Effect on lipid metabolism of a biphasic desogestrel-containing oral contraceptive: Divergent changes in apolipoprotein B and E and transitory decrease in LP(a) levels

Kühl, H.; März, Winfried; Jung-Hoffmann, C.; Weber, J.; Siekmeier, R.; Wl, Gross

doi:10.1016/0010-7824(93)90110-s

Cited by 22 publications

(3 citation statements)

References 30 publications

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“…Overall, PEPI's primary finding is that these impacts were long term. This is in contrast to two previous studies 8,40 that reported treatment effects waned within 1 year.…”

Section: Discussioncontrasting

confidence: 55%

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

Marcovina²,

et al. 1998

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Background-Postmenopausal hormone therapy has been reported to decrease levels of lipoprotein (Lp)(a) in cross-sectional studies and small or short-term longitudinal studies. We report findings from a large, prospective, placebo-controlled clinical trial that allows a broad characterization of these effects for four regimens of hormone therapy. Methods and Results-The Postmenopausal Estrogen/Progestin Interventions study was a 3-year, placebo-controlled, randomized clinical trial to assess the effect of hormone regimens on cardiovascular disease risk factors in postmenopausal women 45 to 65 years of age. The active regimens were conjugated equine estrogens therapy at 0.625 mg daily, alone or in combination with each of three regimens of progestational agents: medroxyprogesterone acetate (MPA) at 2.5 mg daily (ie, continuous MPA), MPA at 10 mg days 1 to 12 (ie, cyclical MPA), and micronized progesterone at 200 mg days 1 to 12. Plasma levels of Lp(a) were measured at baseline (nϭ366), 12 months (nϭ354), and 36 months (nϭ342). Assignment to hormone therapy resulted in a 17% to 23% average drop in Lp(a) concentrations relative to placebo (PϽ.0001), which was maintained across 3 years of follow-up. No significant differences were observed among the four active arms. Changes in Lp(a) associated with hormone therapy were positively correlated with changes in LDL cholesterol, total cholesterol, apolipoprotein B, and fibrinogen levels and were similar across subgroups defined by age, weight, ethnicity, and prior hormone use. Conclusions-Postmenopausal estrogen therapy, with or without concomitant progestin regimens, produces consistent and sustained reductions in plasma Lp(a) concentrations. (Circulation. 1998;97:979-986.)

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“…Overall, PEPI's primary finding is that these impacts were long term. This is in contrast to two previous studies 8,40 that reported treatment effects waned within 1 year.…”

Section: Discussioncontrasting

confidence: 55%

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

Marcovina²,

et al. 1998

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“…This is in contrast to the obser vational study of Nabulsi et al (23) who found 13% lower Lp(a) levels among current estrogen users than among nonusers and with a persistent decrease of Lp(a) from baseline during another study of hor mone replacement therapy (24). It should be remem bered that the effect of sex steroids on Lp(a) may be transient (25) and that we may have missed an eventual decrease in Lp(a). We found no significant correlation between Lp(a) and either LDL choles terol or Apo B.…”

contrasting

confidence: 53%

The effect of medrogestone on plasma lipids and lipoproteins in postmenopausal women using conjugated estrogens: an open randomized comparative study

Leuven¹,

Mooren²,

Buytenhek³

1995

Fertility and Sterility

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O b jectiv e:To test the hypothesis that the progestogen medrogestone has no effect on changes in lipoprotein metabolism evoked by continuous estrogen replacement therapy, paying special attention to high-density lipoproteins (HDL).D e sig n : Open multi center randomized comparative trial. P a tie n ts : Postmenopausal hysterectomized women aged 49 to 64 years. In te r v e n tio n : Continuous oral treatm ent with 0.625 m g d a ily o f conjugated estrogens (CE) alone (n = 55) or CE plus 5 mg of the progestogen medrogestone orally during the last 12 days of each 28-day cycle (n = 59).M a in O u tco m e M ea su res: At baseline and at cycles 3 ,6 , and 13 we m easured the plasm a levels of apolipoprotein (Apo) Al, cholesterol in total HDL and in its subfractions HDL2 and HDL3, using density gradient ultracentrifugation.R e su lts: High-density lipoprotein cholesterol increased from baseline at all assessm ents in both treatm ent groups, being significantly greater in the CE group (+15% a t cycle 13) th a n in the CE and medrogestone group (+8%). However, HDL2-cholesterol increased in both treatm ent groups, but with no significant difference between the two groups. High-density lipoprotein 3 cholesterol increased only in the CE group (+7% at cycle 13); there was no significant change in HDL3-cholesterol in the CE and medrogestone group. Low-density lipoprotein (LDL) cholesterol decreased from baseline at all assessments in both treatm ent groups (-6% and -9%, respec tively, at cycle 13). The change in very low-density (VLDL) lipoprotein cholesterol was not significant in either of the two groups. Medrogestone had no significant effects on the estrogeninduced increases in apo A-l and triglycerides nor on the decreases in ApoB and LDL-cholesterol. Neither hormone significantly affected VLDL-cholesterol or Lp(a) levels.C o n clu sio n : Medrogestone did not eliminate the increase in plasma HDL levels evoked by CE. Fertil Steril 1995;64:525-31 K ey Words: Estrogen, Premarin, progestogen, medrogestone, lipoproteins, menopausePostmenopausal estrogen replacement therapy is associated with a 50% reduction in the incidence of myocardial infarction (1). Although selection, bias (2) and direct effects on the vessel wall and other mech

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“…As VLDLs are converted during lipolysis into rem nants and LDLs, the lacking increase in LDL-CH and total CH may reflect the EE-induced enhancement of remnant and LDL uptake in the liver. It has been demon strated that during treatment with estrogen-dominant ovulation inhibitors, there was a significant reduction in the level of apolipoprotein E [15,17] which is involved in the rapid hepatic eliminaton of 85% of remnants [ 18].…”

Section: Discussionmentioning

confidence: 99%

Short- and Long-Term Effects on Lipid Metabolism of Oral Contraceptives Containing 30 μg Ethinylestradiol and 150 μg Desogestrel or 3-Keto-Desogestrel

Kühl

Jung-Hoffmann²,

Fitzner³

et al. 1995

Horm Res

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During a cross-over study with young female volunteers, the effects of a combination of 30 µg ethinylestradiol (EE) and 150 µg desogestrel (DG) or 3-keto-desogestrel (KDG) upon lipid metabolism were investigated on day 3 of the first cycle (day 3/1) and on day 21 of the third cycle of treatment (day 21/III). As compared to the control cycle, total cholesterol (CH), low-density lipoprotein CH (LDL-CH), and the apolipoproteins A-II and B were reduced already on day 3/1, the effects being more pronounced with the DG-containing formulation. On day 21/III of treatment with EE/DG, the levels of total CH, LDL-CH and apolipoprotein B did not differ from controls, while apolipoprotein A-II was significantly increased. The effects of EE/KDG were similar, except that on LDL-CH which was still reduced on day 21/III. The serum concentrations of total triglycerides (TG), very low-density lipoprotein CH (VLDL-CH), VLDL-TG, LD-TG, high-density lipoprotein CH (HDL-CH), HDL-TG, and apolipoprotein A-I were not significantly affected on day 3/1, but elevated on day 21/III. As during treatment with EE/KDG the peak level of KDG was higher than with EE/DG, the results indicate a more pronounced antagonistic effect of EE/KDG on some EE-induced changes on lipoproteins during the first days of intake. These short-term changes possibly reflect a rapid enhancement of hepatic uptake of remnants and LDL by EE. During long-term treatment, the other effects of EE, e.g. the stimulation of hepatic synthesis of TG, VLDL, and HDL and the inhibition of hepatic lipoprotein lipase, become apparent.

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Effect on lipid metabolism of a biphasic desogestrel-containing oral contraceptive: Divergent changes in apolipoprotein B and E and transitory decrease in LP(a) levels

Cited by 22 publications

References 30 publications

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

The effect of medrogestone on plasma lipids and lipoproteins in postmenopausal women using conjugated estrogens: an open randomized comparative study

Short- and Long-Term Effects on Lipid Metabolism of Oral Contraceptives Containing 30 μg Ethinylestradiol and 150 μg Desogestrel or 3-Keto-Desogestrel

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Effect on lipid metabolism of a biphasic desogestrel-containing oral contraceptive: Divergent changes in apolipoprotein B and E and transitory decrease in LP(a) levels

Cited by 22 publications

References 30 publications

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

Effect of Postmenopausal Hormone Therapy on Lipoprotein(a) Concentration

The effect of medrogestone on plasma lipids and lipoproteins in postmenopausal women using conjugated estrogens: an open randomized comparative study

Short- and Long-Term Effects on Lipid Metabolism of Oral Contraceptives Containing 30 &mu;g Ethinylestradiol and 150 &mu;g Desogestrel or 3-Keto-Desogestrel

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Short- and Long-Term Effects on Lipid Metabolism of Oral Contraceptives Containing 30 μg Ethinylestradiol and 150 μg Desogestrel or 3-Keto-Desogestrel