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Objectives To evaluate the effect on breast density of two low-dose hormone therapy regimens identical in their estrogen component but different in the progestin. Methods A total of 81 non-hysterectomized postmenopausal women were allocated either to 17β-estradiol 1 mg and norethisterone acetate 0.5 mg (E2/NETA, n = 43) or to 17β-estradiol 1 mg and drospirenone 2 mg (E2/DRSP, n = 38). Treatment was continuous and lasted 12 months. The main outcomes were the changes in breast density according to the Wolfe classification between baseline and 12-month mammograms. Results Involution of the fibroglandular tissue was not seen in either of the treatment groups. Under E2/NETA, breast density increased in seven women (16.3%). In contrast, only three women (7.9%) exhibited a density increase under E2/DRSP. Conclusions Although hormone therapy appears to suspend breast involution, it does not increase breast density in the majority of treated women. Progestins differing in pharmacological properties may have a variable impact on breast density. [ABSTRACT FROM AUTHOR]

Objectives Hormone therapy increases the risk of venous thromboembolism, possibly through a negative effect on coagulation inhibitors. The aim of the study was to assess the effect of conjugated equine estrogens alone or in combination with medroxyprogesterone acetate, low-dose 17β-estradiol combined with norethisterone acetate and tibolone on inhibitors of coagulation. Methods Two hundred and sixteen postmenopausal women received orally either conjugated equine estrogens 0.625 mg (CEE, n = 24) or tibolone 2.5 mg (n = 24) or CEE + medroxyprogesterone acetate 5 mg (CEE/MPA, n = 34) or 17β-estradiol 1 mg + norethisterone acetate 0.5 mg (E2/NETA, n = 66) or no therapy (control, n = 68) for 12 months. Plasma antithrombin, protein C and total protein S were measured at baseline and at 12 months. Results CEE, CEE/MPA and E2/NETA treatment were associated with a significant decrease in antithrombin levels (CEE: baseline 235.6 ± 47.6 mg/l, follow-up 221.3 ± 48.3 mg/l, p = 0.0001; CEE/MPA: baseline 251.1 ± 38.6 mg/l, follow-up 225.0 ± 42.6 mg/l, p = 0.009; E2/NETA: baseline 257.1 ± 59.4 mg/l, follow-up 227.1 ± 50.4 mg/l, p = 0.007; tibolone: baseline 252.6 ± 62.4 mg/l, follow-up 261.9 ± 59.1 mg/l, p = 0.39). Protein C decreased significantly in the CEE and CEE/MPA groups (CEE: baseline 3.64 ± 1.17 mg/l, follow-up 2.48 ± 1.47 mg/l, p = 0.004; CEE/MPA: baseline 3.24 ± 1.23 mg/l, follow-up 2.61 ± 1.38 mg/l, p = 0.001; E2/NETA: baseline 3.24 ± 1.10 mg/l, follow-up, 3.15 ± 1.11 mg/l, p = 0.08; tibolone: baseline 3.26 ± 1.25 mg/l, follow-up 3.09 ± 1.32 mg/l, p = 0.37). Protein S decreased significantly only in the CEE/MPA group (CEE: baseline 19.4 ± 2.76 mg/l, follow-up 18.0 ± 2.45 mg/l, p = 0.56; CEE/MPA: baseline 18.4 ± 3.42 mg/l, follow-up 14.5 ± 3.43 mg/l, p = 0.005; E2/NETA: baseline 19.0 ± 3.11 mg/l, follow-up 19.5 ± 3.43 mg/l, p = 0.18; tibolone: baseline 18.5 ± 3.09 mg/l, follow-up 18.0 ± 4.09 mg/l, p = 0.32). Conclusions Estrogen and estrogen-progestin therapy are associated with a reduction in coagulation inhibitors, the extent of which depends on the regimen administered. Tibolone appears to have no effect on inhibitors of coagulation. [ABSTRACT FROM AUTHOR]

Abstract: Objective:: To assess endogenous androgen and insulin resistance status in postmenopausal women receiving continuous combined hormone therapy (HT), tibolone, raloxifene or no therapy. Methods:: A total of 427 postmenopausal women aged 42–71 years were studied in a cross-sectional design. Among them 84 were taking HT (46 women conjugated equine estrogens 0.625mg; medroxyprogesterone acetate, 5mg, CEE/MPA; and 38 women 17β-estradiol 2mg; norethisterone acetate 1mg, E2/NETA); 83 were taking tibolone 2.5mg; 50 were taking raloxifene HCl 60mg; and 210 women were not receiving any therapy. Main outcome measures were FSH, LH, estradiol, total testosterone, SHBG, free androgen index (FAI), Δ4-Androstendione (Δ4-A), Dehydroepiandrosterone sulphate (DHEAS) and HOMA insulin resistance index (HOMA-IR). Results:: In women not on hormone therapy smoking and older age was associated with lower DHEAS levels. FAI values increased linearly with increasing BMI. Age and BMI were positive determinants of HOMA-IR, while no association was identified between endogenous sex steroids and insulin resistance. CEE/MPA therapy was associated with higher SHBG, lower FAI and lower HOMA-IR values compared to women not on therapy (age and BMI-adjusted SHBG: CEE/MPA 148.8nmol/l, controls 58.7nmol/l, p < 0.01; age-adjusted FAI: CEE/MPA 0.8, controls 3.2, p < 0.05; age-adjusted HOMA-IR: CEE/MPA 1.3, controls 2.6, p < 0.05). On the contrary, E2/NETA treatment had no effect on these parameters. Women on tibolone had lower SHBG, higher FAI and similar HOMA-IR values compared to controls (age and BMI-adjusted SHBG: 24.1nmol/l, p < 0.01; FAI: 6.0, p < 0.05; HOMA-IR: 2.3, p = NS). Raloxifene users did not exhibit any difference with respect to sex steroids and HOMA-IR levels. Conclusions:: CEE/MPA users had lower free testosterone and improved insulin sensitivity. Tibolone on the other hand associated with higher free testosterone, while raloxifene did not relate to any of these parameters. [Copyright &y& Elsevier]

The aim of this study was to assess the effect of estrogen, two regimens of continuous combined hormone replacement therapy (HRT), tibolone and raloxifene on serum lipid, apolipoprotein A1 and B and lipoprotein(a) levels in Greek postmenopausal women. A total of 350 postmenopausal women were studied in a prospective open design. Women were assigned to one of the following regimens depending on the presence of risk factors for osteoporosis, climacteric symptoms and an intact uterus: conjugated equine estrogen 0.625 mg (CEE, n = 34), continuous combined CEE 0.625 mg plus medroxyprogesterone acetate (MPA) 5 mg, (n = 80), continuous combined 17β -estradiol 2 mg plus norethisterone acetate (NETA) 1 mg (n = 58), tibolone 2.5 mg (n = 83) and raloxifene HCl 60 mg (n = 50). Forty-five postmenopausal women with no indications for HRT sewed as controls. Total cholesterol (TC), low-density lipoprotein (LDL) cholestrol and high-density lipoprotein (HDL) cholesterol, triglyceride (TG), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB) and lipoprotein(a) (Lp(a)) levels were assessed in each subject at baseline, and at 6 and 12 months of therapy. All therapy regimens lowered TC levels compared to baseline (4.2-8.0% decrease). This effect was more prominent in the subgoup of women with high baseline TC levels (9.1-20.4% decrease,). LDL cholesterol decreased significantly in CEE, CEE/MPA and raloxifene groups (-11.2%, -11.9% and -11.0%, respectively). Hypercholesterolemic women exhibited a steeper decrease in LDL cholesterol (10.6-27.8% in all therapy groups). TG levels increased significantly in the CEE and CEE/MPA groups (23.7% and 21.8%, respectively), while estradiol/NETA had no effect on TG levels. Tibolone decreased TG levels markedly, by 20.6%, while raloxifene had no TG-lowering effect. HDL cholesterol and ApoA1 were increased by CEE and CEE/MPA (HDL cholesterol, 7.4% and 11.8%, respectively; ApoA1, 17.8% and 7.9%, respectively) and decreased by tibolone (HDL cholesterol, -13.6%; and ApoA1, -9.9%). All therapy regimens except raloxifene lowered Lp(a) levels, with tibolone having the more pronounced effect (-13.2 to -29.0%). In conclusion, each therapy regimen had a different effect on lipid-lipoprotein levels, exerting favorable and unfavorable modifications. Hypercholesterolemic women seemed to benefit more from the cholesterol-lowering effect of estrogen replacement therapy/HRT. The choice for a particular regimen should be based on individual needs, indications and lipid-lipoprotein profile. [ABSTRACT FROM AUTHOR]