📋 Key Information Summary
- Autoimmune haemolytic anaemia (AIHA) is caused by autoantibodies directed against red blood cell (RBC) surface antigens, leading to premature RBC destruction.
- The direct antiglobulin test (DAT, Coombs test) is the cornerstone diagnostic investigation; a positive DAT for IgG suggests warm AIHA, while C3 positivity alone suggests cold agglutinin disease (CAD).
- Peripheral blood film shows spherocytes in warm AIHA; polychromasia reflects compensatory reticulocytosis.
- All patients require investigation for secondary causes including lymphoproliferative disorders, systemic lupus erythematosus (SLE), hepatitis C, Epstein–Barr virus, and drug-induced AIHA.
- First-line treatment for warm AIHA is prednisolone 1 mg/kg/day (max 100 mg) PO; taper slowly over 3–6 months once haemoglobin stabilises.
- Avoid RBC transfusion unless life-threatening haemolysis is present; if transfusion is required, use the least incompatible units under specialist guidance.
- Cold agglutinin disease presents with acrocyanosis, Raynaud-like phenomena, and haemolysis triggered by cold exposure; DAT is C3-positive and IgG-negative.
- CAD management centres on cold avoidance and specialist-initiated rituximab (± bendamustine); steroids are generally ineffective in CAD.
- Venous thromboembolism (VTE) risk is significantly elevated in active AIHA; consider thromboprophylaxis in all hospitalised patients.
- Steroid-sparing agents (azathioprine, mycophenolate mofetil, rituximab) are used for steroid-dependent or refractory warm AIHA.
- Splenectomy is a later-line option; patients require pre-operative vaccination against encapsulated organisms (pneumococcus, meningococcus, Haemophilus influenzae type b).
- Aboriginal and Torres Strait Islander peoples may face delayed diagnosis due to access barriers; early referral to haematology is essential in remote and regional settings.
Introduction & Australian Epidemiology
Autoimmune haemolytic anaemia (AIHA) is a group of disorders characterised by autoantibody-mediated destruction of red blood cells. AIHA is classified by the thermal optimum of the causative antibody into warm AIHA (approximately 80–90% of cases), cold agglutinin disease (CAD) (10–15%), and rare mixed-type or paroxysmal cold haemoglobinuria (PCH) subtypes.
In Australia, the estimated annual incidence of AIHA is 1–3 per 100,000 population. AIHA may be idiopathic (primary) or secondary to an underlying condition. Common secondary causes in the Australian context include:
- Lymphoproliferative disorders — chronic lymphocytic leukaemia (CLL), non-Hodgkin lymphoma
- Systemic lupus erythematosus (SLE) and other autoimmune conditions
- Infections — Epstein–Barr virus (EBV), cytomegalovirus (CMV), hepatitis C, Mycoplasma pneumoniae
- Medications — fludarabine, piperacillin–tazobactam, cephalosporins, methyldopa, NSAIDs
- Solid organ transplant (alloimmune haemolysis)
AIHA affects all ages, with a peak incidence in adults aged 40–80 years. There is a slight female preponderance in warm AIHA. CAD has a median age of onset around 65–70 years. Paediatric AIHA is uncommon but may follow viral illness or vaccination and tends to have an acute, often self-limiting course.
The Australian Institute of Health and Welfare (AIHW) data indicate that autoimmune cytopenias contribute to significant hospital admissions, particularly in regional and remote areas where late presentation is more common.
Pathophysiology
AIHA results from loss of immune tolerance to self-antigens on the RBC surface. The mechanism of haemolysis depends on the antibody class and thermal properties:
| Feature | Warm AIHA | Cold Agglutinin Disease | Mixed AIHA |
|---|---|---|---|
| Antibody class | IgG (rarely IgA) | IgM (monoclonal) | IgG + IgM |
| Thermal optimum | 37°C | 3–4°C (range 28–31°C) | Broad range |
| DAT pattern | IgG± / C3± (usually IgG+) | C3 only (IgG−) | IgG+ / C3+ |
| Haemolysis site | Extravascular (splenic) | Extravascular (hepatic) ± intravascular | Both |
| Blood film | Spherocytes, polychromasia | RBC autoagglutination | Mixed features |
| Steroid response | Good initial response | Poor / ineffective | Variable |
Warm AIHA: IgG-coated RBCs are recognised by splenic macrophages via Fcγ receptors. Partial phagocytosis generates spherocytes — rigid, less deformable cells that are eventually trapped and destroyed in the splenic red pulp. If complement (C3b) is also deposited, hepatic Kupffer cells contribute to extravascular haemolysis.
Cold agglutinin disease: Monoclonal IgM (usually targeting the I antigen on RBCs) binds in cooler peripheral vascular beds (fingers, toes, ears, nose). The IgM dissociates upon warming but leaves behind C3b/C4b on the RBC surface. C3b-coated RBCs are phagocytosed by hepatic Kupffer cells (extravascular haemolysis). In severe cases, complement activation proceeds to the membrane attack complex (MAC, C5b–9), causing intravascular haemolysis and haemoglobinuria.
Erythropoietin response: The bone marrow typically mounts a robust reticulocytosis; however, in some cases, a relative reticulocytopenia occurs, worsened by concurrent parvovirus B19 infection or nutritional deficiency (folate, iron), which may exacerbate the anaemia.
Diagnosis
The diagnosis of AIHA requires demonstration of haemolysis together with evidence of immune-mediated RBC destruction. A systematic approach is essential to avoid misdiagnosis, particularly in settings where multiple causes of anaemia coexist.
Diagnostic Criteria
AIHA is diagnosed when all three of the following are present:
- Evidence of haemolysis (biochemical markers — see below)
- Positive direct antiglobulin test (DAT / direct Coombs test)
- Clinical context consistent with autoimmune aetiology (after exclusion of other causes)
DAT-negative AIHA: Up to 5–10% of AIHA cases have a negative standard DAT. Consider DAT-negative AIHA if clinical and laboratory features strongly suggest haemolysis with no alternative cause. Refer to haematology for extended testing (monospecific DAT, flow cytometry, Donath–Landsteiner test for PCH).
Haemolysis Laboratory Markers
| Test | Expected Finding | Notes |
|---|---|---|
| Haemoglobin | ↓ (variable — mild to life-threatening) | May be acutely low in crisis |
| Reticulocyte count | ↑ (usually markedly elevated) | May be inappropriately low in marrow failure or parvovirus |
| Unconjugated bilirubin | ↑ | Predominantly indirect (unconjugated) |
| Lactate dehydrogenase (LDH) | ↑↑ | Non-specific but useful for monitoring disease activity |
| Haptoglobin | ↓↓ (often undetectable) | Low haptoglobin is highly sensitive for haemolysis |
| Urine haemosiderin | Positive in chronic intravascular haemolysis | More relevant in CAD / PCH |
| Folate / Vitamin B12 | Check for concurrent deficiency | Supplement folate if active haemolysis |
Direct Antiglobulin Test (DAT) Interpretation
| DAT Result | Likely Diagnosis | Action |
|---|---|---|
| IgG positive ± C3 positive | Warm AIHA | Investigate secondary causes; start steroids |
| C3 positive only (IgG negative) | Cold agglutinin disease | Cold agglutinin titre; avoid cold exposure; refer haematology |
| IgG positive only (C3 negative) | Warm AIHA (non-complement-binding IgG) | Treat as warm AIHA |
| DAT negative | DAT-negative AIHA, or consider other diagnoses | Extended DAT, haematology referral |
Peripheral Blood Film
- Warm AIHA: Spherocytes (small, round, dense RBCs lacking central pallor), polychromasia (reticulocytes), occasionally nucleated RBCs.
- Cold agglutinin disease: RBC autoagglutination (clumping) — distinguish from rouleaux; agglutination does not disperse on warming to 37°C in CAD.
- PCH: Polychromasia, erythrophagocytosis.
Investigations for Secondary Causes
Essential
Serum protein electrophoresis + immunoglobulins
Screen for lymphoproliferative disorder / CLL
Essential
Flow cytometry (peripheral blood)
If CLL or lymphoma suspected — discuss with haematologist
Essential
ANA, anti-dsDNA, complement (C3/C4)
Screen for SLE and other autoimmune conditions
Available
Hepatitis B, C, HIV serology
Viral-associated AIHA
Available
EBV, CMV serology / PCR
Especially in paediatric or young adult cases
Available
Mycoplasma pneumoniae serology
Associated with cold agglutinin disease (polyclonal)
Specialist
CT chest/abdomen/pelvis
If lymphoma suspected — arrange via haematology
Specialist
Bone marrow biopsy
Not routinely required; consider if cytopenias are multilineage or lymphoma suspected
Specialist
Donath–Landsteiner test
For suspected paroxysmal cold haemoglobinuria (biphasic IgG antibody)
Urgent transfusion situation: If the patient presents with Hb <50 g/L, haemodynamic instability, cardiac failure, or altered consciousness, initiate emergency transfusion with group-compatible (least incompatible) blood. Coordinate with the blood bank and haematology — do NOT delay transfusion in life-threatening anaemia. Send a DAT and antibody screen urgently.
Initial Management — Warm AIHA
Warm AIHA is the most common subtype and is typically responsive to immunosuppressive therapy. Management should be initiated promptly and in consultation with a haematologist.
Treatment Algorithm
1
Confirm Diagnosis & Assess Severity
Positive DAT (IgG±), spherocytes, haemolysis markers. Assess haemodynamic stability and Hb level.
2
Urgent Haematology Referral
All new AIHA diagnoses require haematology input — discuss by phone for acute presentations.
3
Commence Corticosteroids
Start prednisolone 1 mg/kg/day (max 100 mg) PO. IV methylprednisolone for severe/refractory cases.
4
Investigate Secondary Causes
Screen for lymphoma, SLE, hepatitis, drugs — treatment of the underlying cause may resolve AIHA.
5
Supportive Care
Folic acid 5 mg PO daily, VTE prophylaxis, monitor Hb/reticulocytes/LDH daily during acute phase.
First-Line Pharmacotherapy
Prednisolone
Predmix® · Panafcortelone® · Generic · Corticosteroid
Adult dose
1 mg/kg/day PO (max 100 mg) for 1–3 weeks; taper over 3–6 months
Paediatric dose
2 mg/kg/day PO (max 60 mg); taper over weeks to months
Route
Oral (IV methylprednisolone 1 g/day for 1–3 days if severe)
Response rate
~80% initial response; ~20% remain steroid-dependent long-term
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Folic Acid
Generic · Vitamin supplement
Adult dose
5 mg PO daily (required during active haemolysis to support erythropoiesis)
Paediatric dose
2.5–5 mg PO daily
Duration
Ongoing while haemolysis is active
PBS status
✔ PBS General Benefit
Steroid-Sparing Agents (Second-Line)
If the patient is steroid-dependent (unable to taper prednisolone below 15 mg/day within 3–6 months), intolerant of steroid side effects, or relapses after steroid withdrawal, add a steroid-sparing agent:
Rituximab
MabThera® · Ruxience® · Generic · Anti-CD20 monoclonal antibody
Adult dose
375 mg/m² IV weekly × 4 doses (lymphoma schedule) or 1000 mg IV on days 1 and 15
Notes
First-line steroid-sparing agent per 2020 British Society of Haematology (BSH) guidelines. Response rate ~70–80% in warm AIHA.
Key risks
Infusion reactions, hepatitis B reactivation (screen first), hypogammaglobulinaemia
PBS status
✘ Authority Required (Specialist)
Azathioprine
Imuran® · Generic · Purine antimetabolite
Adult dose
2–2.5 mg/kg/day PO (adjust per TPMT/NUDT15 genotype)
Key monitoring
FBC fortnightly initially, then monthly; LFTs; check TPMT/NUDT15 genotype before commencing
Onset
Slow — 3–6 months for full effect
PBS status
✔ PBS General Benefit
Mycophenolate Mofetil
CellCept® · Generic · Immunosuppressant
Adult dose
500 mg PO BD, titrate to 1 g BD as tolerated
Key monitoring
FBC, LFTs; teratogenic — effective contraception required
PBS status
Restricted Benefit (Specialist initiation)
Transfusion in AIHA
Transfusion in AIHA is hazardous. Autoantibodies react with all donor RBCs, making crossmatching difficult. Transfuse only for life-threatening anaemia (Hb <50 g/L with haemodynamic compromise, cardiac failure, or end-organ ischaemia). Always: (1) notify the blood bank of AIHA, (2) request the "least incompatible" units, (3) transfuse slowly with close monitoring, (4) have resuscitation equipment available.
Third-Line Therapies
- Splenectomy: Response rate ~60–70%; reserved for relapsed/refractory cases after rituximab failure. Requires pre-operative vaccination (pneumococcal, meningococcal ACWY + B, Hib). Long-term penicillin V prophylaxis post-splenectomy.
- Cyclophosphamide: 50–100 mg/day PO or IV pulse — used in refractory cases under specialist supervision.
- Thrombopoietin receptor agonists (TPO-RA): Emerging data in AIHA with concurrent thrombocytopenia (Evans syndrome) — specialist use only.
Cold Agglutinin Disease
Clinical Features
Cold agglutinin disease (CAD) is a clonal B-cell lymphoproliferative disorder characterised by monoclonal IgM antibodies (usually targeting the I antigen on RBCs) that bind optimally at temperatures below 31°C. Patients present with symptoms triggered by cold exposure:
- Acrocyanosis: Blue discolouration of fingers, toes, ears, nose, and tip of nose
- Raynaud-like phenomena: Pallor → cyanosis → rubor sequence in digits
- Livedo reticularis: Mottled, net-like skin pattern in cold-exposed areas
- Haemolysis: Chronic, mild-to-moderate anaemia; may worsen acutely in winter or with infection
- Haemoglobinuria: Dark urine after cold exposure (intravascular haemolysis)
- Jaundice: Mild, intermittent
Distinguishing CAD from secondary cold agglutinins: Secondary cold agglutinins (e.g., post-Mycoplasma, EBV) are polyclonal IgM, often transient, and self-resolving. Primary CAD involves monoclonal IgM (usually κ light chain-restricted) and is chronic. Bone marrow biopsy may show clonal B-cell lymphoproliferative disorder (small clone).
Diagnostic Workup for CAD
- DAT: C3 positive, IgG negative — hallmark of CAD
- Cold agglutinin titre: ≥1:64 at 4°C (titres >1:1000 are typical of primary CAD)
- Thermal amplitude testing (specialist): Determines the highest temperature at which the antibody is active — higher thermal amplitude = more clinically significant
- Serum protein electrophoresis: Monoclonal IgMκ paraprotein in ~90% of primary CAD
- Bone marrow biopsy: Not always required but may show clonal lymphoproliferative disorder
Management of CAD
Mild
Cold Avoidance Only
Hb >100 g/L, asymptomatic. Warm clothing, avoid cold drinks and environments. No pharmacotherapy needed.
Setting: Primary care with haematology oversight
Moderate
Rituximab Monotherapy
Hb 80–100 g/L, symptomatic. Rituximab 375 mg/m² IV weekly × 4. Response rate ~50% (lower than warm AIHA).
Setting: Outpatient haematology
Severe
Rituximab + Bendamustine
Hb <80 g/L, transfusion-dependent, or symptomatic despite rituximab monotherapy. Rituximab + bendamustine: response rate ~70–80%, longer remissions.
Setting: Specialist haematology centre
Steroids are ineffective in CAD. Unlike warm AIHA, corticosteroids have minimal activity against cold agglutinins because the primary site of haemolysis is extravascular-hepatic (complement-mediated) rather than splenic (Fc-mediated). Do not use prolonged steroid courses for CAD — refer for rituximab-based therapy.
Supportive Measures for CAD
- Cold avoidance: Warm clothing (thermal gloves, socks, scarves), heated indoor environments, warm fluids
- Avoid cold IV fluids — all IV solutions and blood products must be warmed
- Transfusion with warmed blood if required (blood warmer mandatory)
- Folic acid 5 mg PO daily during active haemolysis
- Eculizumab (anti-C5 monoclonal antibody) — emerging option for transfusion-dependent CAD with intravascular haemolysis (specialist access, limited PBS availability)
Monitoring & Complications
Monitoring During Active Disease
| Parameter | Frequency (Acute) | Frequency (Stable) | Target |
|---|---|---|---|
| Full blood count + reticulocytes | Daily | Every 2–4 weeks then monthly | Hb >100 g/L; reticulocytes normalising |
| LDH | Every 2–3 days | Monthly | Trending toward normal |
| Haptoglobin | Every 2–3 days | Monthly | Normalising (may remain low in CAD) |
| Bilirubin (unconjugated) | Every 2–3 days | Monthly | Normal |
| Renal function + electrolytes | Daily (if severe) | Monthly | Normal (haemoglobinuria can cause AKI) |
| Blood glucose | While on high-dose steroids | At each visit | Steroid-induced hyperglycaemia screening |
| Bone density (DEXA) | Baseline if expected >3 months steroids | 1–2 yearly | Monitor for steroid osteoporosis |
Major Complications
Venous Thromboembolism (VTE): Active AIHA carries a significantly elevated VTE risk (estimated 10–20% in hospitalised patients). Mechanisms include inflammatory cytokine release, complement activation, and immobilisation. Administer thromboprophylaxis (enoxaparin 40 mg SC daily or equivalent) to all hospitalised patients unless contraindicated. Consider extended thromboprophylaxis post-discharge for high-risk patients.
| Complication | Mechanism | Management / Prevention |
|---|---|---|
| VTE (DVT, PE) | Inflammation, complement, endothelial activation | LMWH thromboprophylaxis; DOAC if confirmed VTE |
| Aplastic crisis | Parvovirus B19 infection → transient red cell aplasia | Check parvovirus B19 IgM/PCR; transfuse if severe; isolate in hospital |
| Acute kidney injury | Haemoglobinuria, renal tubular iron deposition | Aggressive IV hydration; monitor U&Es; nephrology if persistent |
| Steroid-induced diabetes | Prednisolone >10 mg/day for >2 weeks | Blood glucose monitoring; HbA1c at 3 months; endocrinology if persistent |
| Steroid-induced osteoporosis | Prolonged corticosteroid use | DEXA baseline; calcium/vitamin D; bisphosphonate if >3 months prednisolone |
| Infection | Immunosuppression (steroids, rituximab, splenectomy) | Vaccination pre-immunosuppression; PJP prophylaxis if combination immunosuppression |
| Post-splenectomy sepsis | Encapsulated organisms (Streptococcus pneumoniae, Neisseria meningitidis) | Vaccination ≥2 weeks pre-op; lifelong penicillin V 500 mg PO BD; patient education |
Vaccination Requirements
If splenectomy is being considered, complete vaccination at least 2 weeks before surgery and ideally 2 weeks after completion of rituximab (if B-cell recovery allows). Required vaccines include:
- Streptococcus pneumoniae: 13-valent conjugate (Prevenar 13®) followed by 23-valent polysaccharide (Pneumovax 23®) — PBS funded
- Neisseria meningitidis: MenACWY (Nimenrix®) + MenB (Bexsero®) — PBS funded for asplenic patients
- Haemophilus influenzae type b: Single dose if not previously received
- Annual influenza vaccination
- COVID-19 vaccination per current ATAGI recommendations
Rituximab and vaccination timing: Rituximab causes B-cell depletion for approximately 6–12 months. Vaccine responses are impaired during B-cell depletion. Ideally, administer vaccines ≥2 weeks before rituximab or wait ≥6 months post-treatment for optimal response. Discuss timing with the treating haematologist.
Special Populations
Pregnancy
AIHA in pregnancy
Warm AIHA may relapse or worsen during pregnancy. IgG crosses the placenta, risking neonatal haemolytic disease of the fetus/newborn (HDFN). Coordinate care between obstetrics, haematology, and neonatology.
Prednisolone
Compatible with pregnancy — preferred first-line agent. Prednisolone is extensively metabolised by placental 11β-HSD2, minimising fetal exposure. Use lowest effective dose.
Azathioprine
Compatible with pregnancy — considered safe based on transplant and IBD data. Do NOT stop abruptly if already established. Avoid allopurinol co-prescription.
Rituximab
Avoid in pregnancy if possible (limited data, potential neonatal B-cell depletion). Use contraception during and for 12 months after treatment. If essential, discuss risks with patient and haematologist.
Mycophenolate mofetil
Contraindicated in pregnancy — teratogenic (microtia, cleft palate). Must be stopped ≥6 weeks before conception. Switch to azathioprine.
Paediatrics
Presentation
Paediatric AIHA is uncommon (~0.2/100,000 children/year). Often acute onset, frequently post-viral. May be self-limiting (resolves within 1–3 months). PCH is more common in children than adults.
Prednisolone
2 mg/kg/day PO (max 60 mg). Taper over 4–6 weeks. Monitor growth, blood pressure, and glucose. Consider bone health if prolonged course.
IV immunoglobulin (IVIg)
May be useful as adjunct in severe paediatric AIHA (1–2 g/kg over 2–5 days). Evidence is limited but used in refractory cases.
Splenectomy
Avoid in children <5 years due to overwhelming post-splenectomy infection risk. Reserve for refractory cases after full immunosuppressive trial.
Elderly
Considerations
Elderly patients are more likely to have secondary AIHA (CLL, lymphoma). Higher risk of steroid adverse effects (diabetes, osteoporosis, infection, delirium). Lower threshold for steroid-sparing therapy.
Rituximab
Preferred early steroid-sparing agent in elderly patients to minimise cumulative steroid exposure. Well tolerated in older adults.
Bone protection
Commence calcium + vitamin D and consider bisphosphonate (e.g., alendronate 70 mg PO weekly) from the start of steroid therapy. DEXA at baseline.
Renal Impairment
Haemoglobinuria and AKI
Intravascular haemolysis (especially in CAD/PCH) can cause acute kidney injury via haemoglobin-mediated tubular damage. Aggressive IV hydration is essential. Monitor U&Es and urine output closely.
Rituximab
No dose adjustment in renal impairment. Use with caution in severe CKD — increased infection risk.
Azathioprine
Consider dose reduction in severe renal impairment (eGFR <30 mL/min). Monitor FBC closely.
Hepatic Impairment
Steroids
Prednisolone is hepatically activated (prednisolone is the active form). No dose adjustment, but monitor LFTs — AIHA itself causes elevated bilirubin.
Azathioprine
Use with caution in hepatic impairment — risk of hepatotoxicity. Monitor LFTs monthly. Avoid in severe hepatic dysfunction.
Hepatitis B screening
Mandatory before rituximab. HBsAg, anti-HBc, anti-HBs. If positive, commence antiviral prophylaxis (entecavir/tenofovir) before immunosuppression and continue for ≥12 months after last rituximab dose.
Immunocompromised
Infection risk
Combination immunosuppression (steroids + rituximab + azathioprine) significantly increases infection risk. Consider PJP prophylaxis (trimethoprim–sulfamethoxazole 160/800 mg PO three times weekly) if on high-dose steroids + another agent.
Live vaccines
Contraindicated during immunosuppression. Check vaccination status before initiating therapy.
Hypogammaglobulinaemia
Prolonged rituximab use may cause IgG deficiency. Monitor immunoglobulin levels. Consider IVIg replacement if recurrent infections and IgG <4 g/L.
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Health Considerations
📚 References
- 1. Hill QA, Stamps R, Massey E, et al. Guidelines on the management of drug-induced immune and secondary autoimmune haemolytic anaemia. Br J Haematol. 2017;177(2):208–220.
- 2. Hill QA, Stamps R, Massey E, et al. The diagnosis and management of primary autoimmune haemolytic anaemia. Br J Haematol. 2017;176(3):395–411.
- 3. Berentsen S, Barcellini W, D'Sa S, et al. Cold agglutinin disease revisited: a multinational, observational study of 232 patients. Blood. 2020;135(6):414–423.
- 4. Berentsen S, Randen U, Vågan AM, et al. High response rate and durable remissions following fludarabine and rituximab combination therapy for chronic cold agglutinin disease. Blood. 2010;116(17):3180–3184.
- 5. Barcellini W, Fattizzo B, Zaninoni A, et al. Clinical heterogeneity and predictors of outcome in primary autoimmune hemolytic anemia: a GIMEMA study of 308 patients. Blood. 2014;124(19):2930–2936.
- 6. Lechner K, Jäger U. How I treat autoimmune hemolytic anemias in adults. Blood. 2010;116(11):1831–1838.
- 7. American Society of Hematology. ASH clinical practice guidelines on management of warm autoimmune hemolytic anemia in adults. Blood Adv. 2024;8(15):4059–4083.
- 8. Chaudhary RK, Das SS. Autoimmune hemolytic anemia: from lab to bedside. Asian J Transfus Sci. 2014;8(1):5–12.
- 9. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health. Canberra; updated 2024.
- 10. Royal Australian College of General Practitioners (RACGP). Management of Anaemia in General Practice. Melbourne: RACGP; 2023.
- 11. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023.
- 12. Fattizzo B, Barcellini W. Autoimmune hemolytic anemia: causes and consequences. Expert Rev Clin Immunol. 2022;18(9):931–945.
- 13. Randen U, Trøen G, Tierens A, et al. Primary cold agglutinin-associated lymphoproliferative disease: a B-cell lymphoma of the bone marrow distinct from lymphoplasmacytic lymphoma. Haematologica. 2014;99(10):1613–1621.
- 14. Maung SW, Leahy M, O'Leary HM, et al. A multi-centre retrospective study of rituximab use in the treatment of relapsed or resistant warm autoimmune haemolytic anaemia. Br J Haematol. 2013;163(1):118–122.