Hemolytic anemia classification: Difference between revisions
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{{Hemolytic anemia}} | {{Hemolytic anemia}} | ||
{{CMG}}; {{shyam}} | |||
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==Overview== | ==Overview== | ||
Hemolytic anemia can be divided into [[intravascular]] and extravascular based on whether the [[Hemolysis|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 anemia]]s 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== | ==Classification== | ||
===Location of Hemolysis=== | |||
*'''Intravascular''': This refers to [[Hemolysis|red blood cell destruction]] within [[Blood vessels|the blood vessels]]. | |||
*'''Extravascular''': This refers to [[Hemolysis|red blood cell destruction]] outside the blood vessels, such as in the [[liver]] or [[spleen]]. | |||
===Types of Hemolytic Anemias=== | |||
*[[Immune hemolytic anemia (patient information)|Secondary immune hemolytic anemia]]<ref name="pmid25705656">{{cite journal| author=Berentsen S, Sundic T| title=Red blood cell destruction in autoimmune hemolytic anemia: role of complement and potential new targets for therapy. | journal=Biomed Res Int | year= 2015 | volume= 2015 | issue= | pages= 363278 | pmid=25705656 | doi=10.1155/2015/363278 | pmc=4326213 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25705656 }} </ref> | |||
*[[Immune hemolytic anemia (patient information)|Idiopathic autoimmune hemolytic anemia]] | |||
*[[Non immune hemolytic anemia (patient information)|Non-immune hemolytic anemia]] caused by [[chemicals]] or [[toxins]] | |||
*[[Microangiopathic hemolytic anemia|Microangiopathic hemolytic anemia (MAHA)]] | |||
*[[Sickle-cell disease (patient information)|Sickle-cell anemia]] | |||
*[[Hemoglobin SC disease]] (similar in symptoms to [[Sickle-cell disease (patient information)|sickle-cell anemia]]) | |||
*[[Thalassemia (patient information)|Thalassemia]] | |||
*Hemolytic anemia due to [[Glucose-6-phosphate dehydrogenase deficiency (patient information)|G6PD deficiency]] | |||
*[[Paroxysmal nocturnal hemoglobinuria (patient information)|Paroxysmal nocturnal hemoglobinuria]] (PNH) | |||
*[[Hereditary elliptocytosis (patient information)|Hereditary elliptocytosis]] | |||
*[[Hereditary]] [[ovalocytosis]] | |||
*[[Hereditary spherocytosis (patient information)|Hereditary spherocytosis]] | |||
*[[Malaria (patient information)|Malaria]]<ref name="pmid25898007">{{cite journal| author=Jauréguiberry S, Thellier M, Ndour PA, Ader F, Roussel C, Sonneville R et al.| title=Delayed-onset hemolytic anemia in patients with travel-associated severe malaria treated with artesunate, France, 2011-2013. | journal=Emerg Infect Dis | year= 2015 | volume= 21 | issue= 5 | pages= 804-12 | pmid=25898007 | doi=10.3201/eid2105.141171 | pmc=4412216 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25898007 }} </ref> | |||
*[[Blood transfusion|Transfusion of blood]] from a donor with a [[Blood type|different blood type]] | |||
Hemolytic anemias can be either genetic or acquired. | '''Hemolytic anemias can be either genetic or acquired.''' | ||
===Genetic=== | ===Genetic=== | ||
*Genetic conditions of RBC membrane | *Genetic conditions of RBC membrane | ||
**[[Hereditary spherocytosis]] | **[[Hereditary spherocytosis]]<ref name="pmid21193012">{{cite journal| author=Hughes MR, Anderson N, Maltby S, Wong J, Berberovic Z, Birkenmeier CS et al.| title=A novel ENU-generated truncation mutation lacking the spectrin-binding and C-terminal regulatory domains of Ank1 models severe hemolytic hereditary spherocytosis. | journal=Exp Hematol | year= 2011 | volume= 39 | issue= 3 | pages= 305-20, 320.e1-2 | pmid=21193012 | doi=10.1016/j.exphem.2010.12.009 | pmc=3404605 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21193012 }} </ref> | ||
**[[Hereditary elliptocytosis]] | **[[Hereditary elliptocytosis]]<ref name="pmid6894932">{{cite journal| author=Tchernia G, Mohandas N, Shohet SB| title=Deficiency of skeletal membrane protein band 4.1 in homozygous hereditary elliptocytosis. Implications for erythrocyte membrane stability. | journal=J Clin Invest | year= 1981 | volume= 68 | issue= 2 | pages= 454-60 | pmid=6894932 | doi= | pmc=370818 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6894932 }} </ref> | ||
*Genetic conditions of RBC metabolism ([[enzyme]] defects) | *Genetic conditions of RBC metabolism ([[enzyme]] defects) | ||
**[[Glucose-6-phosphate dehydrogenase deficiency]] (G6PD or favism) | **[[Glucose-6-phosphate dehydrogenase deficiency]] (G6PD or [[favism]]) | ||
**[[Pyruvate kinase deficiency]] | **[[Pyruvate kinase deficiency]] | ||
*Genetic conditions of hemoglobin | *Genetic conditions of hemoglobin | ||
**[[Sickle cell anemia]] | **[[Sickle cell anemia]] | ||
**[[Thalassemia]] | **[[Thalassemia]] | ||
===Acquired=== | ===Acquired=== | ||
Acquired hemolytic anemia can be further divided into immune and non-immune mediated. | Acquired hemolytic anemia can be further divided into [[immune]] and non-immune mediated. | ||
'''Immune mediated hemolytic | '''Immune-mediated hemolytic anemia''' (direct [[Coombs test]] is positive) | ||
*[[Autoimmune hemolytic anemia]] | *[[Autoimmune hemolytic anemia]]<ref name="pmid26696800">{{cite journal| author=Packman CH| title=The Clinical Pictures of Autoimmune Hemolytic Anemia. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 317-24 | pmid=26696800 | doi=10.1159/000440656 | pmc=4678314 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696800 }} </ref> | ||
**[[Warm antibody autoimmune hemolytic anemia]] | **[[Warm antibody autoimmune hemolytic anemia]] | ||
***Idiopathic | ***[[Idiopathic]] | ||
***[[Systemic lupus erythematosus]] (SLE) | ***[[Systemic lupus erythematosus]] (SLE)<ref name="pmid25949934">{{cite journal| author=Fujii J, Kurahashi T, Konno T, Homma T, Iuchi Y| title=Oxidative stress as a potential causal factor for autoimmune hemolytic anemia and systemic lupus erythematosus. | journal=World J Nephrol | year= 2015 | volume= 4 | issue= 2 | pages= 213-22 | pmid=25949934 | doi=10.5527/wjn.v4.i2.213 | pmc=4419130 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25949934 }} </ref> | ||
***[[Evans' syndrome]] (antiplatelet antibodies and haemolytic antibodies) | ***[[Evans' syndrome]] (antiplatelet antibodies and haemolytic antibodies) | ||
**[[Cold agglutinin disease|Cold antibody autoimmune hemolytic anemia]] | **[[Cold agglutinin disease|Cold antibody autoimmune hemolytic anemia]] | ||
***[[Idiopathic cold hemagglutinin syndrome]] | ***[[Idiopathic cold hemagglutinin syndrome]] | ||
***[[Infectious mononucleosis]] and mycoplasma ( atypical) pneumonia | ***[[Infectious mononucleosis]] and [[Mycoplasma pneumonia|mycoplasma (atypical) pneumonia]] | ||
***[[Paroxysmal cold hemoglobinuria]] (rare) | ***[[Paroxysmal cold hemoglobinuria]] (rare)<ref name="pmid26696800">{{cite journal| author=Packman CH| title=The Clinical Pictures of Autoimmune Hemolytic Anemia. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 317-24 | pmid=26696800 | doi=10.1159/000440656 | pmc=4678314 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696800 }} </ref> | ||
*[[Alloimmune]] hemolytic anemia | *[[Alloimmune]] hemolytic anemia | ||
**[[Haemolytic disease of the newborn]] (HDN) | **[[Haemolytic disease of the newborn]] (HDN) | ||
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***[[Hemolytic disease of the newborn (anti-RhE)|Rhesus E hemolytic disease of the newborn]] | ***[[Hemolytic disease of the newborn (anti-RhE)|Rhesus E hemolytic disease of the newborn]] | ||
***Other [[Blood type|blood group]] incompatibility (RhC, Rhe, [[Kidd antigen system|Kidd]], [[Duffy antigen|Duffy]], MN, P and others) | ***Other [[Blood type|blood group]] incompatibility (RhC, Rhe, [[Kidd antigen system|Kidd]], [[Duffy antigen|Duffy]], MN, P and others) | ||
**Alloimmune hemolytic [[Blood transfusion#Complications|blood transfusion]] reactions (ie from a non-compatible [[blood type]]) | **[[Alloimmune]] hemolytic [[Blood transfusion#Complications|blood transfusion]] reactions (ie from a non-compatible [[blood type]]) | ||
*Drug induced immune mediated hemolytic anemia | *Drug induced immune mediated hemolytic anemia | ||
**[[Penicillin]] (high dose) | **[[Penicillin]] (high dose) | ||
**[[Methyldopa]] | **[[Methyldopa]] | ||
'''Non-immune mediated hemolytic anemia''' (direct [[Coombs test]] is negative) | '''Non-immune mediated hemolytic anemia''' (direct [[Coombs test]] is negative)<ref name="pmid26696800">{{cite journal| author=Packman CH| title=The Clinical Pictures of Autoimmune Hemolytic Anemia. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 317-24 | pmid=26696800 | doi=10.1159/000440656 | pmc=4678314 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696800 }} </ref> | ||
*[[Medication|Drugs]] (i.e., some drugs and other ingested substances lead to hemolysis by direct action on RBCs) | *[[Medication|Drugs]] (i.e., some [[drugs]] and other ingested substances lead to [[hemolysis]] by direct action on [[RBCs]]) | ||
*[[Toxin]]s (e.g., snake venom) | *[[Toxin]]s (e.g., [[Snake venoms|snake venom]]) | ||
*Trauma | *[[Trauma]] | ||
**Mechanical ([[heart valve]]s, extensive vascular surgery, microvascular disease) | **Mechanical ([[heart valve]]s, extensive [[vascular surgery]], and [[microvascular disease]]) | ||
*[[Microangiopathic hemolytic anemia]] (a specific subtype with causes such as TTP, HUS, DIC and HELLP syndrome) | *[[Microangiopathic hemolytic anemia]] (a specific subtype with causes such as [[Thrombotic thrombocytopenic purpura|TTP]], [[Hemolytic-uremic syndrome|HUS]], [[DIC]], and [[HELLP syndrome]]) | ||
*Infections | *[[Infections]] | ||
**[[Malaria]] | **[[Malaria]] | ||
**[[Babesiosis]] | **[[Babesiosis]] | ||
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==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Hematology]] | |||
{{WS}} | |||
{{WH}} | |||
Latest revision as of 17:17, 30 October 2017
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Risk calculators and risk factors for Hemolytic anemia classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Shyam Patel [2]
Overview
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
Location of Hemolysis
- 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
- 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
- Genetic conditions of RBC membrane
- Genetic conditions of RBC metabolism (enzyme defects)
- Genetic conditions of hemoglobin
Acquired
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
- Warm antibody autoimmune hemolytic anemia
- 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)
- Haemolytic disease of the newborn (HDN)
- 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
- Membrane disorders
- Paroxysmal nocturnal hemoglobinuria (rare acquired clonal disorder of red blood cell surface proteins)
- Liver disease
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.