Endocrine Abstracts

We present a case of recurrent troublesome hypothyroidism with three pathologies to vex her medical attendants. This 75 year old lady was treated for Grave’s thyrotoxicosis elsewhere when she was 55 years old. She had positive TSH receptor antibodies and high uniform uptake of radioactive iodine. She presented to us age 65 with relapsed thyrotoxicosis and was maintained on carbimazole 5 mg OD for 8 years which was then stopped. She had been off medication for 2 years when she presented to A&E with hypothermia and bradycardia in February 2017 and was found to be hypothyroid (TSH 7.6, fT4 – 17). She started 25 mcg of levothyroxine and was discharged. Readmitted Jan 2018 with similar signs still on thyroxine 25 mcg (TSH 1.7, fT4 19.2). Treated as possible urosepsis and discharged. Third admission March 2018 with bradycardia and hypothermia but normal TFT. Endocrine advice was not sought during any of these admissions. She had a catastrophic admission to ITU April 2018 with low GCS, hypothermia, bradycardia (TSH 2.5, fT4 14, fT3 2.9). Endocrinology involved with a diagnosis of myxoedema coma. Confirmed compliance, absence of food and drug interaction and of malabsorption symptoms. ECG showed sinus bradycardia. Treated with tri-iodothyronine intravenously, levothyroxine increased to 100 mcg OD with hydrocortisone cover till panhypopituitarism was excluded. Pituitary MR was normal. She recovered dramatically with improved TFT (TSH 1.4, fT4 24.6, fT3 4.1). Four months later she maintained her improvement clinically (TSH undetectable, fT4 27.9, fT3 5.7). Between clinics her worried GP arranged admission in November 2018 with bradycardia, hypothermia and mental slowing (TSH 0.02, fT4 27.2). Gradually increased thyroxine dose to 300 mcg as inpatient over 3 weeks monitoring for signs of thyrotoxicosis. She slowly improved AMTS score, body temperature rose over 36 degrees Celsius and pulse crept over 60/minute. Discharged on 300 mcg thyroxine (TSH <0.01, fT4 33.3, fT3 6.1). In clinic Jan 2019 still bradycardic 60/min, still cold so thyroxine increased to 350 mcg. She posed a challenge heightened by the fact that despite supressed TSH, high fT4 and fT3 she was clinically still hypothyroid. Thus this lady exhibited poor T4 to T3 conversion, isolated TSH deficiency and subsequently both central and peripheral thyroid hormone resistance. Management relied on clinical rather than laboratory assessment for titration of thyroxine in transforming a cold, pale, confused and bradycardic patient slowing to her death into a warm and quick-witted one.