Warm Autoimmune Hemolytic Anemia

Disease Overview

Warm autoimmune hemolytic anemia (wAIHA) is the most common form of autoimmune hemolytic anemia, accounting for approximately 60–75% of cases. It occurs when the immune system mistakenly produces antibodies, primarily immunoglobulin G (IgG), that bind to healthy red blood cells and mark them for premature destruction. The condition is termed “warm” because these antibodies are most active at normal body temperature (37°C), unlike the antibodies involved in certain other forms of autoimmune hemolytic anemia that react more strongly at lower temperatures. Red blood cell destruction, known as hemolysis, occurs primarily in the spleen and liver (extravascular hemolysis). In approximately 30–50% of cases, activation of the complement system also contributes to this process. Normally, red blood cells circulate for about 120 days before being removed from the bloodstream. In wAIHA, their accelerated destruction exceeds the bone marrow’s ability to replace them, resulting in anemia and reduced oxygen delivery to tissues. ^1-3

The estimated incidence of warm AIHA is roughly 0.5–2.3 cases per 100,000 people per year. The condition can occur at any age, but the median age at diagnosis is 52 years, and the risk rises sharply in older adults, up to 10 times higher in people aged 75 or older compared to those under 50. Women are slightly more likely to be affected than men. ^{2, 4, 5}

About half of all cases have no identifiable cause and are called primary (or idiopathic) warm AIHA. The other half are secondary, meaning they are linked to another condition such as a blood cancer (lymphoproliferative disorder), an autoimmune disease, an immune deficiency, an infection, or a medication. ^{1, 3}

Symptoms range from mild fatigue, shortness of breath, and a rapid heartbeat to, in severe cases, chest pain, confusion, and dark urine. Yellowing of the skin (jaundice) and an enlarged spleen may also occur. ^{2, 5}

Effective treatments are available. Corticosteroids are the standard first-line therapy, and medications such as rituximab, immunosuppressants, and other agents are used when additional treatment is needed. ^{1, 3, 5}

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Synonyms

• Warm AIHA
• wAIHA
• warm antibody autoimmune hemolytic anemia

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Signs & Symptoms

wAIHA can develop at any age, but the median age of onset is 52 years. This means that one half of affected individuals will be younger than 52 years of age when the disease begins and that the other half will be above this age. The symptoms of wAIHA usually develop slowly over a period of several weeks to months, but in some people can develop suddenly over a few days. Specific symptoms that occur may vary from one person to another and depend on the rate of onset, the degree of hemolysis and the presence of an underlying disorder. Some individuals, especially those with a gradual onset of anemia, may not have any obvious symptoms (asymptomatic).

When red blood cell destruction happens slowly, the body’s bone marrow can partly keep up by making new red blood cells. This is called compensated, or chronic, hemolysis. When destruction happens quickly, called acute hemolysis,  symptoms appear suddenly and can be much more serious, even at similar levels of anemia. ⁵

The most frequent symptoms are: ⁵

• Fatigue
• Shortness of breath (dyspnea)
• A fast or pounding heartbeat (palpitations)
• These symptoms are directly related to how low the red blood cell count has fallen. ⁵

When red blood cell destruction happens gradually over time (chronic extravascular hemolysis), people often experience: ²

• Fatigue Pale skin (pallor)
• Yellowing of the skin and whites of the eyes (jaundice), caused by a buildup of bilirubin released from destroyed red blood cells
• An enlarged spleen (splenomegaly), because the spleen, an organ that filters the blood, works harder to remove damaged red blood cells.

When red blood cell destruction is rapid (brisk intravascular hemolysis), it can become a medical emergency. Symptoms may include: ⁵

• Chest pain
• Extreme tiredness or lethargy
• Confusion
• Dark or cola-colored urine (hemoglobinuria), caused by hemoglobin released from destroyed red blood cells passing into the urine

A doctor examining someone with warm AIHA may find: ⁵

• Pale skin and jaundice, which are proportional to how much hemolysis is occurring
• A fast heart rate (tachycardia)
• Swelling in the legs or feet (peripheral edema)
• Raised pressure in the neck veins (elevated jugular venous pressure)

These heart and lung signs tend to appear in more severe cases. An enlarged spleen may also be found, especially in people whose warm AIHA is linked to a blood cancer (lymphoproliferative disorder).  ⁵

The level of hemoglobin,  the protein in red blood cells that carries oxygen, varies widely from person to person at the time of diagnosis. Normal hemoglobin is roughly 12–17 g/dL depending on age and sex. ^{2, 6}

The median hemoglobin at presentation is approximately 7–7.5 g/dL  About 27% of people present with a hemoglobin below 6 g/dL, which is severely low.  Some people present with near-normal hemoglobin if the bone marrow is compensating effectively ^{2, 6}

In the most severe cases, hemoglobin can fall below 3 g/dL ^{2, 6}

A serious complication of warm AIHA is the formation of dangerous blood clots (venous thromboembolic events). These include clots in the deep veins of the legs (deep venous thrombosis) and clots that travel to the lungs (pulmonary emboli). This occurs in 15–30% of people with warm AIHA, and the risk is highest in the weeks immediately after diagnosis.  ⁵

Certain features at the time of diagnosis are linked to a worse outlook (poor prognostic factors): ^{2, 5, 6}

• Severe anemia at onset (hemoglobin below 8 g/dL)
• Evans syndrome, a condition in which the immune system attacks both red blood cells and platelets
• A low count of the young red blood cells the bone marrow produces (reticulocytopenia), meaning the marrow is not compensating well
• Acute kidney failure
• The presence of a specific type of autoantibody called warm IgM autoantibodies.

About 30% of people achieve a lasting remission after initial treatment. The remaining people experience a chronic, relapsing course, meaning the disease comes back after periods of improvement. ^{3, 5}

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Causes

Warm AIHA is caused by a malfunction of the immune system. Normally, the immune system makes proteins called antibodies to fight foreign invaders such as bacteria and viruses. In warm AIHA, the immune system mistakenly makes antibodies, called IgG autoantibodies, that target the body’s own red blood cells instead. ^{1, 3}

These IgG autoantibodies attach to red blood cells at normal body temperature (37°C). Once attached, they mark the red blood cells for destruction. ^{1, 3}

The spleen and liver, organs that filter the blood, recognize the marked cells and remove them from circulation. This process of destruction outside the blood vessels is called extravascular hemolysis. ^{1, 3}

The autoantibodies in warm AIHA are polyclonal, meaning they are produced by many different immune cells rather than a single abnormal clone. They also tend to be non-specific, reacting with all red blood cells rather than targeting one particular type. Because of this, they are called panagglutinins. ^{3, 5}

In about 30–50% of cases, a separate arm of the immune system called complement also becomes activated. Complement is a group of proteins that can directly destroy cells. When it is triggered, it adds to the red blood cell destruction already being caused by the autoantibodies. ^{1, 3}

Primary (idiopathic) warm AIHA

In approximately 50% of cases, no underlying cause can be found. These cases are called primary, or idiopathic, warm AIHA. ^{1, 3}

Secondary warm AIHA

In the remaining cases, warm AIHA develops in connection with another condition or trigger. These are called secondary cases. Known associations include: ^{1, 3}

• Lymphoproliferative disorders, blood cancers such as lymphoma or chronic lymphocytic leukemia
• Autoimmune diseases, conditions in which the immune system already attacks the body’s own tissues
• Immunodeficiencies, disorders in which the immune system does not work properly
• Infections
• Medications.

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Affected populations

Warm AIHA is the most common subtype of autoimmune hemolytic anemia, accounting for 60–75% of all AIHA cases. ^{1, 2}

The overall incidence of all forms of AIHA ranges from 0.8 to 3 cases per 100,000 people per year, with a prevalence of approximately 17 per 100,000 people. Because warm AIHA makes up the majority of those cases, its estimated incidence is roughly 0.5–2.3 cases per 100,000 people per year. ^{2, 4, 5}

Warm AIHA can occur at any age. The median age at diagnosis is 52 years. However, the risk rises sharply in older adults, the incidence in people aged 75 or older is up to 10 times higher than in those under 50. ^{2, 5}

Women are slightly more likely to be affected than men. No specific ethnic background has been identified in the source content as carrying a higher or lower risk. ^{2, 4, 5} Primary versus secondary cases About 50% of cases are primary, meaning no underlying cause can be found (also called idiopathic). The remaining 50% are secondary which means that are  linked to another condition such as a blood cancer (lymphoproliferative disorder), an autoimmune disease, an immune deficiency, an infection, or a medication.

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Disorders with Similar Symptoms

Several conditions can look like warm AIHA because they also cause the body to destroy red blood cells too quickly (hemolytic anemia) or share other overlapping symptoms. Blood tests, a look at red blood cells under a microscope (peripheral blood smear), and a key test called the direct antiglobulin test (DAT) which checks whether antibodies or complement proteins are attached to red blood cells can usually help tell these conditions apart. ^{2, 5}

Cold agglutinin disease (CAD) also causes hemolytic anemia, but symptoms may be triggered or made worse by cold temperatures. People with CAD may notice their fingers or toes turning blue in the cold (acrocyanosis) or experience a condition called Raynaud’s phenomenon, where blood vessels in the hands and feet overreact to cold. In warm AIHA, the antibodies involved are usually IgG proteins that react at normal body temperature (37°C). In CAD, the antibodies are typically a different type called IgM, which bind to red blood cells at cooler temperatures and activate a part of the immune system called complement. Blood tests, including specialized antibody testing, and smear findings can help distinguish the two.  ^{2, 3, 5}

Drug-induced immune hemolytic anemia (DIIHA) accounts for about 10% of immune hemolytic anemias and can cause sudden, severe red blood cell destruction. The key difference is a link to a medication,  symptoms may appear days to weeks after starting a drug and often improve after stopping it. Commonly implicated medications include penicillin, cephalosporins, fludarabine, and immune checkpoint inhibitors. Some drugs, such as α-methyldopa and checkpoint inhibitors, can cause antibodies that look identical to those in warm AIHA on lab tests, so a careful medication history is essential to tell them apart. ^{1, 2, 7}

Paroxysmal nocturnal hemoglobinuria (PNH) is a condition in which red blood cells are missing certain protective proteins on their surface, making them vulnerable to destruction by the complement system. People with PNH may notice dark or cola-colored urine (hemoglobinuria) and are at risk of blood clots in unusual places such as the liver veins (Budd-Chiari syndrome) or the veins supplying the intestines. Unlike warm AIHA, the DAT is generally negative in classical PNH, and a specialized blood test called flow cytometry confirms the diagnosis by detecting blood cells lacking certain protective surface proteins, including CD55 and CD59. Notably, one study reported small PNH clones in about 37% of people with warm AIHA, although this finding may not apply to all patients and requires further study to determine its clinical significance. ^{3, 5, 8, 9}

Hereditary spherocytosis (HS) causes chronic hemolytic anemia, an enlarged spleen, and yellowing of the skin (jaundice), symptoms that overlap with warm AIHA. A family history is present in about 75% of cases. The key difference is that HS is an inherited condition caused by variants in red blood cell membrane proteins (spectrin, ankyrin, or band 3), whereas warm AIHA is acquired. The DAT is generally negative in HS, and specific blood tests can confirm the diagnosis. ¹⁰⁻¹²

Microangiopathic hemolytic anemia (MAHA) is a group of conditions , including thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and disseminated intravascular coagulation (DIC), in which red blood cells are physically torn apart as they pass through damaged small blood vessels. People may have acute hemolysis along with a low platelet count (thrombocytopenia), kidney problems, or neurological symptoms. The DAT is usually negative, and a blood smear typically shows fragmented red blood cells called schistocytes. In contrast, warm AIHA more commonly produces round red blood cells called spherocytes. These findings, together with other laboratory tests, help distinguish the conditions. ^2,7

Evans syndrome occurs when the immune system attacks both red blood cells (causing autoimmune hemolytic anemia) and platelets, either at the same time or one after the other. Some people also develop a low count of infection-fighting white blood cells (neutropenia). It is reported in approximately 5–10% of warm AIHA cases. The difference from isolated warm AIHA is the additional presence of a low platelet count (thrombocytopenia), with or without neutropenia. Evans syndrome tends to cause more severe anemia, a worse outlook, and higher mortality than warm AIHA alone, and it is more often linked to underlying immune system disorders, particularly a condition called autoimmune lymphoproliferative syndrome in children. ^{3, 7, 13-15}

Glucose-6-phosphate dehydrogenase (G6PD) deficiency causes episodes of sudden red blood cell destruction triggered by specific stressors such as infections, fava beans, or certain medications (for example, primaquine or rasburicase). Between episodes, most people have no symptoms. Unlike warm AIHA, the DAT is generally negative, the condition follows an X-linked inheritance pattern and mainly affects males, and a specific enzyme test helps confirm the diagnosis. The destruction in G6PD deficiency is caused by oxidative damage to red blood cells, not by the immune system attacking them. ¹⁶⁻¹⁹

Mixed autoimmune hemolytic anemia has features of both warm and cold AIHA and accounts for approximately 5–8% of all AIHA cases. It is driven by both warm-reactive IgG antibodies and cold-reactive IgM antibodies at the same time. Specialized blood tests can identify both types of antibodies, and people may experience hemolysis associated with warm-reactive antibodies as well as cold-triggered symptoms,  a combination that helps distinguish mixed AIHA from typical warm AIHA. ^{2, 5}

Secondary causes of warm AIHA are worth highlighting separately because about 50% of warm AIHA cases are linked to an underlying condition rather than arising on their own. These include blood cancers such as chronic lymphocytic leukemia and lymphoma, autoimmune diseases such as lupus (systemic lupus erythematosus), rheumatoid arthritis, and inflammatory bowel disease, immune deficiencies, infections (including HIV, hepatitis C, Epstein-Barr virus, and SARS-CoV-2), and transplantation. Clues that an underlying condition may be present include swollen lymph nodes, an enlarged liver or spleen, and findings on blood tests or imaging. Identifying a secondary cause matters because treating the underlying condition may improve the AIHA. ¹⁻³

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Diagnosis

Doctors diagnose warm autoimmune hemolytic anemia (warm AIHA) by showing that red blood cells are being destroyed by the immune system (hemolytic anemia with autoimmune pathogenesis). This requires a combination of blood tests and, in some cases, imaging.

The first step is a set of standard blood tests: ^{2, 5}

• A complete blood count (CBC), which measures the number and health of blood cells
• A reticulocyte count (reticulocytes are young red blood cells): a high count shows the bone marrow is working hard to replace destroyed cells
• Lactate dehydrogenase (LDH), a protein released when cells are damaged: levels are elevated in warm AIHA
• Unconjugated bilirubin, a yellow substance produced during the breakdown of red blood cells: levels are elevated in warm AIHA
• Haptoglobin, a protein that clears hemoglobin from the blood: levels are decreased in warm AIHA

The reticulocyte count is usually high, but in up to 20% of people it may be normal or even low. This can happen when the autoantibodies attack not just mature red blood cells but also the early red blood cell precursors in the bone marrow. ^{2, 3}

A doctor may also look at a blood smear, a thin layer of blood examined under a microscope. In about 40% of people with warm AIHA, the smear shows spherocytes, which are red blood cells that have become round and fragile after being partially damaged by the immune system. ²

The direct antiglobulin test (DAT)

The most important single test for warm AIHA is the direct antiglobulin test (DAT), sometimes called the Coombs test. It checks whether antibodies or immune proteins are attached to red blood cells. The DAT is positive in approximately 95% of people with warm AIHA, although results must be considered alongside other evidence of red blood cell destruction. ⁵

When the initial DAT (called a polyspecific DAT) is positive, a follow-up test using more specific reagents (monospecific DAT) is done to identify which immune proteins are attached to the red blood cells. The patterns found are: ^{3, 20}

• IgG antibody alone: found in about 35% of people
• IgG antibody plus a complement protein called C3d: found in about 56% of people
• C3d alone: found in about 9% of people

When the monospecific DAT is positive for C3d but negative for IgG, additional testing is needed to determine the cause. This pattern may occur in cold antibody-mediated hemolysis or certain forms of warm AIHA and does not, by itself, establish a diagnosis of warm AIHA. ³

When the DAT is negative

In 3–10% of people with warm AIHA, the standard DAT comes back negative. These cases may require specialized reference laboratory testing and careful exclusion of other causes of red blood cell destruction. Specialized reference laboratories can run enhanced DAT assays that detect antibodies missed by routine testing.³

A negative standard DAT in warm AIHA may be caused by a very low density of antibodies on the red blood cell surface, by a less common antibody type called IgA, or by antibodies that bind only weakly (low-affinity antibodies). Diagnosis requires compatible clinical findings, laboratory evidence of hemolysis, and exclusion of other causes.⁵

Testing for underlying conditions

Because about half of all warm AIHA cases are linked to another condition, doctors also look for possible underlying causes: ^{2, 5}

• Flow cytometry (a blood test that identifies different types of blood cells) may be recommended to check for blood cancers such as lymphoma or chronic lymphocytic leukemia (lymphoproliferative disorders), particularly when clinical findings suggest an underlying blood disorder.
• Autoimmune panels (blood tests that look for signs of immune system disease) are done when a rheumatologic condition such as lupus is suspected.
• CT imaging (a detailed X-ray scan) may be used when a doctor finds swollen lymph nodes, a very enlarged spleen, or symptoms such as unexplained weight loss or fever (constitutional symptoms).

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Standard Therapies

Warm AIHA is managed by a team led by a hematologist (a doctor who specializes in blood disorders). A hematology consultation is recommended for all people with suspected or confirmed warm AIHA. ⁵

First-line treatment: corticosteroids

The standard first treatment is a corticosteroid called prednisone. About 80% of people respond to this initial therapy. However, only 30–40% stay in remission after the medication is tapered and stopped. ^{1, 3, 5}

For people with severe disease, which includes cases where symptoms, other health conditions, and the degree of anemia together indicate high risk, as well as atypical forms of warm AIHA (such as IgA-mediated or DAT-negative disease) and Evans syndrome, adding rituximab to corticosteroids at the start of treatment may improve long-term response rates compared to corticosteroids alone. Clinical trials have shown substantially higher rates of sustained remission with this combination. ^{1, 3, 5}

Second-line treatment

If rituximab was not used initially, it becomes the preferred second-line therapy for people who do not respond adequately to corticosteroids or whose disease returns when corticosteroids are reduced or stopped. About 70–80% of people respond to rituximab at this stage. The median time to response is 3–6 weeks. However, approximately 30–40% of people may relapse within 3 years. ^{1, 3}

Third-line and later options

When earlier treatments have not worked well enough, several options may be considered: ²⁻³

• Immunosuppressant medications, such as azathioprine, mycophenolate mofetil, or cyclosporine, produce responses in about 50–60% of people, although response rates vary by medication and study. ²⁻³
• Splenectomy (surgical removal of the spleen, the organ that filters and destroys damaged red blood cells) produces a response in approximately 70% of people, but it carries an increased risk of infection and blood clots. It is generally reserved for people who have not responded adequately to other treatments or for whom other options are unsuitable. ²⁻³
• For disease that does not respond to these treatments (refractory disease), the medications bortezomib plus dexamethasone, daratumumab, or fostamatinib may be considered in selected cases, though the evidence supporting their use in warm AIHA is still limited. ¹⁻²

Supportive care

Several supportive measures are an important part of managing warm AIHA.

Red blood cell transfusion is given when clinically needed, based on a person’s symptoms and overall health rather than a fixed hemoglobin number. When a transfusion is urgently needed, for example, when hemoglobin falls below 6 g/dL with severe symptoms or signs of clinical instability,  appropriately selected blood should be given without unnecessary delay. Cross-matching may show an incompatible result because of the panagglutinins (antibodies that react with many or all red blood cells), but this does not mean transfusion should be withheld in an emergency. The blood bank evaluates for other clinically significant antibodies and selects the safest available donor blood. When time allows, extended matching of additional blood group proteins (Rh subgroups, Kell, Kidd, S/s, and Duffy) may be performed, but this should not unnecessarily delay a lifesaving transfusion. In acute settings, the goal is to stabilize the patient and improve symptoms of severe anemia rather than reach a fixed hemoglobin level. ^{1, 5}

Thromboprophylaxis, medication to prevent dangerous blood clots (venous thromboembolism), is recommended for hospitalized people with active hemolysis when there are no contraindications and may also be needed after surgical removal of the spleen. Low-molecular-weight heparin is commonly used for this purpose. The choice and duration of treatment depend on the person’s risk of blood clots and bleeding. ^{1, 5}

Erythropoietin (a hormone that stimulates the bone marrow to make red blood cells) may benefit people whose bone marrow is not producing enough young red blood cells (reticulocytopenic patients). ¹

Acute management

Severe anemia (particularly hemoglobin below 6 g/dL), low oxygen levels (hypoxia), confusion, or unstable blood pressure or heart rate may indicate a medical emergency. Without urgent treatment, these situations can lead to fluid buildup in the lungs (pulmonary edema), a heart attack (myocardial infarction), or a dangerous heart rhythm problem (arrhythmia). Immediate treatment generally includes corticosteroids and, when clinically needed, red blood cell transfusion. Rituximab should also be considered early in people with severe disease, particularly when the response to corticosteroids is inadequate, based on evidence supporting improved sustained responses with combination treatment. ⁵

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Clinical Trials and Studies

Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.

For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:

Tollfree: (800) 411-1222
TTY: (866) 411-1010
Email: [email protected]

Some current clinical trials also are posted on the following page on the NORD website:
https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/

For information about clinical trials sponsored by private sources, contact:
www.centerwatch.com

For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/

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References

1. Murakhovskaya I, Yazdanbakhsh K. Warm Autoimmune Haemolytic Anaemia: Clinical Considerations. British Journal of Haematology. 2026;208(3):841-844. doi:10.1111/bjh.70331.

2. Michel M, Crickx E, Fattizzo B, Barcellini W. Autoimmune Haemolytic Anaemias. Nature Reviews. Disease Primers. 2024;10(1):82. doi:10.1038/s41572-024-00566-2.

3. Berentsen S, Barcellini W. Autoimmune Hemolytic Anemias. The New England Journal of Medicine. 2021;385(15):1407-1419. doi:10.1056/NEJMra2033982.

4. Bozzi S, Umarje S, Hawaldar K, et al. Prevalence and Incidence of Primary Autoimmune Hemolytic Anemia and Cold Agglutinin Disease in the United States, 2016-2023. PloS One. 2025;20(6):e0323843. doi:10.1371/journal.pone.0323843.

5. Brodsky RA. Warm Autoimmune Hemolytic Anemia. The New England Journal of Medicine. 2019;381(7):647-654. doi:10.1056/NEJMcp1900554.

6. 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):2930-6. doi:10.1182/blood-2014-06-583021.

7. Hill QA, Stamps R, Massey E, et al. Guidelines on the Management of Drug-Induced Immune and Secondary Autoimmune, Haemolytic Anaemia. British Journal of Haematology. 2017;177(2):208-220. doi:10.1111/bjh.14654.

8. Goldschmidt V, Apodaca EI, Gálvez KM, Wannesson B, Scheinberg P. Clinical Characteristics and Management of Paroxysmal Nocturnal Haemoglobinuria in Latin America: A Narrative Review. Annals of Hematology. 2025;104(2):867-879. doi:10.1007/s00277-024-05968-6.

9. Fattizzo B, Giannotta J, Zaninoni A, et al. Small Paroxysmal Nocturnal Hemoglobinuria Clones in Autoimmune Hemolytic Anemia: Clinical Implications and Different Cytokine Patterns in Positive and Negative Patients. Frontiers in Immunology. 2020;11:1006. doi:10.3389/fimmu.2020.01006.

10. Bolton-Maggs PH, Langer JC, Iolascon A, et al. Guidelines for the Diagnosis and Management of Hereditary Spherocytosis–2011 Update. British Journal of Haematology. 2012;156(1):37-49. doi:10.1111/j.1365-2141.2011.08921.x.

11. Perrotta S, Gallagher PG, Mohandas N. Hereditary Spherocytosis. Lancet (London, England). 2008;372(9647):1411-26. doi:10.1016/S0140-6736(08)61588-3.

12. Yang L, Shu H, Zhou M, Gong Y. Literature Review on Genotype-Phenotype Correlation in Patients With Hereditary Spherocytosis. Clinical Genetics. 2022;102(6):474-482. doi:10.1111/cge.14223.

13. Fattizzo B, Marchetti M, Michel M, et al. Diagnosis and Management of Evans Syndrome in Adults: First Consensus Recommendations. The Lancet. Haematology. 2024;11(8):e617-e628. doi:10.1016/S2352-3026(24)00144-3.

14. Michel M. Adult Evans’ Syndrome. Hematology/Oncology Clinics of North America. 2022;36(2):381-392. doi:10.1016/j.hoc.2021.12.004.

15. Audia S, Grienay N, Mounier M, Michel M, Bonnotte B. Evans’ Syndrome: From Diagnosis to Treatment. Journal of Clinical Medicine. 2020;9(12):E3851. doi:10.3390/jcm9123851.

16. Luzzatto L, Ally M, Notaro R. Glucose-6-Phosphate Dehydrogenase Deficiency. Blood. 2020;136(11):1225-1240. doi:10.1182/blood.2019000944.

17. Nannelli C, Bosman A, Cunningham J, Dugué PA, Luzzatto L. Genetic Variants Causing G6PD Deficiency: Clinical and Biochemical Data Support New WHO Classification. British Journal of Haematology. 2023;202(5):1024-1032. doi:10.1111/bjh.18943.

18. Noronha SA. Acquired and Congenital Hemolytic Anemia. Pediatrics in Review. 2016;37(6):235-46. doi:10.1542/pir.2015-0053.

19. Pakparnich P, Sudsumrit S, Imwong M, et al. Combined Effects of Double Mutations on Catalytic Activity and Structural Stability Contribute to Clinical Manifestations of Glucose-6-Phosphate Dehydrogenase Deficiency. Scientific Reports. 2021;11(1):24307. doi:10.1038/s41598-021-03800-z.

20. Hill QA, Stamps R, Massey E, et al. The Diagnosis and Management of Primary Autoimmune Haemolytic Anaemia. British Journal of Haematology. 2017;176(3):395-411. doi:10.1111/bjh.14478.

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