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Updated: Sep 20, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
[Effects of a 19-norprogesterone derivative, the fourth decade nomegestrol acetate, on lipids]
C Pélissier1, C Jamin, J-C Colau
1Service de Gynécologie Obstétrique, Hôpital Bichat-Claud-Bernard, Paris.
Abstract:
Dyslipidemia is a cardiovascular risk factor which commonly develops during forty. In Europe, progestins are frequently prescribed for treatment of perimenopausal symptoms in women in this age group, as well as in combination with estrogen replacement therapy in non hysterectomised postmenopausal women. Their complete metabolic tolerance is an important, even if non exclusive, factor to take in consideration for cardiovascular protection. Our aim was to review available data on the effects of a 19-norprogesterone derivative, nomegestrol acetate, on lipid tolerability. In healthy or at risk premenopausal women, clinical studies found no significant changes in lipid parameters (total, HDL and LDL cholesterol, triglycerides, apoprotein B, Lp(a) and LpA-I) with nomegestrol acetate administered in antigonadotropic sequence, alone or combined with estrogen in inverse sequence, during 6 to 9 cycles; there was only a small statistically significant decrease in apoprotein A1, probably due to the induced hypoestrogeny. In clinical studies carried out in postmenopausal women, nomegestrol acetate combined with estrogen replacement therapy in a sequential or continuous combined regimen, did not alter the beneficial estrogen-induced lipid profile: reductions in total and LDL cholesterol, apoprotein B and Lp(a); HDL cholesterol was unchanged and an increase in triglycerides occurred only with oral estrogens. A decrease in apoprotein A1 was found after six months of a cyclic sequential hormone replacement therapy but was associated with a beneficial increase in LpA-I. Nomegestrol acetate has proven its neutral effects on lipid metabolism and does not alter the beneficial estrogen-induced lipid effects.
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