Endocrine Abstracts

Thymic hyperplasia (TH) in Grave’s Disease (GD) is not uncommon. It was first described in 1914 by William Halstead, however incidence has been difficult to establish as most patients remain asymptomatic from the TH and do not routinely undergo chest imaging when managing GD. We present a 49-year-old female with a background of rheumatoid arthritis and hypothyroidism, who presented to Rheumatology with proximal and distal muscle weakness, absent reflexes and weight loss. MRI scan reported widespread myositis in the thigh muscles, and EMG confirmed myopathy for all muscle groups. CT TAP was performed to investigate for malignancy and revealed a thymic mass measuring 2.3x2.6x5 cm and an enlarged thyroid. A PET scan was performed to rule-out metastatic disease from a possible thymoma, which reported increased diffuse uptake in a nodular enlarged thymus and multinodular goitre, metabolically active bilateral pelvic external iliac lymph nodes and marked atrophy of the quadriceps bilaterally. Following Lung MDT, thymectomy was recommended as early-stage cancer or thymoma could not be excluded. Meanwhile, the patient was found to be biochemically hyperthyroid and referred for an endocrinology opinion. She diagnosed with autoimmune hypothyroidism in 2014, and on inspection of thyroid function trend, developed hyperthyroidism in 2018. She was started on levothyroxine 6 months prior but unable to recall why. She reported tiredness, unintentional weight loss but denied palpitations, tremors, diarrhoea or constipation. She had noticed growth of her goitre since starting levothyroxine, but denied difficulty swallowing, breathing or pressure symptoms. There was no family history of thyroid dysfunction. Examination revealed a euthyroid appearance, pulse 60 beats per minute, a diffusely enlarged non-tender goitre with no lymphadenopathy, tremor or thyroid eye disease. Biochemistry confirmed a suppressed TSH, free T4 32.0 pmol/l(11.5-22.7 pmol/l); free T3 17.1 pmol/l(3.5-6.5 pmol/l); thyrotropin receptors antibodies (TRAb) 38.8 U/l(<1.0), and thyroid peroxidase antibodies >1300kIU/l(<61). Despite stopping levothyroxine therapy, the patient remained hyperthyroid, and carbimazole was started. Surgery was halted in view of the likely possibility of TH secondary to GD. Multiple studies describe regression of TH with treatment of hyperthyroidism. If the thymic mass is non-cystic and homogenous, with no calcification or invasion of surrounding structures, TH is likely in the presence of GD. Anti-thyroid treatment should be started for at least 6 months before a follow-up CT is performed. If there is less than 50% regression, a biopsy or thymectomy should be considered to rule out malignancy. Our patient awaits repeat thoracic imaging.