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Biomedical subjects

H Kuhl

Publications and source records attributed to H Kuhl.

At least 73 records · Page 4Linked to original sources
PubMed1994

Lack of effect on the low density lipoprotein receptor in hamsters treated with 17 alpha-ethinyl estradiol.

High pharmacological doses of 17 alpha-ethinyl estradiol are known to increase the number of low density lipoproteins (LDL)-receptors in rats and rabbits, leading to a profound decrease in plasma cholesterol levels. Here, using rats as a positive control, we demonstrate that in hamsters ethinyl estradiol does not upregulate liver LDL-receptors, nor change plasma LDL turnover or plasma LDL-cholesterol. The lack of effect in estradiol-treated hamsters suggests that the hormonal control is different from that in rats.

Animals↗
PubMed1994

[Cardiovascular effects and estrogen/gestagen substitution therapy].

After the menopause there is a profound increase in cardiovascular diseases which is mainly based on an enhanced development of atherosclerosis caused by an estrogen deficiency. The most important pathomechanisms are the rise in LDL-cholesterol and triglycerides as a result of an impaired elimination of LDL and remnants in the liver, and an enhancement of LDL oxidation in the arterial intima. Moreover, at the site of endothelial lesions the occurrence of vasospasms and platelet aggregation is facilitated in estrogen-deficient women which may lead to ischemia. Epidemiological studies revealed that replacement therapy with natural estrogens reduces the risk of cardio-vascular diseases by 30 to 50%, whereby the protective effect is not impaired by the addition of progestogens. The mechanism of action is only partly based on the favorable effect of estrogens on lipid metabolism. Besides an increase in HDL, estrogens may reduce LDL-cholesterol by means of an enhancement of receptor-mediated elimination of LDL and remnants in the liver. A rise in triglycerides is of no clinical relevance, if based on an estrogen-induced increase in triglyceride synthesis and VLDL-LDL turnover. Even in the case of an unfavorable lipid pattern estrogens may protect from atherosclerosis, as they inhibit LDL oxidation by scavenging free oxygen radicals. Finally, estrogens may cause vasodilation which is partly endothelium - dependent, but presumably is also based on the blockade of calcium influx into smooth muscle cells. This may be of particular importance in women with endothelial lesions, e.g. coronary sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

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

[Hormonal contraception and substitution therapy: the importance of progestogen for cardiovascular diseases].

Epidemiological data have demonstrated, that the progestogen component of oral contraceptives is involved in the development of hypertension, ischaemic heart diseases and stroke. It had been suggested, that atherosclerotic lesions due to the unfavourable effect on lipid metabolism of progestogens with androgenic properties, play a causal role. It has, however, been shown, that there is no development of atherosclerosis despite reduced HDL and elevated LDL, presumably because of the induction of hepatic LDL- and remnant-receptors by the strong effect of ethinyl-oestradiol upon the liver. A series of experimental and clinical findings indicates that vasospasms caused by the vasoconstrictory effect of progestogens are involved in the development of arterial thromboses. In postmenopausal women, the additional administration of progestogens to the oestrogen treatment may trigger ischaemic diseases, particularly in the presence of vascular lesions. Oestrogens exercise a pronounced vasodilatory effect and stabilize the vascular tonus--through changes in the responsiveness of endothelium and smooth muscle cells to vasoactive compounds, through modulation of neurotransmitter release from nerve endings, and through direct blocking of calcium channels. The effects depend essentially on an intact endothelium. By a direct action on the vascular wall, progestogens increase the sensitivity of arteries to vasoconstrictory compounds and reduce blood flow. As aldosterone increases the number of beta-adrenergic receptors in the arterial smooth muscle cells and thus act vasodilatorily, it cannot be excluded, that progestogens with high affinity to the aldosterone receptor and antimineralocorticoid properties, may exert a strong vasoconstrictory effect.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiovascular Diseases↗
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↗
PubMed1992

Is 3 alpha, 17 beta-androstanediol-glucuronide a diagnostic marker in women with androgenic manifestations?

3 alpha, 17 beta-androstanediol-glucuronide (Adiol-G) has been described as a marker of local androgen excess due to the increased activity of 5 alpha-reductase in the cells of the hair follicles. In order to test the diagnostic value of Adiol-G, the serum level was compared to that of testosterone, free testosterone, dehydroepiandrosterone sulfate (DHEA-S), androstenedione and to the body mass index in 44 women with androgenic symptoms (Group I), 27 women with menstrual disturbances but no androgenic symptoms (Group II), and 48 healthy women (Group III) who served as controls. Adiol-G was significantly higher (7.8 +/- 5.1 nmol/l) in women with androgenic symptoms than in the other groups, but there was a considerable overlap. Serum testosterone was also found to be higher in Group I than in Groups II and III, respectively. There was a significant correlation between Adiol-G and testosterone, and Adiol-G and DHEA-S. No significant correlation could be shown to exist between androstenedione and Adiol-G. When Adiol-G and testosterone were simply classified as 'normal' or 'increased' (Adiol-G 9.4 nmol/l; testosterone greater than 2.4 nmol/l), higher than normal values of the former were found in the presence of normal testosterone in only 4% of the cases. It is concluded that the level of Adiol-G generally parallels that of testosterone. Consequently, it does not seem to be an effective marker of peripheral androgen excess.

Acne Vulgaris↗