A mistaken case of Primary Hypothyroidism

E Mills, PC Eng, S Hamdulay, K Muralidhara, E Hui, Northwick Park Hospital.

We present the case of a 39-year-old female, who presented to her local hospital complaining of generalized lethargy, weakness, mild chest pains and palpitations. She had been given a diagnosis of Primary Hypothyroidism in Syria 8 years previously during a clinical work-up for subfertility and commenced on Levothyroxine 100mcg. At the time of presentation to our hospital, she had stopped taking Levothyroxine one year previously. On direct questioning, since stopping Levothyroxine, she had become increasingly fatigued and her menstrual cycles irregular. Admission baseline biochemistry was unremarkable, other than serum sodium 120 mmol/L. An echocardiogram for chest pains and palpitations showed a small pericardial effusion, global left ventricular hypokinesia with an ejection fraction of 30-35%, type 2 diastolic dysfunction and a severely dilated left atrium. A subsequent pituitary profile showed 9am cortisol 108 nmol/L, Free T3 < 1.50 pmol/L, Free T4 3 pmol/L, TSH 5.45 mU/L, IGF-1 < 0.4 nmol/L, prolactin 284 mU/L, FSH 6.3 U/L and LH 8.1 U/L. A Pituitary MRI showed the anterior pituitary to be small and laminated along the floor of the pituitary fossa in keeping with an empty sella. A diagnosis of Panhypopituitarism was therefore made and our patient was started on intravenous glucocorticoid replacement, followed by oral levothyroxine. Once established, she was switched to oral hydrocortisone 10mg, 5mg and 5mg, and levothyroxine 75 mcg. A repeat echocardiogram after treatment showed a normal left ventricular function with an ejection fraction of 55%, normal diastolic function and a mildly dilated left atrium. Once her biochemistry had normalized, she was discharged home with adrenal and thyroid axis correction, with further monitoring as an outpatient. Beyond standard consultant care, she was been seen by our local Endocrine Specialist Nurse to empower control of pituitary hormone replacement and promote steroid sick day rule knowledge.

Our case raises a number of interesting points, including the misinterpretation of a normal TSH value in the context of low Free T4 and low Free T3 in Syria as Primary rather than Secondary Hypothyroidism. A correct diagnosis would then have prompted the original physician to investigate for an underlying pituitary abnormality. Furthermore, on stopping Levothyroxine, our patient had an insidious presentation of hypopituitarism over a year, secondary to Empty Sella Syndrome. Hypopituitarism is found in less than 10% of patients with an empty sella, with the majority having normal pituitary function. Finally, our case supports the positive cardiovascular alteration of levothyroxine on cardiac function and structure once a euthyroid state is achieved.