maternal cells settle in the fetus. There is abundant evidence indicating that the thyroid gland is one of the important organs where fetal microchimeric cells may become established.13 The consequences of fetal immune cells within the maternal thyroid gland remain an attractive explanation for the postpartum exacerbation of autoimmune thyroid diseases (AITD), but this influence is far from confirmed.
Consequences of thyroid autoantibodies. The first reports of anassociation between anincrease in early pregnancy loss andthe presence of thyroid autoimmunity came fromour studies more than 15 years ago.14 Since then, the observation has been confirmed in multiple independent studies. This
association, however, exists in the absence of a significant relationship with TSH,15 although women with thyroid autoantibodies (TAbs) to thyroid peroxidase (TPO) and thyoglobulin may have higher plasma TSH levels, within the normal range, reflective of subtle thyroid dysfunction. In contrast, TAbs may be merely reflective of a more general immune diathesis in the women. Although early studies found that levothyroxine (LT4) treatment did not prevent miscarriage in women with TAbs after in vitro fertilization,16 the same investigators recently reported successful prevention of pregnancy loss in euthyroid women using this approach.17 If confirmed, these data suggest that it may be appropriate to start treatment with LT4 at the time of pregnancy in order to reduce the risk of miscarriage and prematurity in euthyroid women with TAbs and suggest that a thyroid diathesis is responsible