Panagiotis Anagnostis1, Johannes Bitzer2, Antonio Cano3, Iuliana Ceausu4, Peter Chedraui5, Fatih Durmusoglu6, Risto Erkkola7, Dimitrios G Goulis8, Angelica Lindén Hirschberg9, Ludwig Kiesel10, Patrice Lopes11, Amos Pines12, Mick van Trotsenburg13, Irene Lambrinoudaki14, Margaret Rees15. 1. Unit of Reproductive Endocrinology, 1st Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Greece. Electronic address: pan.anagnostis@gmail.com. 2. Department of Obstetrics and Gynecology, University Hospital, Basel, Switzerland. 3. Department of Pediatrics, Obstetrics and Gynecology, University of Valencia and INCLIVA, Valencia, Spain. 4. Department of Obstetrics and Gynecology I, "Dr. I. Cantacuzino" Hospital, "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania. 5. Instituto de Investigación e Innovación de Salud Integral (ISAIN), Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador. 6. İstanbul Medipol International School of Medicine, Istanbul, Turkey. 7. Department of Obstetrics and Gynecology, University Central Hospital Turku, Finland. 8. Unit of Reproductive Endocrinology, 1st Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Greece. 9. Department of Women's and Children's Health, Karolinska Institutet and Department of Gynecology and Reproductive Medicine, Karolinska University Hospital, Stockholm, Sweden. 10. Department of Gynecology and Obstetrics, University of Münster, Münster, Germany. 11. Nantes, France Polyclinique de l'Atlantique Saint Herblain. F 44819 St Herblain France, Université de Nantes F 44093 Nantes Cedex, France. 12. Sackler Faculty of Medicine, Tel-Aviv University, Israel. 13. Department of Obstetrics and Gynecology, University Hospital St. Poelten-Lilienfeld, Austria. 14. Second Department of Obstetrics and Gynecology, Aretaieio Hospital, Medical School, National and Kapodistrian University of Athens, Greece. 15. Women's Centre, John Radcliffe Hospital, Oxford, OX3 9DU, UK.
Abstract
INTRODUCTION: Dyslipidemias are common and increase the risk of cardiovascular disease. The menopause transition is associated with an atherogenic lipid profile, with an increase in the concentrations of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), apolipoprotein B (apoB) and potentially lipoprotein (a) [Lp(a)], and a decrease in the concentration of high-density lipoprotein cholesterol (HDL-C). AIM: The aim of this clinical guide is to provide an evidence-based approach to management of menopausal symptoms and dyslipidemia in postmenopausal women. The guide evaluates the effects on the lipid profile both of menopausal hormone therapy and of non-estrogen-based treatments for menopausal symptoms. MATERIALS AND METHODS: Literature review and consensus of expert opinion. SUMMARY RECOMMENDATIONS: Initial management depends on whether the dyslipidemia is primary or secondary. An assessment of the 10-year risk of fatal cardiovascular disease, based on the Systematic Coronary Risk Estimation (SCORE) system, should be used to set the optimal LDL-C target. Dietary changes and pharmacological management of dyslipidemias should be tailored to the type of dyslipidemia, with statins constituting the mainstay of treatment. With regard to menopausal hormone therapy, systemic estrogens induce a dose-dependent reduction in TC, LDL-C and Lp(a), as well as an increase in HDL-C concentrations; these effects are more prominent with oral administration. Transdermal rather than oral estrogens should be used in women with hypertriglyceridemia. Micronized progesterone or dydrogesterone are the preferred progestogens due to their neutral effect on the lipid profile. Tibolone may decrease TC, LDL-C, TG and Lp(a), but also HDL-C concentrations. Low-dose vaginal estrogen and ospemifene exert a favorable effect on the lipid profile, but data are scant regarding dehydroepiandrosterone (DHEA). Non-estrogen-based therapies, such as fluoxetine and citalopram, exert a more favorable effect on the lipid profile than do sertraline, paroxetine and venlafaxine. Non-oral testosterone, used for the treatment of hypoactive sexual desire disorder/dysfunction, has little or no effect on the lipid profile.
INTRODUCTION: Dyslipidemias are common and increase the risk of cardiovascular disease. The menopause transition is associated with an atherogenic lipid profile, with an increase in the concentrations of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), apolipoprotein B (apoB) and potentially lipoprotein (a) [Lp(a)], and a decrease in the concentration of high-density lipoprotein cholesterol (HDL-C). AIM: The aim of this clinical guide is to provide an evidence-based approach to management of menopausal symptoms and dyslipidemia in postmenopausal women. The guide evaluates the effects on the lipid profile both of menopausal hormone therapy and of non-estrogen-based treatments for menopausal symptoms. MATERIALS AND METHODS: Literature review and consensus of expert opinion. SUMMARY RECOMMENDATIONS: Initial management depends on whether the dyslipidemia is primary or secondary. An assessment of the 10-year risk of fatal cardiovascular disease, based on the Systematic Coronary Risk Estimation (SCORE) system, should be used to set the optimal LDL-C target. Dietary changes and pharmacological management of dyslipidemias should be tailored to the type of dyslipidemia, with statins constituting the mainstay of treatment. With regard to menopausal hormone therapy, systemic estrogens induce a dose-dependent reduction in TC, LDL-C and Lp(a), as well as an increase in HDL-C concentrations; these effects are more prominent with oral administration. Transdermal rather than oral estrogens should be used in women with hypertriglyceridemia. Micronized progesterone or dydrogesterone are the preferred progestogens due to their neutral effect on the lipid profile. Tibolone may decrease TC, LDL-C, TG and Lp(a), but also HDL-C concentrations. Low-dose vaginal estrogen and ospemifene exert a favorable effect on the lipid profile, but data are scant regarding dehydroepiandrosterone (DHEA). Non-estrogen-based therapies, such as fluoxetine and citalopram, exert a more favorable effect on the lipid profile than do sertraline, paroxetine and venlafaxine. Non-oral testosterone, used for the treatment of hypoactive sexual desire disorder/dysfunction, has little or no effect on the lipid profile.
Authors: Ekta Kapoor; Juliana M Kling; Angie S Lobo; Stephanie S Faubion Journal: Best Pract Res Clin Endocrinol Metab Date: 2021-09-10 Impact factor: 4.690
Authors: Roshni Joshi; Goya Wannamethee; Jorgen Engmann; Tom Gaunt; Deborah A Lawlor; Jackie Price; Olia Papacosta; Tina Shah; Therese Tillin; Peter Whincup; Nishi Chaturvedi; Mika Kivimaki; Diana Kuh; Meena Kumari; Alun D Hughes; Juan P Casas; Steve E Humphries; Aroon D Hingorani; A Floriaan Schmidt Journal: Ann Clin Biochem Date: 2020-10-21 Impact factor: 2.057