OVARIAN AND PLACENTAL FUNCTION IN ADDISON'S DISEASE<sup>1</sup><sup>2</sup>

Samuels, Leo T.; Evans, Gerald; McKelvey, J.L.

doi:10.1210/endo-32-5-422

Cited by 29 publications

(9 citation statements)

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“…The direction of the concentration gradient between cord and maternal plasma suggests that the plasma 17-ketosteroids of the newborn may be derived from some tissue in the fetal circulation other than from the mother, possibly from the internal cortex of the fetal adrenal or the placenta. It is relevant that several previous workers have observed a progressive increase during pregnancy of urinary 17-ketosteroid excretion in women with proven adrenocortical insufficiency, even though these women had essentially no urinary 17-ketosteroid excretion prior to pregnancy (11)(12)(13) 17-ketosteroids from 19 full-term, newborn infants, and from 20 premature infants. The premature infants had attained weights ranging from 793 to-2381 grams when the samples were taken.…”

Section: Studies On Full-term Newbornsmentioning

confidence: 97%

Plasma 17-Ketosteroids of Full-Term and Premature Infants12

Gardner¹,

Walton²

1954

J. Clin. Invest.

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The adrenal cortex of the newborn exhibits a relative lack of responsiveness to the administration of adrenocorticotrophic hormone which has been the subject of several investigations and is adequately reviewed elsewhere (1). These observations, together with the presence of the fetal reticular zone of the adrenal cortex and the recent report of very low concentrations of compound F-like substances in newborn plasma (2), are all reminiscent of the findings in infants and children with congenital adrenal hyperplasia (3,4).Since children with congenital adrenal hyperplasia have been shown to have markedly elevated concentrations of plasma neutral 17-ketosteroids (5), it was thought desirable to investigate the concentrations of these steroids in the plasma of newborn infants. The purpose of this paper is to describe analytic data obtained when plasma samples from a group of normal full-term infants and a group of premature infants were analyzed for neutral 17-ketosteroids. METHODS

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Section: Studies On Full-term Newbornsmentioning

confidence: 97%

Plasma 17-Ketosteroids of Full-Term and Premature Infants12

Gardner¹,

Walton²

1954

J. Clin. Invest.

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“…However, in S.R. (Case 4) the several determinations during pregnancy indicate a gradual increase in secretion with a subsequent fall, and Samuels, Evans and McKelvey (26) have reported an even more striking rise in another such patient. These workers suggested that this rise was due to secretion by the fetal adrenal.…”

Section: Urinary Excretion Of Hormonesmentioning

confidence: 91%

“…Although in certain of these reports the data given are insufficient to establish the diagnosis of adrenal insufficiency, in the great majority the records are of unquestionable authenticity. In only one such patient has a study of the steroid excretion been reported (26). In this patient, Samuels and associates found that the excretion of estrogens, pregnanediol and of 17-ketosteroids (assayed by a modification of the Zimmermann reaction) during the last two trimesters corresponded to the amounts excreted in normal pregnancy.…”

Section: Introductionmentioning

confidence: 91%

Pregnancy in Addison's Disease: Report of Four Patients

Knowlton

Mudge

Jailer

1949

The Journal of Clinical Endocrinology & Metabolism

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“…Although this is known to occur in normal pregnancy (2), along with a rise in glucocorticoids as determined by bio-assay (1), its occurrence in a patient with adrenal insufficiency is surprising. 3 The third indication of "adrenal activity" is the normal response during pregnancy to epinephrine and ACTH as measured by a fall in circulating eosinophils.…”

Section: Determination Of Acth In Patient's Placentamentioning

confidence: 99%

“…In both reports an unexpected finding has been a rise in 17-ketosteroids which occurred during the latter months of pregnancy in a manner similar to that observed in normal patients. Samuels, Evans and McKelvey (3) suggested that this increase might be accounted for on the basis of fetal secretion of these steroids; however, assays of newborn infants' urine have yielded amounts of these steroids which are inadequate to account for the observed rise in maternal excretion (5,6). Consequently, the possibility may be entertained that the placenta rather than the fetus serves as the source of these steroids.…”

mentioning

confidence: 99%