormone replacement therapy, when, as this research suggests, progesterone might be a more appropriate option.
Article on Pubmed
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25. - Quality of life and costs associated with micronized progesterone and medroxyprogesterone acetate in hormone replacement therapy for non-hysterectomized, postmenopausal women. Ryan N, Rosner A.
Clin Ther 2001; 23(7):1099-115.
This prospective, multicenter, randomized, parallel-group study enrolled 182 postmenopausal women 45 to 65 years of age and evaluated the quality of life (QOL) and menopausal symptoms associated with the use of medroxyprogesterone acetate vs oral micronized progesterone when used as a part of a regular hormone replacement therapy. Menopausal symptoms improved in both groups from baseline to 9 months, as did QOL measures. In addition, patients using micronized progesterone had specific improvements in the areas of cognition and menstrual problems whereas the patients using MPA did not. Micronized progesterone was seen as an effective, cost-comparable alternative to MPA as well as being better tolerated.
Article on Pubmed
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26. - Sleep in menopause: differential effects of two forms of hormone replacement therapy. Montplaisir J, Lorrain J, Denesle R, Petit D.
Menopause 2001; 8(1):10-16.
This randomized clinical trial compared the effects of conjugated equine estrogen (CEE) and medroxyprogesterone acetate to CEE and oral micronized progesterone. Twenty-one postmenopausal women were studied in a sleep lab, with results demonstrating an improvement in subjective measures of menopausal symptoms and sleep in both groups. The group receiving natural progesterone had significantly improved sleep efficiency, whereas the medroxyprogesterone acetate group did not, suggesting that the former might better improve sleep in postmenopausal women.
Article on Pubmed
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27. - Progestins and cardiovascular risk markers. Sitruk-Ware R.
Steroids 2000; 65(10-11):651-8.
This article reviews the effects of various synthetic Progestins and progesterone on cardiovascular health. Many synthetic progestins, especially 19-nortestosterone and some 17-hyroxyprogesterones, have negative effects on cardiovascular risk factors, whereas natural progesterone does not. Further studies utilizing natural and other steroids should be considered.
Article on Pubmed
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28. - Natural progesterone, but not medroxyprogesterone acetate, enhances the beneficial effect of estrogen on exercise-induced myocardial ischemia in postmenopausal women. Rosano GM, Webb CM, Chierchia S, Morgani GL, Gabraele M, Sarrel PM, de Ziegler D, Collins P.
J Am Coll Cardiol 2000;36(7):2154-9.
This randomized crossover study compared the effects of estradiol (E2) (2mg/day), estradiol + progesterone (P4) vaginal gel (2 mg/day + 90 mg on alternate days), and estradiol + medroxyprogesterone acetate (MPA) (2 mg/day + 10 mg/day) on exercise-induced myocardial ischemia in eighteen postmenopausal women with coronary artery disease (CAD) or previous myocardial infarction (MI). Utilizing treadmill testing, patients were evaluated for exercise tolerance after each estradiol phase and at day 10 of each progestogen phase. The results demonstrated an increase in exercise tolerance with both E2 alone and E2 + progesterone, but not by E2 + MPA as compared to baseline. Furthermore, E2 + P4 demonstrated a significant increase in exercise tolerance when compared to MPA. The results suggest that progesterone may be preferred to Progestins for hormone replacement therapy in women at risk for cardiovascular disease.
Article on Pubmed
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29. - Progesterone and Progestins: applications in gynecology. de Ziegler D, Fanchin R.
Steroids 2000;65(10-11):671-9.
This paper reviews the use of a transvaginal progesterone gel as a viable option to other routes of application of natural progesterone (intramuscular, oral micronized), and offered it as a viable option to synthetic Progestins given the low incidence of side effects noted in existing studies.
Article on Pubmed
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30. - Comparison of regimens containing oral micronized progesterone or medroxyprogesterone acetate on quality of life in postmenopausal women: a cross-sectional survey. Fitzpatrick LA, Pace C, Wiita B.
J Women Health Gend Based Med 2000; 9(4):381-7.
A cross-sectional survey was conducted to examine quality of life (QOL) related to physiological, somatic, and vasomotor effects of switching progestogen treatment from medroxyprogesterone acetate (MPA) to micronized progesterone in postmenopausal women already using hormone replacement therapy (HRT). One hundred seventy-six women who were currently using hormone replacement therapy (HRT) containing micronized progesterone for 1-6 months and had previously received HRT containing MPA were surveyed to assess QOL. Women using micronized progesterone-containing HRT experienced significant improvement in vasomotor symptoms, anxiety, somatic complaints and depressive symptoms. Women reported improved control of menopausal symptoms and perceptions of their vaginal bleeding patterns while on the micronized progesterone-containing regimen. Approximately 80% of women reported satisfaction with the progesterone-containing therapy. A micronized progesterone-containing HRT therapy offers the potential for improved QOL with respect to menopausal symptoms.
Article on Pubmed
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31. - Oral micronized progesterone. De Lignieres B.
Clin Ther 1999; 21(1):41-60.
This review article examines the rationale for selecting oral micronized progesterone over synthetic Progestins. It reviews research regarding efficacy and safety and concludes that oral micronized progesterone has fewer side effects than synthetic progestins and is a convenient way to deliver natural progesterone.
Article on Pubmed
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32. - Micronized progesterone: clinical indications and comparison with current treatments. Fitzpatrick LA, Good A.
Fertil Steril 1999;72(3):389-97.
The literature reviewed in this tutorial indicates a potential use for oral micronized progesterone for the treatment of secondary amenorrhea, dysfunctional uterine bleeding, luteal phase disorders, premenopausal bleeding disorders, and as a component of hormone replacement therapy that may provide a better safety profile than commonly utilized synthetic Progestins.
Article on Pubmed
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33. - Progestogen metabolism. Lobo RA.
J Reprod Med 1999; 44(2 Suppl):148-52.
This review clearly elucidates what’s known about the differences in metabolism of various Progestins as compared with endogenous or natural progesterone. Not only are there different pathways for metabolism, but the route of administration also has a significant effect. The physiologic and pathologic state of the patient further influences the metabolism, and there are measurable variations between patients. The authors also review the differences expressed by various tissues in metabolizing progestogens as well as the different biologic potencies of the various progestogens. Most importantly, the authors state the lack of knowledge about the synthetic progestins as compared to natural progesterone, which has a much better understood effect in the body.
Article on Pubmed
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34. - Progestins inhibit the growth of MDA-MB-231 cells transfected with progesterone receptor complementary DNA. Lin VC, Ng EH, Aw SE, Tan MG, Ng EH, Chan VS, Ho GH.
Clin Cancer Res 1999;5(2):395-403.
Progesterone is mainly thought to exert its effects via the estrogen-dependent progesterone receptor (PR), the effects of which may be overshadowed by the presence of estrogen. In order to study the independent effects of progesterone on breast cancer cell lines, PR expression vectors were transfected into a PR and ER negative cell line (MDA-MB-231). The growth of these cells was then studied in response to progesterone and several Progestins. Progesterone was found to significantly inhibit DNA synthesis and cell growth in a dose-dependant fashion. The results of this study indicate that progesterone and progestins independent of estrogen have an antiproliferative effect on breast cancer cells via the progesterone receptor. This suggests a possible role in the treatment of PR negative breast cancer via re-activation of the PR receptor.
Article on Pubmed
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35. - Ovarian steroid protection against coronary artery hyperreactivity in rhesus monkeys. Minshall RD, Stanczyk FZ, Miyagawa K, Uchida B, Axthelm M, Novy M, Hermsmeyer K.
J Clin Endocrinol Metab 1998; 83(2):649-59.
Medroxyprogesterone acetate, but not natural progesterone, negated the protective effects of estradiol against coronary artery hyperreactivity.
Article on Pubmed
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36. - Progestins and breast cancer. Pasqualini JR, Paris J, Sitruk-Ware R, Chetrite G, Botella J.
J Steroid Biochem Mol Biol 1998;65(1-6):225-35.
This review article outlines the many functions of progestogens in hormone-dependent and independent breast cancer and suggests new clinical applications for their use in the treatment of breast cancer.
Article on Pubmed
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37. - Medroxyprogesterone interferes with ovarian steroid protection against coronary vasospasm. Miyagawa K, Rosch J, Stanczyk F, Hermsmeyer K.
Nat Med 1997; 3(3): 324-7.
Ovariectomized rhesus monkeys were treated with physiological levels of 17-beta estradiol in combination with either medroxyprogesterone or progesterone (oral micronized) for four weeks. Following pathophysiological stimulation without injury to induce coronary vasospasm, it was shown that progesterone plus estradiol was protective against vasospasm, whereas estradiol plus medroxyprogesterone allowed vasospasm, concluding that medroxyprogesterone increases risk of coronary vasospasm, while progesterone does not.
Article on Pubmed
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38. - Effects of estrogen or estrogen/Progestin regimens on heart disease risk factors in postmenopausal women. The postmenopausal estrogen/progestin interventions (PEPI) trial. Writing Group for the PEPI Trial.
JAMA 1995; 273(3):199-208.
Bioidentical progesterone (an oral micronized preparation) was used in one group in the PEPI study in place of medroxyprogesterone acetate (MPA). Results showed that the progesterone group had significantly higher HDL cholesterol levels than the MPA group, indicating a different pharmacological effect than the synthetic Progestin with a more favorable effect on blood lipids.
Article on Pubmed
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39. - Differentiating between natural progesterone and synthetic progestogens: clinical implications for premenstrual syndrome management. Martorano JT, Ahlgrimm M, Meyers D.
Compr Ther 1993; 19(3):96-8.
Clinical observations demonstrate that patients suffering from PMS respond to treatment with natural progesterone, whereas synthetic Progestins may exacerbate the condition. The authors review the differences between natural progesterone and synthetic progestins.
Article on Pubmed
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40. - Low-dosage micronized 17 beta-estradiol prevents bone loss in postmenopausal women. Ettinger B, Genant HK, Steiger P, Madvig P.
Am J Obstet Gynecol 1992;166(2):479-88.
The authors evaluated the effects of 17 beta-estradiol (E2) in a randomized, double-blind, dose ranging study of 41 postmenopausal women conducted in 2 phases. Phase one included phased E2 doses (0.5mg, 1.0mg, 2.0mg) plus calcium supplementation (to serum value of 1500mg). Phase two included E2 doses plus random cessation of calcium supplementation. Progestins were added during phase two (total study time of 18 months). Results showed very little change in bone density results for placebo group (0.5 – 0.9%) whereas treatment group showed significant increases from baseline bone density. In phase two the treatment groups showed an annual change in bone density of 2.0%. There was a positive correlation between total calcium intake and the change in bone density results. The study showed a continuous dose-response effect on bone density results. Authors concluded that low dose (1.0mg) beta-estradiol and 1000mg of calcium prevented bone loss in postmenopausal women.
Article on Pubmed
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41. - Sequential use of norethisterone and natural progesterone in pre-menopausal bleeding disorders. Saarikoski S, Yliskoski M, Penttila I.
Maturitas 1990; 12(2):89-97.
This randomized controlled study evaluated the effects of norethisterone (NET) and micronized progesterone (MP) on bleeding disorders in pre-menopausal women. 80 patients were randomized to the trial and all were found via endometrial morphology to need progestogen therapy. They were subsequently treated with NET or MP. In both treatment groups, hyperplastic changes disappeared during the first three cycles, with the duration of treatment being 6 months. NET decreased follicle-stimulating hormone, luteinizing hormone, estradiol and sex-hormone-binding globulin levels (P < 0.001) whereas no changes were seen during MP treatment. High-density-lipoprotein cholesterol and triglyceride levels were also lowered by NET (P< 0.001-0.02) slightly decreased phospholipids. MP treatment had no effect on lipid profiles suggesting it may be a preferred progestogen for the treatment of bleeding disorders.
Article on Pubmed
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42. - Subfractions of high-density lipoprotein cholesterol during estrogen replacement therapy: A comparison between progestogens and natural progesterone. Ottosson UB, Johansson BG, von Schoultz B.
Am J Obstet Gynecol 1985;151(6):746-50.
Fifty-eight postmenopausal women were followed with respect to subfractions of high-density lipoprotein during 3 cycles of unopposed estrogen. The women received either levonorgestrel, medroxyprogesterone acetate, or natural progesterone during the last ten days of the treatment period. Both progestogens significantly lowered HDL cholesterol, whereas natural progesterone had no effect on HDL levels.
Article on Pubmed
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43. - The effect of progesterone and progestogens on the foetus. Dalton K.
Neuropharmacology 1981; 20(12B):1267-9.
This article looks at the differing effects of progesterone and synthetic progestogens on the fetus. Of note in this article is evidence that progesterone supplementation may reduce episodes of pre-eclampsia. Synthetic progestogen supplementation during pregnancy may produce a variety of side effects. Several references are made to articles documenting cases of masculinization of external genitalia in female babies. There are two known cases of true hermaphroditism and several cases of behavioral problems developing in adolescent girls whose mothers took oral synthetic progestogens during pregnancy. More problematic may be administration of oral estrogen-progestogen preparations. Side effects may include spina bifida, esophageal anomalies, heart defects and limb reduction deformities.
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