Endocrine Abstracts

A 23-year-old gentleman with a 9-month history of extreme tiredness, muscle aches and pains, weight gain, cold intolerance and constipation presented to hospital with severe lethargy and dizziness and vacant episodes of increasing frequency. Initial examination revealed him to have a pulse rate of around 66 beats per minute. He was haemodynamically stable. A resting ECG showed an elevated ST segment of more than 2 mm with descent to an upward convexity to an inverted T wave especially prominent in the precordial leads in keeping with type 3 Brugada ECG pattern. The patient was in sinus rhythm with no symptoms of cardiac sounding chest pain. Further investigations revealed raised creatine kinase, deranged liver function in the form of isolated elevated alanine aminotransferase and acute kidney injury. Thyroid function revealed a markedly decreased FreeT4 of 1.6 pmol/l and TSH of greater than 150 miu/l. An echocardiogram showed good left ventricular function and no significant pericardial effusion. The patient was commenced on levothyroxine initially followed by low dose liothyronine. An ultrasound of his kidneys to probe his renal function was normal. An autoimmune screen turned out to be negative. Patient was hospitalised for further management. A 24-h ECG trace showed him to be in sinus rhythm throughout with no cardiac arrythmias. Patient’s stay in hospital was uneventful and he was discharged after 1 week with further review in the endocrine, renal and cardiology outpatient clinics. Endocrine review a month later showed him to have improved with his symptoms though not completely well yet and he had lost the 6 kg which he had gained prior to his hospital admission. He had ongoing muscle aches and tiredness and did not feel mentally sharp. He was asked to wean off his liothyronine over 2 weeks while his levothyroxine was increased. Further cardiology review 3 weeks later showed improving ECG changes especially with settling ST elevation. The patient also had a nephrology review in 2 months which was satisfactory. The raised alanine aminotransferase and creatine kinase was thought to represent metabolic changes due to severe hypothyroidism. A specialist opinion at the inherited arrythmia clinic 8 months later showed resolved ECG changes with now no evidence of Brugada ECG pattern and patient was reassured and discharged. We report on a rare cardiac manifestation of severe hypothyroidism which fortunately was reversible on successful correction of his endocrine abnormality.