Addison's Disease (Primary Adrenocortical Failure)

📋 Key Information Summary

📋

Addison's disease is primary adrenocortical insufficiency characterised by cortisol and aldosterone deficiency due to destruction of the adrenal cortex.
Autoimmune adrenalitis accounts for ~85% of cases in Australia; tuberculosis remains important in immigrant and ATSI populations.
Prevalence in Australia is approximately 45–60 per million; incidence ~5 per million per year, with a female-to-male ratio of 2–3:1.
Classic presentation includes fatigue, weight loss, postural hypotension, hyperpigmentation (due to ACTH excess), salt craving, and hyponatraemia with hyperkalaemia.
Adrenal crisis is a medical emergency — presenting with hypotensive shock, altered consciousness, fever, and abdominal pain — with mortality up to 6% per episode.
Short Synacthen Test (SST) is the gold-standard diagnostic test in Australia; a peak cortisol <450 nmol/L at 30–60 min confirms adrenal insufficiency (MBS Item 66682).
Hydrocortisone is the preferred glucocorticoid replacement (15–25 mg/day divided into 2–3 doses); fludrocortisone replaces aldosterone (50–200 µg once daily).
Sick day rules require patients to double or triple oral hydrocortisone during intercurrent illness; if unable to tolerate oral intake, emergency IM hydrocortisone 100 mg must be administered immediately.
All patients should carry a Steroid Card, an emergency hydrocortisone kit (100 mg IM ampoule + syringe), and an Adrenal Crisis Letter.
Screen for associated autoimmune conditions (thyroid disease, type 1 diabetes, premature ovarian insufficiency, coeliac disease, vitiligo) at diagnosis and periodically.
Emergency department management of adrenal crisis: IV 0.9% sodium chloride bolus 1 L (adult), hydrocortisone 100 mg IV/IM stat, then 50 mg IV/IM 6-hourly until haemodynamically stable.
Patients require lifelong monitoring with annual review of replacement adequacy, bone density, autoimmune screen, and adrenal crisis prevention education.

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Introduction & Australian Epidemiology

Addison's disease, or primary adrenocortical insufficiency, arises from progressive destruction of the adrenal cortex, resulting in deficient production of cortisol, aldosterone, and adrenal androgens. The condition must be distinguished from secondary (pituitary) and tertiary (hypothalamic) causes, which present with cortisol deficiency alone due to insufficient ACTH stimulation.

In Australia, the estimated prevalence is 45–60 cases per million population, with an incidence of approximately 5 per million per year. Autoimmune adrenalitis is the predominant aetiology in Australian tertiary referral centres, accounting for roughly 85% of diagnosed cases. The peak age of onset is between 30 and 50 years, with a marked female predominance (F:M ratio 2–3:1) reflecting the autoimmune basis of the disease.

The insidious onset and non-specific early symptoms mean that diagnosis is frequently delayed by months to years. Studies suggest that up to 50% of adrenal cortex may be destroyed before clinical insufficiency becomes apparent. Once identified, however, the condition is readily treatable with lifelong hormone replacement. The principal ongoing risk is adrenal crisis, which remains a significant cause of morbidity and potentially preventable death.

Given the association with other autoimmune disorders, patients with Addison's disease require screening for polyglandular autoimmune syndromes — particularly autoimmune thyroid disease (present in ~50% of cases), type 1 diabetes mellitus (~10–15%), premature ovarian insufficiency (~10%), coeliac disease (~5–8%), and vitiligo (~10–15%). In the Australian setting, healthcare providers should also consider infectious aetiologies such as tuberculosis, which remains relevant in Aboriginal and Torres Strait Islander communities and in patients from high-burden countries.

Pathophysiology & Causes

Normal Adrenal Function

The adrenal cortex comprises three functional zones: the zona glomerulosa (mineralocorticoid — aldosterone), the zona fasciculata (glucocorticoid — cortisol), and the zona reticularis (androgens — DHEA, androstenedione). Cortisol secretion is regulated by the hypothalamic–pituitary–adrenal (HPA) axis via ACTH, which also drives adrenal melanocortin receptors, explaining the characteristic hyperpigmentation of primary insufficiency.

Aldosterone secretion is primarily controlled by the renin–angiotensin–aldosterone system (RAAS) and serum potassium. Its loss in Addison's disease leads to sodium wasting, potassium retention, and the metabolic derangements that distinguish primary from secondary adrenal insufficiency.

Aetiologies

Aetiology	Frequency (Australia)	Key Features
Autoimmune adrenalitis	~85%	21-hydroxylase antibodies positive; associated with APS-1 & APS-2; lymphocytic infiltration on histology
Tuberculosis	~5–10%	Important in ATSI populations, immigrants from high-burden countries; calcified adrenals on CT
Adrenal haemorrhage / infarction	~2–3%	Waterhouse–Friderichsen syndrome (meningococcal); anticoagulant therapy; antiphospholipid syndrome
Metastatic infiltration	~1–2%	Lung, breast, melanoma; usually bilateral and >90% destruction required
Infectious	Rare	HIV/CMV (in advanced immunosuppression), histoplasmosis, cryptococcosis
Congenital adrenal hyperplasia	Rare	21-hydroxylase deficiency most common; usually diagnosed neonatally or in childhood
Adrenoleucodystrophy	Rare	X-linked; very long-chain fatty acid accumulation; consider in young males
Other (drugs, sarcoidosis, amyloidosis)	Rare	Ketoconazole, etomidate, mitotane; granulomatous disease

Autoimmune Mechanisms

Autoimmune destruction involves CD4+ and CD8+ T-cell mediated cytotoxicity against adrenocortical cells. Circulating antibodies to 21-hydroxylase (CYP21A2) are detectable in ~85% of autoimmune cases and serve as a useful serological marker. Addison's disease may occur in isolation or as part of autoimmune polyendocrine syndromes:

APS-1 (APECED): Autosomal recessive; AIRE gene mutation; triad of chronic mucocutaneous candidiasis, hypoparathyroidism, and Addison's disease. Onset usually in childhood.
APS-2 (Schmidt syndrome): Polygenic; Addison's disease + autoimmune thyroid disease ± type 1 diabetes; adult onset; HLA-DR3/DR4 associated.

Clinical Features & Adrenal Crisis

Gradual Onset — Chronic Insufficiency

The presentation is often insidious over weeks to months, with progressive non-specific symptoms that may be attributed to other diagnoses:

System	Symptoms / Signs	Mechanism
General	Fatigue, malaise, weakness, weight loss, anorexia	Cortisol deficiency; reduced gluconeogenesis
Pigmentation	Generalised hyperpigmentation — creases, buccal mucosa, scars, areolae	ACTH and MSH excess stimulating melanocortin-1 receptors
Cardiovascular	Postural hypotension, dizziness, syncope	Cortisol + aldosterone deficiency → volume depletion, reduced vascular tone
Gastrointestinal	Nausea, vomiting, abdominal pain, salt craving, diarrhoea	Electrolyte disturbance; cortisol deficiency GI effects
Metabolic	Hyponatraemia, hyperkalaemia, hypoglycaemia (especially in children)	Aldosterone loss → Na⁺ wasting, K⁺ retention; cortisol loss → impaired gluconeogenesis
Musculoskeletal	Myalgia, arthralgia	Electrolyte disturbance; androgen deficiency
Psychiatric	Depression, irritability, difficulty concentrating, reduced libido	Cortisol and androgen deficiency

⚠️

Diagnostic pitfall — absence of hyperpigmentation: In patients with dark skin (including many Aboriginal and Torres Strait Islander peoples), hyperpigmentation may be difficult to detect. Similarly, secondary adrenal insufficiency does NOT cause hyperpigmentation (ACTH is low). Always check electrolytes (hyponatraemia + hyperkalaemia) and consider the SST.

Adrenal Crisis

Adrenal (Addisonian) crisis is a life-threatening endocrine emergency characterised by acute haemodynamic compromise due to cortisol deficiency. It may be the presenting feature of undiagnosed Addison's disease or occur in patients on replacement therapy who are inadequately dosed during intercurrent illness.

Moderate

Impending Crisis

Increasing fatigue, nausea, postural dizziness, salt craving. BP normal or mildly postural. Na⁺ 125–132 mmol/L, K⁺ mildly elevated. Able to tolerate oral intake.

Setting: Increase oral hydrocortisone 3×; GP review same day; ED if worsening

Severe

Adrenal Crisis

Hypotension (systolic <90 mmHg), altered consciousness, fever, severe abdominal pain, vomiting. Na⁺ <125 mmol/L, K⁺ >6.0 mmol/L, hypoglycaemia. Unable to tolerate oral intake.

Setting: Emergency department / ICU — IV hydrocortisone 100 mg stat + aggressive fluid resuscitation

Precipitants of Adrenal Crisis

Intercurrent infection or febrile illness (most common — ~40–50% of crises)
Gastroenteritis with vomiting/diarrhoea leading to failure to absorb oral hydrocortisone
Surgery, trauma, or other physiological stress without glucocorticoid stress dosing
Withholding or forgetting replacement therapy
Pregnancy and labour without adequate dose adjustment
Starting medications that accelerate cortisol metabolism (e.g., rifampicin, phenytoin, carbamazepine, mitotane)

🚨

Emergency treatment of adrenal crisis — act immediately:
1. IV access — draw blood for glucose, UEC, cortisol, blood cultures if febrile.
2. Hydrocortisone 100 mg IV bolus (or IM if no IV access). Do NOT wait for cortisol results.
3. IV 0.9% sodium chloride 1 L over 30–60 min (adult). Repeat as needed. Children: 20 mL/kg bolus.
4. Dextrose 10% if hypoglycaemic.
5. Continue hydrocortisone 50 mg IV/IM 6-hourly until haemodynamically stable and tolerating oral intake.
6. Identify and treat the precipitant (antibiotics for infection, etc.).
7. Involve endocrinology early.

Investigations

Initial Screening (Biochemistry)

Essential

Serum UEC — sodium, potassium, creatinine, urea

Hyponatraemia (Na⁺ often <132 mmol/L) + hyperkalaemia (K⁺ often >5.0 mmol/L) is the hallmark biochemical pattern. Urea may be elevated from dehydration. Low-normal creatinine.

Essential

8 AM serum cortisol

Cortisol <100 nmol/L at 8 AM is strongly suggestive of adrenal insufficiency. Cortisol >400 nmol/L essentially excludes it. Values 100–400 nmol/L require dynamic testing.

Essential

Serum ACTH

Elevated (>2× upper limit of normal) in primary insufficiency; low or inappropriately normal in secondary/tertiary. Draw at same time as cortisol (8 AM).

Available

Plasma renin activity (PRA) / serum aldosterone

PRA elevated and aldosterone low/low-normal confirms mineralocorticoid deficiency — confirms primary over secondary. Available at major hospital laboratories.

Available

Blood glucose

Hypoglycaemia may be present, especially in paediatric patients or during crisis.

Short Synacthen Test (SST) — Gold Standard

The SST is the primary confirmatory test in Australia and is available through pathology services (MBS Item 66682 — Synacthen stimulation test).

ℹ️

Protocol (Standard 250 µg SST):
1. Administer IV or IM tetracosactide (Synacthen®) 250 µg.
2. Measure serum cortisol at 0, 30, and 60 minutes.
3. A peak cortisol ≥450 nmol/L (using immunoassay) at 30 or 60 min indicates an adequate adrenal response and excludes adrenal insufficiency.
4. Cortisol below this threshold is diagnostic of adrenal insufficiency.

Notes: The 1 µg (low-dose) SST may be more sensitive for early or partial insufficiency but is not standardised in Australian laboratories. Perform the test at any time of day in suspected crisis; in stable outpatients, an 8 AM baseline cortisol should be drawn first.

Aetiological Investigations

Essential

21-hydroxylase (CYP21A2) antibodies

Positive in ~85% of autoimmune adrenalitis. If negative and autoimmune suspected, may repeat in 6–12 months. Available at reference laboratories (Sullivan Nicolaides, Douglass Hanly Moir).

Available

Adrenal CT scan (non-contrast ± contrast)

Atrophic adrenals in autoimmune disease; enlarged/calcified adrenals suggest TB, haemorrhage, or infiltration. MBS Item 56809.

Available

Chest X-ray and tuberculin skin test / IGRA (QuantiFERON)

If TB suspected — especially in ATSI patients, overseas-born from endemic regions, or immunocompromised patients.

Available

Very long-chain fatty acids (VLCFA)

Screen for adrenoleucodystrophy in young males with unexplained Addison's disease.

Associated Autoimmune Screen (at Diagnosis)

Condition	Screening Test	Frequency
Autoimmune thyroid disease	TSH, free T4, TPO antibodies	At diagnosis, then annually
Type 1 diabetes	Fasting glucose, HbA1c, GAD antibodies	At diagnosis, then annually (fasting glucose/HbA1c)
Coeliac disease	IgA tissue transglutaminase (tTG-IgA) + total IgA	At diagnosis; repeat if new GI symptoms develop
Premature ovarian insufficiency	FSH, oestradiol (if menstruating and <40 years)	At diagnosis; if menstrual irregularity develops
Vitiligo	Clinical inspection	At each review

Management & Sick Day Rules

Long-Term Replacement Therapy

💊

Hydrocortisone

Cortate® · Generic · Glucocorticoid

Adult dose 15–25 mg/day PO divided into 2–3 doses (e.g., 10 mg on waking, 5 mg at midday, 5 mg at 3–4 PM). Total dose individualised to symptom control and body habitus.

Paediatric dose 8–12 mg/m²/day PO divided into 3 doses (e.g., 5 mg/m² morning, 2.5 mg/m² midday, 2.5 mg/m² afternoon). Dose adjusted for growth and pubertal status.

Route Oral (stable); IV or IM (crisis / peri-operative)

Renal adjustment Not required — metabolised hepatically

PBS status ✔ PBS General Benefit

💊

Fludrocortisone

Florinef® · Generic · Mineralocorticoid

Adult dose 50–200 µg PO once daily, usually in the morning. Most adults require 100 µg/day.

Paediatric dose 50–100 µg PO once daily; weight-based dosing 1–3 µg/kg/day.

Monitoring Blood pressure (supine + standing), serum electrolytes, plasma renin activity — titrate to normalise renin if possible.

PBS status ✔ PBS General Benefit

💊

DHEA (dehydroepiandrosterone)

Generic · Adrenal androgen

Adult dose 25–50 mg PO once daily (women only, if persistent fatigue, low mood, or reduced libido despite adequate cortisol/aldosterone replacement).

Paediatric dose Not routinely used in children.

Evidence Cochrane review suggests modest benefit in quality of life; not universally recommended. Trial for 6 months; discontinue if no benefit.

PBS status ✘ Not PBS listed

Dosing Principles

Physiological replacement — aim for the lowest dose that controls symptoms. Over-replacement increases osteoporosis, cardiovascular, and metabolic risk.
Mimic circadian rhythm — two-thirds of the daily hydrocortisone dose in the morning, one-third in the early afternoon. Avoid late-evening dosing (insomnia).
Modified-release hydrocortisone (Plenadren®) — once-daily formulation providing more physiological cortisol profile; superior quality of life in some studies. Not PBS-listed in Australia; limited availability.
Fludrocortisone is not required in secondary adrenal insufficiency (the RAAS is intact as it does not depend on ACTH).

Sick Day Rules

⚠️

Sick day rules must be taught to every patient and reviewed at every clinical encounter. Failure to adjust glucocorticoid dosing during illness is the single most important preventable cause of adrenal crisis.

1

Minor illness (cold, mild URTI, sore throat)

Double the oral hydrocortisone dose (e.g., 10 mg → 20 mg on waking, 5 mg → 10 mg at noon, 5 mg → 10 mg afternoon). Continue for duration of illness. Fludrocortisone dose unchanged.

2

Moderate illness (fever >38°C, significant infection, gastroenteritis)

Triple the oral hydrocortisone dose (e.g., 10/5/5 → 30/15/15 mg). If unable to tolerate oral intake for >2 hours → administer IM hydrocortisone 100 mg from the emergency kit and attend ED.

3

Severe illness / surgery / trauma

IV/IM hydrocortisone 100 mg stat, then 50 mg 6-hourly (or continuous infusion 200 mg/24 h). Fludrocortisone temporarily withheld (hydrocortisone has some mineralocorticoid activity at high doses). Resume usual regimen once stable.

4

Peri-operative dosing

Minor surgery (local anaesthetic, <1 h): hydrocortisone 25 mg IV at induction; resume oral dose next day. Major surgery: hydrocortisone 100 mg IV at induction, then 50 mg IV 6-hourly for 24–48 h, then taper over 1–3 days to usual oral dose.

Emergency Kit & Patient Education

Item	Details
Hydrocortisone ampoule	Hydrocortisone sodium succinate 100 mg powder for injection (Solu-Cortef® or generic). PBS General Benefit.
Syringe + drawing-up needle	5 mL syringe + 21G needle for reconstitution.
IM needle	23G × 25 mm (or 25G × 16 mm for paediatric) for intramuscular injection into the anterolateral thigh.
Steroid emergency card	Card detailing diagnosis, usual medications, and emergency dose. Must be carried at all times.
Adrenal crisis letter	Letter from endocrinologist for ED staff with management instructions — laminated, kept with kit.

✅

All patients should be taught to self-administer IM hydrocortisone. Family members and close contacts should also be trained. In children, parents/carers must be competent in IM injection technique. Access to emergency services (Triple Zero 000) should be reinforced.

Monitoring

Parameter	Frequency	Purpose
Clinical symptoms (fatigue, weight, BP, pigmentation)	Every 3–6 months (first year), then annually	Assess replacement adequacy — under- vs over-replacement
Blood pressure (supine + standing)	Every visit	Postural drop suggests under-replacement of fludrocortisone or hydrocortisone
Serum electrolytes (Na⁺, K⁺)	Every 3–6 months, then annually	Hyponatraemia or hyperkalaemia suggests fludrocortisone under-replacement
Plasma renin activity (if available)	Annually or when adjusting fludrocortisone	Most objective marker of mineralocorticoid replacement adequacy
Weight, BMI	Every visit	Weight gain may indicate over-replacement
Bone mineral density (DEXA scan)	At diagnosis; then every 2–5 years	Glucocorticoid over-replacement increases fracture risk
Autoimmune screen (TSH, HbA1c)	Annually	Screen for associated autoimmune conditions
Sick day rules / emergency kit review	Every visit	Reinforce education; check kit expiry dates; update adrenal crisis letter

Biomarkers of Replacement Adequacy

No single biochemical test perfectly reflects physiological cortisol replacement. In clinical practice, a combination of symptom assessment, body weight trajectory, electrolytes, and ACTH levels is used. Serum cortisol day curves may be helpful in selected patients (e.g., those with persistent symptoms despite apparently adequate dosing).

Over-replacement signs: Weight gain, Cushingoid features (moon face, central adiposity, striae), osteoporosis, hyperglycaemia, hypertension.
Under-replacement signs: Persistent fatigue, weight loss, postural hypotension, hyperpigmentation, hyponatraemia, elevated ACTH.

Special Populations

🤰 Pregnancy

Hydrocortisone — Preferred glucocorticoid in pregnancy (does not cross placenta readily; rapidly inactivated by placental 11β-HSD2). Dose typically increases by 20–40% in the third trimester.

Fludrocortisone — Continue usual dose; may require increase in late pregnancy due to expanded plasma volume and progesterone-mediated mineralocorticoid antagonism.

⚠️ Labour and delivery: Hydrocortisone 100 mg IV at onset of labour/cervical dilation, then 50 mg IV 6-hourly until delivery. Resume oral dosing 24 h post-delivery. Ensure obstetric team and anaesthetist are aware. Elective LSCS — peri-operative hydrocortisone protocol as for major surgery.

⚠️ Prednisolone and dexamethasone cross the placenta and should be avoided as replacement therapy in pregnancy (risk of fetal adrenal suppression and cleft palate).

👶 Paediatrics

Hydrocortisone — 8–12 mg/m²/day PO in 3 divided doses. Neonates: 2–3 mg/kg/day. Use body surface area for dose calculations.

Fludrocortisone — 50–100 µg PO daily; 1–3 µg/kg/day in neonates. Infants may require sodium chloride supplementation (1–4 mmol/kg/day in divided doses) if sodium remains low on fludrocortisone alone.

⚠️ Congenital adrenal hyperplasia (CAH) is the most common cause of primary adrenal insufficiency in children. Management differs — consult paediatric endocrinology. Growth velocity is the most important marker of adequate dosing; over-replacement suppresses growth.

Parental education is critical — parents/carers must be trained in IM hydrocortisone injection. Childcare centres and schools must have an individualised Adrenal Insufficiency Action Plan.

👴 Elderly

Hydrocortisone — Start at the lower end of the dosing range (15 mg/day). Elderly patients are more susceptible to glucocorticoid adverse effects (osteoporosis, glucose intolerance, cognitive effects).

Fludrocortisone — Use cautiously; risk of supine hypertension and oedema. Monitor BP lying and standing.

Fall risk assessment should be performed. DEXA scan at diagnosis. Consider bone-protective therapy (calcium, vitamin D, bisphosphonate) if glucocorticoid exposure is prolonged.

🫘 Renal Impairment

Hydrocortisone — No dose adjustment required (hepatic metabolism). However, cortisol clearance may be reduced in advanced CKD.

Fludrocortisone — Dose may need reduction in CKD (reduced potassium excretion). Monitor K⁺ closely. Hyperkalaemia in CKD + Addison's may be additive and severe.

Patients on dialysis: Fludrocortisone usually not required as dialysis manages electrolytes. Hydrocortisone continues as usual.

🫁 Hepatic Impairment

Hydrocortisone — In severe hepatic impairment, cortisol metabolism may be impaired. Consider lower doses and closer monitoring. Prednisolone (pro-drug not requiring hepatic conversion) may be used as an alternative if needed.

Hypoalbuminaemia may affect cortisol assays (free cortisol may be higher than measured total cortisol). Use clinical assessment alongside biochemistry.

🛡️ Immunocompromised

HIV-associated adrenalitis (CMV, Mycobacterium avium complex) — consider in patients with advanced HIV and unexplained fatigue/hyponatraemia.

Checkpoint inhibitor therapy (nivolumab, pembrolizumab, ipilimumab) can cause immune-related adrenalitis. Monitor cortisol and ACTH in patients on immunotherapy who develop fatigue. Refer to endocrinology.

Hydrocortisone — Standard replacement doses. Stress dosing rules apply as for all patients with adrenal insufficiency.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Epidemiology

Adrenal insufficiency in ATSI populations may be underdiagnosed. Tuberculosis remains an important aetiology — prevalence of active TB in ATSI communities is 6–8 times the non-Indigenous rate (AIHW, 2023). Autoimmune Addison's disease is likely under-recognised due to diagnostic barriers.

Diagnostic challenges

Hyperpigmentation may be difficult to detect in patients with naturally dark skin. Salt craving, fatigue, and weight loss may be attributed to other causes. A low threshold for SST testing is recommended in ATSI patients with unexplained hyponatraemia, hyperkalaemia, or postural hypotension.

Remote & rural access

Access to endocrinology specialists is limited in remote and very remote communities. Telehealth endocrinology consultations (MBS Items 91822/91823) should be utilised. Local health practitioners should be trained in SST administration and interpretation, and in initiating treatment if adrenal crisis is suspected.

TB screening

In ATSI patients presenting with new Addison's disease, consider tuberculous adrenalitis — perform chest X-ray and tuberculin skin test or IGRA (QuantiFERON-TB Gold). Consultation with TB services (RHDAustralia guidelines) is recommended. Calcified adrenals on CT are a clue.

Medication access

Hydrocortisone and fludrocortisone are PBS-listed (General Benefit). In remote communities, ensure adequate supply via Remote Area Aboriginal Health Services (RAAHS) pharmacy or Section 100 (S100) Remote Area Aboriginal Health Service program. Maintain a buffer stock of injectable hydrocortisone at remote clinics.

Cultural safety

Engage Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers in patient education. Use culturally appropriate resources (e.g., NACCHO-endorsed materials). Explain the lifelong nature of treatment in the context of the patient's health beliefs and priorities. Involve family and community in education about adrenal crisis recognition and emergency injection.

Emergency preparedness

In remote communities where ambulance response times may exceed 1 hour, all patients and their close contacts must be trained in IM hydrocortisone self-administration. Ensure the emergency kit is accessible, not expired, and stored appropriately (room temperature, protected from heat in tropical regions). Community clinics should stock emergency hydrocortisone and have protocols for managing adrenal crisis while awaiting retrieval.

📚 References

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