Endocrine Abstracts

Case presentation: A 40-year-old Caribbean woman presented with sudden onset palpitations. She described 3 months of progressive shortness of breath, non-productive cough and 7kg weight loss. She denied chest pain, fevers or night sweats, but reported increased stool frequency, gritty eyes, and occasional visual blurring. She appeared cachectic and had a fine tremor, left eye proptosis and a visible pulsatile goitre. She was afebrile, tachypnoeic, hypoxic, hypotensive with fast atrial fibrillation (HR 240-260bpm). After unsuccessful DC cardioversion, she was admitted to ITU for rate control and high flow oxygen.

Initial investigations: Admission blood tests showed a free T4 of 82.1 pmol/l with supressed TSH. Chest and neck imaging showed a heterogeneously enlarged thyroid gland without substernal extension, extensive ground-glass opacification, mediastinal lymphadenopathy and small bilateral pleural effusions, but no discrete masses. Pulmonary angiography was unremarkable. Thyroid ultrasound was suggestive of thyroiditis.

Progress: Graves’ disease was confirmed (TRAb 25.39units/L). Propylthiouracil (PTU) and dexamethasone were given with good initial response, however the addition of cholestyramine was later required to maintain biochemical euthyroidism. The arrhythmia, initially refractory to treatment, eventually settled with propranol. During her ITU admission, she developed an enlarging left pleural effusion which required chest drain insertion; 500ml of milky transudate was drained (normal LDH, cytology and immunophenotyping). Chylothorax was confirmed biochemically: triglycerides 4.58 mmol/l, cholesterol 0.6 mmol/l. Serum ACE and mycobacterial investigations were negative. There was no histopathological evidence of malignant or granulomatous disease following endobronchial ultrasound. PET-CT on day 25 showed no avidity and near-complete resolution of mediastinal lymphadenopathy and pleural effusion following treatment of Graves’ disease. She was discharged on PTU, propranolol, dexamethasone and cholestyramine, with plans for radioiodine therapy as definitive treatment for Graves’ disease.

Conclusion: Atraumatic chylothorax is rarely described in Graves’ disease. In this case, chylothorax likely occurred due to thoracic duct obstruction by enlarged mediastinal lymph nodes.