Endocrine Abstracts

We would like to report an interesting case of Graves’ disease which presented with thymic hyperplasia, bilateral generalised lymphadenopathy and hypercalcaemia, along with other typical manifestations of hyperthyroidism. A 53 year old lady was admitted following an opioid overdose as she was suffering from depression after a recent slipped disc injury which had resulted in poor mobility. She suffered an out of hospital respiratory arrest, underwent cardiopulmonary resuscitation including treatment with nalaxone and was subsequently admitted. History revealed weight loss, anxiety, sweating and palpitations and she was noted to be in atrial fibrillation. She was found to have hyperthyroidism with TSH <0.01 mU/l (normal range 0.3–4.2 mU/l) and FT4 of 39 pmol/l (normal range 12–22 pmol/l) with positive TSH receptor antibodies. Bloods also showed mild hypercalcaemia with adjusted calcium of 2.72 mmol/l (normal range 2.20–2.60 mmol/l) and supressed PTH of 4 ng/l (normal range 16–65 ng/l) with normal vitamin D. CT thorax, abdomen and pelvis done to rule out malignancy showed generalised small volume lymphadenopathy in the neck, mediastinum and left axilla, nodules in the lung fissures bilaterally and some anterior mediastinal soft tissue. Myeloma screen and tumour markers were negative. She was started on carbimazole and anticoagulation with rivaroxaban and was referred to the Lung and Lymphoma MDTs for imaging review. The MDT discussions suggested a diagnosis of thymic hyperplasia, hypercalcaemia and lymphadenopathy secondary to thyrotoxicosis and did not recommend a biopsy. She responded well to antithyroid drug treatment with resolution of thyrotoxicosis and hypercalcaemia and an interval CT scan at three months showed complete resolution of the thymic hyperplasia and lymphadenopathy. Her symptoms of anxiety have also improved. Thymic hyperplasia is a known but rare manifestation of Graves’ disease which is thought to be caused by the action of TSH receptor antibodies on thyrotropin receptors in the thymus. Similarly, hypercalcaemia has also been reported in severe untreated Graves’ disease. This is thought to be an affect of thyroid hormones causing increased bone resorption. Generalised lymphadenopathy is also described with Grave’s disease. Hypercalcaemia, generalised lymphadenopathy and a neck mass on a background of weight loss would otherwise suggest a malignancy, such as lymphoma, but all of these are known features of severe untreated Graves’ disease. This complex case demonstrates the importance of a multidisciplinary approach to ensure that the patient is not subjected to unnecessary invasive investigations and is managed optimally.