Aspects of Praematurity and Dysmaturity: Groningen 10–12 May by John W. Reynolds (auth.), J. H. P. Jonxis M.D., H. K. A.

By John W. Reynolds (auth.), J. H. P. Jonxis M.D., H. K. A. Visser M.D., J. A. Troelstra M.D. (eds.)

The idea of the foeto-placental unit as an built-in endocrine organ has been outlined lately by way of many in vivo reports on the seventeenth- twentieth week of gestation. A functioning foeto-placental unit is important for many of the elevated oestrogen construction of being pregnant and for the supply of glucocorticoids and aldosterone to the foetus. Neither the foetus nor the placenta on my own have the mandatory enzyme platforms for the synthesis of those teams of steroids. notwithstanding, whilst the foetus and placenta functionality as a unit, the entire enzyme platforms are current for the synthesis of those steroids from circulating ldl cholesterol. The placenta, yet now not the mid-gestation foetal adrenal, can synthesize physiologically a great deal of pregnenolone from circulating ldl cholesterol. a part of the pregnenolone is switched over to progesterone within the placenta by means of the 3~-HSD procedure (absent within the foetus). The progesterone is transferred to the foetus the place it really is reworked by means of C-II, C-17, C-18 and C-21 hydroxylases (all absent within the placenta) to cortisol, corticosterone and aldosterone. Pregnenolone transferred from the placenta to the foetus undergoes 171X-hydroxylation, aspect­ chain splitting and sulfurylation (absent within the placenta) and is switched over to DHAS. The DHAS may possibly endure 161X-hydroxylation (absent within the placenta) within the foetal liver and be transported to the placenta as 161X-OH-DHAS. There it truly is subjected to a impartial steroid sulfatase (absent within the foetus) and is switched over to oestriol through motion of the 3~-HSD procedure and the aromatizing enzyme system.

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Extra info for Aspects of Praematurity and Dysmaturity: Groningen 10–12 May 1967

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Does anybody know what is the placental morphology in chromosomal anomalies, is there any specific morphological variation? And my second question is, would you say that placental aging causes the same degenerative changes that we get for example in toxaemia, infarcts and calcifications? Dr. Gruenwald: I don't think that is to answer either. It has of course been suggested that just about every change you find in the maturing placenta is increased in toxaemia, but every time there has been somebody else who fails to find this.

For this reason malformed fetuses are excluded from further consideration. Obviously, birth weight can be properly evaluated only in relation to gestational age, and pathologic growth retardation is usually recognized if birth weight is below an arbitrary limit such as the 10th percentile, or mean minus 2 standard deviations for the respective week of gestation. The former limit includes 3 to 4 times as many cases as the latter. The question then arises what standards should be used, and the answer depends largely on the problem to be studied.

GRUENWALD Maternal height (N ational Birthday Trust) 3500 3250 3000 2000 33 2 35 31 39 41 36 43 weeks 38 40 42 weeks 3 Fig. 2. Growth curVes derived from birth weights of Swedish (LINDELL, Acta Obstet. et Gynec. Scand. 34: 136, 1956), British (1958, courtesy National Birthday Trust), American (1) and Japanese (4) infants. Fig. 3. Fetal growth curves from birth weights, for groups of mothers of different height. Courtesy National Birthday Trust. of births early in the third trimester are insufficient to make this point with complete assurance.

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