Estrogen metabolism in recurrent jaundice of pregnancy (RJP) and pruritus gravidarum (PG) was studied by determining 12 different estrogens in bile and urine. A uniformly marked fall in the biliary concentrations of all estrogens was observed in RJP. This would suggest that the enterohepatic circulation of these steroids is impaired and offers an explanation for the abnormal pattern of urinary estrogens observed in the two related syndromes. The relative excretion (= percentage of total estrogens) of estriol6 and 16-epiestriol in urine was diminished, whereas that of their respective precursors, 16α-hydroxyestrone and 16β-hydroxyestrone was increased. Rather small or insignificant changes were seen in the urinary excretion of other estrogens. Hence the main alterations occurred in the 16-hydroxylation pathways and included decreased conversion of 16α-hydroxyestrone to estriol and of 16β-hydroxyestrone to 16-epiestriol. The primary cause of these alterations is most likely the decreased biliary excretion of estrogens with consequent impairment of their enterohepatic circulation. This is in accordance with the view that RJP and PG are not caused by a primary abnormality in estrogen production or metabolism in the fetoplacental unit.