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Preeclampsia (PE) is a pregnancy-specific hypertensive syndrome that results in substantial maternal and fetal morbidity and mortality. The exact cause of PE has not been completely elucidate, although abnormal formation of the placenta has been considered. The placenta connects the developing fetus to the uterine wall, producing a large quantity of steroid hormones to maintain pregnancy. Although steroid hormones, particularly progesterone (P4) and estrogen (E2), in the serum of women with PE have been studied, steroidogenesis in the placenta has not well been established. The present study compared the concentrations of steroid hormones, including pregnenolone (PG), P4, dehydroepiandrosterone (DHEA), testosterone (T) and E2, in the serum and placenta of women with PE. PG, P4, DHEA and E2 concentrations tended to be decreased in PE serum and placentas, and the results were statistically significant for P4 and E2 in the serum. Quantification of genes associated with steroidogenesis in the placenta was performed, and the expression of the P4-and E2-synthesizing enzymes testosterone 17-beta-dehydrogenase 3 and 3 beta-hydroxysteroid dehydrogenase/delta 5 4-isomerase type 1 was reduced. Notably, aromatase, an enzyme required for the production of E2, was upregulated in the PE placenta, suggesting that steroidogenic enzymes may be dynamically regulated and may affect the symptoms of PE. In conclusion, the results of the present study suggested that the levels of steroid hormones, including P4 and E2, in the serum and placenta of women with PE are downregulated, which may be mediated by the regulation of steroidogenic enzyme expression in the PE placenta.