Thyroid
.jpeg.jpg "Samyukta Ravi, MD, MA photo")
Samyukta Ravi, MD, MA
Resident physician
Northwell Health/Long Island Jewish Forest Hills Hospital
Albertson, New York, United States
Hashimoto Thyroiditis (HT) and Graves Disease (GD) have historically been considered separate disease processes but are now understood to lie along a spectrum of autoimmune thyroiditis. More recent research suggests that HT is mediated by a cellular immune response and GD by a humoral response. While 10-15% of GD cases have been known to transition to HT, the reverse is much rarer. Here we present the unusual case of a patient with HT who converted to GD and then had oscillating features of both hyper- and hypothyroidism.
A 31-year-old female with history of HT and obesity status post gastric sleeve surgery was seen in 2023. She was diagnosed with hypothyroidism in 2015 by bloodwork. She had positive thyroperoxidase antibody (TPO) levels and took levothyroxine (LT4) for 4 years. In 2019 she had bariatric surgery and LT4 was subsequently discontinued.
On initial presentation she had symptoms of hypothyroidism, including cold intolerance, fatigue, and weight gain. However, thyroid function tests (TFTs) 1 month later revealed: Thyroid stimulating hormone (TSH) < 0.01 ng/dL, free thyroxine (FT4) 4.0 ng/dL, total triiodothyronine (T3) 326 ng/dL. Autoantibody (AAb) workup revealed: Thyroid stimulating immunoglobulin (TSI) 7.56 IU/L, TSH receptor antibody (TRAb) 11.40 IU/L, and TPO 4160.0 IU/L. At that time, she reported symptoms of hyperthyroidism, including panic attacks, palpitations, tremors, facial swelling, and proptosis. She denied using lithium, amiodarone, or recent CT scans. Clinically and biochemically she met criteria for GD though she declined the I-123 thyroid uptake scan for confirmation. She was started on propranolol and methimazole (MMI), but TFTs continued to oscillate between hypo- and hyperthyroid states. Within weeks she was hypothyroid, with TSH 2.57 ng/dL and FT4 0.5 ng/dL. MMI was discontinued but in 1 week she became hyperthyroid (TSH < 0.01 ng/dL and FT4 2.2 ng/dL). AAb titers further increased (TPO 5411 IU/mL, TSI 22 IU/mL, TRAb 23.4 IU/mL), and the patient complained of symptoms spanning both hypo- and hyperthyroid spectrums, reporting weight gain and hospitalization for severe anxiety. Ultimately, the patient elected for complete thyroidectomy, which is to be scheduled.
This patient’s conversion from HT to GD with oscillating signs and symptoms in the absence of thyroid hormone replacement therapy after bariatric surgery is unusual and was challenging to manage. Currently, the pathophysiology of this conversion is not well understood. It is thought that an imbalance between stimulatory and inhibitory antibodies, or recovery after the gland suffers injury from HT, may result in an overt response causing hyperthyroidism. This case illustrates the importance of close investigation to mitigate potential thyrotoxicosis in patients with primary hypothyroidism who develop signs or symptoms of hyperthyroidism.