Serum concentrations of Apolipoprotein A-I and A-II, (Apo A-1 and Apo A-II) HDL-cholesterol (HDL-C), Total Cholesterol (TC), triglycerides (TG) and lipoprotein electrophoresis were assayed serially in the second half of normal pregnancy (21 women), in pre-eclampsia (26 women) and in both groups one and six weeks after delivery. In the normal group we found increased concentrations of Apo A-I and HDL-C, which remained unaltered during pregnancy. Apo A-II was unchanged. Correlation coefficients for Apo A-II vs HDL-C and Apo A-I vs Apo A-II decreased gradually towards delivery while it remained at an elevated and unaltered level for Apo A-I vs HDL-C. The Apo A-I/HDL-C ratio was unaltered during the whole study while the Apo A-I/A-II ratio was elevated during pregnancy and the Apo A-II/HDL-C ratio was reduced. These results may indicate a gradual change in the surface structure of the HDL particle or its subfractions. In pre-eclampsia Apo A-I and HDL-C concentrations were reduced, TG was increased and Apo A-II and TC were unchanged when compared with the normal pregnancy group. A more pronounced correlation coefficient was recorded for Apo A-I vs HDL-C than for Apo A-II vs HDL-C and Apo A-I vs Apo II. The results indicate that from an atherogenic point of view normal pregnancy seems more beneficial than pre-eclampsia.

The transfer of atenolol and metoprolol to human breast milk was studied in 7 lactating women with hypertension. Concentrations of atenolol and metoprolol in maternal plasma and milk and in plasma of the nursed infants were determined. Blood samples were obtained from the women and from the infants during a dose interval. Milk was collected repeatedly from the left breast but only twice from the right breast. The ratio between the area under the milk concentration versus time curve (AUCm) and the area under the plasma concentration versus time curve (AUCp) in the mother varied between 2.0and 3.1 for metoprolol and 1 . 1 and 3.1 for atenolol. The milk concentrations of metoprolol in the right breast were similar to those in the left breast, although the latter had been emptied more frequently. For atenolol the milk concentrations in the right breast were lower than in the left breast. The plasma concentrations of metoprolol and atenolol in the infants were negligible or below the limit of detection. Our results show that exposure of the infant to metoprolol can be minimized if nursing is not undertaken earlier than 3 -4 hours after dose intake.

Peripheral serum levels of unconjugated (E₁ and total (tE₁) oestrone, unconjugated oestradiol-17Β, unconjugated (E₃) and total (tE₃) oestriol, progesterone, unconjugated dehydroepiandrosterone (DHA) and dehydroepiandrosterone sulphate (DHAS), and urinary tE₃ excretion were determined in pre-eclamptic patients at gestational weeks 32 and 36 and in women with normal pregnancy at the corresponding length of gestation. DHA and DHAS were also analyzed in samples taken 6 weeks after delivery. There were no differences between pre-eclamptic and normal subjects in unconjugated oestrogens and progesterone. Serum tE₁ and tE₃ levels and urinary tE₃ were significantly lower, and the E₁/tE₁ and E₃/tE₃ ratios significantly higher in the pre-eclampsia patients. Serum DHA and the DHA/DHAS ratio were significantly elevated in the pre-eclampsia patients during pregnancy, while no differences in these respects were found in the samples taken 6 weeks after delivery. There were no differences in serum DHAS levels. The findings are thought to reflect a general decrease in fetoplacental oestrogen production in combination with a reduced hepatic steroid conjugation in pre-eclamptic subjects.

The relative fatty acid composition of serum lecithin was followed in groups of women during postmenopausal replacement therapy. The effects of estradiol valerate and ethinyl estradiol in two different doses, and the modulating influence of various progestogens and antiestrogens were compared. Unopposed estrogen treatment enhanced liver lecithin synthesis along pathway I, i.e. reduced the amount of stearic acid and increased the amount of palmitic acid. The effect was clearly dose-dependent and even the low dose of 10 µg of ethinyl estradiol was more potent than 2 mg of estradiol valerate. No qualitative difference between the two estrogens was recorded. The sequential addition of the antiestrogen tamoxifen significantly reduced the influence of ethinyl estradiol. Liver lecithin synthesis along pathway I may be stimulated by all estrogens and not only by 17C-alkylated compounds. The prostaglandin precursors, dihomogammalinolenic and arachidonic acid, showed a seemingly dose-dependent increase during estrogen treatment. The comparatively weaker effects of estradiol valerate on lipid metabolism should make this non-alkylated estrogen the first choice in clinical practice.