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Objective To compare the short-term effects of two oral continuous combined oestrogen–progestogen treatment regimens on blood concentrations of several cardiovascular risk markers in healthy postmenopausal women. Study design In a 12-week randomised controlled study, 48 healthy non-hysterectomised postmenopausal women, aged 41–58 years, received either no treatment (control group; n = 16), or daily oral continuous combined treatment with 1 mg micronised 17β-oestradiol plus 5 mg dydrogesterone (E/D group; n = 18) or 0.625 mg conjugated equine oestrogens plus 5 mg medroxyprogesterone acetate (CEE/MPA group; n = 14). Fasting blood sampling was performed at baseline and after 12 weeks of follow-up. Results Compared with the control group, 12-week treatment with E/D or CEE/MPA reduced fibrinogen (−7.7%, p = 0.004 and −3.3%, p = 0.083, respectively), factor VII-act (−8.7%, p = 0.14 and −9.7%, p = 0.06, respectively), homocysteine (−20.5%, p = 0.02 and −26.7%, p = 0.005, respectively), and IGF-1 (−27.9%, p p = 0.002, respectively), but increased factor VII-ag (+10.1%, p = 0.03 and +4.4%, p = 0.46, respectively), endothelin-1 (+15.2%, p = 0.12 and +20.0%, p = 0.13, respectively) and C-reactive protein (+88.8%, p = 0.18 and +71.0%, p = 0.44, respectively). Fibrinolytic factors were not affected by either hormone therapy (HT). Conclusions Short-term oral continuous combined therapy with oestradiol/dydrogesterone and conjugated equine oestrogens/medroxyprogesterone acetate had comparable effects on the investigated cardiovascular risk markers.

Objective: To compare the effects of 17-oestradiol plus dydrogesterone with conjugated equine oestrogens plus medroxyprogesterone acetate on serum lipids, apolipoproteins and lipoprotein(a) in postmenopausal women. Methods: A multi-centre, prospective, randomised, double-blind, comparative one-year study in 362 healthy postmenopausal women aged 39–74 years with an intact uterus. Fasting blood samples were taken at baseline and after 28 and 52 weeks of treatment. Participants received daily oral treatment with continuous combined 1 mg micronised 17-oestradiol/5 mg dydrogesterone (E/D: n = 180) or 0.625 mg conjugated equine oestrogens/5 mg medroxyprogesterone acetate (CEE/MPA:n = 182). Results: Significant differences between the two groups after 52 weeks were observed for total cholesterol (E/D: −1.7%; CEE/MPA: −7.3%), LDL-cholesterol (E/D: −4.5%; CEE/MPA: −11.3%), HDL-cholesterol (E/D: +15.3%; CEE/MPA: +7.5%), triglycerides (E/D: +9.8%; CEE/MPA: +16.6%), VLDL-triglycerides (E/D: −3.3%; CEE/MPA: +10.0%), lipoprotein(a) (E/D: 0.0%; CEE/MPA: −25.2%) and for the ratio apolipoprotein B/LDL-cholesterol (E/D: +0.9%; CEE/MPA +5.9%). Conclusions: E/D and CEE/MPA differ in their anti-atherogenic effects on lipids and lipoproteins. This however can not easily be translated to differences in clinical cardiovascular outcomes. © 2004 Elsevier Ireland Ltd. All rights reserved.

Estrogens influence the independent cardiovascular risk factor homocysteine as well as vasodilatation. Homocysteine alone also influences vasodilatation, indicating a relational triangle that seems important in interpreting the isolated effects of estrogens on homocysteine metabolism and vasoreactivity. This paper gives an overview of the current understanding regarding vasoreactivity, homocysteine metabolism and the role of estrogens. This is placed against the background of the clinical trials on the effect of postmenopausal hormone replacement therapy on homocysteine levels and addresses the importance of the interaction between homocysteine, estrogens and vasoreactivity.

Objective : To investigate the mechanism by which exogenous oestrogen influences the homocysteine metabolism in postmenopausal women. Study design : A randomized placebo controlled trial in which a methionine-loading test was performed, in 25 healthy postmenopausal women, before and after a 12-week oral treatment with placebo or daily 4mg 17s-estradiol with (HRT) or without (ERT) 10mg dydrogesterone. Fasting and post-load homocysteine as well as Vitamins B 6 , B 12 and folate were determined. Results : In both treatment groups a significant 12% decrease in fasting homocysteine was observed. This decrease was accompanied by a post-load homocysteine increase of more than 20%. Vitamin B 6 values were decreased by more than 25%. Conclusion : The hormone therapy induced lowering of fasting homocysteine and Vitamin B 6 levels and an increase in post-load homocysteine, supporting the hypothesis that homocysteine–methionine metabolism is modulated by hormone therapy in postmenopausal women.

Item does not contain fulltext OBJECTIVE:To assess the effect of transdermal vs. oral administration of E2 on plasma homocysteine levels and to evaluate the impact of adding a progestogen to these regimens. DESIGN: Prospective, double-blind, double-dummy, placebo-controlled study. SETTING: Outpatient clinics in two university hospitals and two teaching hospitals in The Netherlands. PATIENT(S): One hundred fifty-two healthy hysterectomized postmenopausal women. INTERVENTION(S): Thirteen 28-day treatment cycles with placebo (n = 49); transdermal 17beta-E2, 50 microg (n = 33), oral E2, 1 mg (n = 37), or oral E2, 1 mg, plus gestodene, 25 microg (n = 33), followed by four cycles of placebo in each group. MAIN OUTCOME MEASURE(S): Fasting plasma total homocysteine concentrations at baseline and cycle 4, 13, and 17. RESULT(S): Mean (+/-SD) homocysteine concentrations in the oral E2 group decreased from baseline to cycle 4 (9.0 +/- 2.5 micromol/L vs. 8.2 +/- 2.0 micromol/L; mean change, -7.6%). Homocystine values in the oral E2 plus gestodene group did not change substantially from baseline to cycle 4 (8.9 +/- 1.6 micromol/L vs. 8.6 +/- 2.0 micromol/L; mean change, -4.4%). No significant changes were observed in the transdermal E2 group. After four washout cycles, the homocysteine concentration had returned to baseline values in all groups. CONCLUSION(S): Oral E2 therapy reduced the homocysteine concentration more than did therapy with transdermal E2 or oral E2 plus gestodene. This finding may indicate a role of liver metabolism and suggests that gestodene has a negative effect on these changes.