SUN-341 - A Challenging Case of Severe Thyrotoxicosis Following Parathyroidectomy: Tracing the Clinical Evolution from Postoperative Thyroiditis and Antibody-Negative Graves' Disease to Alternative Diagnostic Possibilities

Transient thyrotoxicosis after parathyroidectomy is a recognized but uncommon postoperative phenomenon, likely due to intrathyroidal manipulation and release of preformed thyroid hormones. It occurs in ~24–31% of parathyroid surgeries and typically resolves within 4–8 weeks, particularly after bilateral neck exploration, superior parathyroid resection, and lithium therapy. Differentiating this entity from antibody-negative Graves’ disease or thyroiditis can be challenging when thyrotoxicosis is severe or prolonged, further complicating management.

We present a case of a 43-year-old female with schizoaffective disorder, lithium-induced diabetes insipidus, extrapyramidal symptoms from chronic antipsychotic use, and primary hyperparathyroidism due to a left inferior parathyroid adenoma. She underwent left inferior parathyroidectomy without immediate complications. One week later, she developed speech difficulties, anxiety, tremors, and altered mentation. Family history was notable only for maternal hypothyroidism. Laboratory evaluation revealed markedly elevated free T4 >7.7 ng/dL (0.8–1.8) with low TSH 0.4 µIU/mL (0.5–4.5). Given concern for thyroid storm, propylthiouracil was initiated and later transitioned to methimazole. Hydrocortisone was briefly administered but discontinued after ACTH stimulation testing excluded adrenal insufficiency. TSI, TRAb, and TPO antibodies were negative. Thyroid ultrasound demonstrated a heterogeneous, enlarged gland without nodules or increased vascularity.

The patient was hospitalized for 9 days and discharged on methimazole 20 mg daily and propranolol 40 mg daily. Over 1–2 weeks, free T4 declined from >7.7 to 3.78 ng/dL. By 2 months, TSH was 4.52 µIU/mL with free T4 3.0 ng/dL; by 3 months, TSH was 3.13 µIU/mL with free T4 3.8 ng/dL. Radioactive iodine uptake (RAIU) at 4 months showed elevated uptake (4-hour 25.9%, 24-hour 47.8%), consistent with thyroid hyperfunction and suggestive of antibody-negative Graves’ disease.

Persistence of hyperthyroidism with incompletely suppressed TSH, elevated free T4, and increased RAIU argued against destructive thyroiditis. Despite negative antibodies, clinical, biochemical, and imaging features initially supported antibody-negative Graves’ disease, a rare entity ( < 5%). Parathyroid surgery may have triggered immune activation in a predisposed individual, with prior lithium exposure also considered. However, an incomplete biochemical response to methimazole broadened the differential.

Baseline thyroid function was abnormal, and the etiology remains under investigation. Further evaluation includes confirmatory hormone assays, interference testing, assessment for paraproteinemia, and consideration of rare central causes. Hence, postoperative thyrotoxicosis remains diagnostically complex and requires close reassessment as the clinical course evolves.

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