Hemolytic anemia classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Shyam Patel [2]

## Overview

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Hemolytic anemia can be divided into intravascular and extravascular based on whether the destruction of RBCs occurs in the vessels or outside the vessels, usually in spleen and liver. Extravascular hemolytic anemia is more common than intravascular hemolytic anemia. There are many types of hemolytic anemias and the general classification of hemolytic anemia is either acquired or inherited (genetic). Genetic conditions include red blood cell membrane or enzyme defects that predispose the red blood cells to hemolysis.

## Classification

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### Location of Hemolysis

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* Intravascular: This refers to red blood cell destruction within the blood vessels.
* Extravascular: This refers to red blood cell destruction outside the blood vessels, such as in the liver or spleen.

### Types of Hemolytic Anemias

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* Secondary immune hemolytic anemia[1]
* Idiopathic autoimmune hemolytic anemia
* Non-immune hemolytic anemia caused by chemicals or toxins
* Microangiopathic hemolytic anemia (MAHA)
* Sickle-cell anemia
* Hemoglobin SC disease (similar in symptoms to sickle-cell anemia)
* Thalassemia
* Hemolytic anemia due to G6PD deficiency
* Paroxysmal nocturnal hemoglobinuria (PNH)
* Hereditary elliptocytosis
* Hereditary ovalocytosis
* Hereditary spherocytosis
* Malaria[2]
* Transfusion of blood from a donor with a different blood type

Hemolytic anemias can be either genetic or acquired.

### Genetic

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* Genetic conditions of RBC membrane
* Hereditary spherocytosis[3]
* Hereditary elliptocytosis[4]
* Genetic conditions of RBC metabolism (enzyme defects)
* Glucose-6-phosphate dehydrogenase deficiency (G6PD or favism)
* Pyruvate kinase deficiency
* Genetic conditions of hemoglobin
* Sickle cell anemia
* Thalassemia

### Acquired

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Acquired hemolytic anemia can be further divided into immune and non-immune mediated.

Immune-mediated hemolytic anemia (direct Coombs test is positive)

* Autoimmune hemolytic anemia[5]
* Warm antibody autoimmune hemolytic anemia
* Idiopathic
* Systemic lupus erythematosus (SLE)[6]
* Evans' syndrome (antiplatelet antibodies and haemolytic antibodies)
* Cold antibody autoimmune hemolytic anemia
* Idiopathic cold hemagglutinin syndrome
* Infectious mononucleosis and mycoplasma (atypical) pneumonia
* Paroxysmal cold hemoglobinuria (rare)[5]
* Alloimmune hemolytic anemia
* Haemolytic disease of the newborn (HDN)
* Rh disease (Rh D)
* ABO hemolytic disease of the newborn
* Anti-Kell hemolytic disease of the newborn
* Rhesus c hemolytic disease of the newborn
* Rhesus E hemolytic disease of the newborn
* Other blood group incompatibility (RhC, Rhe, Kidd, Duffy, MN, P and others)
* Alloimmune hemolytic blood transfusion reactions (ie from a non-compatible blood type)
* Drug induced immune mediated hemolytic anemia
* Penicillin (high dose)
* Methyldopa

Non-immune mediated hemolytic anemia (direct Coombs test is negative)[5]

* Drugs (i.e., some drugs and other ingested substances lead to hemolysis by direct action on RBCs)
* Toxins (e.g., snake venom)
* Trauma
* Mechanical (heart valves, extensive vascular surgery, and microvascular disease)
* Microangiopathic hemolytic anemia (a specific subtype with causes such as TTP, HUS, DIC, and HELLP syndrome)
* Infections
* Malaria
* Babesiosis
* Septicaemia
* Membrane disorders
* Paroxysmal nocturnal hemoglobinuria (rare acquired clonal disorder of red blood cell surface proteins)
* Liver disease

## References

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1. ↑ Berentsen S, Sundic T (2015). "Red blood cell destruction in autoimmune hemolytic anemia: role of complement and potential new targets for therapy". Biomed Res Int. 2015: 363278. doi:10.1155/2015/363278. PMC 4326213. PMID 25705656.
2. ↑ Jauréguiberry S, Thellier M, Ndour PA, Ader F, Roussel C, Sonneville R; et al. (2015). "Delayed-onset hemolytic anemia in patients with travel-associated severe malaria treated with artesunate, France, 2011-2013". Emerg Infect Dis. 21 (5): 804–12. doi:10.3201/eid2105.141171. PMC 4412216. PMID 25898007.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
3. ↑ Hughes MR, Anderson N, Maltby S, Wong J, Berberovic Z, Birkenmeier CS; et al. (2011). "A novel ENU-generated truncation mutation lacking the spectrin-binding and C-terminal regulatory domains of Ank1 models severe hemolytic hereditary spherocytosis". Exp Hematol. 39 (3): 305–20, 320.e1–2. doi:10.1016/j.exphem.2010.12.009. PMC 3404605. PMID 21193012.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
4. ↑ Tchernia G, Mohandas N, Shohet SB (1981). "Deficiency of skeletal membrane protein band 4.1 in homozygous hereditary elliptocytosis. Implications for erythrocyte membrane stability". J Clin Invest. 68 (2): 454–60. PMC 370818. PMID 6894932.CS1 maint: Multiple names: authors list (link)
5. ↑ 5.0 5.1 5.2 Packman CH (2015). "The Clinical Pictures of Autoimmune Hemolytic Anemia". Transfus Med Hemother. 42 (5): 317–24. doi:10.1159/000440656. PMC 4678314. PMID 26696800.
6. ↑ Fujii J, Kurahashi T, Konno T, Homma T, Iuchi Y (2015). "Oxidative stress as a potential causal factor for autoimmune hemolytic anemia and systemic lupus erythematosus". World J Nephrol. 4 (2): 213–22. doi:10.5527/wjn.v4.i2.213. PMC 4419130. PMID 25949934.CS1 maint: Multiple names: authors list (link)

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