Sporadic Cretinism in One of Twins

Dorff, George B.

doi:10.1001/archpedi.1934.01960190136015

Cited by 29 publications

(3 citation statements)

References 11 publications

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“…Included among these are the assumptions: a) that albumin and TBP each have a single type of binding site for thyroxine at the thyroxine levels employed, b) that there are no interactions between successively bound thyroxine molecules, and c) that zone electrophoresis provides satisfactory estimates of the maximum number of sites on TBP and of the ratio between the intrinsic association constants for the thyroxinealbumin and thyroxine-TBP complexes. These assumptions, as discussed elsewhere (10,15) (32) and, conversely, by the finding of retarded bone age in newborn athyreotic infants of normal mothers (33). The slow passage of maternal thyroxine into the fetus (34) indicates that TBP does not readily pass the placental barrier, if at all, and that the placenta probably does not transfer free thyroxine by any mechanism other than diffusion.…”

Section: Discussionmentioning

confidence: 84%

Thyroxine-Binding by Serum Protein in Pregnancy and in the Newborn

Robbins¹,

Nelson²

1958

J. Clin. Invest.

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Thyroid structure and function in man undergo a number of changes during pregnancy. The thyroid gland may become enlarged and hyperplastic (1, 2), thyroidal uptake of radioiodine is increased (3, 4), "conversion" of blood iodide to organic form is more rapid (4), and the serum proteinbound iodine (PBI) is elevated (5, 6). Although these alterations are like those seen in hyperthyroidism, they appear to be associated, in early pregnancy at least, with an unequivocally euthyroid state. Whereas the PBI rises as early as the first or second month of gestation, and remains at about the same level throughout pregnancy, elevation of the basal metabolic rate (2, 7) begins in the latter half of pregnancy and rises progressively. Circulatory changes, such as increased cardiac output (8), may precede the rise in oxygen consumption but these also change progessively until shortly before term.It has been postulated that alterations in the interaction of thyroid hormone with serum proteins might provide an explanation for these paradoxical findings (6). Inasmuch as circulating thyroxine is largely bound to what appears to be a specific alpha globulin (TBP) (9, 10), attention has been directed toward this protein in pregnancy. It has been demonstrated that TBP in pregnancy has an increased ability to complex thyroxine (10-13).In the present study, the thyroxine-binding capacity of TBP has been quantitated during the course of normal pregnancy and in newborn infants. From these data it has been possible to calculate an approximate concentration of free thyroxine in the serum of these subjects. METHODSSerum was obtained from 16 women during and after uncomplicated pregnancies, usually after an overnight fast, from umbilical vein blood sampled at delivery in three subjects, and from external jugular venipuncture in two infants on the third day after delivery. Mixtures of serum with I13'-labeled L-thyroxine 1 were prepared according to the procedure described previously (14). Prior to use, each of the eight thyroxine preparations employed was tested for radiochemical purity by chromatography, and was repurified, when necessary, to a purity of 90 per cent or better by an extraction procedure (15). Iodine analyses2 were performed by a modification of the method of Zak, Willard, Myers, and Boyle (16). The thyroxine-serum mixtures were subjected to zone electrophoresis on filter paper strips, using barbital buffer, pH 8.6, ionic strength 0.1, and a "reverse-flow" technique (15). This modification of the electrophoresis procedure avoided the inclusion of albumin-bound thyroxine in the alpha globulin zone.For measurement of the thyroxine-binding capacity of TBP, the quantity of thyroxine added to each serum was sufficient to effectively saturate the thyroxine-binding sites on TBP. Actual saturation of these sites is approached asymptotically (15). Analysis of data obtained with normal sera (10), however, had indicated that the amount of thyroxine associated with alpha globulin reaches an effective plateau when less than 60 per cent of t...

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Section: Discussionmentioning

confidence: 84%

Thyroxine-Binding by Serum Protein in Pregnancy and in the Newborn

Robbins¹,

Nelson²

1958

J. Clin. Invest.

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“…Skeletal x-ray provides the most useful test. Epiphyses at the knee and ankle usually appear during the seventh intrauterine month, and these centres should be present at birth (Dorff, 1936;Wilkins, 1962). X-ray of the wrist is helpful after the 3rd to 6th month of life.…”

Section: Discussionmentioning

confidence: 99%

Cretinism: Early diagnosis its relation to mental prognosis

Raiti¹,

Newns²

1971

Archives of Disease in Childhood

139

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“…It is difficult to see how this could happen unless the foetus can develop to the point where its own thyroid begins to secrete, without getting hormone from the mother. In the later stages of pregnancy thyroid hormone seems to be necessary for normal foetal development, at least in humans, since new-born infants with congenital aplasia of the thyroid show some of the signs of thyroid deficiency (Dorff, 1934).…”

Section: Discussionmentioning

confidence: 99%

The passage of thyroxine and triiodothyronine from mother to foetus in pregnant rabbits, with a note on the concentration of protein‐bound iodine in foetal serum

Myant¹

1958

The Journal of Physiology

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Recent evidence suggests that in rabbits the passage of exogenous thyroxine from mother to foetus is very slow during the early stages of pregnancy. Hall & Myant (1956) showed that the foetal:maternal serum concentration ratio (F: M ratio) does not exceed 0x02 at 24 hr after an intravenous injection of radioactive thyroxine into the mother, when the injection is given before the 19th day. Since the thyroid of a foetal rabbit does not begin to make thyroid hormone until the 20th day (Jost, Morel & Marois, 1949), this suggested that the early stages of foetal development take place in the presence of a concentration of thyroxine much lower than that in the mother's serum. However, several points were left in doubt.After the 18th day, the F:M ratio was not measured at intervals of more than 3 hr from the injection. Nor were any observations made on the passage of triiodothyronine across the placenta; therefore we did not exclude the possibility that the foetus gets a supply of triiodothyronine from the mother before its own thyroid begins to function. We also pointed out that the placenta might not be as impermeable to endogenous thyroid hormone, at physiological concentrations, as it is to exogenous thyroxine. Finally, we suggested that the walls of the maternal blood vessels in the placenta constitute the main barrier to the passage of thyroxine from mother to foetus, but the evidence for this was far from conclusive. This paper describes experiments bearing on each of these questions. A few observations on the concentration of protein-bound iodine in the serum of rabbit foetuses are also included.

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Sporadic Cretinism in One of Twins

Cited by 29 publications

References 11 publications

Thyroxine-Binding by Serum Protein in Pregnancy and in the Newborn

Thyroxine-Binding by Serum Protein in Pregnancy and in the Newborn

Cretinism: Early diagnosis its relation to mental prognosis

The passage of thyroxine and triiodothyronine from mother to foetus in pregnant rabbits, with a note on the concentration of protein‐bound iodine in foetal serum

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