Editing Hemolysis

{{Short description|Rupturing of red blood cells and release of their contents}}
{{About|1=medical aspects of hemolysis|2=hemolysis in the culture of microorganisms|3=Hemolysis (microbiology)}}
{{redirect|Laking}}
{{More medical citations needed|date=November 2021}}
{{Infobox medical condition (new)
 |name          = Hemolysis
 |synonym       = Haemolysis (alternative spelling), hematolysis, erythrolysis, or erythrocytolysis
 |image         = HEMOLYSIS.jpg
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 |specialty     = [[Pathology]]
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 |complications = [[Kidney failure]], [[kidney disease]]
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 |causes        = [[Osmosis]]
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[[File:Blausen 0684 OsmoticFlow Hypotonic.png|thumb|170px|A [[red blood cell]] in a hypotonic solution, causing water to move into the cell]]
[[File:Blausen 0683 OsmoticFlow Hypertonic.png|thumb|170px|A [[red blood cell]] in a hypertonic solution, causing water to move out of the cell]]
'''Hemolysis''' or '''haemolysis''' ({{IPAc-en|h|iː|ˈ|m|ɒ|l|ɪ|s|ɪ|s}}),<ref name="lpd">{{cite book|last=Wells|first=John C.|year=2008|title=Longman Pronunciation Dictionary|edition=3rd|publisher=Longman|isbn=978-1-4058-8118-0}}</ref> also known by [[#Nomenclature|several other names]], is the rupturing ([[lysis]]) of [[red blood cell]]s (erythrocytes) and the release of their contents ([[cytoplasm]]) into surrounding fluid (e.g. [[blood plasma]]). Hemolysis may occur [[in vivo]] or [[in vitro]].

One cause of hemolysis is the action of [[hemolysin]]s, toxins that are produced by certain [[pathogenic bacteria]] or [[Fungus|fungi]]. Another cause is intense physical exercise.<ref>{{Cite journal|last1=Witek|first1=K|last2=Ścisłowska|first2=J|last3=Turowski|first3=D|last4=Lerczak|first4=K|last5=Lewandowska-Pachecka|first5=S|last6=Pokrywka|first6=A|date=March 2017|title=Total bilirubin in athletes, determination of reference range|journal=Biology of Sport|volume=34|issue=1|pages=45–48|doi=10.5114/biolsport.2017.63732|issn=0860-021X|pmc=5377560|pmid=28416897}}</ref> [[Hemolysin]]s damage the red blood cell's [[cytoplasmic membrane]], causing lysis and eventually cell death.<ref>{{Cite book|title=Brock Biology of Microorganisms 13th Edition|year=2010|isbn=978-0-321-64963-8|pages=804|last1=Madigan|first1=Michael T.|publisher=Benjamin Cummings }}</ref>

==Etymology==
From hemo- + -lysis, from [[Ancient Greek]] {{lang|grc|αἷμα}} ({{lang|grc-Latn|haîma}}, 'blood') + {{lang|grc|λύσις}} {{lang|grc-Latn|lúsis}}, 'loosening').

==Inside the body==

Hemolysis inside the body can be caused by a large number of medical conditions, including some parasites (''e.g.'', ''[[Plasmodium]]''), some autoimmune disorders (''e.g.'', autoimmune haemolytic anaemia, drug-induced [[hemolytic anemia]], [[atypical hemolytic uremic syndrome]] (aHUS)<ref>{{Cite web|title=Atypical hemolytic-uremic syndrome|url=https://ghr.nlm.nih.gov/condition/atypical-hemolytic-uremic-syndrome|access-date=2020-08-18|website=Genetics Home Reference|language=en}}</ref>),<ref name=":0">{{Cite journal|last=Barcellini|first=Wilma|date=2015|title=Immune Hemolysis: Diagnosis and Treatment Recommendations|journal=Seminars in Hematology|volume=52|issue=4|pages=304–312|doi=10.1053/j.seminhematol.2015.05.001|issn=1532-8686|pmid=26404442}}</ref> some genetic disorders (''e.g.'', [[Sickle-cell disease]] or [[G6PD deficiency]]), or blood with too low a solute concentration ([[Tonicity#Hypotonicity|hypotonic]] to cells).<ref name=":1">{{Cite journal|last1=Beris|first1=Photis|last2=Picard|first2=Véronique|date=2015|title=Non-immune Hemolysis: Diagnostic Considerations|journal=Seminars in Hematology|volume=52|issue=4|pages=287–303|doi=10.1053/j.seminhematol.2015.07.005|issn=1532-8686|pmid=26404441}}</ref>

Hemolysis can lead to [[hemoglobinemia]] due to [[hemoglobin]] released into the [[blood plasma]], which plays a significant role in the [[pathogenesis]] of [[sepsis]]<ref name="Effenberger-Neidnicht 2018 1569–1581">{{Cite journal|last1=Effenberger-Neidnicht|first1=Katharina|last2=Hartmann|first2=Matthias|date=2018|title=Mechanisms of Hemolysis During Sepsis|journal=Inflammation|volume=41|issue=5|pages=1569–1581|doi=10.1007/s10753-018-0810-y|issn=1573-2576|pmid=29956069|s2cid=49526899}}</ref> and can lead to increased risk of infection due to its inhibitory effects on the [[innate immune system]].<ref name="Effenberger-Neidnicht 2018 1569–1581"/>

===Parasitic hemolysis===
Because the feeding process of the ''[[Plasmodium]]'' parasites damages red blood cells, [[malaria]] is sometimes called "parasitic hemolysis" in medical literature.{{citation needed|date=July 2022}}

===HELLP, pre-eclampsia, or eclampsia===
:See [[HELLP syndrome]], [[Pre-eclampsia]], and [[Eclampsia]]

===Hemolytic disease of the newborn===
{{main|Hemolytic disease of the newborn}}
Hemolytic disease of the newborn is an autoimmune disease resulting from the mother's antibodies crossing the placenta to the fetus. This most often occurs when the mother has previously been exposed to blood antigens present on the fetus but foreign to her, through either a blood transfusion or a previous pregnancy.<ref>{{Cite journal|date=2019-02-02|title=Erythrocyte Alloimmunization and Pregnancy: Overview, Background, Pathophysiology|url=https://emedicine.medscape.com/article/273995-overview}}</ref>

===Hemolytic anemia===
{{main|Hemolytic anemia}}
Because ''in vivo'' hemolysis destroys red blood cells, in uncontrolled, chronic or severe cases it can lead to [[hemolytic anemia]].

=== <span id="HemolyticCrisis"></span> Hemolytic crisis===
A hemolytic crisis, or hyperhemolytic crisis, is characterized by an accelerated rate of red blood cell destruction leading to [[anemia]], [[jaundice]], and [[reticulocytosis]].<ref>{{Cite web |url=http://www.innvista.com/health/ailments/anemias/sickle.htm |title=Innvista |access-date=2010-07-04 |archive-url=https://web.archive.org/web/20100624103223/http://www.innvista.com/health/ailments/anemias/sickle.htm |archive-date=2010-06-24 |url-status=dead }}</ref> Hemolytic crises are a major concern with [[sickle-cell disease]] and [[G6PD deficiency]].

===Toxic agent ingestion or poisoning===
''[[Paxillus involutus]]'' ingestion can cause hemolysis.

=== Space hemolysis ===
Spaceflight can cause hemolysis.<ref>{{Cite web |last=Guzman |first=Ana |date=2022-02-24 |title=Scientists Find Increased Red Blood Cell Destruction in Space |url=http://www.nasa.gov/mission_pages/station/research/news/find-increase-red-blood-cell-destruction |access-date=2022-06-09 |website=NASA}}</ref>

===Intrinsic causes===

Hemolysis may result from intrinsic defects in the red blood cell itself:<ref name="Jacobasch Rapoport 1996 pp. 143–70">{{cite journal | last1=Jacobasch | first1=G | last2=Rapoport | first2=SM | title=Hemolytic anemias due to erythrocyte enzyme deficiencies. | journal=Molecular Aspects of Medicine | volume=17 | issue=2 | year=1996 | issn=0098-2997 | pmid=8813716 | pages=143–70| doi=10.1016/0098-2997(96)88345-2 }}</ref><ref name="Bossi Russo 1996 pp. 171–88">{{cite journal | last1=Bossi | first1=D | last2=Russo | first2=M | title=Hemolytic anemias due to disorders of red cell membrane skeleton. | journal=Molecular Aspects of Medicine | volume=17 | issue=2 | year=1996 | issn=0098-2997 | pmid=8813717 | pages=171–88| doi=10.1016/0098-2997(96)88346-4 }}</ref>
* Defects of red blood cell membrane production (as in [[hereditary spherocytosis]] and [[hereditary elliptocytosis]])
* Defects in hemoglobin production (as in [[thalassemia]], [[sickle-cell disease]] and [[congenital dyserythropoietic anemia]])
* Defective red cell metabolism (as in [[glucose-6-phosphate dehydrogenase deficiency]] and [[pyruvate kinase deficiency]])
* [[Paroxysmal nocturnal hemoglobinuria]] (PNH), sometimes referred to as Marchiafava-Micheli syndrome, is a rare, acquired, potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia.

===Extrinsic causes===

Extrinsic hemolysis is caused by the red blood cell's environment:<ref name=":0" /><ref name=":1" />
* Immune-mediated causes could include transient factors as in ''[[Mycoplasma pneumoniae]]'' infection ([[cold agglutinin disease]]) or permanent factors as in [[autoimmune disease]]s like [[autoimmune hemolytic anemia]]<ref name=":0" /> (itself more common in diseases such as [[systemic lupus erythematosus]], [[rheumatoid arthritis]], [[Hodgkin's lymphoma]], and [[B-cell chronic lymphocytic leukemia|chronic lymphocytic leukemia]]).
* [[Spur cell hemolytic anemia]]
* Any of the causes of [[hypersplenism]] (increased activity of the spleen), such as [[portal hypertension]].
* Acquired hemolytic anemia is also encountered in [[burn]]s and as a result of certain infections (e.g. [[malaria]]).
* [[Lead poisoning]] or poisoning by [[arsine]] or [[stibine]] causes non-immune hemolytic anemia.<ref name=":1" />
* [[Running|Runners]] can develop hemolytic anemia due to "[[Mechanical hemolytic anemia|footstrike hemolysis]]", the destruction of red blood cells in feet at foot impact.<ref>{{cite journal |vauthors=Telford RD, Sly GJ, Hahn AG, Cunningham RB, Bryant C, Smith JA |title=Footstrike is the major cause of hemolysis during running |journal=J. Appl. Physiol. |volume=94 |issue=1 |pages=38–42 |date=January 2003 |pmid=12391035 |doi=10.1152/japplphysiol.00631.2001 |s2cid=5750453 }}</ref><ref>{{cite journal |vauthors=Lippi G, Schena F, Salvagno GL, Aloe R, Banfi G, Guidi GC |title=Foot-strike haemolysis after a 60-km ultramarathon |journal=Blood Transfus |pages=377–383 |date=July 2012 |pmc=3417738 |pmid=22682343 |doi=10.2450/2012.0167-11 |volume=10 |issue=3}}</ref>
* Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%.<ref>{{Cite book | url = https://books.google.com/books?id=bJF2zgOhJcoC&q=Biomaterials+Engineering+and+Devices-Human+applications+D.L.Wise&pg=PA203 | title = Biomaterials Engineering and Devices: Orthopedic, dental, and bone graft applications | isbn = 978-0-89603-859-2 | last1 = Wise | first1 = Donald Lee | year = 2000 | publisher = Humana Press }}{{Dead link|date=November 2023 |bot=InternetArchiveBot |fix-attempted=yes }}</ref>

===Intravascular hemolysis===
{{main|Intravascular hemolysis}}

'''Intravascular hemolysis''' describes hemolysis that happens mainly inside the [[vasculature]].<ref name="Stanley 2018">{{cite web | title=Diagnosis of hemolytic anemia in the adult | website=UpToDate | url=https://www.uptodate.com/contents/diagnosis-of-hemolytic-anemia-in-the-adult | access-date=2019-05-04 | author=Stanley L Schrier | editor1=William C Mentzer | editor2=Jennifer S Tirnauer | archive-url=https://web.archive.org/web/20171226181455/http://www.uptodate.com/contents/diagnosis-of-hemolytic-anemia-in-the-adult | archive-date=2017-12-26 | url-status=dead }}</ref> As a result, the contents of the red blood cell are released into the general circulation, leading to [[hemoglobinemia]]<ref name="eClinpath Intravascular hemolysis">{{cite web|url=http://eclinpath.com/hematology/anemia/mechanisms-of-anemia/intravascular-hemolysis-new/|title=Intravascular hemolysis|website=eClinpath|access-date=2019-05-08}}</ref> and increasing the risk of ensuing [[hyperbilirubinemia]].<ref name="Muller Jacobsen Healy McMickan 2006 pp. 229–241">{{cite journal | last1=Muller | first1=Andre | last2=Jacobsen | first2=Helene | last3=Healy | first3=Edel | last4=McMickan | first4=Sinead | last5=Istace | first5=Fréderique | last6=Blaude | first6=Marie-Noëlle | last7=Howden | first7=Peter | last8=Fleig | first8=Helmut | last9=Schulte | first9=Agnes | title=Hazard classification of chemicals inducing haemolytic anaemia: An EU regulatory perspective | journal=Regulatory Toxicology and Pharmacology | publisher=Elsevier BV | volume=45 | issue=3 | year=2006 | issn=0273-2300 | doi=10.1016/j.yrtph.2006.04.004 | pmid=16793184 | pages=229–241 | url=https://rivm.openrepository.com/bitstream/handle/10029/5596/muller.pdf?sequence=1&isAllowed=y | archive-url=https://web.archive.org/web/20190503184457/https://rivm.openrepository.com/bitstream/handle/10029/5596/muller.pdf?sequence=1&isAllowed=y | url-status=dead | archive-date=2019-05-03 | access-date=2019-05-04| hdl=10029/5596 | hdl-access=free }}</ref>

Intravascular hemolysis may occur when red blood cells are targeted by [[Autoantibody|autoantibodies]], leading to [[Complement system|complement]] fixation, or by damage by parasites such as ''[[Babesia]]''.<ref name="eClinpath Bilirubin and hemolytic anemia">{{cite web | title=Bilirubin and hemolytic anemia | website=eClinpath | url=http://eclinpath.com/chemistry/liver/cholestasis/bilirubin/bilirubin-and-hemolysis/ | access-date=2019-05-08}}</ref> Additionally, thrombotic microangiopathy (TMA) can result in hemolysis of red blood cells.<ref>{{Cite web|title=Thrombotic Microangiopathy (TMA)|url=https://unckidneycenter.org/kidneyhealthlibrary/glomerular-disease/thrombotic-microangiopathy-tma/|access-date=2020-08-19|website=UNC Kidney Center|language=en-US}}</ref> TMA is frequently observed in [[Atypical hemolytic uremic syndrome|aHUS]] patients where clots form in the small vessels of the kidney resulting in damaged red blood cells as they attempt to pass through the restricted vessels.<ref>{{Cite web|title=Atypical Hemolytic Uremic Syndrome|url=https://rarediseases.org/rare-diseases/atypical-hemolytic-uremic-syndrome/|access-date=2020-08-19|website=NORD (National Organization for Rare Disorders)|language=en-US}}</ref>

===Extravascular hemolysis===

'''Extravascular hemolysis''' refers to hemolysis taking place in the [[liver]], [[spleen]], [[bone marrow]], and [[lymph nodes]].<ref name="Stanley 2018" /> In this case little hemoglobin escapes into [[blood plasma]].<ref name="Muller Jacobsen Healy McMickan 2006 pp. 229–241" /> The [[macrophages]] of the [[reticuloendothelial system]] in these organs [[phagocytosis|engulf and destroy]] structurally-defective red blood cells, or those with antibodies attached, and release unconjugated bilirubin into the blood plasma circulation.<ref name="Rhodes Varacallo 2019">{{cite journal | last1=Rhodes | first1=Carl E. | last2=Varacallo | first2=Matthew | title=Physiology, Oxygen Transport | website=NCBI Bookshelf | date=2019-03-04 | pmid=30855920 | url=https://www.ncbi.nlm.nih.gov/books/NBK538336/ | access-date=2019-05-04}}</ref><ref name=Sokol81>{{cite journal |vauthors=Sokol RJ, Hewitt S, Stamps BK |title=Autoimmune haemolysis: an 18-year study of 865 cases referred to a regional transfusion centre |journal=Br Med J (Clin Res Ed) |volume=282 |issue=6281 |pages=2023–7 |date=June 1981 |pmid=6788179 |pmc=1505955 |doi=10.1136/bmj.282.6281.2023 }}</ref> Typically, the spleen destroys mildly abnormal red blood cells or those coated with [[Immunoglobulin G|IgG-type antibodies]],<ref name="BRAUNSTEIN.EVAN 2019">{{cite web | author=Braunstein, Evan | title=Overview of Hemolytic Anemia – Hematology and Oncology | website=Merck Manuals Professional Edition | date=2019-05-03 | url=https://www.merckmanuals.com/professional/hematology-and-oncology/anemias-caused-by-hemolysis/overview-of-hemolytic-anemia?query=Autoimmune%20Hemolytic%20Anemia | language=la | access-date=2019-05-05}}</ref><ref name="Hypersplenism 2019">{{cite web | title=Hypersplenism: MedlinePlus Medical Encyclopedia | website=MedlinePlus | date=2019-04-30 | url=https://medlineplus.gov/ency/article/001314.htm | access-date=2019-05-08}}</ref> while severely abnormal red blood cells or those coated with [[Immunoglobulin M|IgM-type antibodies]] are destroyed in the circulation or in the liver.<ref name="BRAUNSTEIN.EVAN 2019" />

If extravascular hemolysis is extensive, [[hemosiderin]] can be deposited in the spleen, bone marrow, kidney, liver, and other organs, resulting in [[hemosiderosis]].<ref name="Muller Jacobsen Healy McMickan 2006 pp. 229–241"/>

==Outside the body==
[[File:Hemolysis.jpg|thumb|Hemolysis of blood samples. Red blood cells without (left and middle) and with (right) hemolysis. If as little as 0.5% of the red blood cells are hemolyzed, the released hemoglobin will cause the [[blood serum|serum]] or [[blood plasma|plasma]] to appear pale red or cherry red in color.<ref>{{Cite web|url=http://www.cdha.nshealth.ca/default.aspx?page=SubPage&centerContent.Id.0=21648&category.Categories.1=411|title=Capital Health}}</ref> Note that the hemolyzed sample appears clearer, because there are significantly fewer cells to scatter light.]]
''[[In vitro]]'' hemolysis can be caused by improper technique during collection of blood specimens, by the effects of mechanical processing of blood, or by bacterial action in cultured blood specimens.

===From specimen collection===
Most causes of ''in vitro'' hemolysis are related to specimen collection. Difficult collections, unsecure line connections, contamination, and incorrect needle size, as well as improper tube mixing and incorrectly filled tubes are all frequent causes of hemolysis.<ref>{{Cite journal|last1=McCaughey|first1=Euan James|last2=Vecellio|first2=Elia|last3=Lake|first3=Rebecca|last4=Li|first4=Ling|last5=Burnett|first5=Leslie|last6=Chesher|first6=Douglas|last7=Braye|first7=Stephen|last8=Mackay|first8=Mark|last9=Gay|first9=Stephanie|date=2017-01-02|title=Key factors influencing the incidence of hemolysis: A critical appraisal of current evidence|journal=Critical Reviews in Clinical Laboratory Sciences|volume=54|issue=1|pages=59–72|doi=10.1080/10408363.2016.1250247|pmid=28013559|s2cid=753640|issn=1040-8363}}</ref> 

''In vitro'' hemolysis during specimen collection can cause inaccurate laboratory test results by contaminating the surrounding plasma with the contents of hemolyzed red blood cells. For example, the concentration of [[potassium]] inside red blood cells is much higher than in the plasma and so an elevated potassium level is usually found in biochemistry tests of hemolyzed blood.

After the blood collection process, ''in vitro'' hemolysis can still occur in a sample due to external factors, such as prolonged storage, incorrect storage conditions and excessive physical forces by dropping or vigorously mixing the tube.

==={{anchor|Mechanical blood processing during surgery}}From mechanical blood processing during surgery===
In some surgical procedures (especially some heart operations) where substantial blood loss is expected, machinery is used for [[intraoperative blood salvage]]. A centrifuge process takes blood from the patient, washes the red blood cells with [[normal saline]], and returns them to the patient's blood circulation. Hemolysis may occur if the centrifuge rotates too quickly (generally greater than 500 rpm)—essentially this is hemolysis occurring outside of the body. Increased hemolysis occurs with massive amounts of sudden blood loss, because the process of returning a patient's cells must be done at a correspondingly higher speed to prevent [[hypotension]], [[pH]] imbalance, and a number of other hemodynamic and blood level factors.  Modeling of fluid flows to predict the likelihood of red cell membrane rupture in response to stress is an active area of research.<ref>{{Cite journal|last1=Faghih|first1=Mohammad M.|last2=Sharp|first2=M. Keith|date=2019-03-07|title=Modeling and prediction of flow-induced hemolysis: a review|journal=Biomechanics and Modeling in Mechanobiology|volume=18|issue=4|pages=845–881|doi=10.1007/s10237-019-01137-1|issn=1617-7940|pmid=30847662|s2cid=73496695}}</ref>

==={{anchor|In microbiology}}From bacteria culture===
{{main|Hemolysis (microbiology)}}
[[File:Streptococcal hemolysis.jpg|thumb|Hemolysis from ''Streptococcus''. Examples of the blood culture patterns created by (from left) alpha-, beta- and gamma-hemolytic streptococci.]]
Visualizing the physical appearance of hemolysis in cultured blood samples may be used as a tool to determine the species of various [[Gram-positive bacteria]] infections (''e.g.'', ''[[Streptococcus]]'').

==Nomenclature==
Hemolysis is sometimes called '''hematolysis''', '''erythrolysis''', or '''erythrocytolysis'''. The words ''hemolysis'' ({{IPAc-en|h|iː|ˈ|m|ɒ|l|ɪ|s|ɪ|s}})<ref name="lpd"/> and ''hematolysis'' ({{IPAc-en|ˌ|h|iː|m|ə|ˈ|t|ɒ|l|ɪ|s|ɪ|s}})<ref>{{cite Merriam-Webster|hematolysis|access-date=8 July 2018}}</ref> both use [[classical compound|combining forms]] conveying the idea of "[[lysis]] of blood" (''[[wikt:haemo-#Prefix|hemo-]]'' or ''[[wikt:haemato-#Prefix|hemato-]]'' + ''[[wikt:-lysis#Suffix|-lysis]]''). The words ''erythrolysis'' ({{IPAc-en|ˌ|ɛr|ə|ˈ|θ|r|ɒ|l|ɪ|s|ɪ|s}})<ref>{{cite web|url=http://www.dictionary.com/browse/erythrolysis|title=erythrolysis|work=American Heritage Stedman's Medical Dictionary|publisher=Houghton Mifflin|access-date=8 July 2018|archive-url=https://web.archive.org/web/20180708162253/http://www.dictionary.com/browse/erythrolysis|archive-date=8 July 2018|url-status=live|df=dmy-all}}</ref> and ''erythrocytolysis'' ({{IPAc-en|ə|ˌ|r|ɪ|θ|r|oʊ|s|aɪ|ˈ|t|ɒ|l|ɪ|s|ɪ|s}})<ref>{{cite web|url=http://www.dictionary.com/browse/erythrocytolysis|title=erythrocytolysis|work=American Heritage Stedman's Medical Dictionary|publisher=Houghton Mifflin|access-date=8 July 2018|archive-url=https://web.archive.org/web/20180708162230/http://www.dictionary.com/browse/erythrocytolysis|archive-date=8 July 2018|url-status=live|df=dmy-all}}</ref> both use combining forms conveying the idea of "[[lysis]] of erythrocytes" (''[[wikt:erythro-#Prefix|erythro-]]'' ± ''[[wikt:cyto-#Prefix|cyto-]]'' + ''[[wikt:-lysis#Suffix|-lysis]]'').

Red blood cells (erythrocytes) have a short lifespan (approximately 120 days), and old ([[wikt:senescent#Adjective|senescent]]) cells are constantly removed and replaced with new ones via [[erythropoiesis]]. This breakdown/replacement process is called erythrocyte turnover. In this sense, erythrolysis or hemolysis is a normal process that happens continually. However, these terms are usually used to indicate that the lysis is [[Pathology|pathological]].

==Complications==
{{see also|Hemolytic anemia#Signs and symptoms}}

Pulmonary hypertension has been gaining recognition as a complication of chronic hereditary and acquired hemolysis.<ref name="Machado Gladwin 2010 pp. 30S–38S II">{{cite journal | last1=Machado | first1=Roberto F. | last2=Gladwin | first2=Mark T. | title=Pulmonary Hypertension in Hemolytic Disorders | journal=Chest | publisher=Elsevier BV | volume=137 | issue=6 | year=2010 | issn=0012-3692 | pmid=20522578 | pmc=2882115 | doi=10.1378/chest.09-3057 | pages=30S–38S}}</ref><ref name="Rother Bell Hillmen Gladwin p=1653">{{cite journal | last1=Rother | first1=Russell P. | last2=Bell | first2=Leonard | last3=Hillmen | first3=Peter | last4=Gladwin | first4=Mark T. | title=The Clinical Sequelae of Intravascular Hemolysis and Extracellular Plasma Hemoglobin | journal=JAMA | publisher=American Medical Association (AMA) | volume=293 | issue=13 | pages=1653–62 | date=2005-04-06 | issn=0098-7484 | pmid=15811985 | doi=10.1001/jama.293.13.1653 | doi-access=free }}</ref><ref name="Reiter Wang Tanus-Santos Hogg 2002 pp. 1383–1389 III">{{cite journal | last1=Reiter | first1=Christopher D. | last2=Wang | first2=Xunde | last3=Tanus-Santos | first3=Jose E. | last4=Hogg | first4=Neil | last5=Cannon | first5=Richard O. | last6=Schechter | first6=Alan N. | last7=Gladwin | first7=Mark T. | title=Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease | journal=Nature Medicine | publisher=Springer Nature | volume=8 | issue=12 | date=2002-11-11 | issn=1078-8956 | pmid=12426562 | doi= 10.1038/nm1202-799| pages=1383–1389| s2cid=19878520 }}</ref> Free hemoglobin released during hemolysis inactivates the [[vasodilator]] nitric oxide (NO).<ref name="Machado Gladwin 2010 pp. 30S–38S II"/> Hemolysis also releases [[arginase]] that depletes [[L-arginine]], the substrate needed for NO synthesis.<ref name="Machado Gladwin 2010 pp. 30S–38S II"/><ref name="Reiter Wang Tanus-Santos Hogg 2002 pp. 1383–1389 III"/> This reduces NO-dependent vasodilation<ref name="Machado Gladwin 2010 pp. 30S–38S II"/> and induces [[platelet]] activation, [[thrombin]] generation, [[procoagulant]] factors and [[tissue factor]] activation,<ref name="Machado Gladwin 2010 pp. 30S–38S II"/> contributing to the formation of [[thrombosis]].<ref name="Machado Gladwin 2010 pp. 30S–38S II"/> This can lead to [[esophageal spasm]] and [[dysphagia]], [[abdominal pain]], [[erectile dysfunction]], [[systemic hypertension]], [[hypoperfusion|decreased organ perfusion]], promotion of [[inflammation]] and [[coagulation]], and [[thrombosis]].<ref name="Rother Bell Hillmen Gladwin 2005 pp. 1653–1662 II">{{cite journal|last1=Rother|first1=Russell P.|last2=Bell|first2=Leonard|last3=Hillmen|first3=Peter|last4=Gladwin|first4=Mark T.|date=2005-04-06|title=The Clinical Sequelae of Intravascular Hemolysis and Extracellular Plasma Hemoglobin|journal=JAMA|volume=293|issue=13|pages=1653–1662|doi=10.1001/jama.293.13.1653|pmid=15811985|issn=0098-7484|quote=The systemic removal of nitric oxide has been shown to contribute to clinical morbidities, including severe esophageal spasm and dysphagia, abdominal pain, erectile dysfunction, and thrombosis.16,17,23-26 In addition, systemic release of hemoglobin is associated with pulmonary and systemic hypertension,17,20,53-55 decreased organ perfusion, and increased mortality.53-58 Plasma hemoglobin and its breakdown product heme can also directly activate endothelial cells and further promote inflammation and coagulation.27|doi-access=free}}</ref>

Chronic hemolysis may also lead to [[endothelial dysfunction]], heightened [[endothelin]]-1-mediated responses and [[vasculopathy]].<ref name="Machado Gladwin 2010 pp. 30S–38S II"/><ref name="Schaer Buehler Alayash Belcher pp. 1276–1284 II">{{cite journal | last1=Schaer | first1=D. J. | last2=Buehler | first2=P. W. | last3=Alayash | first3=A. I. | last4=Belcher | first4=J. D. | last5=Vercellotti | first5=G. M. | title=Hemolysis and free hemoglobin revisited: exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins | journal=Blood | publisher=American Society of Hematology | volume=121 | issue=8 | date=2012-12-20 | issn=0006-4971 | pmid=23264591 | pmc=3578950 | doi=10.1182/blood-2012-11-451229 | pages=1276–1284}}</ref>  The release of [[heme]] leads to the production of [[bilirubin]] and depletion of plasma proteins, such as [[albumin]], [[haptoglobin]], and [[hemopexin]], which may lead to [[jaundice]].<ref name="Smith McCulloh p.">{{cite journal|last1=Smith|first1=Ann|last2=McCulloh|first2=Russell J.|date=2015-06-30|title=Hemopexin and haptoglobin: allies against heme toxicity from hemoglobin not contenders|journal=Frontiers in Physiology|publisher=Frontiers Media SA|volume=6|pages=187|doi=10.3389/fphys.2015.00187|issn=1664-042X|pmc=4485156|pmid=26175690|doi-access=free }}</ref><ref name="Schaer Vinchi Ingoglia Tolosano p.">{{cite journal|last1=Schaer|first1=Dominik J.|last2=Vinchi|first2=Francesca|last3=Ingoglia|first3=Giada|last4=Tolosano|first4=Emanuela|last5=Buehler|first5=Paul W.|date=2014-10-28|title=Haptoglobin, hemopexin, and related defense pathways—basic science, clinical perspectives, and drug development|journal=Frontiers in Physiology|publisher=Frontiers Media SA|volume=5|pages=415|doi=10.3389/fphys.2014.00415|issn=1664-042X|pmc=4211382|pmid=25389409|doi-access=free }} [[File:CC-BY icon.svg|50px]] Material was copied from this source, which is available under a Creative Commons License.</ref> It may also lead to increased levels of the heme breakdown product [[stercobilin]] in the stool.<ref name="BRAUNSTEIN.EVAN 2019" />

[[Splenectomy]] of those with hemolytic disorders appears to increase risk of developing [[pulmonary thrombosis]].<ref name="Machado Gladwin 2010 pp. 30S–38S II"/>

Complications may also arise from the increased workload for the kidney as it secretes [[erythropoietin]] to stimulate the [[bone marrow]] to produce more [[reticulocyte]]s (red blood cell precursors) to compensate for the loss of red blood cells due to hemolysis.<ref name="BRAUNSTEIN.EVAN 2019"/>

==See also==
* [[Hemolysin]]
* [[Glucose-6-phosphate dehydrogenase deficiency]]

==References==
{{Reflist}}

==External links==
* [https://web.archive.org/web/20060515022028/http://www.calgarylabservices.com/HealthcareProfessionals/SpecimenCollection/HemolysisEffects.htm Effects of Hemolysis on Clinical Specimens]

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[[Category:Hematology]]