Endemic Goiter in Western New Guinea. II. Clinical Picture, Incidence and Pathogenesis of Endemic Cretinism

Choufoer, J. C.; Hijn, M. Van; Querido, A

doi:10.1210/jcem-25-3-385

Cited by 84 publications

(31 citation statements)

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“…This would explain the greater severity of the CNS damage caused by iodine deficiency. Thus, the important role of maternal thyroid function (24,25) has been accepted, especially by investigators familiar with endemias where neurological cretins are born: maternal, followed by fetal, hypothyroxinemia, is now considered the major causative factor of their early CNS lesions (2,7,(11)(12)(13)(26)(27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

“…It would be more convincing if it were shown that hypothyroxinemia caused by iodine deficiency during pregnancy actually resulted in alterations of brain morphology, or function, during a period of brain development corresponding to the first half of pregnancy in women. Obtaining such experimental evidence has been elusive for years (24,25), possibly because important phases of human fetal brain development occur after birth in the rat, when compensatory mechanisms mitigate T3 deficiency during the postnatal brain T3 surge despite the low iodine intake (30)(31)(32). For this reason it appeared important to study the brain of iodine-deficient fetuses, which is markedly T3 deficient, whereas the brain of the suckling pup is not.…”

Section: Introductionmentioning

confidence: 99%

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Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

106

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The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

106

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“…In the present context, it is important to realize that iodine-deficient women are hypothyroxinemic, but they are not clinically hypothyroid (9,12), because their circulating 3,5,3′-triiodothyronine (T3) is normal or even slightly elevated and sufficient for euthyroidism of most tissues and organs. TSH rarely increases above normal in these women (24,25).…”

mentioning

confidence: 99%

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Ausó²,

et al. 2003

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“…The most extensive available data on thyroid function during pregnancy in populations with an I intake below 25 µg/d are from New Guinea (Choufoer et al 1965;Pharoah et al 1984) and the Democratic Republic of Congo (RDC; former Zaire; Thilly et al 1978;Delange et al 1982).…”

Section: Thyroid Function In the Mothersmentioning

confidence: 99%

The role of iodine in brain development

Delange¹

2000

Proc. Nutr. Soc.

163

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I is required for the synthesis of thyroid hormones. These hormones, in turn, are required for brain development, which occurs during fetal and early postnatal life. The present paper reviews the impact of I deficiency (1) on thyroid function during pregnancy and in the neonate, and (2) on the intellectual development of infants and children. All extents of I deficiency (based on I intake (μg/d); mild 50–99, moderate 20–49, severe > 20) affect the thyroid function of the mother and neonate, and the mental development of the child. The damage increases with the extent of the deficiency, with overt endemic cretinism as the severest consequence. This syndrome combines irreversible mental retardation, neurological damage and thyroid failure. Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Se deficiency superimposed on I deficiency partly prevents the neurological damage, but precipitates severe hypothyroidism in cretins. I deficiency results in a global loss of 10–15 intellectual quotient points at a population level, and constitutes the world’s greatest single cause of preventable brain damage and mental retardation.

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Endemic Goiter in Western New Guinea. II. Clinical Picture, Incidence and Pathogenesis of Endemic Cretinism

Cited by 84 publications

References 0 publications

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

The role of iodine in brain development

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