Autoimmune hypothyroidism due to thyroid stimulation blocking antibodies (TSB-Ab) is uncommon. When occurring in pregnancy, this condition may be responsible for feto-neonatal complications as a result of both maternal hypothyroidism and trans-placental TSB-Ab transfer to the fetus.
Clinical case: September 2010: a 27 year-old woman was diagnosed with autoimmune severe hypothyroidism (TSH 325 mIU/l (n.v 0.44.0), FT4 1.54 pmol/l (n.v. 11.522.6), FT3 0.67 pmol/l (n.v. 3.78.3); TPOAb and TgAb positive). Levo-thyroxine (L-T4) treatment was started (100 μg/day) and euthyroidism achieved in November 2010 (TSH 0.34 mIU/l, FT4 18.6 pmol/l, FT3 7.0 pmol/l). In December 2010 pregnancy was ascertained (5 weeks) and thyroid function tests revealed lT4 dose inadequacy (TSH 13.9 mIU/l (trimester-specific n.v.: 0.032.3); FT4 10.3 pmol/l (trimester-specific n.v.: 11.9-21)). L-T4 dose was therefore increased (1300 μg/week) with prompt restoration of euthyroidism (January 2011, 8 weeks: TSH 0.16 mIU/l). Thyroid receptor antibodies (TRAb) at 10 weeks of gestation were found to be positive with high titer (>40 UI/l). TSH receptor bioassay revealed these antibodies to be only partially active (30%) in blocking TSH receptors. In the further follow-up L-T4 dose was progressively adjusted to maintain TSH and FT4 within the normal range for pregnancy. Both TRAb titer and Ig-activity proved consistently unchanged (at 20 and 30 weeks).
Fetal/neonatal data. Morphological US, umbilical flowmetry and fetal echo-cardiography were normal for gestational age at 20 and 30 weeks. Fetal thyroid volume and vascularization, bone maturation, and fetal mobility were normal as well, at 32 weeks of gestation. August 2011 (38 weeks): cesarean section delivery. Neonatal data: TSH 29.4, 25.9 e 4.4 μU/ml and FT4 22.0, 31.4 e 16.0 pm/l, at 12 and 36 h and at 3 weeks of post-natal life, respectively. TRAb >40 UI/l at 36 h. Thyroid US was normal.
Severe hypothyroidism in child-bearing age women should advice routinely TRAb bioassay.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology