Two cases of hypophysitis presenting as pseudomacroadenoma and hyponatraemia
Byron Lu Morrell1, Nina Tanna2, Lewis Saunders2, Samantha Anandappa1, Jesse Kumar1, Siva Sivappriyan1, 1Maidstone & Tunbridge Wells NHS Trust, 2King’s College London GKT School of Medical Education
Case 1: A 34-year-old female was admitted to our Hospital unwell, with headache, photophobia and. She also was seen in two other hospitals for similar symptoms.A CT head scan showed mucosal thickening within the paranasal sinuses with ‘bulky pituitary gland’ . Bearing this in mind, pituitary apoplexy was considered the most likely cause, and IV hydrocortisone was initiated.
Blood tests revealed a largely normal FBC, WBC but low MCV. She was hyponatraemic. CRP was 23mg/L. The free T4 was 14.4 pmol/L, with a TSH of 0.09 mIU/L, Prolactin was 1344mIU/l, IGF-1 34.7nmol/L. A pituitary MRI showed a pituitary macroadenoma and patient was referred to local a tertiary centre to undergo transphenoidal surgery. Histology showed a mononuclear inflammatory process consistent with lymphocytic hypophysitis. Further immunostaining with IgG4 revealed a high proportion of IgG4-positive plasma cells within the infiltrate, in keeping with a diagnosis of IgG4 hypophysitis.
Post operatively patient developed hypopituitarism with diabetes insipidus, and treated with levothyroxine 50 mcg daily and desmopressin 100mcg BD and prednisolone. This is currently being weaned off slowly.
Case 2: A 67-year-old gentleman was admitted to Maidstone Hospital with headache for 3 months associated with lethargy, muscle aches and a reduced appetite. Retrospectively, he also had a loss of libido for 4 months with erectile dysfunction. He was on escitalopram for depression.
On admission he was hyponatraemic (Na 122mmol/L) consistent with SIADH picture and thought to be secondary to escitalopram. During his stay, he became bradycardic and hypotensive. His cortisol was low and his cortisol response to synacthen test was inadequate. The rest of the bloods were consistent with panhypopituitarism. His pituitary MRI was reported as Rathke’s cleft or adenoma, with abutting on chiasm with stalk deviation. His visual fields were normal.
The patient was treated with steroid, thyroxine and testosterone and referred to a tertiary centre. While he was waiting for surgery repeat MRI showed spontaneous resolution of the lesion with subtle but more noticeable nodular thickening of the infundibulum which consistent with hypophysitis. Again his replacement is currently being weaned off.
Both these cases presented as hyponatramia but turned out to be pituitary macroadenoma and hyponatraemia. Hypophysitis though rare is an important differential in an acute presentation resembling apoplexy, with raised inflammatory markers.