SAT-380 - Postpartum Storm

Introduction: Hyperthyroidism, a disorder caused by excess thyroid hormone activity, can be classified as true hyperthyroidism and thyrotoxicosis without hyperthyroidism. True hyperthyroidism is characterized by excess thyroid hormone synthesis, most commonly Graves', an autoimmune disorder where thyrotropin receptor antibodies (TRAb) stimulate overproduction of hormones. In contrast, thyrotoxicosis due to thyroiditis results from the release of preformed hormone secondary to thyroid inflammation, including subacute, painless, drug-induced, and postpartum thyroiditis. Postpartum thyroiditis affects approximately 5% of women within one year of pregnancy and is typically associated with elevated thyroid peroxidase and thyroglobulin antibodies. We report a case of a patient who is four-months postpartum, actively breastfeeding, who presented with postpartum thyroiditis with negative antibodies.

Case summary: A 34-year-old G2P1011 woman, four months postpartum with a history of preeclampsia, presented with one day of fever, nausea, and emesis, along with a one-month history of weight loss, hair loss, and heat intolerance. She was tachycardic to the 140s on presentation. Thyroid function tests revealed undetectable TSH with markedly elevated free T4 (>7ug/dL) and T3 (222 ug/dL), yielding a Burch–Wartofsky score of 45. She was treated with propylthiouracil (PTU) and admitted for management of thyroid storm. Given diagnostic uncertainty between true hyperthyroidism and postpartum thyroiditis, she was empirically treated with methimazole, prednisone, and propranolol, resulting in clinical improvement and down trending thyroid hormone levels. Subsequent evaluation demonstrated negative thyroid antibodies, normal inflammatory markers, and a normal thyroid ultrasound.

Discussion: This patient presented with severe thyrotoxicosis associated with clinically significant hyperthyroid symptoms, which prompted immediate treatment despite an unclear diagnosis. Given the severity of symptoms, the treatment strategy was focused on rapid stabilization with propranolol, prednisone, and methimazole. The patients’ postpartum time course heavily favored postpartum thyroiditis, however, the absence of thyroid antibodies complicated her diagnosis. This case is a presentation of antibody-negative postpartum thyroiditis. Differentiation from TRAb-negative Graves' disease, subacute thyroiditis, or other causes of thyrotoxicosis is limited during the postpartum period when radioactive iodine uptake is contraindicated (like in this patient due to breastfeeding) and when Doppler findings are unremarkable. Our approach with this patient demonstrates the importance of a tailored, pragmatic therapeutic approach when the diagnosis remains uncertain, and of maintaining a broad management approach for adequate symptom control and patient safety.

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