Determination of estriol, estriol sulfate, progesterone and neutral steroid mono- and disulfates in umbilical cord blood plasma

Laatikainen, Timo; Peltonen, Jari; Nylander, P.

doi:10.1016/0039-128x(73)90029-9

Cited by 28 publications

(11 citation statements)

References 26 publications

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“…In the newborn with ichthyosiform erythroderma and deafness, the serum 5-androstene-3jS,i7jS-diol sulphate concentration was very high in repeated determinations, but the other steroid sulphate levels were normal. As shown before (Laatikainen, Peltonen & Nylander, 1973), serum 5-androstene-3^,i7^-diol sulphate concentration is normally at a considerably lower level after birth than in this patient. In liver diseases plasma concentrations of reduced sulphated steroids like 5-androstene-3j9,i7j9-diol sulphate are higher than the concentrations of the corresponding keto compounds like dehydroepiandrosterone sulphate (Sjovall & Vihko, 1966).…”

Section: Resultssupporting

confidence: 73%

Serum steroid sulphates in ichthyosis

et al. 1980

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Serum concentrations of pregnenolone sulphate, dehydroepiandrosterone sulphate and 5-androstene-3 beta,17 beta-diol sulphate were measured by radioimmunoassays in twelve patients with various types of ichthyosis. In X-linked ichthyosis (n = 5), ichthyosis vulgaris (n = 5) and lamellar ichthyosis (n = 1), steroid sulphates were not significantly higher than in the control subjects. In one baby with ichthyosiform erythroderma and associated deafness serum 5 -androstene-3 beta,17 beta-diol sulphate concentration was about 60 fold higher (31 microgram/ml) than the mean of the control children. The other steroid sulphate levels were normal in this baby. These results indicate that it is not possible to demonstrate the steroid sulphatase deficiency in X-linked ichthyosis by determining blood steroid sulphates. The cause of the high 5-androstene-3 beta,17 beta-diol sulphate concentration in the baby with ichthyosiform erythroderma needs further evaluation.

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Section: Resultssupporting

confidence: 73%

Serum steroid sulphates in ichthyosis

et al. 1980

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“…Control groups consisted of 30 plasma samples collected after normal pregnancies and deliveries at 38-41 wk of gestation. The results of these analyses were published previously (7). Further, 12 cord plasma samples collected after deliveries at 35-37 wk of gestation after uncomplicated pregnancies were analyzed in this study.…”

Section: Introductionmentioning

confidence: 89%

“…To obtain more detailed information on the metabolism and conjugation of steroids in the fetoplacental unit, we developed a method for determination of progesterone, estriol, estriol sulfate, and 13 neutral steroid monosulfates and 10 neutral steroid disulfates in the cord plasma (7). To study the fetoplacental steroid metabolism in pregnancies complicated by maternal intrahepatic cholestasis, we have analyzed 27 cord plasma samples collected after such pregnancies and compared the steroid levels with those obtained in the cord plasma after uncomplicated pregnancies.…”

Section: Introductionmentioning

confidence: 99%

Effect of Maternal Intrahepatic Cholestasis on Fetal Steroid Metabolism

Laatikainen¹,

Peltonen²,

Nylander³

1974

J. Clin. Invest.

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A B S T R A C T Estriol, estriol sulfate, progesterone, and 17 neutral steroid sulfates, including estriol precursors and progesterone metabolites, were determined in 27 cord plasma samples collected after pregnancies complicated by intrahepatic cholestasis of the mother. The levels of these steroids were compared with those in the cord plasma of 42 healthy controls.In the cord plasma, the steroid profile after pregnancies complicated by maternal intrahepatic cholestasis differed greatly from that seen after uncomplicated pregnancy. Two main differences were found. In the disulfate fraction, the concentrations of two pregnanediol isomers, 5a-pregnane-3a,20a-diol and 5P-pregnane3a,20a-diol, were high after cholestasis. Other investigators have shown that, as a result of cholestasis, these pregnanediol sulfates circulate in greatly elevated amounts in the maternal plasma. Our results indicate that in cholestasis these steroids cross the placenta into the fetal compartment, where they circulate in elevated amounts as disulfates. Secondly, the concentrations of several steroid sulfates known to be synthesized by the fetus were significantly lower in the cholestasis group than in the healthy controls. This was especially true of 16a-hydroxydehydroepiandrosterone sulfate and 16a-hydroxypregnenolone sulfate. These results suggest that, in pregnancies complicated by maternal intrahepatic cholestasis, impairment of fetal steroid synthesis, and especially of 16a-hydroxylation, occurs in the fetal compartment.Thus, the changes in maternal steroid metabolism caused by cholestasis are reflected in the steroid profile of the fetoplacental circulation. Furthermore, maternal intrahepatic cholestasis may result in the production of some substance which crosses the placenta and affects fetal steroid metabolism.

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“…It is widely recognized that the activity of 3 ƒÀ-hydroxysteroid dehydrogenase is lower (Bermudez et al, 1972;Huhtaniemi and Vihko, 1970;Laatikainen et al, 1973), while that of steroid sulfotransferase is higher in the fetal adrenal cortex and peripheral tissues than in those of adults (Korte et al, 1982;Seron-Ferre et al, 1978).…”

mentioning

confidence: 99%