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Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum

Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pre...

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Autores principales: Alameddine, Hind, Palani, Gurunanthan, Zekarias, Kidmealem
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265899/
http://dx.doi.org/10.1210/jendso/bvab048.1898
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author Alameddine, Hind
Palani, Gurunanthan
Zekarias, Kidmealem
author_facet Alameddine, Hind
Palani, Gurunanthan
Zekarias, Kidmealem
author_sort Alameddine, Hind
collection PubMed
description Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pregnant woman, attention should be focused on determining the etiology of the disorder and whether it warrants treatment. Here, we report a case of hyperemesis gravidarum patient presenting with significant elevation of thyroid hormones and a review on diagnosis and management of gestational transient thyrotoxicosis. A 33-year-old female, G4P3 at 8 weeks pregnant admitted for nausea and vomiting. Thyroid labs showed TSH < 0.01 (Reference: 0.4-4.0mU/L) and free T4 is 3.53 (Reference: 0.76-1.46ng/dl). Patient was discharged on antiemetics with a diagnosis of hyperemesis gravidarum. She was re-admitted at 9 weeks pregnant with ongoing nausea and vomiting. She had palpitations, fatigue and reported 15 pound weight loss in 2 weeks. Past medical history included thyroid hormone abnormality noted during pregnancies of 2011 and 2017. Physical exam was significant for tachycardia and diffusely enlarged thyroid gland. Repeat labs showed TSH <0.01, free T4 5.81, total T3 of 317 (Reference: 60-181ng/dl). Thyroid ultrasound showed multiple nodules. Considering significant elevation in free T4 and total T3; empiric therapy with propylthiouracil was recommended. Patient declined anti-thyroid therapy. TSI and TRH antibodies came back later as negative. Patient was treated with enteral feeding for hyperemesis gravidarum. Thyroid labs 3 weeks later improved; FT4 down to 1.63 and TT3 down to 250. Patient delivered healthy baby at 40 weeks of gestation. Although the differential diagnosis of thyrotoxicosis in pregnancy includes any cause that can be seen in a nonpregnant patient, the most likely causes for hyperthyroidism in pregnancy are gestational thyrotoxicosis (GTT) with or without hyperemesis gravidarum or Graves’ disease. GTT is described as an hCG-mediated hyperthyroidism that occurs in the first trimester of pregnancy; it is generally asymptomatic with mild biochemical hyperthyroidism. Distinguishing true overt hyperthyroidism from GTT in a setting of hyperemesis gravidarum is challenging. The absence of clinical signs of hyperthyroidism and negative thyroid antibodies supports the diagnosis of GTT. T3 tends to be disproportionately elevated more than T4 in patients with overt hyperthyroidism. HCG level has not been found to be useful in distinguishing between GTT and GD. Overt hyperthyroidism is treated using anti-thyroid drugs (ATD) whereas supportive therapy without ATD is the accepted standard of treatment of patients with hyperemesis gravidarum and GTT. More studies addressing the best management of these group of patients is needed.
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spelling pubmed-82658992021-07-09 Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum Alameddine, Hind Palani, Gurunanthan Zekarias, Kidmealem J Endocr Soc Thyroid Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pregnant woman, attention should be focused on determining the etiology of the disorder and whether it warrants treatment. Here, we report a case of hyperemesis gravidarum patient presenting with significant elevation of thyroid hormones and a review on diagnosis and management of gestational transient thyrotoxicosis. A 33-year-old female, G4P3 at 8 weeks pregnant admitted for nausea and vomiting. Thyroid labs showed TSH < 0.01 (Reference: 0.4-4.0mU/L) and free T4 is 3.53 (Reference: 0.76-1.46ng/dl). Patient was discharged on antiemetics with a diagnosis of hyperemesis gravidarum. She was re-admitted at 9 weeks pregnant with ongoing nausea and vomiting. She had palpitations, fatigue and reported 15 pound weight loss in 2 weeks. Past medical history included thyroid hormone abnormality noted during pregnancies of 2011 and 2017. Physical exam was significant for tachycardia and diffusely enlarged thyroid gland. Repeat labs showed TSH <0.01, free T4 5.81, total T3 of 317 (Reference: 60-181ng/dl). Thyroid ultrasound showed multiple nodules. Considering significant elevation in free T4 and total T3; empiric therapy with propylthiouracil was recommended. Patient declined anti-thyroid therapy. TSI and TRH antibodies came back later as negative. Patient was treated with enteral feeding for hyperemesis gravidarum. Thyroid labs 3 weeks later improved; FT4 down to 1.63 and TT3 down to 250. Patient delivered healthy baby at 40 weeks of gestation. Although the differential diagnosis of thyrotoxicosis in pregnancy includes any cause that can be seen in a nonpregnant patient, the most likely causes for hyperthyroidism in pregnancy are gestational thyrotoxicosis (GTT) with or without hyperemesis gravidarum or Graves’ disease. GTT is described as an hCG-mediated hyperthyroidism that occurs in the first trimester of pregnancy; it is generally asymptomatic with mild biochemical hyperthyroidism. Distinguishing true overt hyperthyroidism from GTT in a setting of hyperemesis gravidarum is challenging. The absence of clinical signs of hyperthyroidism and negative thyroid antibodies supports the diagnosis of GTT. T3 tends to be disproportionately elevated more than T4 in patients with overt hyperthyroidism. HCG level has not been found to be useful in distinguishing between GTT and GD. Overt hyperthyroidism is treated using anti-thyroid drugs (ATD) whereas supportive therapy without ATD is the accepted standard of treatment of patients with hyperemesis gravidarum and GTT. More studies addressing the best management of these group of patients is needed. Oxford University Press 2021-05-03 /pmc/articles/PMC8265899/ http://dx.doi.org/10.1210/jendso/bvab048.1898 Text en © The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Thyroid
Alameddine, Hind
Palani, Gurunanthan
Zekarias, Kidmealem
Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title_full Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title_fullStr Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title_full_unstemmed Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title_short Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
title_sort gestational thyrotoxicosis in a patient with hyperemesis gravidarum
topic Thyroid
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265899/
http://dx.doi.org/10.1210/jendso/bvab048.1898
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