Cretinism during

Experimental Models of Iodine Deficiency and Cretinism during Development The Role of the Mother... 

Goh KO. Radioiodine treatment during pregnancy chromosomal aberrations and cretinism associated with maternal iodine-131 treatment. J Am Med Womens Assoc 1981 36(8) 262-5. 

In mild and moderate iodine deficiency, endemic cretinism is not observed. However, in a population there is a certain spread of iodine intake, and women at the lower end of the range of iodine intake may still be at risk of insufficient iodine intake during pregnancy. Deficiency of other nutrients and intake of goitrogens from food or from tobacco smoking may increase the risk. 

The demonstration of the prevention of cretinism with iodized oil in a double-blind controlled trial in Papua New Guinea established the causal role of iodine deficiency in cretinism by an effect on the developing fetal brain (Pharoah et al, 1971). Cretinism could not be prevented unless the iodized oil was given before pregnancy, as injection during pregnancy was ineffective (Table 62.2). 

Cretinism is a condition of severe physical and mental retardation due to iodine deficiency, and specifically due to deficiency of thyroid hormones during early pregnancy. This condition is irreversible, even after treatment with thyroid hormones or iodine soon after birth, but can be corrected if treatment with iodine starts prior to or early in gestation. 

Neurological cretinism is caused by severe iodine deficiency during pregnancy and is characterized by severe mental retardation and neurological and motor abnormalities it can be corrected by the administration of iodine before conception. The clinical features of cretinism and CH are different. 

The neurological abnormalities observed in neurological cretinism seem to be caused by maternal hypothyroxinemia during the first period of brain development, early in pregnancy. In iodine deficiency the maternal plasma T4 is low, even if plasma T3 and TSH are normal. 

The importance of the transfer of thyroid hormones from the mother to the fetus during the second half of pregnancy in humans has received increasing attention (Burrow et ai, 1994). Recently, it has become evident that maternal hypothyroxinemia results not only in the birth of children with neurological cretinism, but also in decreased mental and psychomotor development of the rest of the population without cretinism (Beichrodt and Born, 1994). 

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