Reversible pan-hypopituitarism in a case of un-resected non-functioning pituitary adenoma

S Nath, G Das, Department of Endocrinology, Ashford and St Peters Hospital NHS Trust

Abstract: Glucocorticoid replacement therapy is the 1st line treatment in a case of Panhypopituitarism. Administering the right dose and reproducing the pulsatile release of cortisol is still a major challenge. Hyponatremia can occur with worsening hypocortisolemia, but the mechanism is likely multifactorial and also due to inhibition of renal free water clearance. We present a case with on and off subclinical symptoms of cortisol insufficiency for about 10 years before presenting to emergency department with hyponatremia.

Case history: This 56 year old man presented to the emergency department with worsening central abdominal pain, vomiting and loss of appetite for four days. He had a history of on and off abdominal pain and general malaise for about 10 years with no other past medical history. His only medication was Omeprazole which he took when needed. General physical examination revealed slight epigastric pain. His initial blood biochemistry revealed a sodium of 122mmol/L, potassium of 4.2 mmol/L, creatinine 86micromol/L and urea 4.0mmol/L. He was discharged home, but he represented to the emergency department with the same symptoms four days later and was given intravenous fluids. His repeat blood biochemistry revealed sodium of 114mmol/L, potassium of 4.6mmol/L, creatinine 70micromol/L, urea 4.4 mol/L and plasma osmolality-241mmol/kg. Abdominal x-ray was found to be normal. His urine test revealed osmolality of 746mmol/kg and urine sodium of 110mmol/L. On examination he appeared physically exhausted and dry. He was treated with intravenous fluids and his sodium dropped further to 109mmol/L over next 2 days. Further tests revealed his cortisol level was <30nmol/L, TSH 0.21mU/L. FT4 -8.6pmol/L. FT3 -3.0pmol/L, FSH <1IU/L, LH 0.6IU/L, testosterone <0.24nmol/L. Pituitary imaging revealed a pituitary macro adenoma with supra-sellar extension without touching the chiasm.

This patient was then started on hydrocortisone replacement which corrected his sodium to normal levels over the next few days. Interestingly all his gonadal and thyroid hormones recovered with adequate cortisol replacement. Clinically he improved, gained appetite and discharged from hospital.

This patient likely had a very gradual onset cortisol insufficiency due to enlarging non-functioning macro adenoma leading to general decline in health which improved with corticosteroid replacement. The likely explanation for his recovering pituitary-gonadal and pituitary- thyroid axis after hydrocortisone replacement is due to hypocortisolemia affecting the thyrotrophic and gonadotrophic cellular function rather than compression due to tumour. or pituitary stalk effect causing hypogonadism as commonly seen with enlarging pituitary tumours.