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The estradiol metabolism may be of clinical relevance in the pathophysiology of various diseases; the increase in D-ring metabolites over A-ring metabolites in breast cancer patients is of special interest. Since estrogen therapy has been blamed for increasing the risk of breast cancer, the effects of hormonal replacement therapy (HRT) and oral contraception were investigated on the ratio of the main D-ring metabolite, 16alpha-hydroxyestrone (16-OHE1), to the main A-ring metabolite, 2-hydroxyestrone (2-OHE1). In our study, hormone replacement therapy (HRT) in postmenopausal women consisted of administration of estradiol valerate either with or without addition of the progestin dienogest. In the second part of the study, women of reproductive age received ethinylestradiol plus dienogest or ethinylestradiol plus norethisterone acetate as oral contraceptives (OC). 2-OHE1 and 16-OHE1 were measured by enzyme immunoassay in 8 h night-urine collected before and after 3 months of hormone administration. With HRT, that is, estradiol valerate or estradiol valerate plus dienogest, the ratios before treatment were 0.47 and 0.60; after 3 months, they were 0.54 and 0.52, respectively. There were no significant differences. With oral contraception, that is, ethinylestradiol plus dienogest or norethisterone acetate, the ratios before administration were 0.62 and 0.68, vs. 0.31 and 0.54 after 3 months, respectively. The ratio after ethinylestradiol and dienogest was significantly lower after treatment. HRT and OC in the estrogen-progestin combinations tested did not impose any negative effects on estradiol metabolism--they did not elicit a higher D-ring metabolism, which is considered to increase breast cancer risk.

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Magnesium deficiency, prostacyclin deficiency and reduced prostacyclin sensibility of the thrombocytes may possibly play an important pathophysiological role in gestosis/pre-eclampsia. For this reason, we studied the influence of magnesium sulphate (in vitro 2-16 mVal/l) on thromboelastogram, spontaneous and ADP-induced thrombocyte aggregation, prostacyclin sensitivity of the thrombocytes and prostacyclin liberation from umbilical cord vessel preparations. The thromboelastogram showed an inhibitory influence of magnesium sulphate on all measurement parameters. Spontaneous and ADP-induced thrombocyte aggregation were inhibited to a statistically significant extent. The prostacyclin sensibility of the thrombocytes was increased by magnesium-sulphate. Magnesium sulphate enhanced prostacyclin liberation from the vascular wall significantly by 20-36%. It is possible that in gestosis magnesium sulphate may exercise a favourable influence on the disturbed balance between prostacyclin production and prostacyclin sensibility of the thrombocytes by exercising an influence on coagulation, thrombocyte function and prostacyclin liberation, and that it can thus contribute towards stabilising coagulation disturbances.

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