Biomedical subjects

C Jung-Hoffmann

Publications and source records attributed to C Jung-Hoffmann.

At least 19 recordsLinked to original sources

PubMed1998

A randomized cross-over study on various hormonal parameters of two triphasic oral contraceptives.

The effect of two triphasic oral contraceptives (Triquilar [TRQ] and Trisiston [TRS]) containing ethinyl estradiol (EE) and levonorgestrel (LNG) on various hormonal parameters was investigated in 26 women during a cross-over study. TRS consisted of 0.03 mg EE + 0.05 mg LNG (six tablets), 0.04 mg EE + 0.075 mg LNG (six tablets), and 0.03 mg EE + 0.15 mg LNG (nine tablets), whereas TRQ was different in the second phase (five tablets) and third phase (10 tablets). Blood samples were taken on days 6, 11, 21, and 28 of the control and washout cycles and the third treatment cycle. Both formulations inhibited ovulation reliably and decreased the serum levels of gonadotropins, free testosterone, and dehydroepiandosterone sulfate in a time-dependent manner, whereas estradiol and testosterone were already suppressed on day 6, indicating a direct suppressive effect on ovarian steroid synthesis. Prolactin, which rose sporadically in some women, was not significantly changed. In contrast, the levels of sex hormone binding globulin, corticosteroid binding globulin, and cortisol were significantly elevated by 100%. During the hormone-free interval of 7 days, all parameters returned at least partly to baseline. There was no significant difference between the effects of both formulations. The results suggest the possibility of a direct inhibitory effect of contraceptive steroids on ovarian steroid synthesis.

Adult↗

PubMed1998

Effect of two oral contraceptives containing ethinyl estradiol and gestodene or norgestimate on different lipid and lipoprotein parameters.

The effect of a triphasic oral contraceptive containing ethinyl estradiol and gestodene (EE/GSD) on various lipid and lipoprotein parameters was compared with that of a monophasic formulation containing 35 micrograms ethinyl estradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth, and twelfth treatment cycles. There was no significant difference between formulations with regard to the influence on any measured parameter. As compared with controls, a significant increase was observed in the plasma levels of total triglycerides (24-78%), total phospholipids (7-20%), very low density lipoprotein (VLDL) triglycerides (61-76%), VLDL-phospholipids (14-60%), low density lipoprotein (LDL) triglycerides (8-35%), LDL-phospholipids (28-30%), high density lipoprotein (HDL) cholesterol (8-16%), HDL 3-cholesterol (11-20%), HDL-triglycerides (17-66%), HDL-phospholipids, HDL 3-phospholipids (7-11%), apolipoprotein (apo) A-I (5-20%) and apo A-II (10-40%) during treatment with both formulations. In contrast, the LDL-cholesterol levels were significantly decreased. These changes in lipid metabolism appear to reflect a predominance of the effect of the estrogen component. The results indicate that both low dose oral contraceptives containing different progestins and different amounts of EE do not exert a deleterious effect on lipoprotein metabolism, as high HDL-cholesterol and low LDL-cholesterol levels are known as low risk factors of cardiovascular disease. In contrast to endogenous hypertriglyceridemia, an EE-induced rise in triglyceride levels does not appear to increase cardiovascular risk if LDL is not increased.

Adolescent↗

PubMed1995

Effect of two oral contraceptives containing ethinylestradiol and gestodene or norgestimate upon androgen parameters and serum binding proteins.

The effect of a triphasic oral contraceptive containing ethinylestradiol and gestodene (EE/GSD) on various serum hormonal parameters was compared with that of a monophasic formulation containing 35 micrograms ethinylestradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth and twelfth treatment cycle. There was no significant difference in the influence on any hormonal parameter between both formulations. Both EE/GSD and EE/NGM caused a time-dependent suppression of serum dehydroepiandrosterone sulphate (DHEA-S) by 20-30% (p < 0.01) and a reduction of 5 alpha-androstane-3 alpha, 17 beta-diol glucuronide by 50-60% (p < 0.01) during each treatment cycle, while androstenedione levels were reduced by 25% (p < 0.01). There was also a significant decrease in the levels of total testosterone by 30-35% (p < 0.01) and free testosterone by 60% (p < 0.01), while sex hormone-binding globulin (SHBG) was increased by 200-240% on days 11 and 21 (p < 0.01). During the pill-free interval the SHBG levels were reduced to a certain degree but remained elevated by 100% as compared to the pretreatment values. The serum levels of corticosteroid-binding globulin (CBG) which is known to be influenced only by the estrogenic component of combination pills, increased significantly by 170% (p < 0.01) during each treatment cycle. During the pill-free interval of 7 days, the CBG levels decreased but were still elevated by 90-100% as compared to the control cycle. Similarly, the serum levels of cortisol were significantly elevated by 110-140% (p < 0.01) during treatment with both preparations. The results demonstrate a profound suppression of androgen levels and peripheral androgen metabolism.

Adolescent↗

PubMed1995

Gestodene-containing contraceptives.

As GSD is the most potent progestogen used in oral contraceptives, the doses of GSD can be lower than those of other progestogen components. The monophasic (30 micrograms EE + 75 micrograms GSD) and the triphasic formulation (30 micrograms EE + 50 micrograms GSD/40 micrograms EE + 70 micrograms GSD/30 micrograms EE + 100 micrograms GSD) suppress gonadotropin release and ovarian function profoundly and inhibit ovulation reliably. The strong anti-estrogenic and progestogenic effectiveness of GSD is based on the high GSD serum concentrations achieved during daily intake. Because of the weak androgenic properties of GSD, both formulations can be characterized as estrogen-dominant with respect to their hepatic effects. Except for the first cycles, both formulations afford good cycle control, and the rate of side effects is similar to that with comparable low-dose oral contraceptives. The levels of total and free androgens and androgen precursors, as well as of peripheral androgen activity, are significantly reduced, resulting in a reduced incidence of acne. The concentrations of SHBG and other serum-binding globulins are elevated considerably, and thyroid function is almost unaffected. The estrogen-dominant effect on hepatic metabolism of both formulations also is reflected by a significant increase in the levels of triglycerides and VLDL, HDL, and some apolipoproteins, while LDL-CH and total CH remain unchanged. Similar to other low-dose oral contraceptives, the GSD-containing preparations cause a slight impairment of glucose tolerance that does not appear to be of clinical relevance. However, a significant increase exists in pro-coagulatory and fibrinolytic activity that leads to a considerable stimulation of fibrin turnover. In predisposed women, this may contribute to an elevated risk of venous and arterial thromboembolic diseases.

Carbohydrate Metabolism↗

PubMed1995

Short- and long-term effects on lipid metabolism of oral contraceptives containing 30 micrograms ethinylestradiol and 150 micrograms desogestrel or 3-keto-desogestrel.

During a cross-over study with young female volunteers, the effects of a combination of 30 micrograms ethinylestradiol (EE) and 150 micrograms desogestrel (DG) or 3-keto-desogestrel (KDG) upon lipid metabolism were investigated on day 3 of the first cycle (day 3/I) 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/I, 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/I, 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.

Adult↗

PubMed1995

Prodrug versus drug effects of 150 micrograms desogestrel or 3-keto-desogestrel in combination with 30 micrograms ethinylestradiol on hormonal parameters: relevance of the peak serum level of 3-keto-desogestrel.

The pharmacokinetics and pharmacodynamics of 150 micrograms desogestrel (DG) or 150 micrograms 3-keto-desogestrel (KDG) in combination with 30 micrograms ethinylestradiol (EE) were compared in a cross-over study. While the EE levels as well as the area under the curve (AUC) of KDG did not differ, significantly higher peak levels of KDG were observed after intake of the KDG-containing formulation. As compared to the control cycle, LH and FSH were not reduced on day 3 of the first treatment cycle (3/I), but markedly suppressed on day 21 of the third cycle (21/III), the effects being more pronounced with the DG-containing pill. The serum levels of testosterone, free testosterone, androstenedione, androstanediol glucuronide, and dehydroepiandrosterone sulfate (DHEA-S) were significantly reduced already on day 3/I, while sex hormone-binding globulin (SHBG) was unchanged and corticosteroid-binding globulin (CBG) was increased. Thereafter, both SHBG and CBG rose markedly. The progressive decrease in DHEA-S correlated best with free testosterone and androstanediol glucuronide. The results indicate that the peak level of KDG is more important for the biological effectiveness than the AUC of KDG which appears to antagonize the suppressive action of EE on gonadotropin release. The rapid decrease in the androgen levels seems to be due to a direct inhibitory action of the pill on ovarian and adrenal steroid biosynthesis.

Adult↗

PubMed1993

The effect of a biphasic desogestrel-containing oral contraceptive on carbohydrate metabolism and various hormonal parameters.

During 6 cycles of treatment of 19 women, the effect of a low-dose biphasic oral contraceptive containing 40 micrograms ethinylestradiol + 25 micrograms desogestrel (7 tablets) and 30 micrograms ethinylestradiol + 125 micrograms desogestrel (15 tablets) on various hormonal parameters and glucose metabolism was compared with the values of the pre- and post-treatment cycle. There was a profound reduction in gonadotropin secretion and ovarian steroid synthesis. The serum levels of testosterone were reduced by 35%, free testosterone by 55%, and DHEA-S by 30%. Cortisol increased by 100%, SHBG by 250%, and TBG by 60%, while FT3 and FT4 were only marginally influenced. Fasting levels of glucose and insulin did not change significantly, but the glucose load revealed a slight impairment of glucose tolerance. Three weeks after termination of pill intake, the various parameters returned to pretreatment levels, except for SHBG and TBG which were still elevated by 20 to 30%. The results demonstrate a marked preponderance of the effect of the estrogen component, a reliable inhibition of ovulation and very good cycle control during treatment with the biphasic formulation.

Adult↗

PubMed1993

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.

The effect of a low dose biphasic oral contraceptive containing 40 micrograms ethinylestradiol + 25 micrograms desogestrel (7 tablets) and 30 micrograms ethinylestradiol + 125 micrograms desogestrel (15 tablets) on lipid metabolism was investigated in 19 women during 6 cycles of treatment and compared to the values of the pre- and post-treatment cycle. During treatment, all components of HDL increased reversibly by 10 to 30%. The levels of total cholesterol (CH), LDL-CH and IDL-CH rose only slightly, while those of total triglycerides (TG), VLDL-TG and LDL-TG rose continuously by more than 100% until the 6th cycle. At the same time, plasma levels of VLDL-CH increased by 60% and of apolipoprotein B by 20%. Contrary to this, apolipoprotein E decreased by 25% during treatment, and Lp(a) was transitorily reduced during the 3rd cycle. After termination of intake, total CH, LDL-CH, IDL-CH and apolipoprotein B remained elevated, while total TG, VLDL-TG, VLDL-CH and LDL-TG decreased significantly, but were still elevated during the post-treatment cycle. The levels of apolipoprotein E returned to pre-treatment values. The results indicate a marked preponderance of the effect of the estrogen component. The rise in TG and VLDL synthesis seems to be outweighed by an enhanced removal of apolipoprotein E-containing remnants which might offer protection from the development of atherosclerosis.

Adult↗

PubMed1992

Serum concentrations of ethinylestradiol, 3-keto-desogestrel, SHBG, CBG and gonadotropins during treatment with a biphasic oral contraceptive containing desogestrel.

During a cross-over study, the pharmacokinetics of ethinylestradiol (EE) and 3-keto-desogestrel (KDG) were investigated on days 7 and 22 of one cycle of treatment with two biphasic formulations containing 50 micrograms EE (7 tablets) and 50 micrograms EE + 125 micrograms desogestrel (DG) (15 tablets) (50/50 EE) or 40 micrograms EE + 25 micrograms DG (7 tablets) and 30 micrograms EE + 125 micrograms DG (15 tablets) (40/30 EE). Peak serum levels and areas under the curve of EE increased significantly by 50% between days 7 and 22 of those taking 50/50 EE, while during treatment with 40/30 EE, no difference was found between days 7 and 22. Both formulations caused identical KDG levels on day 22. There were only slight differences in the effects of both preparations on sex-hormone-binding globulin (SHBG; +150 to +160%) and on corticosteroid-binding globulin (CBG; +130 to +150%) on day 7. On day 22, the changes were more pronounced with 50/50 EE (SHBG, +310%; CBG, +240%) than with 40/30 EE (SHBG, +250%; CBG, +180%). On day 22 after discontinuation of treatment, the SHBG and CBG levels were still significantly above the control values. Using both formulations, LH and FSH levels were significantly suppressed on day 22, while on day 7 no significant reduction was observed. The rise in the EE levels between days 7 and 22 of 50/50 EE intake and the time course of the EE concentrations during treatment with 40/30 EE appear to be due to an inhibition of hepatic metabolism by the contraceptive steroids, as EE is nearly exclusively bound to albumin which does not change.

Adult↗

PubMed1991

Oral contraceptives containing 20 or 30 micrograms ethinylestradiol and 150 micrograms desogestrel: pharmacokinetics and pharmacodynamic parameters.

The serum concentrations of ethinylestradiol (EE) and 3-keto-desogestrel (KDG) were compared during treatment with a combination of 20 micrograms EE + 150 micrograms DG (20EE/DG) or of 30 micrograms EE + 150 micrograms DG (30EE/DG). During intake of both preparations, the peak levels and the areas under the curve (AUC) of EE increased significantly by approximately 100% between days 1 and 10. In the steady state, the maximal EE levels were 75 +/- 34 pg/ml (20EE/DG) and 136 +/- 55 pg/ml (30EE/DG), and the AUC were 464 +/- 236 pg.h/ml and 840 +/- 492 pg.h/ml. The KDG levels, which were identical with both preparations, increased between days 1 and 21 by approximately 300% up to values of 4.5 +/- 1.6 ng/ml. There were large interindividual variations in the AUC of EE and KDG and no correlation between the levels of EE and KDG. On day 21 of intake of 30EE/DG, the serum concentrations of sex-hormone- and corticosteroid-binding globulin were higher by 16% and 12%, respectively than with 20EE/DG. Although the morning peak levels of cortisol did not differ, the decrease which occurred thereafter, according to the circadian rhythm, was slower with 30EE/DG. There was no relationship between the serum concentrations of EE and/or KDG and the occurrence of irregular bleedings, which was similar during treatment with both preparations. As most of the women who bled had bleedings both with 20EE/DG and 30EE/DG, an influence of predisposition can be assumed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Time-dependent alterations in lipid metabolism during treatment with low-dose oral contraceptives.

The effect of sex steroids on lipid metabolism depends on the type and dose of the compounds, the route of administration, and the duration of treatment. Therefore the composition of an oral contraceptive determines the resultant effect on lipids and lipoproteins. During 12 months of treatment, the effects of two oral contraceptives containing 30 micrograms of ethinyl estradiol and 150 micrograms of desogestrel (EE/DG) or 75 micrograms of gestodene (EE/GSD) on 19 serum parameters of lipid metabolism were followed in 11 women each. There was no change in total cholesterol and phospholipids. Total triglyceride levels were significantly elevated only by EE/GSD. After 3 and 6 months of intake of both preparations, a transitory increase in the triglyceride content of very low-density lipoprotein and low-density lipoprotein and a decrease in low-density lipoprotein-phospholipids was observed. After 12 months, very low-density lipoprotein cholesterol, very low-density lipoprotein phospholipids, and apolipoprotein B were significantly elevated, whereas very low-density lipoprotein triglycerides and all components of low-density lipoprotein were unchanged. Most of the components of high-density lipoprotein (HDL) were increased as a result of a rise in HDL3 and apolipoprotein A2, whereas HDL2 and apolipoprotein A1 were not altered. There was no significant difference between the effects of the two preparations, although those of EE/GSD were mostly more pronounced. The increase in high-density lipoprotein, very low-density lipoprotein, and total triglycerides reflects a slight preponderance of the effect of the estrogen component. Because low-density lipoprotein cholesterol and total cholesterol were not changed, treatment with both formulations is in all probability not associated with an elevated risk of atherosclerosis.

Adolescent↗

PubMed1990

Intra- and interindividual variations in contraceptive steroid levels during 12 treatment cycles: no relation to irregular bleedings.

During one year of treatment with oral contraceptives containing 30 micrograms ethinylestradiol and 150 micrograms desogestrel (EE/DG) or 30 micrograms EE and 75 micrograms gestodene (EE/GSD), the serum concentrations of EE, 3-keto-desogestrel (KDG) and GSD were determined on day 1, 10 and 21 of the 1st, 3rd, 6th and 12th cycle. The areas under the time-versus-concentration curves were calculated from the levels before and 0.5, 1, 1.5, 2, 3, 4 and 24 hours after intake of a tablet. There were large intra- and interindividual variations both revealing coefficients of variation (C.V.) between 25% and 80% (EE),, 30% and 50% (KDG) and 30% and 65% (GSD). During each cycle, the EE levels increased significantly between day 1 and 10 by 70% on average reaching a steady-state, while the progestogen concentrations rose by 100% (KDG) and 150% (GSD) up to a steady-state between day 10 and 21. After reaching the steady-state, the C.V. were generally lower. The ratios between the levels of EE and the progestogens showed still higher variations indicating different influences on the estrogen and progestogen component. There was no correlation between the steroid levels and weight, height or age. In spite of the large intraindividual variations, most of the women showed a distinct pattern of the levels of EE and the progestogens throughout the year of treatment indicating a genetic or acquired predisposition. The difference in the average AUC of EE, KDG and GSD between the women was 300% at most. During the first cycle of treatment with EE/DG and EE/GSD, about half of the women recorded intermenstrual bleedings which decreased thereafter. There was no relation between the occurrence of irregular bleedings and the average serum levels of EE and the progestogens of the individual women, neither during the first cycle nor during the whole treatment period of 12 cycles. It is concluded that spottings or breakthrough bleedings during treatment with oral contraceptives are not dependent on a distinct pattern of the serum levels of EE and the progestogen.

Adolescent↗

PubMed1990

Changes in lipid metabolism during 12 months of treatment with two oral contraceptives containing 30 micrograms ethinylestradiol and 75 micrograms gestodene or 150 micrograms desogestrel.

The effect of two oral contraceptives containing 30 micrograms ethinylestradiol + 75 micrograms gestodene (EE/GSD) or 30 micrograms ethinylestradiol + 150 micrograms desogestrel (EE/DG) upon serum lipids and lipoproteins were measured in 11 women each on days 1, 10, and 21 of the first, third, sixth, and twelfth treatment cycle and compared to the levels on days 1, 10, and 21 of the preceding control cycle. There was no change in total cholesterol (CH) and phospholipids (PL), while total triglycerides (TG) were significantly elevated only during treatment with EE/GSD. After 3 and 6 months of intake of both oral contraceptives, a transitory increase in the TG content of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), and a decrease in LDL-PL was observed. After 12 months, VLDL-CH, VLDL-PL, and apolipoprotein B were significantly elevated, while VLDL-TG and all components of LDL were unchanged. Most of the components of high-density lipoprotein (HDL) were increased due to a rise in HDL3 and apolipoprotein A-II, while HDL2 and apolipoprotein A-I were not altered. There was no significant difference between the effects of the two preparations, although those of EE/GSD were mostly more pronounced. The time-dependent change in the effects of the oral contraceptives on various parameters of lipid metabolism demonstrates that the relevance of results of short-time studies may be questionable. There was also a significant alteration in some parameters between day 1 and 10 of the treatment cycles and a tendency to return to the pretreatment levels during the pill-free week, e.g., in total TG and in the PL component of VLDL, LDL and HDL. The increase in HDL, VLDL, and total TG reflects a slight preponderance of the effect of ethinylestradiol on lipid metabolism. The unchanged total CH and LDL-CH and the elevated HDL levels indicate that the risk of the development of atherosclerosis is in all probability not increased during treatment with both preparations.

Adolescent↗

PubMed1989

Interaction with the pharmacokinetics of ethinylestradiol and progestogens contained in oral contraceptives.

The serum concentrations of ethinylestradiol (EE) during the first 4 h and 24 h after intake of an oral contraceptive containing 30 micrograms EE and 75 micrograms gestodene (EE/GSD) were compared to those after intake of a preparation containing the same EE dose and 150 micrograms desogestrel (EE/DG) in each of 11 women on days 1, 10, and 21 of their 1st, 3rd, 6th, and 12th cycles. There were great interindividual variations, but during treatment with EE/GSD the EE levels were higher and the EE peaks occurred by 30 min later than during treatment with EE/DG. The areas under the EE serum concentration-versus-time curves (AUC) between 0 and 4 h were higher by 37% (p less than 0.03) and between 0 and 24 h higher by 70% (p less than 0.002) during treatment with EE/GSD. During each treatment cycle, the EE levels rose between day 1 and 10. The serum levels of corticosteroid-binding globulin (CBG), which is known to be influenced only by the estrogenic component of the combination pill, increased significantly (p less than 0.01) during each treatment cycle. CBG was elevated on day 21 of the 6th and 12th cycle by 150 to 155% and by 120 to 130% with EE/GSD and EE/DG, respectively. The difference between the two drugs was significant (p less than 0.02). During the pill-free intervals of 7 days between the treatment cycles, the CBG levels decreased but were still elevated by 85% with EE/GSD and 50% with EE/DG at the beginning of the following cycle as compared to the control cycle. The serum levels of cortisol were also significantly more elevated (p less than 0.05) during treatment with EE/GSD as compared to EE/DG. Despite the same EE dose during treatment, the higher EE levels with EE/GSD as compared to EE/DG seem to be due to a retardation of the inactivation and elimination of EE caused by the progestogen component. The rise in the EE levels during each cycle seems to be due to a reduction in the oxidative metabolism by EE itself.

Adolescent↗

PubMed1988

Effect of two oral contraceptives containing 30 micrograms ethinylestradiol and 75 micrograms gestodene or 150 micrograms desogestrel upon various hormonal parameters.

The effect of two oral contraceptives containing 30 micrograms ethinylestradiol + 75 micrograms gestodene or 30 micrograms ethinylestradiol + 150 micrograms desogestrel upon various hormonal parameters were measured in 11 women each on days 1, 10, and 21 of the first, second, third, sixth, and twelfth treatment cycle and compared to the levels on days 1, 10, and 21 of the preceding control cycle. There was no significant difference in the clinical effects or in the influence on the serum hormone parameters between both formulations. A significant decrease in the serum concentrations of luteinizing hormone and follicle stimulating hormone was observed during each cycle which was dependent on the duration of intake. Contrary to this, prolactin was not significantly altered, but 6 out of the 22 women showed episodically elevated prolactin levels. Serum estradiol and progesterone were profoundly suppressed, except one woman who ovulated during the twelfth cycle probably due to a therapy with metamizol, trimethoprim and sulfamethoxazole. The concentrations of dehydroepiandrosterone-sulphate were significantly and time-dependently reduced by 20 to 25% during each treatment cycle. There was also a significant decrease in the serum levels of testosterone by 20 to 30% and of free testosterone by 40 to 60%, while sex hormone-binding globulin increased by 250 to 300%. It could be observed that during the pill-free interval of 7 days the pituitary and ovarian function recovered, while the sex hormone-binding globulin levels remained elevated by 100%.

Adolescent↗

PubMed1988

Alterations in the serum levels of gestodene and SHBG during 12 cycles of treatment with 30 micrograms ethinylestradiol and 75 micrograms gestodene.

The serum concentrations of gestodene have been measured radioimmunologically in 11 female volunteers on Day 1, 10, and 21 of the 1st, 3rd, 6th, and 12th cycle of treatment with an oral contraceptive containing 30 micrograms ethinylestradiol and 75 micrograms gestodene during the first 4 hours and 24 hours after intake. During the 1st cycle the maximal gestodene levels increased from 2.1 to 6.2 ng/ml on Day 1 to values between 7.5 and 22.0 ng/ml on Day 21. During the 3rd and 6th treatment cycle the levels were still higher with maxima between 10.1 and 26.3 ng/ml, while during the 12th cycle the gestodene concentrations were slightly lower. The serum levels of SHBG rose significantly during intake of the pill up to values between 210 and 240 nmol/l on Day 21 of each cycle, and were reduced to a certain degree during the pill-free interval. The SHBG concentrations correlated closely with the area under the gestodene concentration-versus-time curves (AUC) indicating a pronounced influence of serum protein binding upon the pharmacokinetics of gestodene. The gestodene levels of the individual women remained relatively constant during the 12 treatment cycles, although great interindividual differences were found. It is concluded that the relatively high serum concentrations of gestodene are not only based on the binding to SHBG, but probably also on an impeded metabolism of gestodene.

Adolescent↗

PubMed1988

Serum levels of 3-keto-desogestrel and SHBG during 12 cycles of treatment with 30 micrograms ethinylestradiol and 150 micrograms desogestrel.

The serum concentrations of 3-keto-desogestrel (KDG) have been determined radioimmunologically in 11 female volunteers on Day 1, 10, and 21 of the 1st, 3rd, 6th, and 12th cycle of treatment with 30 micrograms ethinylestradiol and 150 micrograms desogestrel during the first 4 hours and 24 hours after intake. On the first day of each cycle the KDG levels were low, but increased thereafter until Day 21. Highest serum concentrations were measured on Day 21 of the 3rd and 6th cycle with peak levels between 1.5 and 6.2 ng/ml. Contrary to this, the KDG levels were significantly reduced during the 12th treatment cycle. The serum concentrations of SHBG rose significantly between Day 1 and Day 21 of each cycle reaching values which were 3-fold of those at the beginning of treatment. During the pill-free intervals, SHBG levels decreased but remained elevated as compared to controls. There was a significant correlation between the SHBG levels and the area under the KDG-concentration-versus-time curves (AUC) indicating a pronounced influence of the serum steroid-binding protein upon the pharmacokinetics of KDG. There were great interindividual differences in the KDG levels. The serum levels of the individual woman remain, however, in a relatively constant range throughout the treatment period of 12 months, possibly due to genetic factors.

Adult↗

PubMed1988

[Effect of 2 low-dosage Gestodene or desogestrel containing ovulation inhibitors on sex hormones and lipid metabolism].

In a randomised study on 20 healthy female subjects we compared the effect of two low-dosage antiovulants containing gestodene or desogestrel on ovarial and adrenal function and on fatty metabolism. Both antiovulants produced a moderate inhibition of gonadotropin secretion and a marked suppression of serum levels of oestradiol, testosterone and free testosterone; there was a strong increase in sex hormone-binding globulin, and an increase in cortisol--probably due to the increase on corticosteroid-binding globulin--and a continuous drop in dehydroepiandrosterone S. In all cases there was no significant difference between the effect of both preparations. Whereas there was no change in total and LDL cholesterol, total phospholipids and VLDL triglycerides, there was a significant increase in the concentrations of apolipoprotein B, total triglycerides, the cholesterol and phospholipid properties of VLDL as well as of all components of HDL. The LDL triglycerides were also elevated, whereas the LDL phospholipids dropped. On the whole the changes in lipid metabolism, which indicate a certain predominance of the oestrogen effect, were low. However, it became that the duration of intake exercises considerable influence.

Adolescent↗