SFEBES2023 Poster Presentations Thyroid (63 abstracts)
Department of Diabetes and Endocrinology, Chesterfield Royal Hospital, Chesterfield, United Kingdom
Background: There is a well-documented relationship between lithium exposure and thyroid dysfunction via multiple mechanisms. Lithium is commonly associated with goitre, hypothyroidism, and subclinical hypothyroidism. Lithium-induced autoimmune hyperthyroidism is rare and poorly understood. We report a case of autoimmune thyroiditis, Graves disease (GD), in a patient with longstanding primary hypothyroidism believed to be induced by Lithium.
Case report: A 77-year-old lady presented to her GP with a 5-month history of thyrotoxic symptoms, including weight loss and palpitations. Medical history included a 20 year history of hypothyroidism, treated with Levothyroxine, type 2 diabetes, chronic kidney disease, and longstanding depressive psychosis, controlled with lithium. Levothyroxine was stopped; despite this thyroid function (TFT) remained abnormal (serum-free T3 16.4 pmol/l; serum-free T4 37.3 pmol/l; and serum TSH < 0.05 mIU/l. She was referred to Endocrine outpatient clinic and started on Carbimazole 20mg once-daily pending her appointment. She had high Thyroid-specific Antibodies, with TSH receptor antibodies at 18.10 IU/l(Range) and Thyroid peroxidase antibodies at 544 IU/mL(Range). Thyroid Technetium scanning confirmed increased uptake and diffuse toxic goitre, features suggestive of GD. She continued titrated dose Carbimazole guided by regular TFT and clinical thyroid status. Due to concerns about declining renal function, lithium was withheld by the psychiatric team. The plan is to treat definitively once her thyroid status stabilises with Antithyroid medication.
Discussion: This case is noteworthy, given the rare association between lithium exposure and autoimmune hyperthyroidism. The presentation of GD was also unusual as our patient had previously been managed for primary hypothyroidism for several years, which raises discussion points on lithium affecting circulating thyroid autoantibodies and potentially converting existing autoantibodies from a suppressing to an activating form.