DIFFERENTIATING TRANSIENT GESTATIONAL THYROTOXICOSIS Thyroid Function Tests and Pregnancy: AUTHOR FIRST, MD, AUTHOR SECOND MD and LAST AUTHOR MD Department of Medicine. Jersey Shore University Medical Center, Neptune NJ LEARNING OBJECTVES LABORATORY DATA (Reference 3) 10 Weeks 14 Weeks HCG (mIU/mL) 99,308 TSH (0.45-4.5 uU/mL) <0.005 <0.004 Total T4 (4.5-12 ug/dL) 17.5 Free T4 (0.93-1.71 ng/dL) 1.32 Thyroid Stimulating Immunoglobulin (TSI: 0-129%) 112% Thyroid Peroxidase Ab (0-34 IU/mL) <10 Discuss the impact of normal pregnancy on thyroid function tests (TFTs). Distinguish transient hyperthyroidism of hyperemesis gravidarum from other causes of hyperthyroidism during pregnancy. CASE PRESENTATION 27 year old G1P0 with twin gestation presented at 10 weeks gestation complaining of vomiting which began at week 5 of pregnancy. She lost 10 pounds (~8% weight loss). Thyroid stimulating hormone (TSH) was suppressed. Her sister has Graves’ disease. Our patient saw an endocrinologist at 14 weeks where she denied tremor, diarrhea, heat intolerance, palpitations, skin, hair, nail changes, or neck pain. The vomiting had resolved and she had re-gained 4 pounds. PATHOPHYSIOLOGY The Pregnancy related increase in estradiol levels increases thyroxine binding globulin (TBG), Total T4 and T3 levels. HCG is is a glycoprotein hormone with a homologous alpha–subunit to TSH. HCG can bind to the TSH receptor stimulating the output of thyroid hormone. HCG-mediated hyperthyroidism can be associated with hyperemesis gravidarum which is characterized by excessive, persistent nausea and vomiting that causes weight loss of more than 5%, ketonuria and typical onset is before 12 weeks of gestation. CONCLUSIONS The lack of symptoms, normal exam, low TSH, normal Free T4, and negative antibodies clarified the diagnosis of gestational transient hyperthyroidism in the setting of hyperemesis gravidarum. Graves’ must be clinically excluded because when not controlled it is associated with maternal and fetal complications such as thyroid storm, fetal goiter, and pregnancy loss. PHYSICAL EXAMINATION SUMMARY DIFFERENTIATING TRANSIENT GESTATIONAL THYROTOXICOSIS FROM GRAVES DISEASE Vital signs were normal. HR 80 She did not have proptosis, lid lag, periorbital edema, thyromegaly, thyroid nodules, tremor, or hyperreflexia. The history, examination and laboratory data are essential for distinguishing between gestational transient hyperthyroidism and Graves’ disease. Gestational transient hyperthyroidism (HCG mediated) does not require therapy, whereas Graves disease (autoimmune) requires anti-thyroid medications. Hyperemesis gravidarum associated gestational transient hyperthyroidism is self limited and typically resolves by 18 weeks gestation. Gestational Graves History of Thyroid Disease - + Goiter/Thyroid Bruit + + Ophthalmopathy Tremor TPO/TSI Antibodies TSH Low Suppressed Resolution 2nd Trimester 12-18 Months REFERENCES 1. Abnormal stimulation of the thyrotrophin receptor during gestation. Patrice Rodien. Human Reproduction Update 10 (2);95-105, 2004 2. TSH suppression by hcg during early pregnancy. Haddow et al J Clin Endocrin Metab, Sep 2008 93(9);3341-3347 3. Biochemical tests for abnormalities in pregnancy. Huy A.Tran. Australian Prescriber, 2006;29:48-52