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Endocrine Abstracts (2016) 44 OC6.2 | DOI: 10.1530/endoabs.44.OC6.2

SFEBES2016 Oral Communications Pregnancy and Reproductive Health (6 abstracts)

The thyroidal response to hCG stimulation is impaired in women with subclinical hypothyroidism and is influenced by BMI, fetal sex and parity

Tim Korevaar 1, , Layal Chaker 1, , Theo Visser 1, & Robin Peeters 1,


1Erasmus University Medical Center, Rotterdam, The Netherlands; 2Rotterdam Thyroid Center, Rotterdam, The Netherlands.


Introduction: Although hCG is an important determinant of gestational thyroid function, it is unknown to what extent hCG is a risk factor for thyroid disease and we also lack knowledge on which characteristics influence the thyroidal response to hCG stimulation.

Methods: hCG, TSH, FT4 and TPOAbs were measured in 5435 pregnant women (<18 weeks) in a prospective cohort. Subclinical disease entities were defined according to P2.5-P97.5 in TPOAb negative women. We investigated the association of hCG with the risk of thyroid disease, and the association of subject characteristics with thyroidal hCG response by using multivariable logistic and linear regression models adjusting for age, smoking, BMI, parity, ethnicity, education and fetal sex.

Results: hCG was not associated with subclinical hypothyroidism (P=0.29). As compared to euthyroid women, the association of hCG with FT4 was strongly attenuated in women with subclinical hypothyroidism (P=0.047). Higher hCG was associated with a lower risk of hypothyroxinemia (P<0.0001) and a higher risk of subclinical as well as overt hyperthyroidism (both P<0.0001). As compared to euthyroid women, the association of hCG with TSH was similar in women with hypothyroxinemia, and the association of hCG with FT4 was similar in women with subclinical hyperthyroidism (P=0.72 and P=0.22, respectively). In the whole population, higher BMI was associated with a lower thyroidal response to hCG stimulation in a dose-dependent manner (P=0.068 for FT4 and 0.003 for TSH). Also, male fetal sex and high maternal parity (>2) were associated with a lower thyroidal response to hCG stimulation (P=0.0006 & 0.0064; and P=0.036 & 0.019 for FT4 and TSH, respectively). Iodine status, smoking and maternal age were not associated with differences in the thyroidal response to hCG stimulation. All results remained similar after exclusion of TPOAb positive women.

Conclusion: Women with subclinical hypothyroidism exhibit a thyroidal hCG response that fits with a decreased thyroid functional capacity. In contrast to subclinical hypothyroidism, hCG was an important determinants of other disease entities. In the whole population, BMI, male fetal sex and a high parity are associated with a lower thyroidal response to hCG stimulation.

Volume 44

Society for Endocrinology BES 2016

Brighton, UK
07 Nov 2016 - 09 Nov 2016

Society for Endocrinology 

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