A 21 year-old woman was found to have a pituitary macroadenoma following an episode of haemophilus meningitis. Biochemical TSH and GH excess was noted, although with no clear clinical correlates. She was treated with a somatostatin analogue (SSA), which restored the euthyroid state and controlled GH hypersecretion, but she re-presented with a further episode of cerebrospinal fluid (CSF) leak and recurrent meningitis. Histology following transsphenoidal adenomectomy revealed a Pit-1 lineage plurihormonal adenoma expressing GH, TSH and PRL. Such plurihormonal pituitary tumours are uncommon and even more unusual to present with spontaneous bacterial meningitis. The second episode of CSF leak and meningitis appears to have been due to SSA therapy-induced tumour shrinkage, which is not a well-described phenomenon in the literature for this type of tumour.
Pit-1 lineage GH/TSH/PRL-expressing plurihormonal pituitary adenomas are uncommon. Moreover, this case is unique as the patient first presented with bacterial meningitis.
Inmunohistochemical plurihormonality of pituitary adenomas does not necessarily correlate with biochemical and clinical features of hormonal hypersecretion.
Given that plurihormonal Pit-1 lineage adenomas may behave more aggressively than classical pituitary adenomas, accurate pathological characterization of these tumours has an increasing prognostic relevance.
Although unusual, a CSF leak and meningitis may be precipitated by SSA therapy of a pituitary macroadenoma via tumour shrinkage.
A 56-year-old man was brought to the Emergency Department after being found collapsed at his office with a reduced level of consciousness. From clinical examination and initial investigations, he was diagnosed as having bacterial meningitis and was promptly commenced on empirical i.v. antibiotics. Computed tomography of the brain revealed a parenchymal mass at the base of the skull and subsequent magnetic resonance imaging of the head 4 days later confirmed a large soft tissue mass, which extended through to the cavernous sinus. Examination of the cerebrospinal fluid (CSF) following lumbar puncture confirmed pneumococcal meningitis and antibiotics were continued for 2 weeks in total. During the admission, hormone profiling revealed a grossly elevated prolactin. When coupled with the initial results of the brain imaging, this result helped to confirm a macroprolactinoma that was invading the postnasal space. A final diagnosis of pneumococcal meningitis secondary to invading prolactinoma was made. The patient was started on cabergoline and was followed up in the outpatient clinic upon discharge. He made a full recovery from the meningitis. Over the next few months, prolactin levels returned to be normal and the prolactinoma shrank significantly in size. The patient remains on cabergoline that will most likely be continued indefinitely.
Bacterial meningitis is a rare first presentation of pituitary macroprolactinoma.
Patients with invasive macroprolactinoma do not always present with CSF leakage.
Prompt treatment with antibiotics and a dopamine agonist is of great importance for a favourable outcome.
Close monitoring of the patient for signs of raised intracranial pressure is essential in the management of macroprolactinoma.
Note the risk of CSF leakage after initiation of dopamine agonist therapy irrespective of concomitant meningitis in macroprolactinoma.