Endocrine Abstracts

In euthyroid women normal pregnancy is associated with a rise in free thyroxine and fall in TSH levels attributable to high levels of hCG in the first trimester. In hypothyroid women free thyroxine tends to fall and TSH rises if the dose of thyroxine is not raised, due to further pregnancy - associated changes including a rapid rise in thyroxine-binding globulin and increased renal clearance and placental metabolism of thyroid hormone. Fetal thyroid development occurs by 12 weeks gestation and thyroid hormone secretion not till later. Organogenesis particularly of the nervous system is dependent on adequate thyroxine levels in the fetal circulation, implying transplacental transport of maternal thyroxine to the fetus. If this is inadequate potential impairment of various aspects of mental development ensues, best seen in areas of endemic iodine deficiency but also suggested in offspring of under or untreated hypothyroid women.

Since there is debate about how early appropriate changes in thyroxine doseage should be made we audited the practice in our recently established endocrine/antenatal clinic for the first 2½ years. 83 hypothyroid women were seen. The first visit to the joint clinic occurred after 12 weeks gestation in 50 women (60.2%), over the years of observation this appeared to increase (52.8%, 64% and 71.4%). Overall 9 woman were seen at 12 weeks (10.8%) and 19 women (22.8%) were seen before 12 weeks gestation. At the first visit 56 women (67.4%) had their thyroxine doseage increased. These findings prompt concern that possibly important adjustments in thyroxine doseage were delayed beyond an optimal stage in pregnancy in many hypothyroid women. We plan to pilot preconception advice and early assessment in selected primary care centres and in the longterm to monitor what, if any, the timing of thyroxine doseage adjustment has on the outcome of children born to these women.