Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2021) 73 AEP604 | DOI: 10.1530/endoabs.73.AEP604

1CHU Mohammed VI, Marrakech, Maroc, Endocrinologie, Metabolic Diseases and Nutrition, Marrakech, Morocco; 2CHU Mohammed VI, Marrakech, Maroc, Maternity Resuscitation, Marrakech, Morocco


Introduction

Hyperthyroidism during pregnancy can be caused by an hydatiform mole in its partial or total form. The biochemical particularities between hcg (human corionic gonadotropin) and Tsh (thyreo-stimulating hormone) in gestational trophoblastic disease can explain the thyrostimulating effect in it. We report a case of hyperthyroidism on molar pregnancy through an observation.

Observation

Patient of 27 years old, with a history of an intrauterine fetal death 5 years ago, admitted for incoercible vomiting on pregnancy estimated at 11 weeks with partial hydatiform mole. At the examination agitated patient without exophthalmia. She presented tachycardia at 118 beats per minute, fine tremor of the extremities, and no goiter. Laboratory results showed a stunt TSH at 0.01 mui/ml; T4l: 28.3 pmol/l, T3:7.9 pmol/l, HCG 540984 or +1.9 N. An obstetrical echography conclude on uterus increased in size, fetus in flattened death, placenta abnormally large with snowflake image reminiscent of a partial mole. Thyroid echography was normal. EKG: sinus tachycardia at 120 bpm. The rest of the balance sheet is without particularities, in particular the Ac anti RTS and TPO. The management consisted in the initiation of carbimazol 30 mg/day and propanolol 40 mg/d to obtain euthyroidism before uterine extraction. At day 4 we had improved symptoms and biological euthyroidism with T4L at 13 pmol/l after uterine evacuation.

Discussion

Clinical hyperthyroidism is a common complication of a hydatiform mole, in our case presented by incoercible vomiting and tachycardia. The structural homology between the TSH and HCG subunits and between their receptors gives HCG a thyroid-stimulating action. The presence of intrauterine fetal death could be attributed to the direct effects of thyroid hormones on the fetus. The treatment of hyperthyroidism induced by hydatiform mole is an uterine evacuation although in our case we first particularly used ATS and blockers.

Conclusion

The diagnosis of hyperthyroidism secondary to hydatiform mole is retained before a low or undetectable TSH, T4l elevated after eliminating transient hyperthyroidism from the large ratio to term, TRACK negativity and cervical ultrasound without hypervascularization. This is a resolutive table after uterine extraction.

Volume 73

European Congress of Endocrinology 2021

Online
22 May 2021 - 26 May 2021

European Society of Endocrinology 

Browse other volumes

Article tools

My recent searches

No recent searches.

My recently viewed abstracts