![]() |
JOURNAL TOOLS |
Publishing options |
eTOC |
To subscribe |
Submit an article |
Recommend to your librarian |
ARTICLE TOOLS |
Reprints |
Permissions |
Share |


YOUR ACCOUNT
YOUR ORDERS
SHOPPING BASKET
Items: 0
Total amount: € 0,00
HOW TO ORDER
YOUR SUBSCRIPTIONS
YOUR ARTICLES
YOUR EBOOKS
COUPON
ACCESSIBILITY
REVIEWS
Minerva Endocrinologica 2005 June;30(2):71-88
Copyright © 2005 EDIZIONI MINERVA MEDICA
language: English
Thyroid disease in pregnancy and childhood
Lazarus J. H.
The subject of thyroid disease in pregnancy is receiving increasing attention from many scientific disciplines. Thyroid function in pregnancy is characterised by a T4 surge at 12 weeks declining thereafter. Serum thyroid hormone concentrations fall in the second half of pregnancy but there are few data on normal reference ranges. Fetal brain development depends on T4 transport into the fetus which in turn depends on sufficient maternal iodine supply. There is current concern that adequate iodisation is not present in large parts of Europe. There is increasing evidence that thyroid autoimmunity is associated with fetal loss but the mechanism is unclear and therapy requires carefully conducted studies. While hyperthyroidism in pregnancy is uncommon, effects on both mother and child are critical if untreated. The use of propylthiouracil is recommended together with measurement of TSH receptor antibodies at 36 weeks gestation. Women receiving thyroxine therapy for hypo-thyroidism or as suppressive therapy should have their dose increased by up to 50% during pregnancy. There are now substantial data to show deleterious effects on child IQ resulting from low maternal T4 (or high TSH) during gestation. Major advances in molecular biology have contributed to elucidation of many genetic causes of congenital hypothyroidism. However, the aetiology of the majority of cases is still unclear and further research is required. The presence of TPO antibodies in about 10% of pregnant women in early gestation is a predictor of an increased incidence of subclinical hypothyroidism during pregnancy and also of postpartum thyroid dysfunction. The latter condition occurs in 5-9% of women and 25-30% progress to permanent hypothyroidism. This review suggests that screening for thyroid function in early pregnancy and levothyroxine intervention therapy for maternal subclinical hypothyroidism should be considered but evidence is awaited. Screening for both thyroid dysfunction and thyroid antibodies ideally at a preconception clinic but certainly in early gestation is recommended.