Hyperemesis Gravidarum and Thyroid: What Role for the Endocrinologist?

Special Article - Thyroid Gland

Annals Thyroid Res. 2019; 5(1): 174-177.

Hyperemesis Gravidarum and Thyroid: What Role for the Endocrinologist?

Brucker-Davis F¹, Rougier C1,2, Trastour C2, Panaïa-Ferrari P3, Hiéronimus S1*

¹Department of Endocrinology, University Hospital of Nice, France

²Department of Obstetrics, University Hospital of Nice, France

³Department of Biochemistry and Hormonology, University Hospital of Nice, France

*Corresponding author: Sylvie Hiéronimus, Centre Hospitalier Universitaire de Nice, Université Côte d’Azur, Hôpital l’Archet 2, CHU Nice, 151 route de Saint-Antoine 06200 Nice, France

Received: November 27, 2018; Accepted: January 11, 2019; Published: January 18, 2019


Objective: To characterize a population of women with Hyperemesis Gravidarum (HG) and abnormal thyroid tests.

Methods: We report 60 women with HG referred to a specialized clinic for assessment of abnormal thyroid tests early in pregnancy. They underwent thyroid ultrasound and thyroid tests (TSH, FT4, FT3, thyroid auto-antibodies) at each trimester when possible. Obstetrical and neonatal information were collected prospectively.

Results: 40% of women had a severe form of HG requiring hospitalization, 23.3% had a personal thyroid history (two Graves, six nodules, five hypothyroidisms). They were nine twin pregnancies. Ultrasound revealed 14.8% of increased thyroid volume and 26% of solid nodules. At first visit, 56 (93.3%) had a TSH<0.1mU/l. 11. 9% had at least one positive anti-thyroid antibody. 23.5% of TSH remained suppressed throughout pregnancy. HG coexisted in at least 10 cases with an underlying cause of hyperthyroidism, different from transient gestational hyperthyroidism: three active Graves’ disease, five autonomous thyroid nodules, and two over-treatment with levothyroxine.

Conclusion: Hyperthyroidism is quite common in HG, but the etiology is not univocal with the possibility of underlying thyroid condition. Given the stakes of maternal hyperthyroidism and the risks of unnecessary treatment on the fetus, a precise etiological diagnosis is required, ideally by an endocrinologist, with a follow up when necessary.

Keywords: Hyperemesis gravidarum; Pregnancy; Thyroid; Transient gestational hyperthyroidism; Graves’ disease; Toxic nodules


HG: Hyperemesis Gravidarum; FT4: Free T4; FT3: Free T3; TPO: Anti Thyroperoxidase; Tg: Thyroglobulin; PTU: Propylthiouracyl; WA: Weeks of Amenorrhea; ART: Assisted Reproductive Techniques


Hyperemesis Gravidarum (HG) is characterized by incoercible vomiting occurring in the first part of pregnancy and not related to other causes. Its diagnosis is clinical with additional criteria not universally accepted: dehydration, electrolyte imbalance, ketonuria and weight loss of 5% or more of body weight [1,2]. Its prevalence is estimated to 0.3 to 3% of pregnancies depending on diagnostic criteria and ethnic variation [3]. It is considered as a transient, self-limited condition [1]. However, there is a continuum between the usual mild “morning sickness” and the severe debilitating form, which requires hospitalization(s) and extends throughout pregnancy. HG is often downplayed by doctors, while the perception of women is often excruciating [4] and the true prognosis is unclear. Its physiopathology, obscure until recently, has improved with a better understanding of the role of tachykinins, such as placental endokinin or Substance P, which can cause nausea by activation of NK1R receptor in the area postrema of the brain [5].

HG is associated with gestational hyperthyroidism during the first trimester in up to 66% of cases according to Goodwin [6]. Because of its similarity of structure with TSH, hCG can bind to the TSH receptor on the thyroid, and stimulate thyroid secretion [7]. This is one of the adaptive mechanisms to the pregnancy state, allowing an increase of the thyroid hormone secretion to meet the needs of the woman and her embryo. This explains the “mirror image” between TSH and hCG concentrations at that stage of pregnancy. The prevalence of gestational hyperthyroidism increases with hCG concentrations [8], with a TSH usually suppressed when hCG is >200,000 and always when >400,000 [9]. Thus, gestational hyperthyroidism is more frequent in situations where hCG is higher (twin or molar pregnancies), or in case of molecular variants (such as reduced sialylation of hCG) [7], or exceptionally in case of mutation of TSH-receptor [10].

Currently, despite this knowledge, there is no consensus for thyroid imbalance screening in HG women, unless clinical signs of thyrotoxicosis are present [11]. We report here our experience stemming from a clinic for pregnant women with abnormal thyroid tests to discuss the role of endocrinologist in the care of this population.

Patients and Methods

Design of the study

We describe 60 women referred to our clinic dedicated to thyroid disease in pregnancy for HG and abnormal thyroid tests (TSH <0.1 mUI/l or on thyroid medication). First assessment usually occurred during the first trimester. We collected information on: personal and family medical history, obstetrical past, clinical presentation and treatment. Thyroid assessment included a hormonal and antithyroid antibody screening, and a thyroid ultrasound (see methods in reference 12). Thyroid tests were repeated at the second and third trimester, and in post-partum, when appropriate or possible. We recorded also the term at delivery, gender and weight of the newborn, mode of delivery.

As previously described [12], free T4 (FT4), free T3 (fT3), TSH, hCG, Anti-Thyroperoxidase (TPO) and anti-Thyroglobulin (Tg) antibodies were measured by chemiluminescence (ADVIA Centaur, Siemens Healthcare Diagnostics, France), and anti-TSH receptor antibodies by radio immunologic assay (Brahms Thermo Fisher, Germany). Reference ranges were established in our laboratory for fT4 and TSH during the first trimester of pregnancy (2.5 and 97.5 percentiles): fT4 11.3-19.23 pmol/l and TSH 0.1-3.23 mUI/l. The other reference ranges were provided by the manufacturer outside pregnancy: fT3 3.0-7.0 pmol/l; anti-TPO antibodies <60 UI/l, antithyroglobulin <60UI/l, anti TSH receptor<1.5UI/l.

Statistical analysis

Quantitative variables are expressed as medians and range. Qualitative variables are expressed as counts and percentages.


Clinical characteristics are shown on (Table 1). Half the women were nulliparous. Among the women with previous pregnancies, 77% reported a personal history of HG, and 61% a family history of HG. Nine women had twin pregnancies. Eight pregnancies (13%) were induced by medically assisted procreation techniques. The mean loss of weight was 10.6% (standard deviation 5.3%, max 22.9%). 24 (40%) women needed one or more hospitalizations for rehydration and conservative care. Hypokaliemia was common (31.6%), often requiring IV supplementation. 15 women had digestive complications (eight liver abnormalities and eight pancreatitis, including two symptomatic cases). A personal history of thyroid disease was found in 14 women (two Graves’ disease, five hypothyroidisms, including one after total thyroidectomy for thyroid cancer and one after lobectomy for nodule, one postpartum thyroiditis with transient hypothyroidism -untreated at first visit-, and six nodules known before pregnancy).