A longitudinal study of thyroid autoantibodies in pregnancy — ASN Events
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A longitudinal study of thyroid autoantibodies in pregnancy (#72)

Elif I Ekinci 1 2 3 , Wei-Ling Chiu* 4 , Ken Sikaris 5 , Zhong X Lu 6 7 , Intissar Bittar 8 , Que Lam 9 , Nick Crinis 8 , Christine A Houlihan 10 11
  1. MBBS, FRACP, PhD; Department of Endocrinology, Austin Health, Melbourne
  2. Department of Medicine, University of Melbourne, Melbourne
  3. Menzies School of Health Research, Darwin
  4. MBChB, BSci; Department of Medicine, Eastern Health, Melbourne
  5. MBBS, FRCPA; Department of Chemical Pathology, Melbourne Pathology, Melbourne
  6. MBBS, FRCPA, PhD; Department of Chemical Pathology, Melbourne Pathology, Melbourne
  7. Department of Medicine, Monash University, Melbourne
  8. BSci; Department of Biochemistry, Austin Health, Melbourne
  9. MBBS, FRCPA; Department of Biochemistry, Austin Health, Melbourne
  10. MBBS, FRACP, MD; Department of Endocrinology, Austin Health, Melbourne
  11. Mercy Hospital for Women, Melbourne

*Equal first author contribution, presenting author

Background: Thyroid-peroxidase (TPOAb) and anti-thyroglobulin (TGAb) antibodies are frequently measured during investigation of thyroid dysfunction in pregnancy, with no specific recommendation on timing of testing, despite recognition of decreasing titers throughout gestation 1, 2 .  We thus aimed to assess the longitudinal changes of TPOAb and TGAb in a cohort of healthy women throughout gestation and post-partum.

Methods: Healthy women were recruited into a longitudinal study of thyroid function during pregnancy.  Serum TPOAb, TGAb, TSH and free T4 (fT4) were measured at trimester-1 (T1), trimester-2 (T2), trimester-3 (T3) and post-partum (PP) using Roche assays.  Post-partum thyroid dysfunction (PPTD) was determined as TSH outside normal non-pregnant interval (0.5-5.0 mU/L). 

Results: Data were available for T1: 142 women at 11.9±0.2 (mean±SE, weeks); T2: 96 at 24.4±0.3; T3: 80 at 35.9±0.2; PP: 86 at 12.9±0.4.  At T1, 13 (9%) and 15 (11%) individuals had positive TPOAb and TGAb, respectively.  Compared to those with negative TPOAb at T1, women with positive TPOAb had higher TSH at T1 (1.60 versus 0.71 mU/L, p=0.01), and higher fT4 at PP (21.3 versus 15.7 mmol/L, p=0.002).  Of those with positive TPOAb at T1, 33% (3/9) at T2 and 43% (3/7) at T3 remained positive, and all (9/9) were positive again at PP (χ2, p<0.001).  Similarly, of those with positive TGAb at T1, 27% (3/11) and 33% (3/9) remained positive at T2 and T3, respectively, and 92% (11/12) were positive again at PP (χ2, p<0.001).  Of the 14 women with PPTD, 23% (3/13) and 54% (7/13) had positive TPOAb and TGAb, respectively, at T1. 

Conclusions: As the majority of pregnant women lose their TPOAb and TGAb positivity after T1, testing for these antibodies should occur at T1 or post-partum; a negative thyroid autoantibody result at T2 or T3 does not exclude autoimmune thyroid disease, and is thus of limited value.   

  1. Glinoer D RM, Grün JP, Kinthaert J. Risk of subclinical hypothyroidism in pregnant women with asymptomatic autoimmune thyroid disorders. J Clin Endocrinol Metab. 1994;79(1):197-204.
  2. Smyth PP, Wijeyaratne CN, Kaluarachi WN, Smith DF, Premawardhana LD, Parkes AB, et al. Sequential studies on thyroid antibodies during pregnancy. Thyroid. 2005 May;15(5):474-7.
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