A 58-year-old woman presented to the emergency room with palpitations and a 20-kg weight loss over 5 months. Physical examination revealed a diffusely enlarged thyroid gland (estimated weight of 50 g), resting heart rate of 150 beats per minutes, fine tremors of her fingers, and brisk deep tendon reflexes. Electrocardiogram showed atrial fibrillation. Thyroid-stimulating hormone was suppressed to less than 0.01 mIU/L (reference range: 0.3–4.2) and free thyroxine and total triiodothyronine were elevated to more than 99.1 pmol/L (reference range: 11.6–21.9) and more than 806 nmol/L (reference range: 123–307), respectively. Thyrotropin receptor antibody was elevated to more than 40 IU/L (reference range: 0–1.75). Chest computed tomography angiogram to rule out pulmonary embolism was obtained prior to the thyroid function test results, which incidentally revealed an anterior mediastinal mass (Fig. 1A). The iodine-123 uptake scan demonstrated a symmetrically enlarged thyroid with diffuse homogeneous uptake (71% at 24 hours, reference range: 8–29%), without ectopic uptake in the chest. Graves’ disease (GD) was diagnosed and she was started on methimazole 20 mg, 3 times daily, and propranolol immediately, and was eventually treated with radioactive iodine ablation (20 mCi) at 7-month follow-up. Her symptoms and thyroid function have gradually improved. Repeat chest computed tomography at 3 months and 12 months demonstrated a significant decrease of the thymic volume (Fig. 1B and 1C).
Figure 1.
Computed tomography scan of the chest showing a homogenous anterior mediastinal mass (red arrows). A: At initial presentation. B: At 3-month follow-up, when free thyroxine was 23.2 pmol/L and total triiodothyronine was 338 nmol/L. C: At 12-month follow-up, when free thyroxine was 18.0 pmol/L and total triiodothyronine was 154 nmol/L.
Thymic hyperplasia in Graves’ disease is commonly discovered incidentally by chest imaging for other reasons, as in our case. The pathogenesis is thought to be related to a direct trophic effect from excess thyroid hormones, as well as autoimmunity from the thyrotropin receptor antibody, leading to increased proliferation of cortical epithelia cells and medullary lymphoid follicles [1, 2]. It is a benign condition and usually improves after successful treatment of hyperthyroidism. Biopsy and thymectomy are recommended to be deferred in the setting of thyrotoxicosis to avoid triggering a thyroid storm, and should be reconsidered if the thymus fails to regress with treatment to rule out malignancy [3].
Acknowledgments
Author Contributions: D.L. prepared the manuscript. D.L. and J.C.M. were involved in the clinical care of the patient. All authors read and approved the final submitted version. Written informed consent was obtained from the patient.
Additional Information
Disclosure Summary: The authors have nothing to disclose.
Data Availability
All data generated or analyzed during this study are included in this published article or in the data repositories listed in the References.
References and Notes
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Data Availability Statement
All data generated or analyzed during this study are included in this published article or in the data repositories listed in the References.