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3,5,3 - Triiodothyronine maternal

In Papua New Guinea, Pharoah and Connolly (1987) have described varying scenarios ranging from stillbirths to cretinism, and less severe neurological defects of motor and cognitive performance. These effects could be correlated with the level of maternal thyroxine (T4), but not with maternal triiodothyronine (T3), indicating the importance of maternal T4 to the fetus. [Pg.600]

For the purposes of our study, the neuro-intellectual and behavioral outcome of all the ID and IS children was related to the thyroid function of their mothers over the first half of gestation. Average values of maternal T3, T4, free triiodothyronine (FT3), free thyroxine (FT4),TSH and TBG saturation by T4 at 8, 13 and 20 weeks of gestation in both the ID area ADHD+ and ADHD— subgroups,... [Pg.657]

Figure 88.2 The possible pathway of maternal-fetal TH metabolism influenoed by excess iodine. Abbreviations T4, thyroxine T3, triiodothyronine T2, 3,3 -L-diiodothyronine rl3, reverse triiodothyronine D1, type 1 iodothyronine deiodinase D2, type 2 iodothyronine deiodinase D3, type 3 iodothyronine deiodinase. Figure 88.2 The possible pathway of maternal-fetal TH metabolism influenoed by excess iodine. Abbreviations T4, thyroxine T3, triiodothyronine T2, 3,3 -L-diiodothyronine rl3, reverse triiodothyronine D1, type 1 iodothyronine deiodinase D2, type 2 iodothyronine deiodinase D3, type 3 iodothyronine deiodinase.
Some research indicates (Calvo et ai, 2002 Morreale de Escobar et ai, 1991, 2004) that human fetuses acquire the ability to synthesize THs at 10—12 weeks of gestation. In the second and third trimester, the fetus can potentially derive TH both from its own thyroid and the thyroid of the mother. Prior to 12 weeks gestation, the mother is the sole source of TH for the developing fetus. Current evidence indicates that there is substantial transfer of maternal TH across the placenta, and fetal TH exists in first trimester embryonic units (Contempre et ai, 1993). The mother provides small amounts ofT4 throughout the pregnancy. The main active TH, triiodothyronine (T3), is converted from T4 and the concentration is strictly regulated by a complex system. After birth, the neonate produces TH independendy. [Pg.1047]

Dussault JH, Row VV, Lickrish G, Volp6 R, Studies of serum triiodothyronine concentration in maternal and cord blood Transfer of triiodothyronine across human placenta. J Clin Endocrinol 29 595 (1969)... [Pg.200]

The first 3 cases (serial nos 604, 638, 515) in the table had hormonal profiles entirely consistent with severe hypothyroidism although these women did not exhibit the clinical features of hypothyroidism In all three cases the pregnancy outcome was a stillblrth/early neonatal death In the succeeding 3 cases (serial nos 568, 245, 430) the maternal total and free thyroxine values were low but triiodothyronine values were within the normal range In one of these the outcome was a stillbirth/early neonatal death and one child has a hearing/speech defect but no other abnormality and, by our definition, cannot be labelled as an endemic cretin ... [Pg.346]

Another case (serial no 398) is of particular interest in that the child exhibits the clinical features of cretinism The maternal thyroxine and TSH values were abnormal and consistent with hypothyroidism but the triiodothyronine values were within the normal... [Pg.346]

There is a spectrum of Impairment ranging from death through clinical endemic cretinism and subclinical deficits of motor and cognitive performance, to normality. This spectrum of effects appears to be associated with maternal thyroxine during pregnancy. No association with maternal triiodothyronine was found. [Pg.351]


See other pages where 3,5,3 - Triiodothyronine maternal is mentioned: [Pg.42]    [Pg.321]    [Pg.93]    [Pg.1095]    [Pg.477]    [Pg.608]    [Pg.655]    [Pg.676]    [Pg.860]    [Pg.860]    [Pg.159]    [Pg.185]    [Pg.209]    [Pg.177]    [Pg.313]   
See also in sourсe #XX -- [ Pg.34 , Pg.251 , Pg.256 , Pg.341 , Pg.343 ]




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