Endocrine Abstracts

Background: The clinical manifestations of thyrotoxicosis do not always correlate with the extent of thyroid biochemical abnormalities. Here, we report the case of a COVID-19 positive patient who presented with congestive heart failure as a first-time presentation of thyrotoxicosis.

Case report: A 40-year-old female presented to Emergency Department with two days history of lower limb oedema and abdominal distension. She denied dyspnoea, chest pain, palpitations, weight loss or heat intolerance. She had history of cervical cancer 3 years prior, treated with oophorectomy and hysterectomy and 10 pack-year smoking. On clinical examination, diffusedly enlarged thyroid gland, irregularly irregular pulse and signs of congestive cardiac failure (raised JVP, gallop rhythm, reduced air entry in lower zones of the lungs, pitting oedema up to hips bilaterally) were observed. ECG showed atrial fibrillation with atrial flutter; chest X-ray showed bilateral moderate pleural effusion. Laboratory work-up revealed deranged liver biochemistry (bilirubin 38 umol/l, ALT 13 U/l, GGT 120 U/l, alkaline phosphatase 339 U/l), normal troponin, elevated d-dimer (1340 ng/ml), markedly elevated pro-BNP (7421 pg/ml), markedly elevated free T4 73 pmol/l (range 8.3-19 pmol/l), free T3 27 pmol/l (range 3.8-6 pmol/l) and suppressed TSH <0.01 mIU/l (range 0.38-5.33 mIU/l). She had positive SARS-CoV-2 PCR on surveillance testing but no symptoms of COVID-19 infection. Transthoracic echocardiogram demonstrated left ventricular dysfunction (ejection fraction 35%), impaired right ventricular systolic function, dilated left and right atria. CT pulmonary angiogram/abdomen/pelvis showed no evidence of pulmonary embolism but demonstrated moderate to large bilateral pleural effusion with extensive free intra-abdominal fluid, an enlarged thyroid gland and heterogeneous liver parenchymal enhancement. She was treated with IV metoprolol, IV furosemide and anticoagulation on admission, later commenced on oral carbimazole 20 mg bd, propranolol and IV furosemide infusion (180 mg/24hr) for further diuresis. Heart failure medications were adjusted as per cardiology team. Metolazone, spironolactone, bumetanide, ramipril and dapagliflozin were commenced. TPO and anti-TSH receptor antibodies returned positive, consistent with Graves’ hyperthyroidism. She was discharged home 8 days after admission with close follow-ups with Endocrinology and Cardiology teams. Upon discharge, she was euvolaemic (14 kg weight loss) with improved thyroid function (free T4 34.6 pmol/l, free T3 9.9 pmol/l, TSH 0.01 mIU/l) and pro-BNP (2176 pg/ml).

Discussion: Our case highlights that thyrotoxicosis can present with congestive cardiac failure without classical symptoms of hyperthyroidism. Thyrotoxicosis should be considered in cases with a new presentation of heart failure. There is evidence that COVID-19 may be associated with high risk of thyrotoxicosis. It remains unclear if COVID-19 infection was coincidental or precipitated thyrotoxicosis with heart failure in our case.