Prolactinoma
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Direct answer
Cabergoline, not surgery, is the first-line treatment for prolactinomas of every size — it normalises prolactin and shrinks macroprolactinomas in the large majority of patients, reversing mass effects and restoring fertility. Diagnosis rests on a clearly elevated serum prolactin with pituitary imaging, after excluding pregnancy and hyperprolactinaemic drugs, with two laboratory traps to disarm first: macroprolactinaemia (benign complexes causing spuriously high readings, unmasked by polyethylene glycol precipitation) and the hook effect (extremely high prolactin under-reported in standard assays, solved by diluting the sample). Women classically present early with amenorrhoea, galactorrhoea and infertility; men present later with libido loss, erectile dysfunction and visual field compromise.
What you must remember
- Microprolactinoma <10 mm; macroprolactinoma ≥10 mm — the anatomic distinction that dictates follow-up intensity.
- Rough prolactin-size correlation: microadenomas typically 25–200 ng/mL; levels above ~200 ng/mL usually mean a true prolactinoma, and macroadenomas often exceed 500 ng/mL into the thousands.
- Hook effect: a giant tumour with "modest" prolactin should prompt sample dilution before believing non-adenoma diagnoses.
- Macroprolactinaemia: request PEG precipitation; if recovery reveals macroprolactin, the patient needs no pituitary workup at all.
- Drug causes: antipsychotics (risperidone the worst), metoclopramide, domperidone, methyldopa, opioids, verapamil, high-dose oestrogen — usually prolactin <100–150 ng/mL, stalk-effect range.
- Cabergoline 0.25–0.5 mg twice weekly, titrated monthly by prolactin; superior to bromocriptine in efficacy and tolerance.
- Surgery (transsphenoidal) is reserved for dopamine-agonist resistance or intolerance, apoplexy, or CSF leak; radiotherapy is a distant third option.
- Echocardiographic surveillance for valvulopathy is advised for patients on high cumulative cabergoline doses, per current guidance — a modern exam point.
How dopamine agonists transform the case
A 28-year-old woman has amenorrhoea for two years, galactorrhoea expressible on examination, prolactin 480 ng/mL, and MRI showing a 14 mm macroadenoma touching but not compressing the optic chiasm. She wants to conceive. Start cabergoline 0.5 mg twice weekly; by three months prolactin is 22 ng/mL, menses return, and the tumour has shrunk clear of the chiasm. She conceives — cabergoline is stopped once pregnancy is confirmed (bromocriptine has the longer safety record if continued therapy is needed). Because her tumour was a macroadenoma, she gets formal visual fields each trimester; with a microadenoma, that intensity would be unnecessary since symptomatic growth in pregnancy is rare.
The male mirror-image teaches the presentation gap: a 42-year-old man with two years of waning libido and recent headaches has a 3 cm macroadenoma, prolactin 2,600 ng/mL (after dilution — the first assay reported 300 ng/mL, a hook effect worth naming), and bitemporal field loss. Men tolerate months of vague symptoms, so their tumours arrive bigger; dopamine agonist therapy still succeeds in most, with fields often improving within weeks.
Two exclusion steps precede any of this. Confirm the patient is not pregnant and audit the drug list — the psychiatric inpatient on risperidone with prolactin of 90 ng/mL needs a conversation with the psychiatrist about alternatives, not an MRI. And run the PEG precipitation on borderline-high samples in asymptomatic people; idiopathic macroprolactinaemia explains a real share of "hyperprolactinaemia" reports and needs nothing but reassurance.
Where students slip
First, prescribing bromocriptine by habit: cabergoline is the preferred agent — once- or twice-weekly dosing, better normalisation and shrinkage, and far less nausea — and stating that earns the mark. Second, missing the two assay traps: the giant tumour with "unimpressive" prolactin (hook effect — dilute) and the healthy person with incidental mild hyperprolactinaemia (macroprolactinaemia — PEG). Third, forgetting that prolactin elevation from stalk compression (masses other than prolactinomas) usually stays under ~150 ng/mL, so a craniopharyngioma with prolactin 100 ng/mL is not a prolactinoma, and its treatment is surgical. Finally, in pregnancy, over-monitoring microadenomas or under-monitoring macroadenomas: the rule is fields-driven follow-up for macros, reassurance for micros.
Frequently asked questions
What is the first-line treatment for a macroprolactinoma with visual field defects?
A dopamine agonist — cabergoline — which shrinks most macroprolactinomas rapidly and restores vision; surgery is reserved for resistance, intolerance, apoplexy or progressive deficit despite therapy.
What are macroprolactinaemia and the hook effect?
Macroprolactinaemia is high-molecular-weight prolactin complexed with IgG, causing falsely raised assays in people without disease (unmasked by PEG precipitation); the hook effect under-reports extremely high prolactin in standard assays, corrected by diluting the sample.
How is prolactinoma managed during pregnancy?
Cabergoline is stopped after conception in most patients; microadenomas need only reassurance, macroadenomas trimesterly visual field assessment, with bromocriptine or surgery reserved for symptomatic growth.
Which drugs commonly raise serum prolactin?
Antipsychotics (especially risperidone and phenothiazines), metoclopramide and domperidone, methyldopa, reserpine, verapamil, opioids and high-dose oestrogens — usually to modest levels consistent with stalk effect.
When is surgery indicated in prolactinoma?
For dopamine-agonist resistance (failure to normalise prolactin or shrink the tumour), intolerance of all available agonists, pituitary apoplexy with deteriorating vision or neurological deficit, and CSF rhinorrhoea during medical shrinkage.