Today urinary excretion of estrogen äs an indicator of possible pregnancies at risk is an accepted parameter. For a long time excretion of estrogen was considered äs a so-called fetoplacental indicator; since both fetus and placenta participate in estriol synthesis. However, recent findings indicate [7,22,23] that the fetus is, to some extent, independent of the placenta äs far äs the synthesis of estriol precursors is concerned. It has also been demonstrated that the capacity of the placenta to form aromatic compounds is not decreased but rather elevated in severely impaired nutrition [21]. Heüce decreased estrogen excretion is more probably due to limited synthesis in the fetus than in the placenta. The lack of placental sulfatase is an exception that is hardly of quantitative importance [6,8]. Hence the rate of estrogen excretion may be considered a fetal rather than a fetoplacental parameter. Usually an impairment of the nutritive function of the placenta that is chronic in nature is the basis of the endocrinologically assayable danger to the fetus. If urinary estrogen excretion is decreased it must be assumed that the fetus has already been damaged. Hence for perinatal diagnostic purposes it is desirable to use a purely placental indicator that might indicate danger earlier than estrogen excretion and that permits us to distinguish between fetal and placental malfunction. Three hormone tests are usually applied: HPL (human placental lactogen) in serum; pregnandiol in urine äs an indicator of progesteron metabolism and plasma progesteron. HPL indicates the rate of proteinsynthesis in the placenta and pregnandiol its steroid biosynthesis. The introduction of radioimmunological tests for HPL has feduced pregnandiol determinations with their well known drawbacks related to urinary analyses. Pregnandiol determinations very often gave false normal J. Perinat. Med. 3 (1975) Curriculum vitae

Ovarian follicular activity was significantly suppressed during treatment with levonorgestrel 100 micrograms/ethinylestradiol 20 micrograms. Similarly, endogenous ovarian steroid production was almost uniformly decreased. A 'dissociation' of ovarian and endometrial development was also seen during this therapy.

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