Autoimmune hemolytic anemia

Short description: Blood disorder in which antibodies target red blood cells

Autoimmune hemolytic anemia

Other names| Autoimmune haemolytic anaemia

Autoimmune hemolytic anemia (AIHA) occurs when a person's immune system produces antibodies directed against their own red blood cells (RBCs). These antibodies attach to red cells, causing them to break down (lyse), and reducing the number of oxygen-carrying red blood cells in circulation (anemia).[1][2] The antibodies are usually directed against common red cell antigens, therefore they also bind to allogenic or transfused red cells and cause them to lyse. (ref).[3][4][5] Autoimmune haemolytic anaemia can be caused by different types of antibodies with reactivity at different temperatures. The one caused by IgG antibodies is called warm-immune haemolytic anaemia and has an incidence of 5-10 cases per million whereas ‘cold agglutinin disease’ is caused by IgM antibodies with an incidence of 1-1.8 cases per million.

The terminology used in this disease is somewhat ambiguous. Although MeSH uses the term "autoimmune hemolytic anemia",[6] some sources prefer the term "immunohemolytic anemia" so drug reactions can be included in this category.[7][8] The National Cancer Institute considers "immunohemolytic anemia", "autoimmune hemolytic anemia", and "immune complex hemolytic anemia" to all be synonyms.[9]

## Contents

* 1 Signs and symptoms
* 2 Causes
* 3 Pathophysiology
* 4 Laboratory features and Diagnosis
* 4.1 Classification
* 4.2 Evidence for hemolysis
* 5 Treatment
* 6 History
* 7 Summary
* 8 In children
* 9 See also
* 10 References
* 11 External links

## Signs and symptoms

Symptoms of AIHA may be due to the underlying anemia; including shortness of breath or dyspnea, fatigue, headache, muscle weakness and pallor.[10]

Jaundice is a common sign of haemolytic anemia. It is caused by the accumulation of bilirubin in skin, and sclera. Bilirubin is produced by degradation of heme molecule and as red cells lyse and release intracellular contents, the free heme decomposes to bilirubin causing jaundice. Jaundice can also be accompanied by dark (tea coloured) urine due to free hemoblogin.

In cold agglutinin disease (cold antibody type), agglutination and impaired passage of red blood cells through capillaries in the extremities causes acrocyanosis and Raynaud phenomenon with a rare complication of gangrene[4]

Spherocytes are found in immunologically mediated hemolytic anemias.[11] Signs of hemolysis that are present in AIHA include low hemoglobin (blood count), alterations in levels of cell markers of hemolysis; including elevated lactate dehydrogenase (LDH), decreased haptoglobin and elevated unconjugated bilirubin.[4] Reticulocytosis, or an increase in circulating immature red blood cells, may be seen.[4]

## Causes

The causes of AIHA are poorly understood. The disease may be primary, or secondary to another underlying illness. The primary AIHA is idiopathic (the two terms used synonymously) and accounts for more than 60% of unselected cases.[12]

Secondary AIHA can result from many other illnesses usually the ones that also affect immune system. The most common causes of secondary AIHA include lymphoproliferative disorders (e.g., chronic lymphocytic leukemia, lymphoma), immune dysregulation disorders such as autoimmune lymphoproliferative syndrome (ALPS) and common variable immunodeficiency (CVID) and other autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma, Crohn's disease, ulcerative colitis), infections (as HIV, EBV, hepatitis, mycoplasma, viral pneumonia, and other respiratory infections) and drugs.[13] Less common causes of warm-type AIHA include neoplasms other than lymphoid, and bone marrow / solid organ transplant. Secondary warm type AIHA has been observed in cases of Covid-19.[4] Secondary cold type AIHA is also caused primarily by lymphoproliferative disorders but is also commonly caused by infection, especially by mycoplasma, viral pneumonia, infectious mononucleosis, and other respiratory infections. Less commonly, it can be caused by concomitant autoimmune disorders.[14]

Drug-induced AIHA, though rare, can be caused by a number of drugs. More than 130 drugs have been implicated in causing AIHA.[15]

In about half of cases, the cause of autoimmune hemolytic anemia cannot be determined (idiopathic or primary). This condition can also be caused by or occur with another disorder (secondary) or rarely, occur following the use of certain drugs (such as penicillin) or after a person has a blood and marrow stem cell transplant.[16]

Secondary causes of autoimmune hemolytic anemia include:[16]

* Autoimmune diseases, such as lupus
* Chronic lymphocytic leukemia
* Non-Hodgkin's lymphoma and other blood cancers
* Epstein-Barr virus
* Cytomegalovirus
* Mycoplasma pneumonia
* Hepatitis
* HIV[16]

## Pathophysiology

AIHA can be caused by different antibody classes with IgG and IgM antibodies being the primary antibody types. IgA autoantibodies can also rarely cause AIHA.

Pathophysiology of warm or IgG mediated AIHA differs from cold or IgM mediated AIHA. Warm AIHA means immune haemolysis is caused by auto-antibodies which bind to red cells at body temperature (37 degree Celsius). These are usually IgG but can be IgM in rare cases.[17] In warm AIHA, red cells coated by IgG undergo antibody mediated cell death in the reticuloendothelial system of liver and spleen leading to extravascular haemolysis. These IgG antibodies are also capable of activating the complement cascade with variable efficacy, further leading to opsonisation and destruction of red cells in reticuloendothelial system (RE) system or intravascular haemolysis via terminal complement.[18]

Red cell autoantibodies causing cold agglutinin disease are of IgM class. These bind to RBC antigens at lower temperatures (e.g. in the acral parts of body such as hands, feet, ears, nose). The antibody/RBC antigen complex then activates the classical complement pathway leading to complement mediated hemolysis of RBCs in RE system.[19]

Rarely, a biphasic IgG antibody leads to complement mediated intravascular lysis. This antibody binds to red cells in acral regions along with first two components of complement. As the blood moves to central regions of the body and warms up, the IgG dissociates but the complement remains attached to red cell causing intravascular hemolysis.[20] The antibody causing this biphasic hemolysis is commonly IgG but IgM and IgA have also been reported.[21]

Paroxysmal Cold Hemoglobinuria (PCH) is primarily a pediatric disease and usually occurs with Mycoplasma pneumonia infection or other viral infections. It can also occur with chronic lymphocytic leukemia and lymphomas in adults.

Pathophysiologic mechanisms involved in drug induced haemolysis include:  drug-dependent autoantibodies due to an immuno-allergic mechanism, drug-independent autoantibodies due to molecular mimicry, or nonspecific stimulation of the immune system.[22][23]

When DAT is performed, the typical presentations of AIHA are as follows. Warm-type AIHA shows a positive reaction with antisera to IgG antibodies with or without complement activation. Cases may also arise with complement alone or with IgA, IgM or a combination of these three antibody classes and complement. Cold-type AIHA usually reacts with antisera to complement and occasionally to the above antibodies. This is the case in both cold agglutinin disease and cold paroxysmal hematuria. In general, mixed warm and cold AIHA shows a positive reaction to IgG and complement, sometimes IgG alone, and sometimes complement alone. Mixed-type can, like the others, present unusually with positive reactions to other antisera.[14]

## Laboratory features and Diagnosis

Diagnosis of AIHA should be suspected in a patient presenting with acute onset of anemia (fatigue, pallor, SOB), jaundice, dark urine etc. It is essential to consider the secondary causes of AIHA such as infections, lymphoproliferative conditions, drugs, immune dysregulation and autoimmune conditions. Laboratory investigations are carried out to determine the aetiology of the anemia. These include complete blood count, reticulocyte count, markers of hemolysis (haptoglobin, LDH and bilirubin) and red cell morphology on peripheral smear.

Laboratory investigations are carried out to determine the etiology of the disease. Following confirmation of hemolysis (seen with laboratory markers of low hemoglobin, elevated LDH, decreased haptoglobin, and elevated unconjugated bilirubin).

The diagnosis of AIHA in a patient is confirmed via direct antiglobulin test (DAT) also known as the Coombs test. This test assesses for presence of IgG or IgM antibodies attached to the surface of RBCs. Red cells from patient are incubated with antiglobulin reagent at 37 degree Celsius. If positive, further testing is undertaken to determine if hemolysis is IgM/complement mediated or IgG mediated.[4][5]

A bone marrow biopsy is used in AIHA to identify a possible underlying lymphoproliferative disorder.[4]

### Classification

AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin disease and paroxysmal cold hemoglobinuria. These classifications are based on the characteristics of the autoantibodies involved in the pathogenesis of the disease. Each has a different underlying cause, management, and prognosis, making classification important when treating a patient with AIHA.[24]

* * *

Autoimmune hemolytic anemia

* Warm AIHA (IgG mediated)

* Primary (No underlying secondary cause)
* Secondary (lymphoproliferative disorders, autoimmune disordersstem cell transplant, infections, immune dysregulation, drugs)[25]: 259

* Cold AIHA

* Primary cold agglutinin disease
* Secondary cold agglutinin syndrome

* Associated with malignant disease
* Acute, transient,[25] infection-associated (acute cold antibody mediated AIHA complicating Mycoplasma pneumoniae or viral infections[26])
* Chronic (lymphoproliferative disorders)[25]: 259

* Paroxysmal cold hemoglobinuria[25]: 259

* Idiopathic
* Secondary

* Acute, transient (Infections other than syphilis)[25]: 259
* Chronic (syphilis)[25]: 259

* Mixed cold- and warm-antibody type

* Idiopathic
* Secondary (lymphoproliferative disorders, autoimmune disorders)[25]

* Drug-induced immune hemolytic anemia[25]: 259

* Autoimmune type
* Drug absorption type
* Neoantigen type[27]

### Evidence for hemolysis

The following findings may be present:[28][29]

* Increased red cell breakdown
* Elevated serum bilirubin (unconjugated)
* Excess urinary urobilinogen
* Reduced plasma haptoglobin
* Raised serum lactic dehydrogenase (LDH)
* Hemosiderinuria
* Methemalbuminemia
* Spherocytosis
* Increased red cell production:
* Reticulocytosis
* Erythroid hyperplasia of the bone marrow

Specific investigations

* Positive direct Coombs test

## Treatment

Steroids are the first line treatment in warm AIHA; with oral prednisone achieving an 80% initial response rate, with a 30-40% sustained remission rate at 1 year.[4] Steroids may be decreased at 3 weeks and tapered at 3–6 months depending on the response.[4] Rituximab may be added to initial management to increase the response rate, or it may be used in cases of severe disease such as IgA mediated warm AIHA, mixed AIHA, Evans syndrome or in cases of high hemolysis levels).[4] If a response cannot be achieved with steroids or rituximab, other third line options are considered which include azathioprine, cyclophosphamide, cyclosporine, mycophenolate mofetil, sirolimus and bortezomib.[4] The treatments for secondary warm AIHA are generally the same as primary warm AIHA, but with the addition of treating the underlying disease if possible.[4] Splenectomy can be considered for refractory disease.

Steroids are not indicated in the treatment of cold agglutinin disease due to low response rates.[4] Cases of cold agglutinin disease with mild anemia with limited and compensated hemolysis can be monitored with adjunct supportive care (such as avoidance of cold exposure or thermal protection to prevent against hemolysis).[4] Rituximab is used to treat pathogenic B-cell clones in cold agglutinin disease with response rates of 45-60%.[4] Relapses are common upon discontinuation of rituximab, but the medication can be restarted to achieve subsequent remission.[4] Rituximab can be combined with bendamustine to achieve a 71% overall and 40% complete response rate with an increased response seen with prolonged therapy (with a time to best response at a median of 30 months) due to the drugs' effect on long lived plasma cells.[4] Splenectomy is less efficacious in cold agglutinin disease.[30]

Special considerations are required when treating people with AIHA using blood transfusion. In cold agglutinin disease and PCH; the patient and the extremity should be kept warm during transfusion to prevent agglutination and hemolysis of the donor and patient red blood cells.[4] In warm AIHA; cross-matching of blood will show incompatibility so it is recommended to perform a bedside in vivo compatibility test prior to infusion.[4] Erythropoietin (EPO) has been shown to increase hemoglobin levels in cold and warm AIHA.[4]

## History

"Blood-induced icterus" produced by the release of massive amounts of a coloring material from blood cells followed by the formation of bile was recognized and described by Vanlair and Voltaire Masius' in 1871. About 20 years later, Hayem distinguished between congenital hemolytic anemia and an acquired type of infectious icterus associated with chronic splenomegaly. In 1904, Donath and Landsteiner suggested a serum factor was responsible for hemolysis in paroxysmal cold hemoglobinuria. French investigators led by Chauffard stressed the importance of red-cell autoagglutination in patients with acquired hemolytic anemia. In 1930, Lederer and Brill described cases of acute hemolysis with rapid onset of anemia and rapid recovery after transfusion therapy. These hemolytic episodes were thought to be due to infectious agents. A clear distinction between congenital and acquired hemolytic anemia was not drawn, however, until Dameshek and Schwartz in 1938, and, in 1940, they demonstrated the presence of abnormal hemolysins in the sera of patients with acquired hemolytic anemia and postulated an immune mechanism.[31]

## Summary

A hemolytic state exists whenever the red cell survival time is shortened from the normal average of 120 days. Hemolytic anemia is the hemolytic state in which anemia is present, and bone marrow function is inferentially unable to compensate for the shortened lifespan of the red cell. Immune hemolytic states are those, both anemic and nonanemic, which involve immune mechanisms consisting of antigen-antibody reactions. These reactions may result from unrelated antigen-antibody complexes that fix to an innocent-bystander erythrocyte, or from related antigen-antibody combinations in which the host red cell or some part of its structure is or has become antigenic. The latter type of antigen-antibody reaction may be termed "autoimmune", and hemolytic anemias so produced are autoimmune hemolytic anemias.[2]

## In children

In general, AIHA in children has a good prognosis and is self-limiting. However, if it presents within the first two years of life or in the teenage years, the disease often follows a more chronic course, requiring long-term immunosuppression, with serious developmental consequences. The aim of therapy may sometimes be to lower the use of steroids in the control of the disease. In this case, splenectomy may be considered, as well as other immunosuppressive drugs. Infection is a serious concern in patients on long-term immunosuppressant therapy, especially in very young children (less than two years).[32]

## See also

* Hematology
* Hemolytic anemia
* List of circulatory system conditions
* List of hematologic conditions
* Splenomegaly

## References

1. ↑ Shoenfield, Y (2008). Diagnostic Criteria in Autoimmune Disease. Humana Press.
2. ↑ 2.0 2.1 "Disease-associated autoimmune hemolytic anemia". Bull N Y Acad Med 46 (6): 411–26. June 1970. PMID 5267234.
3. ↑ "Autoimmune hemolytic anemia". Am. J. Hematol. 69 (4): 258–71. April 2002. doi:10.1002/ajh.10062. PMID 11921020.
4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 Berentsen, Sigbjørn; Barcellini, Wilma (7 October 2021). "Autoimmune Hemolytic Anemias". New England Journal of Medicine 385 (15): 1407–1419. doi:10.1056/NEJMra2033982. PMID 34614331.
5. ↑ 5.0 5.1 Kokori, SI; Ioannidis, JP; Voulgarelis, M; Tzioufas, AG; Moutsopoulos, HM (2000-02-15). "Autoimmune hemolytic anemia in patients with systemic lupus erythematosus.". The American Journal of Medicine 108 (3): 198–204. doi:10.1016/S0002-9343(99)00413-1. ISSN 0002-9343. PMID 10723973.
6. ↑ Autoimmune+hemolytic+anemia at the US National Library of Medicine Medical Subject Headings (MeSH)
7. ↑ Wright MS (1999). "Drug-induced hemolytic anemias: increasing complications to therapeutic interventions". Clin Lab Sci 12 (2): 115–8. PMID 10387489.
8. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. pp. 636. ISBN 978-0-7216-0187-8.
9. ↑ "Definition of immunohemolytic anemia". NCI Dictionary of Cancer Terms. http://www.cancer.gov/templates/db_alpha.aspx?CdrID=523291.
10. ↑ "Autoimmune hemolytic anemia | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program". https://rarediseases.info.nih.gov/diseases/5870/autoimmune-hemolytic-anemia.
11. ↑ "HbSC hemoglobinopathy suspected by chest x-ray and red blood cell morphology". Acta Clin Belg 60 (6): 377–82. 2005. doi:10.1179/acb.2005.057. PMID 16502600.
12. ↑ "Epidemiology of Secondary Warm Autoimmune Haemolytic Anaemia-A Systematic Review and Meta-Analysis". Journal of Clinical Medicine 10 (6): 1244. 2021. doi:10.3390/jcm10061244. PMID 33802848.
13. ↑ Bride, Karen; Teachey, David (2017-11-01). "Autoimmune lymphoproliferative syndrome: more than a FAScinating disease". F1000Research 6: 1928. doi:10.12688/f1000research.11545.1. ISSN 2046-1402. PMID 29123652.
14. ↑ 14.0 14.1 "Autoimmune haemolysis: an 18-year study of 865 cases referred to a regional transfusion centre". Br Med J (Clin Res Ed) 282 (6281): 2023–7. June 1981. doi:10.1136/bmj.282.6281.2023. PMID 6788179.
15. ↑ Garbe, Edeltraut; Andersohn, Frank; Bronder, Elisabeth; Klimpel, Andreas; Thomae, Michael; Schrezenmeier, Hubert; Hildebrandt, Martin; Späth-Schwalbe, Ernst et al. (2011-07-12). "Drug induced immune haemolytic anaemia in the Berlin Case-Control Surveillance Study". British Journal of Haematology 154 (5): 644–653. doi:10.1111/j.1365-2141.2011.08784.x. ISSN 0007-1048. PMID 21749359. https://doi.org/10.1111/j.1365-2141.2011.08784.x.
16. ↑ 16.0 16.1 16.2 "Autoimmune hemolytic anemia". 2014-02-24. https://rarediseases.info.nih.gov/diseases/5870/autoimmune-hemolytic-anemia. This article incorporates text from this source, which is in the public domain.
17. ↑ Berentsen, Sigbjørn (2016-12-02). "Cold agglutinin disease". Hematology 2016 (1): 226–231. doi:10.1182/asheducation-2016.1.226. ISSN 1520-4391. PMC 6142439. https://doi.org/10.1182/asheducation-2016.1.226.
18. ↑ Packman, Charles H. (January 2008). "Hemolytic anemia due to warm autoantibodies". Blood Reviews 22 (1): 17–31. doi:10.1016/j.blre.2007.08.001. ISSN 0268-960X. PMID 17904259. https://doi.org/10.1016/j.blre.2007.08.001.
19. ↑ Zilow, G.; Kirschfink, M.; Roelcke, D. (1994). "Red Cell Destruction in Cold Agglutinin Disease". Transfusion Medicine and Hemotherapy 21 (6): 410–415. doi:10.1159/000223021. ISSN 1660-3796. https://doi.org/10.1159/000223021.
20. ↑ Jacobs, Jeremy W.; Figueroa Villalba, Cristina A.; Booth, Garrett S.; Woo, Jennifer S.; Stephens, Laura D.; Adkins, Brian D. (2023-06-02). "Clinical and epidemiological features of paroxysmal cold hemoglobinuria: a systematic review". Blood Advances 7 (11): 2520–2527. doi:10.1182/bloodadvances.2022009516. ISSN 2473-9529. PMC 10248093. https://doi.org/10.1182/bloodadvances.2022009516.
21. ↑ Karafin, Matthew S.; Shirey, R. Sue; Ness, Paul M.; King, Karen E.; Keefer, Jeffrey (2012-05-02). "A case study of a child with chronic hemolytic anemia due to a Donath–Landsteiner positive, IgM anti-I autoantibody". Pediatric Blood & Cancer 59 (5): 953–955. doi:10.1002/pbc.24185. ISSN 1545-5009. https://doi.org/10.1002/pbc.24185.
22. ↑ Maquet, Julien; Lafaurie, Margaux; Michel, Marc; Lapeyre-Mestre, Maryse; Moulis, Guillaume (2024-02-13). "Drug-induced immune hemolytic anemia: detection of new signals and risk assessment in a nationwide cohort study". Blood Advances 8 (3): 817–826. doi:10.1182/bloodadvances.2023009801. ISSN 2473-9529. PMC 10874903. https://doi.org/10.1182/bloodadvances.2023009801.
23. ↑ Garratty, G.; Arndt, P.A. (2014-01-01). "Drugs that have been shown to cause drug-induced immune hemolytic anemia or positive direct antiglobulin tests: some interesting findings since 2007". Immunohematology 30 (2): 66–79. doi:10.21307/immunohematology-2019-100. ISSN 1930-3955. https://doi.org/10.21307/immunohematology-2019-100.
24. ↑ Zanella, A.; Barcellini, W. (2014-09-30). "Treatment of autoimmune hemolytic anemias". Haematologica (Ferrata Storti Foundation (Haematologica)) 99 (10): 1547–1554. doi:10.3324/haematol.2014.114561. ISSN 0390-6078. PMID 25271314.
25. ↑ 25.0 25.1 25.2 25.3 25.4 25.5 25.6 25.7 Gehrs, B. C.; Friedberg, R. C. (2002). "Concise review: Autoimmune Hemolytic Anemia". American Journal of Hematology (Wiley) 69 (4): 258–71. doi:10.1002/ajh.10062. PMID 11921020.
26. ↑ Berentsen, Sigbjørn; Beiske, Klaus; Tjønnfjord, Geir E. (2007-07-21). "Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy". Hematology (Amsterdam, Netherlands) (Informa UK Limited) 12 (5): 361–370. doi:10.1080/10245330701445392. ISSN 1607-8454. PMID 17891600.
27. ↑ Berentsen, Sigbjørn; Sundic, Tatjana (2015-01-29). "Red Blood Cell Destruction in Autoimmune Hemolytic Anemia: Role of Complement and Potential New Targets for Therapy". BioMed Research International (Hindawi Limited) 2015: 363278-1–363278-11. doi:10.1155/2015/363278. ISSN 2314-6133. PMID 25705656.
28. ↑ Clinical Medicine (6th ed.). Elsevier Saunders. 2005. p. 437.
29. ↑ "Autoimmune Hemolytic Anemia". https://www.lecturio.com/concepts/autoimmune-hemolytic-anemia/.
30. ↑ Go R. S., Winters J. L., Kay N. E. (2017). "How I treat autoimmune hemolytic anemia". Blood 129 (22): 2971–2979. doi:10.1182/blood-2016-11-693689. PMID 28360039.
31. ↑ Dameshek, William; Schwartz, Steven O. (1938-01-13). "The Presence of Hemolysins in Acute Hemolytic Anemia: Preliminary Note" (in en). New England Journal of Medicine 218 (2): 75–80. doi:10.1056/NEJM193801132180205. ISSN 0028-4793. http://www.nejm.org/doi/abs/10.1056/NEJM193801132180205.
32. ↑ "Rituximab for the treatment of refractory autoimmune hemolytic anemia in children". Blood 101 (10): 3857–61. May 2003. doi:10.1182/blood-2002-11-3547. PMID 12531800.

## External links

Classification|

* ICD-10: D59.0-D59.1
* ICD-9-CM: 283.0
* OMIM: 205700
* MeSH: D000744

|

External resources|

* Orphanet: 98375

* v
* t
* e

Diseases of red blood cells

| Polycythemia|

* Polycythemia vera

|

| Anemia|

| Nutritional|

* Micro-: Iron-deficiency anemia
* Plummer–Vinson syndrome

* Macro-: Megaloblastic anemia
* Pernicious anemia

|

Hemolytic
(mostly normo-)|

| Hereditary|

* enzymopathy: Glucose-6-phosphate dehydrogenase deficiency
* glycolysis
* pyruvate kinase deficiency
* triosephosphate isomerase deficiency
* hexokinase deficiency

* [[Biology:Hemoglobinopathemoglobinopathy]]: Thalassemia
* alpha
* beta
* delta
* Sickle cell disease/trait
* Hereditary persistence of fetal hemoglobin

* membrane: Hereditary spherocytosis
* Minkowski–Chauffard syndrome
* Hereditary elliptocytosis
* Southeast Asian ovalocytosis
* Hereditary stomatocytosis

|

Acquired|

| AIHA|

* Warm antibody autoimmune hemolytic anemia
* Cold agglutinin disease
* Donath–Landsteiner hemolytic anemia
* Paroxysmal cold hemoglobinuria
* Mixed autoimmune hemolytic anemia

|

* membrane
* paroxysmal nocturnal hemoglobinuria

* Microangiopathic hemolytic anemia
* Thrombotic microangiopathy
* Hemolytic–uremic syndrome

* Drug-induced autoimmune
* Drug-induced nonautoimmune

* Hemolytic disease of the newborn

Aplastic
(mostly normo-)|

* Hereditary: Fanconi anemia
* Diamond–Blackfan anemia

* Acquired: Pure red cell aplasia
* Sideroblastic anemia
* Myelophthisic

Blood tests|

* Mean corpuscular volume
* normocytic
* microcytic
* macrocytic
* Mean corpuscular hemoglobin concentration
* normochromic
* hypochromic

Other|

* Methemoglobinemia
* Sulfhemoglobinemia
* Reticulocytopenia

Template:Autoimmune diseases

0.00

(0 votes)

Original source: https://en.wikipedia.org/wiki/Autoimmune hemolytic anemia. Read more

|

Retrieved from "https://handwiki.org/wiki/index.php?title=Medicine:Autoimmune_hemolytic_anemia&oldid=4018730"
*[v]: View this template
*[t]: Discuss this template
*[e]: Edit this template