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B De Lignieres

Publications and source records attributed to B De Lignieres.

6 recordsLinked to original sources
PubMed1991

Changes in plasma lipoprotein and apolipoprotein composition in relation to oral versus percutaneous administration of estrogen alone or in cyclic association with utrogestan in menopausal women.

Sixty-three postmenopausal women were assigned to four treatment groups and received either Premarin or percutaneous 17 beta-estradiol (Oestrogel) alone or in combination with micronized progesterone (Utrogentan). The oral administration of estrogen alone to hysterectomized women resulted in: 1) a significant increase in triglyceride levels in plasma and all major lipoprotein fractions, 2) a significant increase in very low density lipoprotein cholesterol, 3) a significant decrease in low density lipoprotein (LDL) cholesterol but not LDL apo B concentration, 4) a significant increase in all the lipid components of high density lipoprotein (HDL) as well as apo AI, 5) and a significant increase in HDL2 cholesterol. In contrast, percutaneous administration of estrogen to hysterectomized women only increased HDL2 cholesterol and the triglyceride and cholesterol content of the whole HDL fraction. These results suggest that the route of estrogen administration is important in determining effects on lipoprotein metabolism. The same two estrogens were given to women with natural menopause, along with utrogestan, a micronized progesterone. The simultaneous administration of Utrogestan reversed the HDL cholesterol elevating effect of percutaneous estrogen alone, but it had no effect on other plasma lipoproteins. On the other hand, utrogestan in combination with oral estrogen had several potential beneficial effects on plasma lipoproteins. This combination did not negate the effects of oral estrogen alone on HDL, rather it further increased the concentrations of HDL cholesterol and apo AI. It also did not negate the LDL cholesterol lowering effect of oral estrogen alone. Furthermore, utrogestan lowered the magnitude of hypertriglyceridemia induced by oral estrogen alone. These results suggest that Utrogestan has lower potency of androgenic action and has desirable effects when given in cyclic combination with estrogen.

Administration, Cutaneous↗
PubMed1987

Oral micronized progesterone. Bioavailability pharmacokinetics, pharmacological and therapeutic implications--a review.

Progesterone (P), the natural hormone, binds to its specific receptors to induce specific progestational effects. In addition to this binding, P is able to interfere with the binding sites of other steroids. Therefore the natural hormone exhibits an anti-estrogenic activity, and anti-androgenic activity and also exerts anti-mineralocorticoid effects. For a long time progesterone could not be used in clinical applications because of a rapid liver inactivation after oral administration. An oral micronized preparation of progesterone is now available which produces adequate plasma and tissue levels of progesterone. The preparation reproduces the anti-estrogenic effect of the natural hormone on the endometrium at the dose of 200 mg daily. It also reproduces the anti-mineralocorticoid effect and has no androgenic action. No side effects have been reported as far as lipids profile, coagulation factors and blood pressure are concerned. Therefore oral micronized progesterone appears suitable for hormonal replacement therapy in various areas, essentially postmenopause therapy, premenstrual syndrome, correction of irregular cycles and pregnancy maintenance.

Administration, Oral↗
PubMed1986

Biological effects of estradiol-17 beta in postmenopausal women: oral versus percutaneous administration.

To determine whether the route of administration or the type of estrogen used in estrogen replacement therapy (ERT) is more important in avoiding effects on hepatic function, 24 postmenopausal women were studied before and at the end of 2 months of oral or percutaneous administration of the same estrogen, estradiol-17 beta (E2). The treatments studied were oral micronized E2, 2 mg/day (9 women); oral E2 valerate, 2 mg/day (5 women), and percutaneous E2, 3 mg/day (10 women). Specific plasma biological and biochemical markers of estrogenic action were evaluated, namely, E2, estrone (E1), LH, FSH, sex steroid binding protein (SBP), renin substrate, antithrombin activity, and lipoproteins (high density lipoprotein cholesterol, low density lipoprotein cholesterol, very low density lipoprotein triglycerides). Both oral and percutaneous administration of E2 increased plasma E2 levels up to midfollicular values and decreased LH and FSH levels into the same range. Oral administration of E2 led to substantial increases in plasma E1, SBP, renin substrate, and VLDL levels, whereas AT decreased significantly. Percutaneous administration of E2 led to a physiological plasma E1/E2 ratio and did not induce any change in hepatic proteins. These data suggest that the route of administration of E2 determines the biochemical response to ERT in postmenopausal women. SBP is the most sensitive marker of the liver action of estrogen, and triglycerides also are simple and useful markers for this effect. Percutaneous E2 therapy is an effective method of ERT, and has no measurable effects on hepatic markers of estrogen action.

Administration, Oral↗
PubMed1983

Differential lipemic and hormonal responses to oral and parenteral 17 beta-estradiol in postmenopausal women.

To determine the influence of the route of administration on the hormonal and lipemic responses to 17 beta-estradiol, 50 postmenopausal women were studied before and after various regimens of replacement therapy. The effects on plasma lipids and lipoproteins and on estrone and estradiol levels of the oral administration of micronized estradiol or estradiol valerate (2 mg/24 hours) were compared to those of percutaneously administered estradiol (3 mg/24 hours). These treatments were given during two cycles of 3 weeks separated by a 1-week interval. Circulating levels of estradiol and estrone increased significantly (p less than 0.05) in all groups while follicle-stimulating hormone levels decreased significantly. The posttreatment estradiol/estrone ratio was significantly (p less than 0.05) greater in the parenteral group (0.8 +/- 0.1) than in both oral estrogen groups (0.3 +/- 0.1 and 0.4 +/- 0.1, respectively). Oral administration of estradiol resulted in a significant increase in triglycerides (20% to 44%, p less than 0.05) and very low-density lipoprotein (VLDL) triglycerides (30% to 40%, p less than 0.05) and a decrease in low-density lipoprotein cholesterol (14% to 17%, p less than 0.05). In contrast, despite a substantial increase in serum estrogen levels, percutaneous estradiol induced a significant decrease in triglyceride (from 0.78 +/- 0.04 to 0.67 +/- 0.05 mmol/L, p less than 0.001) and VLDL triglyceride (from 0.44 +/- 0.16 to 0.35 +/- 0.12 mmol/L p less than 0.05) levels and no significant change in cholesterol levels. The increases of high-density lipoprotein cholesterol levels observed in the three groups were not significant. These data indicate that the route of administration modulates the metabolic and hormonal responses to estrogen therapy.

Administration, Oral↗
PubMed1981

Estradiol, progesterone and plasma lipids during the menstrual cycle.

Epidemiological data tend to relate some of the sex differences in plasma lipid levels to the physiological secretion of estrogens and progesterone. The influence of sex hormones on plasma lipoprotein metabolism has not been extensively investigated. Precise correlation between plasma lipids and circulating hormones levels are still lacking. The short term effect on plasma lipids of large variations in estradiol and progesterone plasma levels occurring during the menstrual cycle has been studied in eight fertile women over a total of 18 cycles. Concentrations of plasma lipids, particularly triglycerides and HDL cholesterol levels were remarkably stable in the three hormonal situations studied, namely during menstruation (low estradiol and progesterone levels), in the follicular phase of the cycle (high estradiol and low progesterone levels) and in the luteal phase (high estradiol and progesterone levels). Considerable variation of plasma estradiol levels (400%) did not modify, the plasma lipid values on a short term basis (8-21 days). The physiological role of 17-beta estradiol and progesterone in the sex differences of blood lipid levels remains to be clarified. If this metabolic effect exists, it does not seen to be influenced by short term variation in hormone levels.

Adult↗