Thyroid-pituitary function in eight anencephalic infants

Grasso, Sebastiano; Mazzone, D; Pezzino, V.; Vigo, R. Carmona; Vigneri, Riccardo

doi:10.1530/acta.0.0930396

Cited by 15 publications

(8 citation statements)

References 14 publications

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“…By contrast, hypothalamic factors do not appear necessary for thyrotrophic and lactotrophic pituitary cell development [Leroyer-Alizon et al, 1980;Begeot et al, 19841. Other than a few thyroid dysplasias (Table IX), the thyroids of our AN sample were normal. Other studies have found that AN pituitary thyroid-secreting hormone (TSH)-secreting cells and the thyroid gland develop normally in the absence of the hypothalamus and are able to function if adequately stimulated [Grasso et al, 1980;Leroyer-Alizon et al, 1980;Cavallo et al, 198 I]. Interestingly, extrahypothalamic brain thyroid-releasing hormone (TRH) known to be independent of the hypothalamus and synthesized in situ [Jackson and Reichlin, 19771, has been demonstrated in a cell line from the sera cerebrovasculosa of an AN fetus [Ishikawa et al, 19761. One of the principal features of AN is adrenal hypoplasia.…”

Section: Malformations In Other Organ Systemsmentioning

confidence: 99%

Studies in neural tube defects II. Pathologic findings in a prospectively collected series of anencephalics

Melnick

Myrianthopoulos

1987

Am. J. Med. Genet.

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This report presents the pathologic anatomy of a prospectively collected series of 36 anencephalic infants. This series provides an opportunity to investigate the epidemiology of organ system pathology in anencephaly (AN) as well as other facets of its natural history. AN infants had a mean gestational age 2.5 weeks younger than normal controls, though birthweight was normal for gestational age. Nearly 1/3 of the liveborn infants with AN died within 15 minutes, 2/3 within 3 hours; 3 AN infants survived to 48 hours. Details and discussions of the pathologic findings and their physiologic significance are presented. Regarding those AN infants who received detailed neurologic examinations, correlations are made between the brain pathology and neurologic function prior to death.

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Section: Malformations In Other Organ Systemsmentioning

confidence: 99%

Studies in neural tube defects II. Pathologic findings in a prospectively collected series of anencephalics

Melnick

Myrianthopoulos

1987

Am. J. Med. Genet.

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“…Foetal TSH was positively correlated with foetal fT 4 (r ¼ 0.896, P , 0.001) 27 . Foetal TSH has a higher bioactivity than maternal TSH, and its synthesis is not under hypothalamic control, as shown by the high cord serum TSH concentration found in anencephalic foetuses 28,29 . 31 and are believed to mediate cyclic AMP-independent biological effects of TSH that might be acting as a growth factor for brain development 32 .…”

Section: Introductionmentioning

confidence: 99%

Iodine deficiency and brain development in the first half of pregnancy

Escobar

Obregón

Rey

2007

Public Health Nutr.

277

213

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An inadequate supply of iodine during gestation results in damage to the foetal brain that is irreversible by mid-gestation unless timely interventions can correct the accompanying maternal hypothyroxinemia. Even mild to moderate maternal hypothyroxinemia may result in suboptimal neurodevelopment. This review mainly focuses on iodine and thyroid hormone economy up to mid-gestation, a period during which the mother is the only source for the developing brain of the foetus. The cerebral cortex of the foetus depends on maternal thyroxine (T 4 ) for the production of the 3 0 ,3,5-tri-iodothyronine (T 3 ) for nuclear receptor-binding and biological effectiveness. Maternal hypothyroxinemia early in pregnancy is potentially damaging for foetal brain development. Direct evidence has been obtained from experiments on animals: even a relatively mild and transient hypothyroxinemia during corticogenesis, which takes place mostly before mid-gestation in humans, affects the migration of radial neurons, which settle permanently in heterotopic locations within the cortex and hippocampus. Behavioural defects have also been detected. The conceptus imposes important early changes on maternal thyroid hormone economy that practically doubles the amount of T 4 secreted something that requires a concordant increase in the availability of iodine, from 150 to 250-300 mg I day 21 . Women who are unable to increase their production of T 4 early in pregnancy constitute a population at risk for having children with neurological disabilities. As a mild to moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia, the birth of many children with learning disabilities may be prevented by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible, in order to ensure that their requirements for iodine are met.

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“…There is not a lack of TRH receptors in the pituitaries of the fetal or newborn rats since they have a prompt rise in plasma TSH in re sponse to exogenous TRH [26]. Anencephalic human in fants also appear to have normal pituitary-thyroid func tion, in support of the rat data [27][28][29], TRH is produced in many cells in the body other than the PVN. However, whatever TRH may be in the systemic circulation does not reach the thyrotrophs in sufficient concentration to stimulate TSH secretion, nor does hypothalamic or other central nervous system TRH outside the PVN have any significant effect on TSH secretion [30][31][32],…”

Section: Discussionmentioning

confidence: 96%

Evidence that the Major Physiological Role of TRH in the Hypothalamic Paraventricular Nuclei May Be to Regulate the Set-Point for Thyroid Hormone Negative Feedback on the Pituitary Thyrotroph

et al. 1993

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If a primary physiologic action of TRH is to regulate the set-point for negative feedback, a sudden drop in plasma thyroid hormone concentration should stimulate the same rate of in vivo increase in TSH secretion from normal and TRH-deprived thyrotrophs. To test this hypothesis, 3 experiments were performed in which young adult female rats were divided into 3 groups of 6-10 rats each: intact controls, hypothalamic paraventricular nuclei ablation (PVN) and sham-ablated (Sham). Sham and PVN rats were thyroparathyroidectomized 2-4 weeks after brain lesions and serial blood samples taken in all groups at frequent intervals from 0 to 58 days post-thyroidectomy. Plasma TSH was significantly higher than in intact controls by 3 days post-thyroidectomy in both the Sham and PVN groups (p < 0.05). At 14 days PVN plasma TSH was 4 × higher and at 30 days 8 × higher than in intact controls and remained consistently at 50% of that of the Sham group. There was no statistical difference between PVN and Sham in the rate of increase in TSH. Plasma T4 was 40% lower in PVN than in Sham at the time of thyroidectomy and became undetectable in both by day 3. The prompt parallel rate of rise of plasma TSH in Sham and PVN groups following thyroidectomy indicates that a primary physiologic action of TRH in the thyrotroph is to control the set-point for thyroid hormone negative feedback on TSH secretion. However, this does not appear to be the sole mechanism by which TRH influences TSH secretion since even by 2 months post-thyroidectomy, when plasma TSH concentration had plateaued, plasma TSH was 50% lower in PVN than in Sham rats.

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Thyroid-pituitary function in eight anencephalic infants

Cited by 15 publications

References 14 publications

Studies in neural tube defects II. Pathologic findings in a prospectively collected series of anencephalics

Studies in neural tube defects II. Pathologic findings in a prospectively collected series of anencephalics

Iodine deficiency and brain development in the first half of pregnancy

Evidence that the Major Physiological Role of TRH in the Hypothalamic Paraventricular Nuclei May Be to Regulate the Set-Point for Thyroid Hormone Negative Feedback on the Pituitary Thyrotroph

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