Endocrine Abstracts

A 37-year-old Nigerian lady was referred to the endocrinology clinic with worsening dyspnoea, weight loss, poor sleep and palpitations over the preceding few months. She had a past history of depression treated with citalopram. She was clinically and biochemically thyrotoxic with a TSH <0.01 μ/l [0.4–5] and free T₄ 49.3 pmol/l [9–19]. TSH receptor antibodies were positive. She was commenced on carbimazole 40 mg once daily and propranolol 40 mg twice daily. After 2 months of therapy her free T₄ had improved to 23.4 pmol/l and her therapy was altered accordingly.

Despite significant improvement in her thyroid function, she experienced ongoing dyspnoea, nocturnal sweating and cough. Her general practitioner referred her to the respiratory clinic, where she described occasional haemoptysis after prolonged coughing. Induced sputum testing for Acid–Alcohol Fast Bacilli was negative. A CT scan showed a diffuse soft tissue mass in the anterior and prevascular mediastinum but importantly no lymphadenopathy was evident in her thorax, abdomen or pelvis. Acetylcholine receptor antibodies were negative. She was diagnosed as having thymic hyperplasia as a result of Graves’ thyrotoxicosis. The thymic hyperplasia reduced significantly in volume on interval scans after optimal medical management of her thyrotoxicosis, and we were able to reassure her without the need for invasive investigations such as mediastinoscopy or thymic biopsy.

This case reminds us that thyrotoxicosis is a possible cause of dyspnoea. Thymic hyperplasia associated with Graves’ disease is rare, but has been reported in the literature. Routine assessment for thymic hyperplasia is not recommended but with increasing use of CT scanning, may be identified as an incidental finding.

This case highlights the need to be aware of Graves’ disease as a cause for thymic hyperplasia and invasive management is not necessarily required, assuming there are no features concerning for myasthenia gravis or underlying malignancy.