Abstract

The excretion of oestriol in the maternal urine increases approximately a thousandfold from conception to term. During the first weeks of pregnancy, the oestriol is derived from the metabolism of oestrone and oestradiol produced by the corpus luteum. Later, the placenta becomes the major site of oestrogen production, and synthesises oestriol as well as oestrone, oestradiol and other oestrogens. From this time, the urinary oestriol is derived in two ways—directly from placental oestriol and indirectly from the metabolism of the other oestrogens. The placenta, in turn, derives many of the steroid precursors required for oestrogen synthesis from other sites, the most important being the foetus. The levels of oestriol in the urine therefore reflect the combined functional capacity of the foeto‐placental unit.SUMMARYThe urinary oestriol excretion in 265 patients with complicated pregnancies (30 perinatal deaths) and 211 normal pregnancies is presented.In the 70 patients with oestriol values below the normal range there were 21 foetal deaths, and 6 of the 49 surviving infants showed placental insufficiency. Ery‐throblastosis was the cause of 6 of the 9 deaths which occurred in patients with normal oestriol values.Low oestriol excretion was present in the majority of patients with impending intra‐uterine death and therefore the test is of value in selection of the optimum time for termination of such pregnancies. However, low oestriol excretion did not always signify that an infant at birth would appear placentally insufficient nor did a normal oestriol value exclude the possibility that an infant would exhibit this syndrome.

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