📋 Key Information Summary
- Hypopituitarism is partial or complete deficiency of anterior pituitary hormones (± posterior pituitary); ACTH and TSH deficiencies are most life-threatening if untreated.
- Common causes in Australia include pituitary adenomas (functioning or non-functioning), transsphenoidal surgery, cranial radiotherapy ≥30 Gy, traumatic brain injury (TBI), and Sheehan syndrome.
- Loss of hormones follows a characteristic order: GH → LH/FSH → ACTH → TSH; GH is most vulnerable and ACTH deficiency is the most dangerous.
- Cortisol must be replaced BEFORE levothyroxine — initiating thyroxine in undiagnosed ACTH deficiency precipitates adrenal crisis.
- Acute adrenal crisis (pituitary apoplexy or undiagnosed deficiency) presents with hypotension, hyponatraemia, hypoglycaemia; treat IV hydrocortisone 100 mg bolus then 50 mg 6–8 hourly.
- Dynamic testing confirms axis failure: short Synacthen test (ACTH), GnRH stimulation test (LH/FSH), insulin tolerance test or glucagon stimulation test (GH), TRH stimulation test (TSH).
- Hydrocortisone replacement 15–25 mg/day in divided doses (10 mg / 5 mg / 5 mg) for secondary adrenal insufficiency; no mineralocorticoid replacement required.
- Levothyroxine 1.6 µg/kg/day for central hypothyroidism; monitor free T4 (not TSH) as TSH is unreliable.
- Gonadal replacement: testosterone enantate 250 mg IM every 2–4 weeks or transdermal gel for males; cyclical oestrogen–progestogen HRT for premenopausal females.
- GH replacement (somatropin) requires Authority PBS approval; retest in adulthood if childhood-onset; initiation under endocrinologist supervision.
- All patients need a crisis plan, MedicAlert identification, and education on stress dosing of hydrocortisone (double dose for minor illness; triple dose + seek medical review for febrile illness).
- Aboriginal and Torres Strait Islander peoples have higher rates of TBI and may face barriers to specialist endocrinology access; culturally safe outreach and education are essential.
🎧 Audio Brief
Introduction & Australian Epidemiology
Hypopituitarism is the partial or complete deficiency of one or more anterior pituitary hormones, with or without posterior pituitary involvement (diabetes insipidus). It may present insidiously with non-specific fatigue and weight gain, or acutely with life-threatening adrenal crisis. The condition carries significant morbidity from untreated hormone deficiencies and excess mortality — primarily driven by untreated ACTH deficiency and cardiovascular disease.
| Epidemiological Parameter | Data |
|---|---|
| Prevalence | 45.5 per 100,000 population (European data; Australian estimates similar) |
| Incidence | 4.2 per 100,000 per year |
| Commonest cause | Pituitary adenoma (including post-surgical/radiotherapy) |
| Most vulnerable axis | GH → Gonadotrophin → ACTH → TSH (in order of susceptibility) |
| Excess mortality | SIR 1.2–2.2; higher in females, younger patients, and those with craniopharyngioma |
| TBI-related | Up to 30% of moderate–severe TBI develop some pituitary dysfunction |
In Australia, the most common aetiologies encountered in specialist practice are non-functioning pituitary macroadenomas managed with transsphenoidal surgery, prolactinomas treated medically, and craniopharyngiomas. Post-radiotherapy hypopituitarism is increasingly recognised as a late effect of cranial irradiation in survivors of childhood and adult cancers. Traumatic brain injury is an emerging cause, with Australian trauma registries documenting significant rates of post-TBI pituitary dysfunction.
Aetiology & Pathophysiology
Hypopituitarism results from destruction or dysfunction of the anterior pituitary gland (secondary) or impairment of hypothalamic releasing factors (tertiary). The anterior pituitary is particularly susceptible to compression, ischaemia, and radiation damage due to its confined anatomical position within the sella turcica.
| Aetiological Category | Examples | Mechanism |
|---|---|---|
| Pituitary tumours | Non-functioning adenoma, craniopharyngioma, Rathke cleft cyst, meningioma, metastasis | Compression and destruction of normal pituitary tissue |
| Post-surgical | Transsphenoidal surgery, craniotomy | Direct surgical trauma, stalk damage, vascular compromise |
| Radiotherapy | Cranial irradiation ≥30 Gy (brain tumours, nasopharyngeal CA, ALL) | Progressive vascular fibrosis; GH most vulnerable (onset 2–5 yr post-RT) |
| Vascular | Pituitary apoplexy, Sheehan syndrome, subarachnoid haemorrhage, DIC | Haemorrhagic infarction of pituitary; Sheehan: postpartum haemorrhage |
| Infiltrative / Inflammatory | Lymphocytic hypophysitis, sarcoidosis, haemochromatosis, Langerhans cell histiocytosis, IgG4 disease | Immune-mediated destruction or iron deposition |
| Traumatic brain injury | Closed head injury, blast injury | Stalk transection, hypothalamic contusion, vascular spasm |
| Infections | Tuberculosis, fungal (aspergillosis), abscess | Granulomatous destruction or abscess formation |
| Genetic / Developmental | Combined pituitary hormone deficiency (PROP1, PIT1, HESX1 mutations), septo-optic dysplasia | Defective transcription factor signalling |
| Empty sella | Primary or secondary empty sella syndrome | Arachnoid herniation into sella with pituitary compression |
Pathophysiological Cascade
Anterior pituitary cell types have differential sensitivity to insult. Somatotrophs (GH) are the most vulnerable, followed by gonadotrophs (LH/FSH), then thyrotrophs (TSH), and finally corticotrophs (ACTH) — the most resistant. This hierarchy explains why GH deficiency typically appears first, and ACTH deficiency last, in progressive pituitary destruction. However, in acute insults (pituitary apoplexy, surgery), multiple axes may fail simultaneously.
Pituitary apoplexy is an endocrine emergency. Acute haemorrhage or infarction within a pituitary adenoma causes sudden headache, visual field defects, ophthalmoplegia, and rapid-onset hypopituitarism (particularly ACTH deficiency). Immediate IV hydrocortisone is required before confirmatory testing.
The posterior pituitary may also be affected in craniopharyngioma, surgery near the stalk, and traumatic brain injury, leading to central diabetes insipidus (ADH deficiency). Posterior pituitary function is generally preserved in adenoma-related hypopituitarism and after radiotherapy.
Clinical Features by Hormone Deficiency
Presentation depends on the number and type of hormone deficiencies, speed of onset, and underlying aetiology. Chronic deficiencies present insidiously; acute pituitary apoplexy presents as an emergency.
| Hormone Deficiency | Key Clinical Features | Distinguishing Features |
|---|---|---|
| ACTH deficiency (secondary adrenal insufficiency) | Fatigue, weakness, anorexia, nausea, weight loss, postural hypotension, hyponatraemia, hypoglycaemia | Hyperpigmentation ABSENT (unlike primary adrenal insufficiency); aldosterone secretion preserved (no hyperkalaemia, no salt-wasting) |
| TSH deficiency (central hypothyroidism) | Fatigue, cold intolerance, constipation, weight gain, dry skin, bradycardia | TSH may be low, normal, or mildly elevated (inappropriately low for the fT4 level); normal TSH does NOT exclude central hypothyroidism |
| LH/FSH deficiency (hypogonadotropic hypogonadism) | Males: erectile dysfunction, decreased libido, reduced shaving frequency, muscle wasting, gynaecomastia. Females: amenorrhoea or oligomenorrhoea, infertility, vaginal dryness, osteoporosis | In premenopausal women, amenorrhoea is an early and prominent sign; in males, symptoms may be attributed to ageing |
| GH deficiency | Fatigue, reduced exercise capacity, central adiposity, decreased lean mass, reduced bone mineral density, impaired quality of life, dyslipidaemia | Most non-specific symptoms; often the last axis tested but the first to fail; significant impact on cardiovascular risk profile |
| Prolactin deficiency | Inability to lactate postpartum (Sheehan syndrome) | Rarely clinically significant outside lactation; prolactin is usually the last anterior hormone to be lost |
| ADH deficiency (central diabetes insipidus) | Polyuria (>3 L/day), polydipsia, nocturia, dilute urine (USG <1.005), hypernatraemia | Usually post-surgical or craniopharyngioma; transient DI may occur post-operatively with triphasic response |
Adrenal crisis — Suspect in any patient with known hypopituitarism presenting with hypotension, altered consciousness, severe hyponatraemia, or hypoglycaemia. Do NOT wait for confirmatory cortisol results — give IV hydrocortisone 100 mg immediately.
Investigations (Dynamic Testing)
Diagnosis of hypopituitarism requires demonstration of low target gland hormones in the setting of inappropriately low or normal pituitary trophic hormones (TSH, ACTH, LH/FSH). Dynamic stimulation tests are required to confirm ACTH and GH reserve, as basal levels may be misleading.
Baseline Investigations
ESSENTIAL
9 AM serum cortisol
Screening test; <100 nmol/L highly suggestive of insufficiency; >400 nmol/L virtually excludes it; 100–400 nmol/L requires dynamic testing
ESSENTIAL
Free T4 and TSH
Low fT4 with low/inappropriately normal TSH = central hypothyroidism. TSH alone is unreliable
ESSENTIAL
LH, FSH, oestradiol (F) or testosterone (M)
Low sex steroids with low/inappropriately normal gonadotrophins = hypogonadotropic hypogonadism
AVAILABLE
IGF-1 (insulin-like growth factor 1)
Low age- and sex-adjusted IGF-1 supports GH deficiency but is not diagnostic; dynamic testing required for confirmation. MBS item 66730
AVAILABLE
Prolactin
Low in stalk destruction; elevated in stalk compression (disinhibition); useful to differentiate sellar mass aetiologies
AVAILABLE
Electrolytes, glucose, FBC
Hyponatraemia (dilutional in ACTH deficiency), hypoglycaemia, normochromic normocytic anaemia
ESSENTIAL
MRI pituitary (with gadolinium)
Gold standard for structural assessment; identifies adenoma, craniopharyngioma, empty sella, infiltrative disease. MBS item 63071
AVAILABLE
Visual field assessment
Formal perimetry for any suprasellar or macroadenoma (chiasmal compression → bitemporal hemianopia)
Dynamic Stimulation Tests
| Test | Protocol | Diagnostic Threshold | Notes |
|---|---|---|---|
| Short Synacthen test (ACTH reserve) | Synacthen 250 µg IV/IM; measure cortisol at 0 and 30 min | Peak cortisol <450 nmol/L = insufficient | Most widely used in Australia; adequate screening for secondary adrenal insufficiency. MBS item 66727 |
| Insulin tolerance test (ITT — gold standard for GH & ACTH) | Insulin 0.1–0.15 U/kg IV bolus; target symptomatic hypoglycaemia (glucose <2.2 mmol/L); measure cortisol and GH at 0, 30, 60, 90, 120 min | Peak GH <3 µg/L = GH deficiency; Peak cortisol <500 nmol/L = ACTH deficiency | Requires inpatient setting, continuous monitoring; contraindicated in epilepsy, ischaemic heart disease, elderly |
| Glucagon stimulation test (alternative to ITT) | Glucagon 1 mg IM (or 1.5 mg if >90 kg); measure GH and cortisol at 0, 90, 120, 150, 180 min | Peak GH <3 µg/L = GH deficiency; Peak cortisol <500 nmol/L = ACTH deficiency | Preferred outpatient alternative when ITT contraindicated; nausea is common |
| GnRH stimulation test | GnRH 100 µg IV; measure LH and FSH at 0, 30, 60 min | Inadequate LH rise (<2× baseline) with low sex steroids = hypothalamic/pituitary gonadotrophin failure | Rarely required clinically; basal gonadotrophins + sex steroids usually sufficient |
| TRH stimulation test | TRH 200 µg IV; measure TSH at 0, 20, 60 min | Absent or delayed TSH rise with low fT4 = central hypothyroidism | Largely superseded by fT4 + TSH interpretation; TRH availability in Australia may be limited |
| Water deprivation test (diabetes insipidus) | 8-hour fluid deprivation; measure urine osmolality, serum osmolality, body weight hourly; desmopressin 2 µg SC at end | Urine osmolality <300 mOsm/kg after dehydration, rising >50% after desmopressin = complete central DI | Requires specialist supervision; plasma copeptin (if available) is emerging as an alternative |
Order of testing matters: If adrenal insufficiency is suspected, confirm cortisol deficiency or empirically start hydrocortisone BEFORE performing thyroid function testing or starting levothyroxine. Thyroxine replacement unmasks cortisol deficiency and may precipitate adrenal crisis.
Replacement Therapy
Hormone replacement must be initiated in a physiologically logical order: cortisol first, then thyroid, then sex hormones and GH. The goal is to mimic normal physiology as closely as possible using the minimum effective doses.
Cortisol Replacement (ACTH Deficiency)
Secondary adrenal insufficiency does NOT require mineralocorticoid replacement — aldosterone secretion is primarily regulated by the renin–angiotensin system, which remains intact. Only glucocorticoid replacement is needed.
Hydrocortisone
Hydrocortisone · Generic · Glucocorticoid
Adult dose
15–25 mg/day PO in 2–3 divided doses (e.g., 10 mg on waking, 5 mg at lunch, 5 mg at 4 pm)
Paediatric dose
8–12 mg/m²/day PO in 3 divided doses
Route
Oral (routine); IV/IM (adrenal crisis)
Renal adjustment
No dose adjustment required
PBS status
✔ PBS General Benefit
Prednisolone
Panafcortelone® · Generic · Glucocorticoid
Adult dose
3–5 mg/day PO as single morning dose (longer acting alternative)
Notes
Less physiological than hydrocortisone; used when compliance with multiple doses is difficult
PBS status
✔ PBS General Benefit
Adrenal crisis management:
- IV hydrocortisone 100 mg bolus immediately
- Then 50 mg IV every 6–8 hours
- IV normal saline 0.9% — aggressive fluid resuscitation (1 L over 30–60 min, then titrate)
- Monitor glucose; dextrose infusion if hypoglycaemic
- Taper to oral hydrocortisone over 2–3 days when stable
Stress Dosing (Sick Day Rules)
| Situation | Hydrocortisone Adjustment |
|---|---|
| Minor illness (cold, low-grade fever) | Double oral dose until recovered (usually 2–3 days) |
| Moderate illness (fever >38.5°C, gastroenteritis, UTI) | Triple oral dose; if unable to take orally → IM hydrocortisone 100 mg and present to ED |
| Major illness / surgery | IV hydrocortisone 50–100 mg stat then 50 mg 6–8 hourly; taper over 2–3 days post-op |
| Minor dental procedure | Extra 20–25 mg PO on day of procedure |
| Vomiting / unable to take oral meds | IM hydrocortisone 100 mg (self-administered emergency injection) → attend ED |
Thyroid Replacement (Central Hypothyroidism)
Levothyroxine
Oroxine® · Eutroxsig® · Thyronorm® · Synthetic T4
Adult dose
1.6 µg/kg/day PO (adjusted by fT4); typical range 75–150 µg/day
Paediatric dose
Neonates 10–15 µg/kg/day; children 4–5 µg/kg/day
Route
Oral — on empty stomach, 30–60 min before breakfast
Monitoring
Free T4 (aim mid-upper normal range); TSH is NOT reliable for dose titration in central hypothyroidism
Renal adjustment
No dose adjustment
PBS status
✔ PBS General Benefit
Critical safety rule: Never initiate levothyroxine without first confirming adequate cortisol replacement (or simultaneously starting hydrocortisone). Thyroxine increases cortisol metabolism and can precipitate life-threatening adrenal crisis in ACTH-deficient patients.
Sex Hormone Replacement
Males — Testosterone Replacement
Testosterone enantate
Primoteston Depot® · IM injection
Adult dose
250 mg IM every 2–4 weeks (most commonly every 3 weeks)
Monitoring
Serum testosterone mid-cycle (aim 15–25 nmol/L); haematocrit, lipids, LFTs, PSA annually
PBS status
✔ PBS Restricted Benefit — Authority Required for confirmed hypogonadism
Testosterone undecanoate
Reandron 1000® · Deep IM injection
Adult dose
1000 mg deep IM; initial dose, repeat at 6 weeks, then every 10–14 weeks
Advantages
Less fluctuation in serum levels; fewer injections per year
PBS status
✔ PBS Restricted Benefit — Authority Required
Testosterone gel
Testogel® · Androfeme® (F) · Topical
Adult dose
50 mg gel applied daily to shoulders/upper arms
Notes
Avoid skin-to-skin contact for 6 hours after application; risk of transfer to women and children
PBS status
✔ PBS Restricted Benefit — Authority Required
Females — Oestrogen–Progestogen Replacement
For premenopausal women with hypogonadotropic hypogonadism, physiological oestradiol replacement is essential to maintain bone density, cardiovascular health, and quality of life. Combined oral contraceptive pill (COCP) is often used as a convenient alternative to physiological HRT, though it provides supraphysiological oestradiol.
Oestradiol valerate + levonorgestrel
Progynova® + Provera® or Climaval® Sequential
Adult dose
Oestradiol 2 mg/day PO (or transdermal patch 50–100 µg/24hr) with cyclical progestogen (medroxyprogesterone acetate 10 mg/day for 10–12 days/month)
Key principle
Cyclical progestogen essential in any woman with an intact uterus to prevent endometrial hyperplasia
PBS status
✔ PBS General Benefit
Fertility — Gonadotrophin Therapy
When fertility is desired, sex steroid replacement must be stopped and replaced with gonadotrophin therapy under specialist reproductive endocrinology supervision:
- Males: FSH (recombinant or hMG) + hCG to stimulate spermatogenesis; treatment duration 6–18 months; MBS authority required
- Females: FSH ± LH (recombinant gonadotrophins) with ultrasound monitoring for ovulation induction; high multiple pregnancy risk
Growth Hormone Replacement
Somatropin
Norditropin® · Genotropin® · Omnitrope® · Recombinant GH
Adult dose
Start 0.1–0.3 mg SC daily (evening); titrate by 0.1–0.2 mg every 4 weeks based on IGF-1 and clinical response; typical maintenance 0.2–0.6 mg/day
Paediatric dose
0.025–0.05 mg/kg SC daily; adjusted for growth response and IGF-1
Route
Subcutaneous injection (pen device)
Monitoring
IGF-1 every 4–6 weeks during titration (aim mid-normal for age/sex); fasting glucose, HbA1c, lipids annually
Contraindications
Active malignancy; active proliferative diabetic retinopathy; acute critical illness
PBS status
✔ PBS Authority Required — Specialist-initiated; documented GH deficiency on dynamic testing required
Re-assessment of GH status in adulthood: Patients diagnosed with GH deficiency in childhood require re-testing after completion of linear growth (usually ≥18 years) before continuing GH replacement into adulthood. Only ~30% of childhood-onset cases persist on re-testing.
Desmopressin (Central Diabetes Insipidus)
Desmopressin
Minirin® · DDAVP® · Synthetic ADH analogue
Adult dose (oral)
100–200 µg PO 2–3 times daily
Adult dose (intranasal)
10–20 µg intranasally once or twice daily
Paediatric dose
Oral 50–300 µg/day in divided doses; intranasal 5–20 µg/day
Monitoring
Serum sodium (risk of hyponatraemia if over-replaced); instruct patients to drink to thirst, not on a schedule
PBS status
✔ PBS General Benefit
Hyponatraemia risk: Desmopressin over-replacement without adequate water intake restriction can cause dilutional hyponatraemia. Patients should be instructed to drink to thirst rather than on a fixed schedule. Monitor sodium within 1 week of initiation or dose change.
Monitoring
Lifelong monitoring is essential as replacement doses may change over time, and the underlying condition (e.g., adenoma) may progress. All patients should have an individualised management plan and emergency action plan.
| Parameter | Frequency | Target / Notes |
|---|---|---|
| Clinical review | Every 6–12 months (endocrinologist) | Symptoms, weight, BP, well-being assessment, QoL questionnaire |
| 9 AM cortisol or day-curve | Annually or after dose change | If on prednisolone; hydrocortisone day curve (3-point) if symptoms of under/over-replacement |
| Free T4 | Every 6–12 months | Aim mid-upper reference range; do NOT use TSH for dose titration |
| Testosterone (males) | Mid-cycle if IM; trough if gel | Aim 15–25 nmol/L; also monitor haematocrit (polycythaemia risk) |
| Oestradiol / withdrawal bleed (females) | Every 6–12 months | Confirm physiological replacement; ensure regular withdrawal bleeds if on cyclical HRT |
| IGF-1 | Every 4–6 weeks during titration; every 6–12 months once stable | Aim mid-normal for age and sex; avoid supraphysiological levels |
| Fasting glucose / HbA1c | Annually | GH replacement may impair glucose tolerance |
| Lipid profile | Annually | GH and sex steroid deficiency contribute to dyslipidaemia |
| DEXA bone density | At diagnosis; then every 2 years | Osteoporosis risk in GH and sex hormone deficiency |
| MRI pituitary | Per underlying pathology (e.g., 3–6 months post-surgery; annually for residual adenoma) | Assess tumour recurrence/residual mass; visual fields if chiasmal compression |
| Sodium (if on desmopressin) | Within 1 week of dose change; then 3–6 monthly | Hyponatraemia risk |
| PSA (males on testosterone) | Annually (age >50 or >40 if FHx) | Prostate screening per RACGP guidelines |
Patient Education & Crisis Plan
- All patients with ACTH deficiency must carry a MedicAlert bracelet/necklace
- Provide a written steroid emergency card and individualised adrenal crisis action plan
- Patients (and family) should be trained in IM hydrocortisone self-injection
- Supply an emergency hydrocortisone kit (Hydrocortisone 100 mg powder for injection or prefilled syringe)
- Educate on sick day rules (see stress dosing table above)
- Advise all healthcare providers of adrenal insufficiency before any procedure or illness
Special Populations
Pregnancy
Hydrocortisone
Safe in pregnancy; dose requirements may increase in 2nd–3rd trimester (increased CBG); increase by 20–30% from first trimester; stress dose for labour (hydrocortisone 100 mg IV at onset of active labour, then 50 mg 6–8 hourly until delivery, then rapid taper)
Levothyroxine
Requirements increase by 30–50% in pregnancy; increase dose as soon as pregnancy confirmed; monitor fT4 each trimester
Testosterone
Contraindicated in pregnancy (virilisation of female foetus); ensure contraception if on replacement
Oestradiol
Stop once pregnancy confirmed; no teratogenic risk from prior use; progesterone support may be considered in early pregnancy if history of miscarriage
GH (somatropin)
Discontinue as soon as pregnancy confirmed; no evidence of teratogenicity from inadvertent exposure in early pregnancy
Paediatrics
Combined pituitary hormone deficiency
Consider genetic testing (PROP1, POU1F1, HESX1) in congenital CPHD; GH deficiency is usually the first and most clinically significant deficiency in children
GH replacement
Higher doses required in children (0.025–0.05 mg/kg/day); monitored by paediatric endocrinologist; re-test in adulthood
Pubertal induction
If hypogonadotropic hypogonadism: low-dose testosterone (males) or oestradiol (females) from age 12–13, gradually increasing over 2–3 years to adult replacement
Elderly
Hydrocortisone
Lower replacement doses may be appropriate (10–15 mg/day); higher falls risk with over-replacement; avoid prednisolone if possible (osteoporosis risk)
Testosterone
Monitor haematocrit closely (polycythaemia risk); assess cardiovascular risk before initiating; PSA monitoring essential
GH
Benefit less well-established in elderly; lower starting doses; monitor glucose tolerance closely
Renal Impairment
All pituitary hormones
No significant dose adjustments required for hydrocortisone, levothyroxine, or testosterone in CKD. GH may require dose reduction in CKD-associated growth failure. Monitor sodium carefully with desmopressin in CKD.
Hepatic Impairment
Levothyroxine
May require dose adjustment in severe liver disease (altered T4 to T3 conversion); monitor fT4 closely
Testosterone
Avoid oral testosterone (17α-alkylated formulations); use parenteral (IM) or transdermal preparations. Intramuscular testosterone enantate is preferred in hepatic impairment.
Immunocompromised
Hydrocortisone
Physiological replacement doses do NOT cause clinically significant immunosuppression. Patients should follow standard vaccination schedules. Stress dosing remains essential during intercurrent infections.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
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