Iron Deficiency & Metabolism

📋 Key Information Summary

📋

Iron deficiency is the most common nutritional deficiency worldwide and the leading cause of anaemia in Australia, particularly affecting premenopausal women, Aboriginal and Torres Strait Islander peoples, the elderly, and those with chronic disease.
Diagnosis requires a combination of tests: serum ferritin (most sensitive single test), serum iron, transferrin saturation (TSAT), and total iron-binding capacity (TIBC). Ferritin <30 µg/L confirms iron deficiency; ferritin 30–100 µg/L with TSAT <20% is suggestive.
Ferritin is an acute-phase reactant — in the setting of inflammation, infection, or liver disease, a ferritin level <100 µg/L may still indicate true iron deficiency.
Investigation of the underlying cause is mandatory, not optional. In men and postmenopausal women, gastrointestinal blood loss must be excluded with bidirectional endoscopy.
Oral iron (ferrous sulfate 325 mg [~65 mg elemental iron] PO daily to TDS) is first-line for non-severe deficiency without malabsorption or intolerance. Alternate-day dosing may improve absorption and reduce side effects.
IV iron is indicated when oral iron is ineffective, poorly tolerated, contraindicated (e.g., IBD flare, CKD on ESA), or when rapid repletion is needed (e.g., perioperative, pregnancy in third trimester).
Ferric carboxymaltose (Ferinject®) and iron polymaltose (Ferrosig®) are commonly used IV iron preparations in Australia. Ferric carboxymaltose allows up to 1000 mg in a single infusion.
Expected haemoglobin rise: 10–20 g/L over 2–4 weeks with adequate treatment. Reticulocyte response peaks at days 5–10. Aim to replenish iron stores (target ferritin >100 µg/L) even after haemoglobin normalises.
Iron requirements increase substantially in pregnancy (additional ~1000 mg total), rapid growth periods (infancy, adolescence), and chronic blood loss (menorrhagia, GI bleeding).
Oral iron should not be taken with tea, coffee, calcium supplements, proton pump inhibitors, or antacids — all reduce absorption. Vitamin C (ascorbic acid) enhances non-haem iron absorption.
IV iron carries a small risk of anaphylaxis (estimated <1:200,000 for ferric carboxymaltose), hypophosphataemia (particularly ferric carboxymaltose), and infusion reactions. Monitoring during and after infusion is essential.
Aboriginal and Torres Strait Islander peoples have disproportionately higher rates of iron deficiency driven by nutritional inadequacy, chronic infection, hookworm infestation in remote communities, and barriers to healthcare access.

Introduction & Australian Epidemiology

Iron deficiency is the most common cause of anaemia worldwide and a leading contributor to the global burden of disease. It presents classically with microcytic hypochromic anaemia and manifests clinically with fatigue, pallor, dyspnoea on exertion, pica, restless legs syndrome, koilonychia, and angular cheilitis. In Australia, iron deficiency affects approximately 12% of premenopausal women, 5–8% of men, and up to 20% of Aboriginal and Torres Strait Islander women of reproductive age.

The Australian Institute of Health and Welfare (AIHW) estimates that iron deficiency anaemia contributes to significant healthcare utilisation, particularly in primary care and emergency departments. Populations at greatest risk include premenopausal women (due to menstrual losses), pregnant women (increased fetal and placental demands), infants and adolescents (rapid growth), the elderly (chronic disease, nutritional inadequacy, occult GI blood loss), blood donors, vegetarians and vegans, and individuals with chronic gastrointestinal conditions such as coeliac disease or inflammatory bowel disease.

Iron deficiency exists on a spectrum: depleted iron stores precede iron-deficient erythropoiesis, which in turn precedes frank iron deficiency anaemia (IDA). Early identification and treatment of iron deficiency — before anaemia develops — is important to prevent symptomatic morbidity, impaired cognitive function in children, adverse pregnancy outcomes, and reduced quality of life. This guideline provides a comprehensive overview of iron metabolism, causes, investigation, and management aligned with Australian practice.

Iron Metabolism & Stores

Iron is an essential element required for oxygen transport (haemoglobin and myoglobin), electron transfer in the mitochondrial respiratory chain (cytochromes), DNA synthesis, and numerous enzymatic reactions. Total body iron in a healthy adult is approximately 3–4 g, distributed as follows:

Compartment	Amount (approx.)	% of Total	Function
Haemoglobin iron	2.0–2.5 g	~65%	Oxygen transport
Storage iron (ferritin, haemosiderin)	0.5–1.0 g	~20–25%	Reserve pool (liver, spleen, bone marrow macrophages)
Myoglobin iron	~200 mg	~5%	Muscle oxygen storage
Tissue iron (cytochromes, enzymes)	~150 mg	~4%	Cellular respiration, enzymatic function
Transport iron (transferrin-bound)	~3 mg	<1%	Iron delivery to erythroid precursors

Key Regulatory Proteins

Divalent metal transporter 1 (DMT1): Located on the apical membrane of duodenal enterocytes; mediates uptake of non-haem (ferrous) iron.
Ferroportin: The sole known cellular iron exporter, located on the basolateral membrane of enterocytes and on macrophages. Regulated by hepcidin.
Hepcidin: A 25-amino-acid peptide hormone synthesised by the liver. The master regulator of systemic iron homeostasis. Hepcidin binds to ferroportin, triggering its internalisation and degradation, thereby reducing iron absorption from the gut and iron release from macrophages.
Transferrin: The plasma iron transport glycoprotein. Each molecule binds two ferric (Fe³⁺) ions. Transferrin saturation (TSAT) reflects the proportion of transferrin binding sites occupied by iron.
Ferritin: An intracellular iron storage protein; serum ferritin is proportional to total body iron stores (in the absence of inflammation).
Hephaestin and caeruloplasmin: Ferroxidases that oxidise Fe²⁺ to Fe³⁺ for loading onto transferrin.

Iron Absorption

Dietary iron exists in two forms: haem iron (from animal sources: red meat, poultry, fish) and non-haem iron (from plant sources, fortified foods). Haem iron is absorbed intact via the haem carrier protein 1 (HCP1) at 15–35% efficiency. Non-haem iron must be reduced from Fe³⁺ to Fe²⁺ by duodenal cytochrome b (DcytB) and then absorbed via DMT1 at 2–20% efficiency. Non-haem iron absorption is enhanced by ascorbic acid, citric acid, and animal protein, and inhibited by phytates, polyphenols (tea, coffee), calcium, and certain medications (PPIs, antacids).

Daily iron losses are approximately 1–2 mg/day (desquamation of GI mucosal cells, skin, urinary losses). Menstruating women lose an additional 0.5–1 mg/day on average (higher with heavy menstrual bleeding). The recommended daily intake (NHMRC Nutrient Reference Values) is 8 mg/day for adult men, 18 mg/day for premenopausal women, 27 mg/day in pregnancy, and 9 mg/day for lactating women.

Causes of Iron Deficiency

Iron deficiency results from an imbalance between iron intake/absorption and iron losses/demand. The three principal aetiological categories are blood loss, malabsorption, and increased physiological demand. In clinical practice, multiple factors often coexist.

1. Blood Loss (Most Common Cause)

⚠️

Critical: In men and postmenopausal women with confirmed iron deficiency, gastrointestinal malignancy must be excluded. Up to 10–15% of patients with iron deficiency without anaemia and GI symptoms harbour a significant GI lesion, including colorectal cancer. Bidirectional endoscopy (OGD and colonoscopy) is mandatory unless an alternative clear cause is identified.

Gastrointestinal blood loss: Colorectal cancer, gastric cancer, oesophagitis/gastritis, peptic ulcer disease, angiodysplasia, inflammatory bowel disease, NSAID gastropathy, hookworm infestation (particularly in ATSI remote communities), hereditary haemorrhagic telangiectasia, Meckel's diverticulum.
Gynaecological: Heavy menstrual bleeding (HMB) — the most common cause in premenopausal women. Defined as >80 mL blood loss per cycle or symptoms of excessive menstrual flow. Causes include fibroids, adenomyosis, endometrial polyps, coagulopathy (e.g., von Willebrand disease), and anovulatory cycles.
Other: Frequent blood donation, chronic haematuria (e.g., IgA nephropathy), intravascular haemolysis (e.g., mechanical heart valves, paroxysmal nocturnal haemoglobinuria), post-surgical blood loss.

2. Malabsorption

Coeliac disease: Affects ~1% of the Australian population; frequently presents with iron deficiency as the sole manifestation. All patients with unexplained iron deficiency should be screened with tissue transglutaminase (tTG) IgA and total IgA.
Helicobacter pylori infection: Causes iron deficiency through altered gastric acid secretion (impairing non-haem iron absorption), increased iron utilisation by the bacterium, and chronic blood loss from gastritis.
Atrophic gastritis / auto-immune gastritis: Reduced gastric acid impairs Fe³⁺ → Fe²⁺ conversion. May coexist with pernicious anaemia (vitamin B12 deficiency).
Inflammatory bowel disease: Active inflammation of the duodenum/proximal ileum, chronic blood loss, and hepcidin-mediated iron sequestration.
Bariatric surgery: Roux-en-Y gastric bypass and sleeve gastrectomy reduce the absorptive surface and bypass the duodenum (primary site of iron absorption).
Medications: Proton pump inhibitors (PPIs), H2-receptor antagonists, calcium supplements, and antacids reduce non-haem iron absorption by raising gastric pH.
Other: Chronic diarrhoea, previous gastrectomy, small bowel resection.

3. Increased Demand

Pregnancy: Total iron requirement ~1000 mg (expanded maternal red cell mass ~450 mg, fetal/placental iron ~300 mg, blood loss at delivery ~250 mg). Without supplementation, most women become iron deficient.
Lactation: Additional 0.5–1 mg/day lost in breast milk.
Rapid growth periods: Infancy (particularly premature neonates with low iron stores), adolescence (especially with HMB onset).
Athletes: Endurance athletes with increased GI losses (runner's colitis), haemolysis (foot-strike), and sweat iron losses.

4. Reduced Dietary Intake

Vegetarian and vegan diets (non-haem iron with lower bioavailability ~5–12%).
Restricted diets — elderly living alone, food insecurity, eating disorders.
Inadequate dietary diversity in remote ATSI communities.

5. Functional Iron Deficiency

In chronic inflammatory conditions (CKD, CHF, cancer, chronic infections), elevated hepcidin impairs iron absorption and macrophage iron release, leading to iron-restricted erythropoiesis despite adequate or even elevated iron stores. This is termed functional iron deficiency and is distinct from true (absolute) iron deficiency. TSAT <20% with ferritin >100 µg/L in the setting of inflammation suggests functional deficiency.

Investigations

Iron Studies — Core Tests

Test	Normal Range	Iron Deficiency	Notes
Serum Ferritin	20–300 µg/L (M) 20–200 µg/L (F)	<30 µg/L (definite) 30–100 µg/L (probable, if TSAT <20%)	Best single marker of iron stores. Acute-phase reactant — may be falsely normal/elevated with inflammation.
Serum Iron	10–30 µmol/L	↓ Low (often <10 µmol/L)	Diurnal variation (higher in AM). Non-specific — low in inflammation, infection.
TIBC	45–80 µmol/L	↑ High (>80 µmol/L)	Reflects transferrin concentration. Rises in iron deficiency as liver produces more transferrin.
Transferrin Saturation (TSAT)	20–50%	<20% (often <15%)	Calculated: (serum iron ÷ TIBC) × 100. Key indicator of iron availability for erythropoiesis.
Soluble Transferrin Receptor (sTfR)	0.8–1.8 mg/L	↑ Elevated	Not affected by inflammation. Useful to distinguish true iron deficiency from anaemia of chronic disease. sTfR/log ferritin index >2 suggests true ID.

Interpreting Iron Studies in the Setting of Inflammation

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Ferritin <30 µg/L: Confirms iron deficiency regardless of CRP.
Ferritin 30–100 µg/L with TSAT <20% and elevated CRP: Probable iron deficiency in the setting of coexisting inflammation.
Ferritin >100 µg/L with TSAT <20%: Functional iron deficiency (CKD, CHF, cancer) — iron stores present but inaccessible to erythroid precursors.
When ferritin interpretation is uncertain, sTfR or the sTfR/ferritin index can help distinguish true deficiency from anaemia of chronic disease.

Full Blood Examination (FBE)

Haemoglobin: Low (anaemia); normal in early iron depletion.
MCV: Low (<80 fL) — microcytosis (late finding).
MCH: Low (<27 pg) — hypochromia.
RDW: Elevated — anisocytosis (helps distinguish from thalassaemia trait where RDW is typically normal).
Blood film: Microcytic hypochromic red cells, pencil cells (elliptocytes), target cells.
Reticulocyte count: Low or inappropriately normal relative to degree of anaemia.

MBS-Itemised Investigations for Underlying Cause

Available

FBE + Iron Studies (MBS 65070, 65090)

First-line. Bulk-billed in most practices.

Available

Coeliac serology — tTG IgA + total IgA (MBS 69456, 69452)

All patients with unexplained IDA. High sensitivity and specificity.

Available

H. pylori test — faecal antigen (MBS 69330) or urea breath test (MBS 69324)

Consider in all patients; eradicate if positive.

Available

Stool FOB / FIT (MBS 69486)

Colorectal cancer screening; positive result mandates colonoscopy.

Available

CRP / ESR

Assess for coexisting inflammation affecting ferritin interpretation.

Available

Renal function + Urinalysis (MBS 66510, 66512)

Exclude CKD, chronic haematuria as iron loss source.

Available

Vitamin B12 and Folate (MBS 66542, 66543)

Co-existing deficiencies common (coeliac disease, malabsorption, pregnancy).

Referral

Bidirectional endoscopy (OGD + colonoscopy)

Mandatory in men and postmenopausal women with confirmed IDA. MBS items: 30473 (colonoscopy), 30471 (OGD). Refer all patients with positive FIT, alarm features, or age >50.

Referral

Capsule endoscopy (MBS 30673)

If bidirectional endoscopy negative and ongoing iron deficiency — small bowel evaluation.

Specialist

Bone marrow iron stores

Rarely required; gold standard for iron store assessment. Consider if diagnostic uncertainty persists.

Pathophysiology

Iron deficiency develops through a predictable sequence of depletion:

Stage 1 — Iron store depletion: Storage iron (ferritin) is consumed to meet ongoing erythropoietic demand. Ferritin falls below normal. No functional deficit yet — haemoglobin and TSAT remain normal.
Stage 2 — Iron-deficient erythropoiesis: Iron supply to the erythroid marrow becomes insufficient. TSAT falls below 20%. RBC precursors show impaired haem synthesis. Haemoglobin may remain normal or begin to decline.
Stage 3 — Iron deficiency anaemia: Haemoglobin falls below sex-specific reference ranges. Microcytic, hypochromic anaemia develops. Marrow erythroid hyperplasia with absent stainable iron. Clinical symptoms (fatigue, dyspnoea, pallor) become apparent.

At the cellular level, iron deficiency impairs:

Haem synthesis: Reduced haem leads to decreased haemoglobin production, smaller RBCs, and impaired oxygen delivery.
Myoglobin synthesis: Results in impaired muscle function and exercise intolerance.
Mitochondrial function: Iron-containing cytochromes and iron-sulphur cluster proteins are essential for oxidative phosphorylation. Deficiency causes cellular energy deficit.
Immune function: Impaired lymphocyte proliferation and neutrophil bactericidal activity.
Neurological function: Iron is a cofactor for tyrosine hydroxylase and tryptophan hydroxylase (dopamine and serotonin synthesis). Deficiency causes cognitive impairment, restless legs syndrome, and pica.
Epithelial integrity: Glossitis, angular cheilitis, koilonychia, Plummer–Vinson syndrome (oesophageal web, dysphagia, iron deficiency triad).

Hepcidin–Ferroportin Axis

Hepcidin is the central regulator of iron homeostasis. In iron-replete states, hepcidin binds ferroportin on enterocytes and macrophages, causing its internalisation and lysosomal degradation, thereby reducing iron absorption and release. In iron deficiency, hepcidin production is suppressed (mediated by decreased BMP-SMAD signalling and increased erythroferrone from erythroid precursors), allowing maximal iron absorption and macrophage iron recycling. In inflammation, IL-6 drives hepcidin production via the JAK-STAT3 pathway, leading to functional iron deficiency — iron is trapped in macrophages and enterocytes, unavailable for erythropoiesis.

Clinical Presentation & Diagnostic Criteria

Symptoms

Iron deficiency may be asymptomatic in early stages. Symptoms include:

General: Fatigue, weakness, lethargy, reduced exercise tolerance, dyspnoea on exertion.
Neurological: Poor concentration, impaired memory, irritability, restless legs syndrome (up to 25% of patients with IDA).
Pica/pagophagia: Compulsive craving for ice, starch, or dirt — highly specific for iron deficiency.
Dermatological: Pallor (conjunctival, palmar), koilonychia (spoon nails), angular cheilitis, hair loss.
Oral: Glossitis, atrophic tongue papillae.
ENT: Dysphagia (Plummer–Vinson syndrome — oesophageal web, typically postmenopausal women).
Gynaecological: Menorrhagia (may be both cause and consequence).
Cardiovascular: Tachycardia, palpitations, flow murmur (with severe anaemia).

Diagnostic Criteria

ℹ️

Iron deficiency: Ferritin <30 µg/L (or ferritin 30–100 µg/L with TSAT <20% and elevated CRP).
Iron deficiency anaemia: Iron deficiency (as above) PLUS haemoglobin below reference range: <120 g/L (non-pregnant women), <110 g/L (pregnant women), <130 g/L (men).
Functional iron deficiency: TSAT <20% with ferritin >100 µg/L in the context of chronic inflammation or erythropoiesis-stimulating agent (ESA) therapy.

Differential Diagnosis of Microcytic Anaemia

Condition	Ferritin	TSAT	RDW	Hb Electrophoresis
Iron deficiency anaemia	↓	↓	↑	Normal
Thalassaemia trait (α or β)	Normal/↑	Normal	Normal/↑ slightly	↑ HbA2 (β), abnormal (α)
Anaemia of chronic disease	Normal/↑	↓	Normal	Normal
Sideroblastic anaemia	↑	↑	↑	Normal
Lead poisoning	Normal/↑	Normal/↓	↑	Normal

Management — Oral & IV Iron Replacement

The goals of iron replacement therapy are: (1) correct anaemia and restore haemoglobin to target; (2) replenish iron stores (ferritin >100 µg/L); and (3) identify and treat the underlying cause. Concurrent investigation and treatment of the underlying cause is essential — iron replacement alone without addressing ongoing losses or malabsorption will result in recurrent deficiency.

Oral Iron — First-Line Therapy

Oral iron is the initial treatment for most patients with iron deficiency without severe anaemia, malabsorption, intolerance, or need for rapid repletion.

💊

Ferrous Sulfate (325 mg tablet = ~65 mg elemental iron)

Ferro-Gradumet® · Various generics · Oral iron

Adult dose 325 mg (1 tablet) PO once daily to TDS. Alternate-day dosing (e.g., every second day) achieves similar absorption with fewer GI side effects.

Paediatric dose 3–5 mg/kg/day elemental iron, divided BD–TDS. Ferrous sulfate liquid (e.g., Ferro-Liquid® 5 mL = 15 mg elemental iron).

Route Oral

Duration 3–6 months after haemoglobin normalisation (to replenish stores). Total duration often 4–9 months.

Renal adjustment No dose adjustment. Consider IV iron if CKD stage 4–5.

PBS status ✔ PBS General Benefit

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Ferrous Fumarate (325 mg tablet = ~107 mg elemental iron)

Ferro-Tab® · Various generics

Adult dose 325 mg PO once daily.

PBS status ✔ PBS General Benefit

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Ferrous Gluconate (300 mg tablet = ~35 mg elemental iron)

Various generics

Adult dose 300–600 mg PO BD–TDS. Lower elemental iron content — better tolerated GI.

PBS status ✔ PBS General Benefit

💡

Tips to optimise oral iron therapy:

Take on an empty stomach (1 hour before or 2 hours after food) for maximal absorption.
Pair with vitamin C (250–500 mg ascorbic acid) to enhance non-haem iron absorption.
Separate from tea, coffee, calcium supplements, and antacids/PPIs by at least 2 hours.
Alternate-day dosing (once every 2 days) reduces hepcidin-mediated suppression and improves fractional absorption by up to 40%, while halving GI side effects.
Expect reticulocyte rise by days 5–10 and haemoglobin rise of 10–20 g/L by 2–4 weeks. Recheck FBE and iron studies at 4–8 weeks.

When to Consider IV Iron

Oral iron intolerance (refractory GI side effects).
Inadequate response to oral iron after 4–8 weeks (haemoglobin rise <10 g/L).
Malabsorption (coeliac disease, IBD, bariatric surgery, atrophic gastritis).
Chronic kidney disease (stage 4–5, particularly on erythropoiesis-stimulating agents).
Need for rapid repletion: perioperative, severe anaemia (Hb <70–80 g/L), late pregnancy (3rd trimester), chronic heart failure.
Ongoing blood loss exceeding oral iron replacement capacity.
Inflammatory bowel disease with active disease.

IV Iron Preparations — Australian Formulary

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Ferric Carboxymaltose

Ferinject® · IV iron

Adult dose Up to 1000 mg IV in 15 minutes infusion. May repeat after ≥7 days if total iron deficit >1000 mg. Maximum 1000 mg per infusion.

Iron deficit calculation Ganzoni formula: Body weight (kg) × (target Hb − actual Hb) (g/L) × 0.24 + 500 mg (stores).

Key side effect Hypophosphataemia (occurs in 5–50% — usually transient and asymptomatic). Monitor phosphate at 2–4 weeks post-infusion.

PBS status ⚠ PBS Restricted Benefit — authority required for: oral iron intolerance/inefficacy, CKD stage 4–5, IBD, pregnancy (3rd trimester), preoperative.

💉

Iron Polymaltose

Ferrosig® · IV iron

Adult dose 200 mg IV diluted in 200 mL NaCl 0.9%, infused over 60 minutes. Repeat as needed.

Key side effect Lower risk of hypophosphataemia compared to ferric carboxymaltose. Infusion reactions possible.

PBS status ⚠ PBS Restricted Benefit — as per ferric carboxymaltose criteria.

💉

Ferric Derisomaltose (Monofer®)

Monofer® · IV iron

Adult dose Up to 20 mg/kg IV (max 1500 mg) in a single infusion over 30–60 minutes. Can replete total iron deficit in one visit.

Key side effect Low hypophosphataemia risk. Infusion reactions (rare).

PBS status ⚠ PBS Restricted Benefit

🚨

IV iron safety: Anaphylaxis risk is very low (<1:200,000 for ferric carboxymaltose). Resuscitation equipment and trained staff must be available. Patients should be observed for ≥30 minutes post-infusion. Do not use IV iron in first trimester of pregnancy, active systemic infection, or iron overload (ferritin >500 µg/L or TSAT >50%). Hypophosphataemia monitoring is recommended at 2–4 weeks after ferric carboxymaltose infusions.

Monitoring Response to Treatment

Days 5–10

Reticulocyte count peaks (reticulocyte crisis). First evidence of therapeutic response.

Weeks 2–4

Haemoglobin rise of 10–20 g/L expected. Recheck FBE. If <10 g/L rise, reassess adherence, ongoing losses, malabsorption, or alternative diagnosis.

Weeks 4–8

Repeat iron studies (ferritin, TSAT). Haemoglobin should be normalising.

Months 3–6

Continue oral iron for at least 3 months after haemoglobin normalisation. Target ferritin >100 µg/L.

Ongoing

Recheck iron studies 3–6 months after cessation. Monitor for recurrence, especially if underlying cause persists (e.g., HMB, CKD).

Special Populations

🤰

Pregnancy

Screening:

Iron studies at booking visit and 28 weeks. All pregnant women should receive iron supplementation (30–60 mg elemental iron/day) if stores are low.

Oral iron:

Ferrous sulfate 325 mg PO daily with vitamin C. Alternate-day dosing tolerated better.

IV iron:

Ferric carboxymaltose safe in 2nd and 3rd trimesters. Avoid in first trimester. Indicated if severe IDA, intolerance, or late presentation.

Target:

Hb >110 g/L by delivery. Ferritin >30 µg/L.

Iron requirements peak in 3rd trimester (~6–7 mg/day absorbed needed). Post-partum iron loss from delivery averages 250 mg. Recheck at 6-week postnatal visit.

👶

Paediatrics

High-risk groups:

Premature infants, low-birthweight, exclusive breastfeeding beyond 6 months without iron-containing complementary foods, cow's milk introduction <12 months, poor dietary intake.

Oral iron:

Ferrous sulfate drops 3–5 mg/kg/day elemental iron, divided BD–TDS, on empty stomach.

Duration:

Continue for 2–3 months after haemoglobin normalisation.

IV iron:

Ferric carboxymaltose not PBS-listed for children <14 years. Iron sucrose or polymaltose in specialist settings.

Iron deficiency in infancy is associated with irreversible cognitive impairment if untreated. Delayed cord clamping at birth reduces incidence of infant iron deficiency.

👴

Elderly

Common causes:

GI blood loss (malignancy, NSAIDs, angiodysplasia), nutritional inadequacy, chronic disease.

Threshold for investigation:

Lower — must exclude GI malignancy. Bidirectional endoscopy recommended even with mild iron deficiency.

Treatment:

Oral iron may be poorly tolerated (constipation common). IV iron often better tolerated and effective. Address contributing medications (NSAIDs, anticoagulants).

🫘

Chronic Kidney Disease

Functional iron deficiency:

Common in CKD stage 4–5. TSAT <20%, ferritin >100 µg/L. Iron trapped in stores due to hepcidin.

Oral iron:

Generally ineffective in CKD stage 4–5 (reduced absorption, hepcidin-mediated blockade).

IV iron:

First-line in CKD 4–5 and dialysis patients. Target TSAT 20–30%, ferritin 200–500 µg/L. Ferric carboxymaltose or iron sucrose per renal unit protocols.

Caution:

Avoid ferritin >500 µg/L or TSAT >50% (iron overload risk). Monitor FBC, ferritin, TSAT regularly.

🛡️

Inflammatory Bowel Disease

Prevalence:

Up to 70% of IBD patients have iron deficiency (blood loss, malabsorption, inflammation-driven hepcidin).

Oral iron:

Often worsens GI symptoms (diarrhoea, cramping, bloating). Ferrous sulfate particularly poorly tolerated.

IV iron:

Preferred in moderate–severe IBD, active flares, or oral intolerance. Ferric carboxymaltose is first-line in this setting.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Prevalence

Iron deficiency anaemia is 2–3 times more prevalent in Aboriginal and Torres Strait Islander populations compared to non-Indigenous Australians, particularly in women of reproductive age, children, and remote communities. The AIHW reports significantly higher rates of iron deficiency-related hospitalisations in ATSI peoples.

Key contributors

Nutritional inadequacy (food insecurity, limited access to fresh iron-rich foods in remote areas), chronic infection burden (Helicobacter pylori, soil-transmitted helminths including hookworm in tropical/remote NT and QLD), chronic inflammatory disease, chronic kidney disease (higher prevalence in ATSI communities), higher rates of HMB without gynaecological access.

Hookworm (Necator americanus)

Endemic in some remote tropical communities. Causes chronic GI blood loss and iron deficiency. Stool microscopy and/or PCR testing should be considered in ATSI patients in endemic areas with unexplained iron deficiency. Treatment with albendazole 400 mg stat is indicated. RHDAustralia guidelines recommend consideration of hookworm in all remote ATSI patients with IDA.

Barriers to care

Geographic isolation and limited specialist services (gastroenterology, haematology) in remote and very remote communities. Cultural and language barriers — interpreter services should be used where needed. Distrust of health services due to historical and ongoing systemic inequities. Cost of medications and transport to health services. Lower health literacy regarding iron supplementation adherence and dietary modification.

Cultural considerations

Respect for family and community decision-making processes. Involve Aboriginal Health Workers and Aboriginal Liaison Officers in care planning. Traditional foods rich in iron (kangaroo, shellfish, bush foods) may be culturally appropriate dietary advice. Yarning-based education approaches may be more effective than written materials. Ensure female patients can see female providers for gynaecological assessments where preferred.

Management approach

Oral iron therapy is appropriate first-line if accessible and tolerated. IV iron via outreach services (ferric carboxymaltose allows single-visit infusion) is particularly valuable for remote patients unable to attend multiple appointments. Telehealth follow-up for monitoring iron studies. Collaborate with local Aboriginal Community Controlled Health Organisations (ACCHOs) for ongoing care coordination. Address food security through community programs and Close the Gap PBS co-payment initiatives.

Screening

NHMRC guidelines recommend iron studies as part of routine health assessments for ATSI peoples. All ATSI pregnant women should have iron studies at first antenatal visit and at 28 weeks. Annual screening for iron deficiency in ATSI children at health checks. Lower threshold for investigation of iron deficiency in ATSI adults of any age.

📚 References

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