Five-year follow-up for women with subclinical hypothyroidism in pregnancy.
BACKGROUND
Increasing numbers of women are being treated with l-thyroxine in pregnancy for mild thyroid dysfunction because of its association with impaired neuropsychological development in their offspring and other adverse obstetric outcomes. However, there are limited data to indicate whether treatment should be continued outside of pregnancy.


OBJECTIVE
We aimed to determine whether subclinical hypothyroidism and maternal hypothyroxinemia resolve postdelivery.


METHODS
A total of 523 pregnant healthy women with no known thyroid disorders were recruited during routine antenatal care and provided blood samples at 28 weeks of pregnancy and at a mean of 4.9 years postpregnancy.


METHODS
TSH, free T₄, free T₃, and thyroid peroxidase antibody levels were measured in serum taken in pregnancy and at follow-up.


RESULTS
Subclinical hypothyroidism in pregnancy (TSH >3 mIU/L) was present in 65 of 523 (12.4%) women. Of these, 49 (75.4%) women had normal thyroid function postpregnancy; 16 of 65 (24.6%) had persistent high TSH (TSH >4.5 mIU/L postpregnancy) with 3 women receiving l-thyroxine treatment. A total of 44 of 523 (8.4%) women had isolated maternal hypothyroxinemia in pregnancy (free T₄ <10th centile and TSH ≤3 mIU/L). Only 2 of 44 (4.5%) had TSH >4.5 mIU/L outside pregnancy. Of the women with subclinical hypothyroidism in pregnancy with antibody measurements available, those with thyroid peroxidase antibodies in pregnancy were more likely to have persistently elevated TSH or be receiving l-thyroxine replacement after pregnancy (6 of 7 [86%] vs 10 of 57 [18%], P < .001).


CONCLUSIONS
The majority of cases of subclinical hypothyroidism in pregnancy are transient, so treatment with l-thyroxine in these patients should be reviewed because it may not be warranted after pregnancy.
Department of Endocrinology, Royal Devon and Exeter Hospital, Exeter, EX2 5DW, United Kingdom. b.vaidya@exeter.ac.uk.
Beverley M
BM
Shields
Bridget A
BA
Knight
Anita V
AV
Hill
Andrew T
AT
Hattersley
Bijay
B
Vaidya
D000328:Adult; D001323:Autoantibodies / Q000032:analysis; D001324:Autoantigens; D015331:Cohort Studies; D016903:Drug Monitoring; D004739:England / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D020249:Hormone Replacement Therapy; D006801:Humans; D007037:Hypothyroidism / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology*; D007453:Iodide Peroxidase / Q000037:antagonists & inhibitors; D033862:Iron-Binding Proteins / Q000037:antagonists & inhibitors; D049590:Postpartum Period; D011247:Pregnancy; D011248:Pregnancy Complications / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology*; D015995:Prevalence; D012720:Severity of Illness Index; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood / Q000378:metabolism / Q000627:therapeutic use; D014284:Triiodothyronine / Q000097:blood / Q000378:metabolism
D001323:Autoantibodies; D001324:Autoantigens; D033862:Iron-Binding Proteins; D014284:Triiodothyronine; D013972:Thyrotropin; C056658:TPO protein, human; D007453:Iodide Peroxidase; D013974:Thyroxine