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Letter to the Editor
2021
:16;
3
doi:
10.25259/GJMPBU_1_2021

Gestational Transient Thyrotoxicosis Associated with Hyperemesis Gravidarum

Department of General Medicine, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
Department of Pediatrics, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
Department of Obstetrics and Gynaecology, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka, India
Corresponding author: H. S. Kiran, Department of General Medicine, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysore, Karnataka, India. drhskiran@gmail.com
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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Kiran HS, Rashmi N, Rajani HS, Nandish M. Gestational Transient Thyrotoxicosis Associated with Hyperemesis Gravidarum. Glob J Med Pharm Biomed Update 2021;16:3.

Dear Sir,

A 28-year-old primigravida presented with history of amenorrhea for 2 months; complaints of nausea and vomiting since 1 week - aggravated since 1 day with weight loss of 3 kg. She was diagnosed to have hyperemesis gravidarum. The case was referred to General Medicine in view of altered thyroid profile. She did not have any symptoms of thyroid disorders at present or in the past and was apparently healthy thus far. There were no clınıcal sıgns of hyperthyroidism (no tachycardia, no eye signs, no goiter, etc.). Pulse rate was 86 bpm; Blood pressure was 100/60 mm Hg; she was afebrile and Systemic examination was unremarkable. Complete hemogram, random blood sugar, renal function test, liver function test and Urine routine examination - within normal limits; ketone bodies present in urine. USG was unremarkable; consistent with 2 months of gestation with single intra-uterine pregnancy. Her thyroid profile was consistent with thyrotoxicosis (Free triiodothyronine FT3 - 3.99 (2.3-4.2 pg/ml), Free thyroxine FT4 – 2.77 (0.89-1.76 ng/ml), Serum thyroid stimulating hormone – 0.008 (0.27-4.2 µIU/ml), Anti thyroid peroxide (TPOAb) – 7.80 (0-34 IU/ml) – Negative, TRAb (TSH Receptor Antibody) assay – Negative). Ultrasound of thyroid was normal, and radioisotope scan of thyroid was not considered in view of pregnancy. With a diagnosis of gestational transient thyrotoxicosis associated with hyperemesis gravidarum,[1] intravenous fluids and antiemetics were given and discharged with advice to get a thyroid profile in out patients department after 1 month which normalized.

Goldman et al use a broad term “transient nonimmune hyperthyroidism of early pregnancy” since there are many causes such as twin/multiple pregnancies, mutation in the TSH receptor, hyperplacentosis, hyperreactio luteinalis, hydatidiform mole, and choriocarcinoma, though the entity associated with hyperemesis gravidarum is the most common one.[2] Goldman and Mestman call it “transient thyrotoxicosis of hyperemesis gravidarum.”[2] Goldman and Mestman define this entity as follows: “Hyperthyroidism diagnosed for the first time in early pregnancy,transient, without evidence of thyroid autoimmunity, lack of physical findings consistent with Graves’ disease, resolving spontaneously by the end of the first or early second trimester of pregnancy.”[2]

The clinical challenge is to differentiate this from Graves’ disease. Investigations usually reveal low or undetectable serum TSH associated with elevated serum FT4 and negative tests for autoimmunity (TPO and TRAb).[2]

With the increase in human chorionic gonadotropin levels during the first trimester of pregnancy, there is a concomitant reciprocal decrease in TSH that continues into the mid-trimester of pregnancy.[2,3] hCG levels being elevated, there is a weak binding of hCG with TSH receptors resulting in this phenomenon.[3] This may be associated with hyperemesis gravidarum.[3] Thyrotoxicosis has been attributed to the thyrotropic action/thyroid-stimulating activity of hCG (with either high levels of hCG or hCG molecule variant with high biological activity).[2] However, serum hCG levels are not used as a diagnostic marker, except in hydatidiform mole and choriocarcinoma.[2] Ultrasound should be done to exclude other etiologies such as multiple pregnancies and trophoblastic disease.[2] Antithyroid drugs are not indicated in this condition; Patients may be treated with only i.v.fluids and symptomatic supportive treatment.[2,3] There is no effect on obstetrical outcome while some studies have indicated lower birth weight of the baby.[2,4]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

  1. . Transient hyperthyroidism of hyperemesis gravidarum (a sheep in wolf's clothing) J Am Board Fam Pract. 2000;13:35-8.
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  2. , . Transient non-autoimmune hyperthyroidism of early pregnancy. J Thyroid Res. 2011;2011:142413.
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  3. , , . Thyroid gland physiology and testing In: Harrison's Principles of Internal Medicine (20th ed). New Delhi: Mc Graw Hill Education; . p. 2694.
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  4. , , , , , , et al. The effects of gestational transient thyrotoxicosis on the perinatal outcomes: A case-control study. Arch Gynecol Obstet. 2017;295:87-93.
    [CrossRef] [PubMed] [Google Scholar]

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