Thyroid Dysfunction: Reproduction and Postpartum Thyroiditis

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Abstract
Thyroid function during pregnancy is characterized by changes in circulating thyroid hormone concentrations related to alterations in thyroxine binding globulin (TBG), human chorionic gonadotropin (hCG), and iodine status. The immunology of normal pregnancy shows a reduction in antibody titer during gestation and an increase in T helper-2 (TH2) immune responses. Thyroid dysfunction may cause menstrual disturbances in hyper- and hypothyroidism but less marked disturbances of sexual function in men. Fertility is reduced in hypo- and hyperthyroid females. Accumulating evidence suggests a strong association between the presence of thyroid antibodies and fetal loss, although the data relating to recurrent abortion are not so convincing. Asymptomatic maternal gestational hypothyroidism may occur in up to 2.5% of women; studies have shown a significant impact of this condition in causing a decrease of child IQ, suggesting that screening for maternal hypothyroidism with intervention may be justified. Postpartum thyroid disease occurs in 5 to 9% of women and thyroid dysfunction postpartum is seen in 50% of thyroid peroxidase antibody positive (TPO Ab+ve) women. There is a significant rate of hypothyroidism in long-term follow-up of women who have transient postpartum thyroid dysfunction.

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