A 42-year-old house wife presented with worsening headaches over 6 months i
n the absence of visual symptoms or symptoms suggestive of focal neurology.
She was a life-long smoker. Systems review was unremarkable apart from sec
ondary amenorrhoea and galactorrhoea of 6 months duration. Her serum prolac
tin was found to be 620 mU/I (60-400), FT4 12.6 nmol/l (9.8-23.1), TSH 1.38
mU/l (0.35-5.5), oestradiol < 73 pmol/l, LH and FSH of 4.4 and 12.6 mlU/l,
respectively. She was on bromocriptine. A presumptive diagnosis of pneumon
ia, based on pyrexia and CXR findings, was made and she was started on IV a
ntibiotics. Two days later she developed meningism and deterioration of con
scious level. (Lumbar puncture results: no organisms, 312 neutrophils and 1
64 lymphocytes). CT scan revealed a 2.5-cm pituitary adenoma, with suprasel
lar extension. A repeat hormonal profile revealed FSH 1.4, LH < 0.3 mU/l, o
estradiol <73 pmol/l, prolactin 488 mU/I (60-400), and low random cortisol
at 29 nmol/l.
T1-weighted MR1 revealed a large pituitary mass with evidence of haemorrhag
e.
The patient subsequently underwent a transsphenoidal exploration with resec
tion of the pituitary lesion. Whilst awaiting the histopathology results, C
T of chest revealed a 1.5-cm diameter rounded well defined density in the r
ight lower lobe associated with hilar, pre-and right para-tracheal lymphade
nopathy.
The histopathology of the pituitary lesion, obtained piecemeal, revealed fr
agments of fibrous tissue infiltrated by sheets of acidophilic prolactin-po
sitive cells, in keeping with a prolactinoma. In addition, other fragments
with blood clot included highly atypical epithelial cells with mitotic figu
res. These were negative for prolactin but showed HMFG-and CEA-positivity,
excluding them from a pituitary lineage. Transbronchial biopsy revealed mod
erately differentiated adenocarcinoma, with evidence of lymphatic spread. T
he overall conclusion was of bronchogenic adenocarcinoma, metastasizing to
a prolactinoma and complicated by apoplexy.