Med2Date β€” Clinical Guidelines
Home Clinical Examination The Endocrine System

The Endocrine System

Last updated 31 May 2026 Β· Endocrinology

πŸ“‹ Key Information Summary

πŸ“‹
  • Endocrine history must systematically screen for weight change, sweating, heat/cold intolerance, palpitations, skin and hair changes, sexual dysfunction, polyuria/polydipsia, and menstrual irregularity β€” these are the cardinal symptom clusters that localise endocrine pathology.
  • Thyroid examination proceeds through inspection β†’ palpation β†’ auscultation; a solitary nodule carries ~5–15 % malignancy risk and requires ultrasound Β± fine-needle aspiration (FNA) per the Bethesda classification.
  • Goitre is classified as diffuse or nodular; the commonest causes in Australia are iodine deficiency (re-emerging post-2010 cessation of voluntary iodisation), autoimmune thyroiditis, and Graves' disease.
  • Graves' disease β€” the leading cause of thyrotoxicosis in Australia β€” produces characteristic eye signs (lid lag, exophthalmos, lid retraction), fine tremor, tachycardia, warm moist skin, and pretibial myxoedema.
  • Causes of thyrotoxicosis include Graves' disease, toxic multinodular goitre, toxic adenoma, subacute thyroiditis (de Quervain's), factitious thyrotoxicosis, and amiodarone-induced thyrotoxicosis (Types 1 and 2).
  • Hypothyroidism examination reveals bradycardia, dry coarse skin, delayed relaxation of reflexes, periorbital oedema, macroglossia, and non-pitting oedema (myxoedema); Hashimoto's thyroiditis is the commonest cause in iodine-replete populations.
  • Acromegaly signs include enlarged hands/feet, frontal bossing, prognathism, macroglossia, and widened palmar creases; screen with IGF-1 and confirm with oral glucose tolerance test (OGTT) β€” GH should suppress to < 1 Β΅g/L.
  • Cushing's syndrome presents with central obesity, moon face, buffalo hump, purple striae (> 1 cm), proximal myopathy, easy bruising, and hypertension; differentiate ACTH-dependent from ACTH-independent causes.
  • Adrenal insufficiency (Addison's disease) β€” look for hyperpigmentation (palmar creases, buccal mucosa, scars), postural hypotension, salt craving, and vitiligo; primary adrenal insufficiency is autoimmune in ~80 % of Australian cases.
  • Hypopituitarism may present with fatigue, failure to lactate, loss of secondary sexual characteristics, or features of specific hormone deficiency; investigate with 9 am cortisol, thyroid function, gonadotrophins, IGF-1, and prolactin.
  • Diabetes screening should be considered during any endocrine consultation β€” HbA1c, fasting glucose, or oral glucose tolerance test β€” particularly in patients with Cushing's, acromegaly, phaeochromocytoma, or thyrotoxicosis.
  • Aboriginal and Torres Strait Islander peoples have higher rates of thyroid dysfunction, type 2 diabetes, and later presentation of endocrine disease; culturally safe examination techniques and access to specialist endocrine services in rural/remote areas remain critical gaps.

Introduction & Australian Epidemiology

The endocrine system comprises a network of glands that secrete hormones directly into the bloodstream, regulating metabolism, growth, reproduction, and homeostasis. A systematic endocrine history and examination β€” encompassing the thyroid, pituitary, adrenal, gonadal, and pancreatic axes β€” is fundamental to clinical practice in Australian primary care and specialty settings.

Endocrine disorders are highly prevalent in Australia. The Australian Institute of Health and Welfare (AIHW) reports that thyroid disease affects approximately 1 in 10 Australians, with autoimmune thyroiditis and iodine deficiency disorders being the most common causes. Diabetes mellitus (predominantly type 2) affects over 1.3 million Australians, with significantly higher prevalence among Aboriginal and Torres Strait Islander peoples. Cushing's syndrome, although uncommon (estimated incidence 0.7–2.4 per million per year), is frequently unrecognised for years. Acromegaly has an estimated prevalence of 40–130 per million, with a diagnostic delay averaging 7–10 years.

Iodine deficiency has re-emerged as a public health concern in Australia following the cessation of mandatory iodisation of bread in 2010 (replaced by voluntary measures). National surveys show that pregnant women and children in parts of Victoria, New South Wales, and Tasmania are at particular risk. Conversely, areas of Queensland and the Northern Territory have historical iodine sufficiency.

This article provides a structured approach to the endocrine history and clinical examination, covering thyroid, pituitary, and adrenal assessment, with emphasis on Australian clinical practice, common presentations, and differentiation of endocrine syndromes.

Condition Estimated Australian Prevalence Key Risk Groups
Hypothyroidism (subclinical + overt) ~5–10 % of adults; higher in women > 60 Women, elderly, Down syndrome, Turner syndrome, type 1 diabetes, coeliac disease
Hyperthyroidism ~1–2 % of women; 0.1–0.2 % of men Women aged 20–50, smokers (Graves'), amiodarone users
Type 2 diabetes ~5.3 % (1.3 million); higher in ATSI populations (~14 %) Obesity, age > 40, ATSI, Pacific Islander, South Asian descent, PCOS, GDM history
Cushing's syndrome ~0.7–2.4 per million per year Exogenous corticosteroid use (commonest cause), pituitary adenoma, adrenal adenoma
Acromegaly ~40–130 per million Adults 30–50, pituitary adenoma; rarely MEN1
Primary adrenal insufficiency ~100–140 per million Autoimmune (Addison's), bilateral adrenal haemorrhage, TB (immigrants), medications (ketoconazole, etomidate)

Endocrine History

A thorough endocrine history is the cornerstone of diagnosis. Endocrine diseases are protean in their presentation and frequently masquerade as psychiatric, cardiac, or musculoskeletal conditions. The clinician must systematically elicit symptoms relating to each major axis.

Cardinal Symptom Domains

1
Weight Change
Quantify change (kg) over timeframe (weeks/months). Unintentional weight loss suggests thyrotoxicosis, phaeochromocytoma, uncontrolled diabetes, adrenal insufficiency, or hypopituitarism. Weight gain suggests hypothyroidism, Cushing's syndrome, insulinoma, or PCOS. Ask about appetite changes β€” hyperphagia with weight loss (thyrotoxicosis) vs. hyperphagia with weight gain (Cushing's, insulin resistance).
2
Sweating & Temperature Intolerance
Heat intolerance and increased sweating β†’ thyrotoxicosis, phaeochromocytoma, menopause. Cold intolerance and decreased sweating β†’ hypothyroidism, hypopituitarism. Night sweats may suggest phaeochromocytoma, carcinoid syndrome, or menopause. Ask specifically about the need for extra blankets or fans.
3
Palpitations & Cardiovascular Symptoms
Palpitations, exertional dyspnoea, and exercise intolerance suggest thyrotoxicosis, phaeochromocytoma, or acromegalic cardiomyopathy. Orthostatic dizziness β†’ adrenal insufficiency, autonomic neuropathy (diabetes), or phaeochromocytoma. Chest pain in a young patient with thyrotoxicosis warrants urgent assessment for atrial fibrillation and cardiac failure.
4
Skin, Hair & Nail Changes
Dry skin, brittle hair, and hair loss β†’ hypothyroidism, iron deficiency, hypopituitarism. Hyperpigmentation (especially palmar creases, buccal mucosa, scars) β†’ Addison's disease or ectopic ACTH. Acne and hirsutism β†’ PCOS, Cushing's, congenital adrenal hyperplasia. Easy bruising β†’ Cushing's. Vitiligo β†’ autoimmune thyroid disease or Addison's.
5
Sexual & Reproductive Dysfunction
Erectile dysfunction, decreased libido β†’ hypogonadism (primary or secondary), hyperprolactinaemia, hypothyroidism, diabetes. Menstrual irregularity (oligomenorrhoea, amenorrhoea) β†’ PCOS, hyperprolactinaemia, thyroid disease, Cushing's, hypothalamic amenorrhoea. Infertility β†’ assess all axes. Galactorrhoea β†’ hyperprolactinaemia (prolactinoma, hypothyroidism, medications).
6
Polyuria, Polydipsia & Fluid Balance
Polyuria (β‰₯ 3 L/day) and polydipsia β†’ diabetes mellitus, diabetes insipidus (cranial or nephrogenic), hypercalcaemia, or psychogenic polydipsia. Nocturia is common. Ask about urine volume, colour, and frequency. Polyuria with dilute urine and hypernatraemia β†’ diabetes insipidus. Polyuria with glycosuria β†’ diabetes mellitus.
7
Musculoskeletal & Neurological
Proximal myopathy β†’ Cushing's, thyrotoxicosis, osteomalacia/hyperparathyroidism. Bone pain β†’ hyperparathyroidism, osteoporosis, Paget's disease. Carpal tunnel syndrome β†’ hypothyroidism, acromegaly. Headache and visual field defects β†’ pituitary macroadenoma. Paraesthesiae and tetany β†’ hypoparathyroidism, hypocalcaemia.
8
Medication & Family History
Always ask about: corticosteroids (oral, inhaled, topical β€” iatrogenic Cushing's), amiodarone (thyrotoxicosis/hypothyroidism), lithium (thyroid disease), metoclopramide/prochlorperazine (hyperprolactinaemia), combined oral contraceptives, and antipsychotics. Family history of autoimmune endocrine disease (thyroid, Addison's, type 1 DM, coeliac) clusters under autoimmune polyglandular syndromes.
⚠️
Red-flag symptoms requiring urgent investigation: Acute thyrotoxic storm (fever > 40Β°C, delirium, cardiac failure), myxoedema coma (hypothermia, bradycardia, reduced consciousness), adrenal crisis (severe hypotension, vomiting, confusion β€” often precipitated by illness, surgery, or steroid withdrawal), and pituitary apoplexy (sudden headache, visual loss, ophthalmoplegia).

Symptom Correlation by Endocrine Axis

Axis Hyperfunction Symptoms Hypofunction Symptoms
Thyroid Weight loss, heat intolerance, tremor, palpitations, diarrhoea, anxiety, oligomenorrhoea Weight gain, cold intolerance, constipation, fatigue, menorrhagia, dry skin, hoarse voice
Adrenal cortex Central obesity, striae, proximal myopathy, easy bruising, hypertension, psychosis (Cushing's) Fatigue, weight loss, postural hypotension, salt craving, nausea, hyperpigmentation (Addison's)
Adrenal medulla Episodic headache, sweating, palpitations, hypertension, anxiety (phaeochromocytoma) Not clinically relevant (adrenal medullary insufficiency alone is rare)
Pituitary Acromegaly features, galactorrhoea (prolactinoma), Cushing's (ACTH adenoma), visual field defects Fatigue, amenorrhoea, loss of libido, failure to lactate, growth failure (paediatric)
Parathyroid Stones (renal), bones (pain), groans (constipation), psychic moans (depression/confusion) Tetany, paraesthesiae, seizures, Chvostek's and Trousseau's signs, prolonged QT
Pancreatic islets Hyperglycaemia: polyuria, polydipsia, weight loss, blurred vision (diabetes) Hypoglycaemia: sweating, tremor, confusion, seizures (insulinoma, sulfonylurea excess)

Thyroid Examination & Causes of Goitre

A systematic thyroid examination proceeds through four phases: inspection, palpation, auscultation, and assessment of regional lymph nodes. Always position the patient sitting upright with the neck slightly extended. Ask the patient to swallow water during palpation to elevate the gland.

Step-by-Step Thyroid Examination

1
Inspection
Stand in front of the patient. Ask them to extend the neck slightly and swallow water. Observe for visible swelling, asymmetry, or a mass in the anterior neck that moves with swallowing. Note any surgical scars (thyroidectomy). Assess for midline vs. lateral swelling β€” thyroid masses move with swallowing; lymph nodes and branchial cysts do not. A retrosternal goitre may cause engorgement of neck veins and facial plethora (Pemberton's sign β€” ask patient to raise both arms above the head for 60 seconds).
2
Palpation β€” From Behind (Preferred)
Stand behind the patient. Place fingertips of both hands on either side of the trachea at the level of the cricoid cartilage. Ask the patient to swallow and feel for the thyroid isthmus rising under your fingers. Assess each lobe separately β€” slide fingers laterally from the trachea. Note: size (WHO grading: Grade 0 = not palpable, Grade 1a = palpable, Grade 1b = visible with neck extended, Grade 2 = visible at normal neck position), consistency (soft/firm/hard), tenderness, nodularity, and whether it moves with swallowing.
3
Palpation β€” From the Front (Alternative)
If standing behind is impractical (e.g., patient in bed), use the same technique from the front. Hook your thumb around the trachea and palpate the lobes with the remaining fingers. Palpate each lobe independently.
4
Auscultation
Place the bell of the stethoscope over each thyroid lobe. A thyroid bruit indicates increased vascularity β€” classically found in Graves' disease (due to increased thyroid blood flow, sometimes with a palpable thrill). A bruit may also be heard in Hashitoxicosis and large hypervascular goitres.
5
Lymph Node Assessment & Completion
Palpate the cervical and supraclavicular lymph nodes (central compartment, lateral neck, Virchow's node). Assess for tracheal deviation (deviation away from a large goitre). Check for Horner's syndrome (ipsilateral ptosis, miosis, anhidrosis β€” suggests advanced thyroid malignancy with cervical sympathetic chain involvement).

Solitary Thyroid Nodule Assessment

⚠️
Solitary thyroid nodule: A palpable solitary nodule warrants ultrasound assessment. Approximately 5–15 % of solitary nodules are malignant. Features raising suspicion for malignancy include: hard consistency, irregular borders, fixation to surrounding structures, cervical lymphadenopathy, rapid growth, history of head/neck irradiation, age < 20 or > 60, male sex, and family history of thyroid cancer (MEN2, familial papillary). Use the ACR Thyroid Imaging Reporting and Data System (TI-RADS) to guide FNA biopsy.
TI-RADS Category Risk of Malignancy Recommended Action
TR1 β€” Benign < 2 % No FNA; routine follow-up
TR2 β€” Not suspicious < 2 % No FNA; routine follow-up
TR3 β€” Mildly suspicious 2–5 % FNA if β‰₯ 2.5 cm; follow-up if 1.5–2.5 cm
TR4 β€” Moderately suspicious 5–20 % FNA if β‰₯ 1.5 cm; follow-up if 1–1.5 cm
TR5 β€” Highly suspicious > 20 % FNA if β‰₯ 1 cm; consider FNA if 0.5–1 cm

Causes of Goitre

Category Causes Key Features
Diffuse goitre β€” euthyroid Iodine deficiency, Hashimoto's thyroiditis (early), physiological (puberty, pregnancy), lithium, amiodarone Symmetrically enlarged, smooth, non-tender; TFTs initially normal
Diffuse goitre β€” hyperthyroid Graves' disease, Hashitoxicosis, gestational thyrotoxicosis Symmetrically enlarged, may have bruit/thrill; eye signs in Graves'
Multinodular goitre Multinodular goitre (simple/toxic), long-standing iodine deficiency Irregular, nodular, may become very large; toxic MNG β†’ autonomous hot nodules
Solitary nodule Colloid nodule, thyroid cyst, follicular adenoma, papillary/follicular/medullary/anaplastic carcinoma Single discrete nodule; ultrasound and FNA required for risk stratification
Inflammatory / Acute Subacute thyroiditis (de Quervain's), acute suppurative thyroiditis, Riedel's thyroiditis Tender, may have fever; post-viral onset (de Quervain's); very hard/"woody" (Riedel's)

Hyperthyroidism Examination & Causes of Thyrotoxicosis

Thyrotoxicosis refers to the clinical state of excess thyroid hormone action, regardless of the source. Hyperthyroidism is a subset where the thyroid gland itself is the source. The distinction is clinically important β€” treatment differs depending on the underlying cause.

Examination Findings in Hyperthyroidism

1
General Appearance
Patient appears anxious, restless, and may have significant weight loss despite a good appetite. Warm, moist skin with increased sweating. Fine hair with possible diffuse hair loss. Onycholysis (Plummer's nails). Warm peripheries with a wide pulse pressure.
2
Eye Signs (Graves' Ophthalmopathy)
Lid retraction β€” visible sclera above the superior limbus (due to sympathetic stimulation of MΓΌller's muscle). Lid lag β€” upper lid lags behind the globe on downward gaze (von Graefe's sign). Exophthalmos β€” proptosis measured with an exophthalmometer (normal < 20 mm in Caucasians). Periorbital oedema and chemosis. Conjunctival injection. Assess for ophthalmoplegia β€” restriction of eye movements (inferior rectus most commonly affected β†’ difficulty looking up). Diplopia. Severe sight-threatening orbitopathy: optic neuropathy (reduced visual acuity, colour desaturation, relative afferent pupillary defect).
3
Cardiovascular
Tachycardia β€” resting heart rate > 100 bpm; may have atrial fibrillation (especially in elderly). Wide pulse pressure. Flow murmurs β€” systolic flow murmur at the apex and over the thyroid. High-output cardiac failure in severe or prolonged cases. Bruit over the thyroid (increased vascularity). Check for peripheral oedema and signs of cardiac failure.
4
Neurological / Tremor
Fine tremor β€” ask the patient to extend their fingers with a piece of paper resting on the dorsum; the paper will tremble. Hyperreflexia with shortened relaxation phase. Proximal myopathy β€” difficulty rising from a squat or climbing stairs. Emotional lability and difficulty concentrating. Choreoathetosis (rare β€” thyrotoxic chorea).
5
Dermatological
Warm, moist skin. Pretibial myxoedema (Graves' specific) β€” non-pitting, waxy, orange-peel texture over the shins. Diffuse hyperpigmentation. Onycholysis. Diffuse alopecia. Note: Graves' dermopathy can also affect the forearms and dorsum of feet.

Graves' Disease β€” Specific Signs

ℹ️
Graves' disease is the most common cause of thyrotoxicosis in Australia (60–80 % of cases). It is an autoimmune condition with TSH-receptor stimulating antibodies (TRAb). The classic triad includes: (1) diffuse goitre with thyroid bruit, (2) ophthalmopathy (present in 25–50 %), and (3) dermopathy (present in 1–5 %). Graves' may also present with thyroid acropachy (digital clubbing and periosteal new bone formation β€” very rare). A family history of autoimmune thyroid disease is common. Smoking significantly worsens ophthalmopathy.

Causes of Thyrotoxicosis

Cause Mechanism Key Differentiating Features
Graves' disease TRAb-stimulated diffuse thyroid hyperplasia Diffuse goitre, ophthalmopathy, dermopathy, positive TRAb
Toxic multinodular goitre (TMNG) Autonomous hyperfunctioning nodules Elderly, long-standing nodular goitre, gradual onset; scan shows patchy uptake
Toxic adenoma (Plummer's disease) Single autonomous hyperfunctioning nodule Solitary hot nodule on scintigraphy; remainder of gland suppressed
Subacute thyroiditis (de Quervain's) Inflammatory destruction β†’ release of preformed hormone Painful tender thyroid, post-viral, elevated ESR/CRP; self-limiting (weeks)
Amiodarone-induced thyrotoxicosis (AIT) Type 1: iodine-driven synthesis; Type 2: destructive thyroiditis On amiodarone; can be difficult to treat; Type 2 β†’ corticosteroids; may coexist
Factitious thyrotoxicosis Exogenous thyroid hormone ingestion Suppressed thyroglobulin, absent goitre, low radioiodine uptake
Thyrotoxicosis of pregnancy hCG-mediated (hyperemesis gravidarum) or Graves' First trimester; hyperemesis; transient; check TRAb to distinguish from Graves'
TSH-secreting pituitary adenoma Excess TSH β†’ thyroid stimulation Rare; elevated TSH with elevated T4/T3; MRI pituitary

Hypothyroidism Examination & Causes

Hypothyroidism results from insufficient thyroid hormone production or action. It may be primary (thyroid gland failure), secondary (pituitary TSH deficiency), or tertiary (hypothalamic TRH deficiency). Primary hypothyroidism accounts for > 95 % of cases in Australia.

Examination Findings in Hypothyroidism

1
General Appearance
Patient appears lethargic, overweight, and may have a hoarse or deep voice. Slow movements, slow speech, and delayed responses. Hair is coarse, dry, and brittle with possible lateral eyebrow thinning (Queen Anne's sign). Skin is dry, cool, pale, and may have a yellowish tinge (carotenaemia). Non-pitting oedema (myxoedema) β€” especially periorbital, hands, and feet.
2
Cardiovascular
Bradycardia. Diastolic hypertension (narrowed pulse pressure). Pericardial effusion β€” may have muffled heart sounds and globular heart on CXR. Reduced cardiac output. Hypothyroidism is a reversible cause of heart failure and dyslipidaemia (elevated LDL cholesterol).
3
Neurological
Delayed relaxation of deep tendon reflexes (pseudomyotonic β€” the classic sign, best elicited at the biceps, supinator, or knee jerk). Carpal tunnel syndrome. Cerebellar ataxia (rare). Peripheral neuropathy. Cognitive slowing and depression. Macroglossia β€” enlarged tongue with teeth indentations.
4
Other Systems
Constipation (reduced gut motility). Menorrhagia (common cause in premenopausal women). Goitre β€” may be present (Hashimoto's, iodine deficiency) or absent (post-ablative, post-surgical). Anaemia (normocytic or macrocytic β€” consider associated pernicious anaemia). Hypothermia (especially in myxoedema coma).

Causes of Hypothyroidism

Category Causes Key Features
Primary β€” Autoimmune Hashimoto's thyroiditis (most common cause in Australia), post-partum thyroiditis Anti-TPO antibodies positive; may have goitre; associated with other autoimmune conditions
Primary β€” Iatrogenic Post-radioiodine ablation, post-thyroidectomy, post-external beam radiotherapy (head/neck) History of treatment; no goitre; lifelong thyroxine needed
Primary β€” Drugs Amiodarone, lithium, tyrosine kinase inhibitors, immune checkpoint inhibitors (pembrolizumab, nivolumab), iodine excess (contrast) Medication history essential; checkpoint inhibitor thyroiditis may be painless or destructive
Primary β€” Nutritional Iodine deficiency (re-emerging in parts of Australia) Goitrous hypothyroidism; urinary iodine excretion low; pregnant women at highest risk
Primary β€” Infiltrative Amyloidosis, sarcoidosis, haemochromatosis, Riedel's thyroiditis Rare; hard goitre (Riedel's); consider in multisystem disease
Central (secondary/tertiary) Pituitary tumour/surgery, Sheehan's syndrome, cranial irradiation, infiltrative disease, hypothalamic dysfunction Low T4 with inappropriately low/normal TSH; other pituitary hormone deficiencies present
Congenital Thyroid agenesis, dyshormonogenesis, maternal antithyroid medications Neonatal screening (Guthrie test at 48–72 hours); early treatment prevents intellectual disability
🚨
Myxoedema coma is a life-threatening emergency (mortality 30–60 %). Features include: hypothermia (< 35Β°C), reduced consciousness/coma, bradycardia, hypotension, hypoventilation, hyponatraemia, and hypoglycaemia. Precipitated by infection, cold exposure, surgery, or sedative medications. Immediate management includes IV levothyroxine (loading dose 200–500 Β΅g), IV hydrocortisone (100 mg bolus then 50 mg Q8H β€” to cover potential adrenal insufficiency), passive rewarming, and intensive care admission. Refer to the Australian Resuscitation Council guidelines.

Pituitary Assessment: Acromegaly, Cushing's Disease & Hypopituitarism

The pituitary gland β€” the "master gland" β€” regulates the thyroid, adrenal, gonadal, and growth axes. Pituitary pathology presents with features of hormone excess (functioning adenomas), hormone deficiency (compression of normal tissue), or mass effects (headache, visual field defects). A systematic examination must assess for signs of each anterior pituitary hormone axis.

Acromegaly

Acromegaly results from chronic excess growth hormone (GH), almost always from a pituitary somatotroph adenoma. It has an insidious onset, with a diagnostic delay of 7–10 years being typical. In Australia, it affects approximately 40–130 per million people.

1
Hands & Feet
Enlarged, spade-like hands β€” increased ring and glove size is a patient-reported clue. Increased shoe size. Soft tissue swelling with doughy texture. Increased hand breadth (measure; compare with old photographs). Widened palmar creases.
2
Face & Head
Frontal bossing (frontal bone prominence). Prognathism β€” protrusion of the mandible with resultant underbite and widened dental spacing (increased interdental gap). Macroglossia. Nasal bone enlargement (broadened nose). Coarsened facial features β€” compare with old photographs (Google "time progression acromegaly"). Zygomatic arch prominence. Skin tags (associated with colonic polyps β€” consider colonoscopy).
3
Systemic Complications
Cardiovascular: Hypertension (30–40 %), cardiomegaly, acromegalic cardiomyopathy (biventricular hypertrophy, diastolic then systolic dysfunction, arrhythmias), heart failure. Respiratory: Obstructive sleep apnoea (70 % β€” screen with Epworth Sleepiness Scale), upper airway obstruction. Metabolic: Glucose intolerance/diabetes (up to 50 %). MSK: Arthropathy (large joints), carpal tunnel syndrome (50 %), proximal myopathy. Endocrine: Hyperprolactinaemia (co-secretion), hypogonadism (stalk compression), hypopituitarism.
4
Visual Assessment
Bitemporal hemianopia β€” due to compression of the optic chiasm by a macroadenoma (> 10 mm). Test visual fields by confrontation. Assess visual acuity and colour vision (red desaturation). Fundoscopy β€” papilloedema is rare but optic atrophy may occur.

Investigation of Acromegaly

Essential IGF-1 (insulin-like growth factor 1) Age- and sex-matched; the best screening test. Elevated IGF-1 is suggestive.
Essential Oral glucose tolerance test (OGTT) with GH 75 g glucose load; GH should suppress to < 1 Β΅g/L (or < 0.4 Β΅g/L with ultrasensitive assay). Failure to suppress confirms acromegaly. MBS Item 66540.
Referral MRI pituitary with gadolinium Identifies adenoma size and relationship to the optic chiasm and cavernous sinuses.
Available Pituitary function panel TSH, free T4, 9 am cortisol, FSH, LH, testosterone/oestradiol, prolactin β€” to assess for co-existing hypopituitarism or hyperprolactinaemia.

Cushing's Syndrome

Cushing's syndrome results from chronic glucocorticoid excess. The commonest cause in Australia is exogenous corticosteroid use (iatrogenic). Endogenous causes are classified as ACTH-dependent (80 % β€” Cushing's disease from pituitary ACTH adenoma, or ectopic ACTH from small-cell lung cancer, carcinoid) and ACTH-independent (20 % β€” adrenal adenoma, adrenal carcinoma, bilateral adrenal hyperplasia).

1
Body Habitus
Central obesity β€” truncal fat deposition with relatively thin limbs. Moon face (plethoric, round face). Buffalo hump (dorsocervical fat pad). Supraclavicular fat pads. Madelung's lipomatosis (rare, alcohol-related).
2
Skin
Purple/violaceous striae > 1 cm wide β€” particularly on the abdomen, thighs, breasts, and axillae (red/purple in early stages). Easy bruising (thin, fragile skin). Poor wound healing. Fungal skin infections (tinea, candida β€” especially in intertriginous areas). Acne and hirsutism (androgen excess, especially in adrenal carcinoma). Hyperpigmentation (if ACTH is elevated β€” ectopic ACTH or Cushing's disease with very high ACTH).
3
Musculoskeletal
Proximal myopathy β€” difficulty rising from a squat (Gower's sign), climbing stairs, or lifting arms above head. Osteoporosis β€” vertebral compression fractures (dorsal kyphosis). Avascular necrosis of femoral head (especially with exogenous steroids).
4
Metabolic & Endocrine
Hypertension (70–80 %). Glucose intolerance / diabetes mellitus (50–80 %). Hypokalaemia (especially ectopic ACTH β€” cortisol overwhelms 11Ξ²-HSD2). Menstrual irregularity and erectile dysfunction. Psychiatric β€” depression, psychosis, insomnia, cognitive impairment. Growth retardation in children (exogenous steroids).

Cushing's Syndrome β€” Screening Investigations

Essential 1 mg overnight dexamethasone suppression test (ONDST) Take 1 mg dexamethasone at 11 pm; measure serum cortisol at 9 am next day. Cortisol < 50 nmol/L excludes Cushing's. Best initial screening test. MBS Item 66540.
Essential 24-hour urinary free cortisol (UFC) Collect on 2 separate occasions. Elevated > 3Γ— upper limit of normal is highly suggestive. Mild elevations can occur in depression, obesity, and alcoholism.
Essential Late-night salivary cortisol Collection at 11 pm–midnight. Elevated salivary cortisol has high sensitivity. Two collections recommended.
Referral ACTH level, high-dose dexamethasone suppression test, MRI pituitary, CT adrenals After confirmation of hypercortisolism; differentiate ACTH-dependent vs. ACTH-independent. Inferior petrosal sinus sampling (IPSS) may be needed for localisation (available at specialist centres).

Hypopituitarism

Hypopituitarism β€” deficiency of one or more anterior pituitary hormones β€” may result from pituitary tumours, surgery, radiotherapy, Sheehan's syndrome (postpartum pituitary necrosis), traumatic brain injury, or infiltrative diseases. Loss of hormones follows a characteristic order: GH > LH/FSH > TSH > ACTH > prolactin. Posterior pituitary involvement (ADH, oxytocin) is less common but can cause central diabetes insipidus.

1
GH Deficiency
Fatigue, reduced exercise capacity, increased visceral fat, decreased lean muscle mass, reduced bone density, impaired quality of life. In children: short stature, growth failure, delayed bone age.
2
Gonadotrophin (LH/FSH) Deficiency
Women: amenorrhoea/oligomenorrhoea, infertility, vaginal atrophy, decreased libido, osteoporosis. Men: erectile dysfunction, decreased libido, reduced facial/body hair, testicular atrophy, infertility, osteoporosis. Prepubertal: delayed/absent puberty.
3
TSH Deficiency (Central Hypothyroidism)
Fatigue, cold intolerance, weight gain, constipation, dry skin β€” milder than primary hypothyroidism. Goitre is absent. Low free T4 with inappropriately low/normal TSH.
4
ACTH Deficiency (Secondary Adrenal Insufficiency)
Fatigue, nausea, weight loss, postural hypotension β€” but NO hyperpigmentation (ACTH is low, unlike primary adrenal insufficiency). Risk of adrenal crisis during intercurrent illness. Hyponatraemia (cortisol deficiency β†’ impaired free water excretion).
5
Prolactin Deficiency
Inability to lactate postpartum (Sheehan's syndrome β€” classic presentation). Very rare in other contexts.
⚠️
Pituitary apoplexy: Acute haemorrhage or infarction within a pituitary adenoma presents with sudden severe headache, visual loss, ophthalmoplegia (III, IV, VI nerve palsies), and reduced consciousness. Hydrocortisone 100 mg IV bolus must be given immediately, followed by urgent MRI and neurosurgical assessment. This is a neurosurgical emergency.

Adrenal Assessment: Addison's Disease & Cushing's Syndrome

Addison's Disease (Primary Adrenal Insufficiency)

Addison's disease results from destruction of the adrenal cortex, leading to deficiency of cortisol, aldosterone, and adrenal androgens. In Australia, autoimmune adrenalitis accounts for approximately 80 % of cases. Other causes include bilateral adrenal haemorrhage (Waterhouse-Friderichsen syndrome β€” meningococcal septicaemia), tuberculosis, metastatic disease (lung, breast, melanoma), medications (ketoconazole, etomidate, mitotane), and congenital adrenal hyperplasia.

1
Hyperpigmentation
The hallmark of primary adrenal insufficiency (distinguishes it from secondary). Due to excess ACTH and melanocyte-stimulating hormone (MSH, derived from the same POMC precursor). Check: palmar creases (most reliable site), buccal mucosa and tongue, scars (hyperpigmented), areolae, pressure points (belt line, bra line, knuckles), nail beds, and vermilion border of the lips. Also look for vitiligo (autoimmune depigmentation β€” associated in ~10–15 % of autoimmune Addison's).
2
Cardiovascular & Postural Assessment
Postural hypotension β€” measured as a drop of β‰₯ 20 mmHg systolic or β‰₯ 10 mmHg diastolic on standing. Due to cortisol and aldosterone deficiency (volume depletion, impaired vascular reactivity). Dehydration. Tachycardia (compensatory).
3
General Features
Weight loss and anorexia. Fatigue and weakness (profound). Nausea, vomiting, abdominal pain. Salt craving (aldosterone deficiency β†’ sodium wasting). Arthralgia and myalgia. Psychiatric symptoms β€” depression, irritability, confusion. Hyperkalaemia and hyponatraemia (aldosterone deficiency).

Cushing's Syndrome β€” Revisited (Adrenal Perspective)

When Cushing's syndrome is confirmed, the clinician must determine the aetiology. The investigation algorithm begins with ACTH levels to separate ACTH-dependent (pituitary or ectopic) from ACTH-independent (adrenal) causes.

ACTH-Independent
Adrenal Adenoma
Suppressed ACTH (< 5 pmol/L). Unilateral adrenal mass on CT. Typically less severe hypercortisolism. DHEA-S usually normal. Usually managed surgically (laparoscopic adrenalectomy).
Setting: Endocrine surgical referral
ACTH-Dependent
Cushing's Disease (Pituitary)
Elevated/normal ACTH (5–50 pmol/L). Pituitary microadenoma on MRI (may be occult β€” 40 %). High-dose dex suppression test β†’ cortisol suppresses (> 50 %). IPSS confirms central source. First-line: transsphenoidal surgery.
Setting: Pituitary neurosurgery centre
ACTH-Dependent
Ectopic ACTH / Adrenal Carcinoma
Very high ACTH (> 50 pmol/L) β†’ ectopic ACTH (small-cell lung cancer, bronchial carcinoid). OR very high cortisol with large adrenal mass (> 4 cm), calcification, heterogeneous enhancement β†’ adrenal carcinoma (rare but aggressive). Metyrapone, ketoconazole, or mitotane for adrenal carcinoma. Chemotherapy for SCLC.
Setting: Tertiary oncology / endocrine centre
🚨
Adrenal crisis (Addisonian crisis): Life-threatening emergency presenting with severe hypotension, vomiting, abdominal pain, confusion, and cardiovascular collapse. Most commonly precipitated by physiological stress (infection, surgery, trauma) in patients with known adrenal insufficiency who have not increased their glucocorticoid dose, or in patients with undiagnosed adrenal insufficiency. Immediate treatment: IV hydrocortisone 100 mg bolus, followed by 50 mg every 6–8 hours. IV normal saline (0.9 % NaCl) for fluid resuscitation. Monitor glucose and electrolytes. Do NOT wait for cortisol results to treat. Treat the precipitant (e.g., antibiotics for infection).

Comparison: Primary vs. Secondary Adrenal Insufficiency

Feature Primary (Addison's) Secondary (Pituitary)
ACTH level ↑↑ Elevated ↓ Low / inappropriately normal
Hyperpigmentation Present (classic) Absent
Aldosterone ↓ Low (zona glomerulosa destroyed) Usually normal (RAAS intact)
Hyperkalaemia Common Uncommon
Hyponatraemia mechanism Cortisol + aldosterone deficiency Cortisol deficiency (impaired free water excretion)
Other pituitary deficiencies No Commonly present (GH, TSH, LH/FSH)
Associated conditions Autoimmune polyglandular syndromes, vitiligo, type 1 DM, coeliac Pituitary tumour, post-surgery, cranial irradiation, Sheehan's

Other Adrenal Incidentalomas

Adrenal incidentalomas are discovered in approximately 5 % of abdominal CT scans performed for unrelated indications. The key clinical question is whether the lesion is functioning (secreting cortisol, aldosterone, or catecholamines) or malignant. All adrenal incidentalomas β‰₯ 4 cm with unenhanced CT attenuation > 10 Hounsfield units require further characterisation and may need adrenalectomy.

Must Rule Out (Biochemical)
  • Phaeochromocytoma β€” 24-hour urinary catecholamines/metanephrines or plasma free metanephrines
  • Cushing's β€” 1 mg ONDST
  • Conn's syndrome (primary aldosteronism) β€” aldosterone/renin ratio (if hypertensive)
Suspicious Features for Adrenal Carcinoma
  • Size > 4 cm
  • Unenhanced CT attenuation > 10 HU
  • Irregular margins, calcification, necrosis
  • Rapid growth on serial imaging
  • Contrast washout < 50 % at 15 minutes

Special Populations

🀰 Pregnancy
Thyroid: hCG has TSH-like activity β†’ TSH falls in first trimester (normal). Use trimester-specific reference ranges. Hypothyroidism requires increased levothyroxine dose (↑ 25–50 % as soon as pregnancy confirmed). Uncontrolled hypothyroidism associated with miscarriage, pre-eclampsia, and impaired neurodevelopment.
Graves' disease: TRAb crosses the placenta β†’ neonatal thyrotoxicosis risk. Monitor TRAb at 18–22 weeks. PTU preferred in first trimester (teratogenicity risk with methimazole/carbimazole β€” aplasia cutis). Switch to carbimazole after first trimester.
Adrenal: Hydrocortisone is inactivated by placental 11Ξ²-HSD2 β€” higher doses needed. Prednisolone and dexamethasone cross the placenta. Stress-dose steroids during labour (hydrocortisone 100 mg IV every 6–8 hours).
Diabetes: Gestational diabetes mellitus (GDM) screen at 24–28 weeks (OGTT); manage with metformin or insulin. HbA1c target < 6.5 % (or < 6.0 % if safely achievable).
Note: Radioiodine is contraindicated in pregnancy and breastfeeding. Thyroid ultrasound and FNA are safe.
πŸ‘Ά Paediatrics
Congenital hypothyroidism: Detected on neonatal screening (Guthrie test 48–72 hours). Levothyroxine 10–15 Β΅g/kg/day started within 2 weeks of birth prevents intellectual disability. Monitor TSH and free T4 every 1–2 months in first year.
Short stature: Assess growth velocity, bone age (left wrist X-ray), IGF-1, GH provocation tests. GH deficiency treatment with somatotropin.
Precocious puberty: Girls < 8 years, boys < 9 years with secondary sexual characteristics. Assess GnRH stimulation test, bone age, and brain MRI.
Diabetes: Type 1 DM is the commonest endocrine disease in childhood. Diabetic ketoacidosis (DKA) is a medical emergency in children β€” use the ISPAD/ADIPS fluid and insulin protocols.
Note: Dose adjustments are weight-based. Consult paediatric endocrinology for all children with endocrine disorders.
πŸ‘΄ Elderly
Thyroid: Subclinical hypothyroidism is common (TSH 4.5–10 mIU/L with normal free T4); treatment is controversial. The TRUST trial showed no benefit of levothyroxine in over-65s with subclinical hypothyroidism. Overtreatment risks atrial fibrillation and osteoporosis.
Hyperthyroidism: "Apathetic thyrotoxicosis" β€” presents with weight loss, atrial fibrillation, and heart failure without classic adrenergic symptoms. Amiodarone-induced thyrotoxicosis is increasingly common.
Adrenal: Cortisol levels rise with age. The ONDST may be less specific in the elderly (higher false-positive rate). Secondary adrenal insufficiency is common after prolonged corticosteroid use β€” wean slowly.
Falls & frailty: Overtreatment of thyroid disease, adrenal insufficiency, and hypogonadism all contribute to falls and frailty. Assess bone density (DEXA) in patients on long-term thyroxine with suppressed TSH.
Note: Start low, go slow with hormone replacement in the elderly. Regular review of polypharmacy is essential.
🫘 Renal Impairment
Thyroid: "Sick euthyroid" / non-thyroidal illness syndrome in CKD β€” low T3, low/normal T4, normal/low TSH. Interpret TFTs with caution. Levothyroxine does not require renal dose adjustment but absorption may be altered.
Calcium/phosphate: Secondary hyperparathyroidism is extremely common in CKD (stages 3–5). Check PTH, calcium, phosphate, and vitamin D. Treat with phosphate binders, calcitriol, and cinacalcet (PBS Authority Required).
Adrenal: Cortisol metabolism is prolonged in CKD β€” lower replacement doses may be needed. Hyperkalaemia risk is compounded by aldosterone deficiency.
Note: Metformin is contraindicated if eGFR < 15 mL/min/1.73 mΒ² (dose reduction at eGFR 30–45). Adjust insulin doses in renal impairment.
🫁 Hepatic Impairment
Thyroid: Cirrhosis alters thyroid-binding globulin β†’ low total T4, low T3 (euthyroid sick). Free T4 is usually normal. Diagnosis relies on free T4 and TSH together.
Glucocorticoids: Prednisolone is preferred over prednisone in severe liver disease (prednisone requires hepatic conversion to prednisolone). Hepatic clearance of corticosteroids is prolonged.
Diabetes: Hepatogenous diabetes occurs in 20–40 % of cirrhosis patients. Metformin should be used cautiously in cirrhosis (risk of lactic acidosis). Insulin is often required.
Note: Amiodarone (hepatotoxic) should be used cautiously in patients with liver disease and thyroid dysfunction.
πŸ›‘οΈ Immunocompromised
Immune checkpoint inhibitors (ICPi): Pembrolizumab, nivolumab, ipilimumab β†’ immune-mediated thyroiditis, hypothyroidism, hypophysitis, primary adrenal insufficiency, and type 1 DM. Monitor TFTs, cortisol, glucose before each cycle. Hypophysitis is more common with ipilimumab.
HIV: Increased risk of adrenal insufficiency (CMV adrenalitis, TB, ketoconazole/ritonavir interactions). Central hypothyroidism. Lipodystrophy with antiretroviral therapy.
Transplant: Post-transplant diabetes mellitus (PTDM) with tacrolimus and corticosteroids. New-onset diabetes after transplantation (NODAT) affects 10–30 % of renal transplant recipients.
Note: Immune-mediated endocrinopathies from ICPi may be irreversible (especially hypothyroidism, type 1 DM) and require lifelong hormone replacement.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander peoples experience a disproportionate burden of endocrine disease in Australia. Type 2 diabetes is the single most prevalent chronic condition, and thyroid disorders are underrecognised. Culturally safe, trauma-informed examination and communication are essential.

Diabetes burden
Type 2 diabetes prevalence is approximately 14 % in ATSI adults (vs. 5 % non-Indigenous) and is rising in younger age groups. Diabetic complications β€” nephropathy, retinopathy, neuropathy, and lower limb amputation β€” occur at significantly higher rates. Culturally appropriate diabetes education and support programmes (e.g., Tackling Indigenous Smoking, Deadly Choices) are vital. PBS-subsidised glucose-lowering agents (metformin, SGLT2 inhibitors, GLP-1 receptor agonists) should be offered as per PBS indications. HbA1c targets may need individualisation (e.g., < 7 % or < 8 % depending on comorbidity and hypoglycaemia risk).
Thyroid disease
Iodine deficiency remains a concern in some remote communities, particularly in pregnant women and young children. Iodine supplementation (150 Β΅g/day recommended in pregnancy) is not uniformly accessible. Autoimmune thyroid disease may present later in ATSI populations. Thyroid function testing (TSH, free T4) is available through Medicare-funded pathology services, but access to specialist endocrine services is limited in remote areas β€” use telehealth through the Australian Government's specialist outreach programmes.
Adrenal & pituitary disease
Autoimmune polyglandular syndromes (including Addison's disease) may be underdiagnosed in ATSI populations. Rheumatic fever prophylaxis (intramuscular benzathine penicillin) and chronic corticosteroid use for autoimmune conditions may contribute to secondary adrenal suppression β€” always screen for adrenal insufficiency before steroid withdrawal. Cushing's syndrome from exogenous corticosteroids (for asthma, COPD, rheumatic conditions) is a particular concern in communities with high rates of respiratory disease.
Social & cultural determinants
Housing insecurity, food insecurity (limited access to fresh food in remote communities β€” "food deserts"), and cost of medications are significant barriers to endocrine disease management. Optimal pharmacotherapy may be inaccessible without closing the gap provisions (PBS Co-payment Measure for eligible ATSI patients in remote areas). Always ask about social circumstances in a non-judgemental, culturally safe manner. Involve Aboriginal and Torres Strait Islander health workers and liaison officers in endocrine consultations. Use of yarning (narrative-based communication) may improve patient engagement and understanding of complex endocrine diagnoses.
Screening & prevention
Recommend annual HbA1c (or fasting glucose) for all ATSI adults from age 18 (earlier if risk factors present) as per RACGP guidelines. Annual diabetic foot checks (MBS Item 721/723). Thyroid function screening should be considered in pregnant ATSI women and those with autoimmune conditions. Ensure routine vaccination (influenza, pneumococcal) is up to date, as endocrine patients are at increased infection risk. Engage with local Aboriginal Community Controlled Health Organisations (ACCHOs) for coordinated endocrine care.

πŸ“š References

  1. 1. Royal Australian College of General Practitioners (RACGP). Management of type 2 diabetes: A handbook for general practice. Melbourne: RACGP; 2020.
  2. 2. Australian Institute of Health and Welfare (AIHW). Diabetes: Australian facts. AIHW Cat. No. CVD 83. Canberra: AIHW; 2023.
  3. 3. Grossman A, Johannsson G, Quinkler M, Zelissen P. Therapy of endocrine disease: Perspectives on the management of adrenal insufficiency: clinical insights from across Europe. Eur J Endocrinol. 2013;169(6):R165–R175.
  4. 4. Fleseriu M, Hashim IA, Karavitaki N, et al. Hormonal replacement in hypopituitarism in adults: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(11):3888–3921.
  5. 5. Katznelson L, Laws ER Jr, Melmed S, et al. Acromegaly: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2014;99(11):3933–3951.
  6. 6. Nieman LK, Biller BM, Findling JW, et al. The diagnosis of Cushing's syndrome: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008;93(5):1526–1540.
  7. 7. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343–1421.
  8. 8. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200–1235.
  9. 9. Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association management guidelines for adult patients with thyroid nodules and differentiated thyroid cancer. Thyroid. 2016;26(1):1–133.
  10. 10. Husebye ES, Allolio B, Arlt W, et al. Consensus statement on the diagnosis, treatment and follow-up of patients with primary adrenal insufficiency. J Intern Med. 2014;275(2):104–115.
  11. 11. Li M, Eastman CJ. The changing epidemiology of iodine deficiency. Nat Rev Endocrinol. 2012;8(7):434–440.
  12. 12. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023.
  13. 13. Stimson RH, Anderson AJ, Macfarlane DP, et al. Thyroid disease in pregnancy β€” a clinical update. Intern Med J. 2023;53(5):654–662.
  14. 14. Ha CE, Bhagavan NV. Essentials of Medical Chemistry and Biochemistry. 2nd ed. Amsterdam: Academic Press; 2021. [Chapter on endocrine biochemistry and laboratory diagnostics].
  15. 15. Guidelines Development Committee of the Endocrine Society of Australia. Clinical practice guidelines for the diagnosis and management of primary hyperparathyroidism. Med J Aust. 2023;219(8):380–387.
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, LandewΓ© RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

πŸ“š References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, LandewΓ© RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing β€” misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFΞ± blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).