Hypopituitarism as the presenting feature of bronchogenic carcinoma with metastases to the pituitary gland
A 78-year-old male presented with a four month history of general lethargy and one stone weight loss. He had a history of well controlled type 2 diabetes mellitus, hypertension and Barrett's oesophagus. He was an ex-smoker of 50 pack years. On clinical examination he had a blunted affect, grade 2 finger clubbing, a palpable liver edge and appeared unsteady on his feet; visual fields were normal and visual acuity was N5 bilaterally. Initial biochemical investigations, revealed normal renal function and central hypothyroidism fT4 8.3 pmol/L (NR: 9.4-18.6), TSH 0.21 mu/L (NR: 0.3- 4.4). Five months prior to admission, he was biochemically euthyroid fT4 14.0 pmol/L, TSH 1.16 mu/L, on routine testing at his general practitioner. On further questioning, he had no headache, visual disturbance, galactorrhoea or polyuria. The presence of a rapid progression of central hypothyroidism, as well as a sub-optimal short synacthen response [], prompted gadolinium-enhanced brain and pituitary magnetic resonance imaging (MRI). This revealed cerebral and cerebellar metastases and a sellar mass measuring 9.5 mm in AP dimension [Figures and ], with invasion into the floor of the sella consistent with a pituitary metastatic deposit. Hypopituitarism (secondary hypothyroidism, hypoadrenalism and hypogonadism was confirmed biochemically []. The rise in prolactin was attributable to pituitary stalk compression.\nHe was commenced on hydrocortisone 30 mg at 8 am and 10 mg at 5 pm initially, and subsequently levothyroxine 100 mcg was cautiously introduced. As there were no clinical symptoms of hypogonadism, testosterone replacement was not commenced in the initial treatment phase. A computed tomography (CT) scan of chest [] revealed a 4.3 Χ 3.3 cm right hilar mass consistent with bronchogenic carcinoma. In addition, features of liver and bilateral adrenal metastases were also present. There was no evidence of diabetes insipidus present possibly attributed to by the low serum cortisol levels, which can mask this condition. His admission was complicated by a brief episode of psychosis attributed to high dose dexamethasone (8 mg bd) for treatment of brain metastases, which resolved upon dose reduction. After discussion with the multidisciplinary team and given the extent of his disseminated disease he was treated with palliative measures. He subsequently died shortly after his admission.