Abstract

Background: Neonatal thyrotoxicosis is rare but can be life threatening. This usually has an autoimmune etiology occurring due to transplacental passage of TSH receptor-stimulating immunoglobulins (TSI) from mother to fetus. Perinatal monitoring for fetal hyperthyroidism is therefore prompted by a maternal history of Grave’s disease. Case: We present here a premature baby born at 33 weeks of gestation in a community hospital. Mother had no known medical conditions but received limited prenatal care. She had normal prenatal labs except a urine drug screen positive for marijuana. Baby presented with tachycardia and irritability since birth which was thought to be an effect of maternal drug use. Birth weight was appropriate for gestational age. There were concerns for cardiac failure necessitating transfer to our neonatology unit on day of life 4. Persistent tachycardia prompted endocrine work up revealing suppressed TSH, significantly elevated free T4 and TSI. Methimazole and Lugol’s iodine were started. Baby’s echocardiogram showed mitral and tricuspid regurgitation with no output failure. Mother’s labs subsequently revealed normal TSH but elevated TSI. The child was taken off Methimazole at four months of age when all labs normalized including TSI. Conclusion: Women with a prior history of hyperthyroidism are routinely monitored in pregnancy to determine the risk for fetal or neonatal hyperthyroidism. The lack of any maternal history of thyroid dysfunction, along with marijuana use in pregnancy, made recognizing neonatal thyrotoxicosis in our patient a challenge. Early diagnosis and commencement of therapy is necessary to prevent short-term and potential long-term adverse outcomes of neonatal thyrotoxicosis.

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