A 36-year-old male presented with complaints of headache for 3 months in May 2008 for which he underwent MRI brain that revealed a 14.4×20×16 mm sellar mass with peripheral hyperintense ring, stalk thickening and dural enhancement (). On examination, he was afebrile with body mass index of 26 kg/m2. His blood pressure was 90/70 mm Hg, and had no signs of meningeal irritation. On investigation his serum electrolytes and haemogram were within normal range. Hormonal work up showed 800 h cortisol of 11.5 nmol/l (N, 140–690), total T3 1.23 nmol/l (N, 0.92–2.78), total T4 55 nmol/l (N, 58–140), TSH 1.24 mU/l (N, 0.5–5), LH 1.61 IU/l (N, 1.3–13), FSH 2.7 IU/l (N, 0.9–15), testosterone <0.69 nmol/l (N, 10–35) and prolactin of 7 μg/l (N, 2–15). Paired serum (280 mOsmol/kg) and urine osmolality (350 mOsmol/kg) were within normal range. A diagnosis of lymphocytic hypophysitis was considered. He was started on glucocorticoids, L-thyroxine and testosterone replacement therapy. He presented to us again in August 2008 with headache and fever for 2 days. On examination, he had neck rigidity and early papilledema. A possibility of acute meningitis was considered and he was treated with intravenous antibiotics and stress dosages of glucocorticoids. Lumbar puncture was planned after neuroimaging. He showed clinical improvement within 24 h and repeat MRI done after 3 days showed reduction in size of the mass (10×3.5×7 mm). With this rapid clinical and radiological improvement, lumbar puncture was deferred and antibiotics were continued for 2 weeks.
Pituitary MR T1 weighted contrast enhanced coronal section showing peripheral ring enhancement with central heterogeneous intensity and stalk thickening suggestive of pituitary abscess.
He was again admitted in October 2008 with severe headache, fever and meningism. On evaluation, cerebrospinal fluid (CSF) examination showed protein 2.69 g/l, glucose 2.83 mmol/l with corresponding blood glucose of 6.39 mmol/l and 300 cells with neutrophilic pleocytosis. CSF Gram's stain, culture, Indian ink stain and adenosine deaminase levels (6 U/l) were non-contributory. He was started on intravenous antibiotics and stress doses of glucocorticoids while levothyroxine was continued. With this therapy his symptoms resolved. Radionuclide cysternography did not reveal any CSF fistula.
In December 2008, he was again admitted with complaints of headache, fever and abnormal behavior. On examination he had neck rigidity and papilledema. CSF examination after decompressive measures showed protein 2.2 g/l, glucose 4 mmol/l and 1920 cells with predominant neutrophils, while CSF Gram's stain and culture were non-contributory. MRI showed mild increase in size of lesion (19×12×10 mm) in comparison to August 2008 with peripheral enhancement and sphenoid sinusitis.