Endocrine Abstracts

JOINT2101

Introduction: Autoimmune thyroid diseases (AITDs), including Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), are distinct yet interrelated conditions. While HT typically causes hypothyroidism and GD results in hyperthyroidism, their coexistence in a single patient is rare. This case highlights the diagnostic and therapeutic complexities of overlapping HT and GD

Case Report: A 26-year-old woman with a positive family history of autoimmune thyroid disease and a personal history of chronic lymphocytic thyroiditis, diagnosed three years prior and managed with 50 µg of L-thyroxine daily, was referred to the endocrinology outpatient clinic for symptoms suggestive of hyperthyroidism. These symptoms persisted despite the progressive reduction and eventual discontinuation of treatment. On initial evaluation, the patient reported diarrhea, palpitations, and increased appetite. Physical examination revealed a non-enlarged thyroid and no exophthalmos. Thyroid function tests showed suppressed TSH levels (<0.001 mIU/l) and elevated free thyroxine (FT4) levels (48 pmol/l; normal range 10–28 pmol/l), persisting despite complete cessation of treatment. Both thyroperoxidase antibodies and TSH receptor antibodies were elevated at 115 IU/l (normal <8 IU/l) and 12.9 IU/l (normal <1.5 IU/l), respectively. Thyroid ultrasound revealed a slightly enlarged gland with irregular edges and increased vascular flow on Doppler, suggestive of thyroiditis. The patient was started on 10 mg of thiamazole and beta-blockers, resulting in significant improvement in clinical symptoms.

Discussion: The coexistence of GD and HT is rare but well-documented in several case reports (1–3). These autoimmune thyroid disorders share pathogenic mechanisms, including genetic and environmental factors, T-cell-mediated autoimmunity, and the presence of autoantibodies (1). Patients with simultaneous GD and HT may exhibit alternating phases of hyperthyroidism and hypothyroidism due to shifting antibody profiles (1). In this patient, hyperthyroidism was suspected when persistently suppressed TSH levels were observed despite reducing and eventually discontinuing L-thyroxine therapy. Diagnosing coexisting GD and HT can be challenging, requiring a thorough evaluation of clinical presentation, thyroid function tests, antibody assays, and imaging studies (3). Notably, our patient lacked classic clinical signs of GD, such as exophthalmos or a homogeneous goiter. Ultrasound findings were indicative of both HT (irregular gland edges, mild enlargement) and GD (increased vascular flow). Coexisting autoimmune thyroid diseases have been associated with other autoimmune conditions, including inflammatory bowel diseases, albeit rarely (4). Long-term monitoring of patients with autoimmune thyroid diseases is essential, even in the absence of clinical manifestations, due to the potential for disease progression (2).