Desogestrel- and levonorgestrel-containing oral contraceptives have different effects on urinary excretion of prostacyclin metabolites and serum high density lipoproteins.

Prostacyclin synthesis is stimulated in vitro by high density lipoproteins (HDL), which themselves are differently affected by desogestrel (DG)- and levonorgestrel (LN)- containing oral contraceptives. In this study we measured the urinary excretion of the metabolites of prostacyclin [6-keto-prostaglandin F 1 alpha(6-keto) and 2,3-dinor-6-keto-prostaglandin F1 alpha (dinor)] and of thromboxane A2 [thromboxane B2 (TxB2)] as well as serum HDL- and HDL2 cholesterol concentrations before and during DG and LN administration alone or in combination with ethinyl estradiol (EE) in 26 women. Before the trial, urinary dinor excretion correlated with serum total HDL cholesterol (r = 0.499; P less than 0.01) and HDL2 cholesterol levels (r = 0.668; P less than 0.001; n = 26). Administration of DG (150 micrograms/day; 14 women) or LN (150 micrograms/day; 12 women) for 2 weeks caused no changes in the excretion of these prostanoids, but LN administration decreased serum HDL cholesterol levels. After that, the women underwent a monophasic regimen of 150 micrograms DG or LN plus 30 micrograms EE for 3 months and thereafter polyphasic regimens of the same steroids for a further 3 months. The DG-containing pills increased urinary dinor excretion by 25-40%, but caused no changes in 6-keto and TxB2 excretion, as measured on days 19-21 of the cycles. LN-containing pills reduced urinary 6-keto excretion by 22% at the end of polyphasic treatment, but caused no changes in dinor and TxB2 output. DG plus EE, but not LN plus EE, increased serum total HDL and HDL2 cholesterol concentrations by a maximum of 25%. Thus, a DG plus EE combination may stimulate PGI2 synthesis by increasing the levels of HDL/HDL2. Theoretically, this stimulation protects against occlusive vascular disorders.