The thyroid and pregnancy - fertility, management and physiological changes

A McGregor

Department of Medicine, GKT School of Medicine of KCL, LONDON

Endocrine Nurses Training Course 9-11 September 2004
Wills Hall, Stoke Bishop, Bristol, BS9 1AE

Normal thyroid function both in the non-pregnant and pregnant state requires adequate dietary iodine intake to ensure the necessary production of thyroid hormones. In pregnancy, at least during the first trimester and therefore prior to the development and functioning of the foetal hypothalamic-pituitary-thyroid axis; foetal development and particularly that of the nervous system is critically dependent on the passage of maternal thyroxine (T4) across the placenta and the local monodeiodination of maternal T4 to triiodothyronine (T3). Abnormal thyroid function (hyper- or hypo- thyroidism, autoimmune thyroid disease (AITD) or iodine deficiency) may not only impact on the health of the pregnant mother and the developing foetus but may also compromise the ability of an otherwise healthy young woman of re-productive age to become pregnant.

Infertility (an inability to conceive after 12months of regular intercourse without contraception) occurs in about 12% of the female population capable of becoming pregnant. Hypothyroidism undoubtedly leads to an interference in the menstrual cycle and to ovulatory dysfunction (through a number of mechanisms) and thus to infertility. In contrast, whilst there may be changes in the menstrual cycle in women who are hyperthyroid; most remain ovulatory. There is an increasing recognition that the presence of autoimmune thyroid disease (detectable thyroid auto- antibodies,with or without significant alterations in thyroid function ) may itself be associated with an increased risk of infertility, with endometriosis being found more commonly in infertile women with AITD, as compared with infertile women without AITD.

Assuming the successful achievement of pregnancy in women with normal thyroid function, a major series of physiological adjustments occur, which allow the mother to respond to the increased demands of the foetus for iodine and thyroid hormone. During pregnancy an increased loss of iodine due to an increase in renal iodide clearance requires an increase in thyroid gland uptake of iodide of up to 60%. This increased requirement and the increasing transfer of iodide from the maternal circulation to the foetus, clearly requires adequate dietary iodine intake in pregnancy. The major increase in oestrogen production during pregnancy produces a marked increase in thyroxine- binding globulin (TBG) concentration which allows a marked increase in hormone binding capacity and therefore a transient decrease in free thyroid hormone levels to stimulate a small increase in TSH (within the normal range). This change in free thyroid hormone levels is off set by a compensatory increase in thyroid hormone secretion, in the first trimester of pregnancy, when increased levels of human chorionic gonadotropin (hCG) lead to an increase in free T4 concentrations. In women on T4 replacement for previously diagnosed hypothyroidism; the inability of their own thyroid gland (because of its destruction) to increase iodide uptake or respond to hCG, may predispose to a period of maternal hypothyroxinaemia, which may have consequences for normal foetal nervous system development, unless T4 replacement is increased to an appropriate dose to compensate.

The opinions expressed in this paper are those of the speaker and do not necessarily reflect the views of the Society