Nonfunctioning Pituitary Adenoma

Nonfunctioning pituitary adenoma is a pituitary tumour without clinical hormone excess. Most are of gonadotroph lineage, with the rest null cell or silent corticotroph and somatotroph tumours.

It accounts for about one third of clinically apparent pituitary adenomas and usually presents in adults aged 40 to 60 years as a macroadenoma, found by visual or neurological symptoms or incidentally.

Macroadenomas enlarge over time, and regrowth after surgery occurs in a substantial share of residual tumours. Microadenomas rarely progress.

Pathophysiology.

Monoclonal expansion compresses the normal gland, the optic chiasm and the cavernous sinus. Stalk compression raises prolactin mildly.

Hormone secretion is inefficient, so there is no excess syndrome. Lineage is defined by transcription factors (SF1, T-PIT, PIT1) on histology.

• Bitemporal hemianopia or reduced acuity, headache, and double vision from cranial nerve palsies.
• Hypopituitarism: fatigue, hypogonadism, hypothyroidism, adrenal insufficiency, with mild hyperprolactinaemia.

Red flags.

• Sudden severe headache with visual loss, ophthalmoplegia, vomiting or collapse (apoplexy).
• Progressive visual field loss.

• Pituitary MRI with contrast. Formal visual fields, acuity and optical coherence tomography if the tumour touches the chiasm.
• Prolactin, IGF-1, morning cortisol (a short stimulation test with tetracosactide 250 micrograms for intermediate values), thyroid stimulating hormone with free thyroxine, LH, FSH, testosterone or oestradiol, and serum sodium.
• Exclude hormone excess before labelling the adenoma non-functioning.
• Histology with immunostaining and transcription factors after surgery.

Differential diagnosis.

• Prolactinoma, meningioma, craniopharyngioma and Rathke cleft cyst.
• Hypophysitis, metastasis, lymphoma and germinoma.
• Carotid aneurysm and empty sella.

• Transsphenoidal surgery for visual compromise, chiasmal compression, apoplexy with deficits, or progressive growth. Observe small asymptomatic tumours away from the chiasm.
• Replace deficits: hydrocortisone first (15 to 25 mg daily in two or three divided doses), then levothyroxine (about 1.6 micrograms/kg daily, starting 25 to 50 micrograms in older adults or heart disease) with free thyroxine in the mid to upper reference range, then sex steroids. Growth hormone replacement in selected patients.
• Apoplexy: hydrocortisone 100 mg intravenously, then 50 mg every 6 hours (or 200 mg over 24 hours by infusion), fluid and electrolyte care, and urgent neurosurgical review if there is visual loss, falling consciousness or ophthalmoplegia. Stable patients may be managed conservatively.
• After surgery: morning cortisol on day 1 to 3 (cover with hydrocortisone until axis tested), sodium and fluid balance for delayed hyponatraemia around days 5 to 7, and screen for diabetes insipidus.
• Stereotactic radiotherapy for residual tumour or regrowth. Dopamine agonists give limited shrinkage.

Special groups. Women planning pregnancy: macroadenomas may enlarge; treat before conception when compressive.

Monitoring. MRI at 3 to 6 months after surgery, then at 1 year, then every 1 to 2 years. Annual pituitary function and visual fields.

Referral and escalation. Pituitary multidisciplinary team; neurosurgical and ophthalmic review for visual compromise.