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| Hemolysis | |
|---|---|
| Other names | Haemolysis (alternative spelling), hematolysis, erythrolysis, or erythrocytolysis |
 | |
| Specialty | Pathology |
| Complications | Kidney failure,kidney disease |
| Causes | Osmosis |
Hemolysis orhaemolysis (/hiːˈmɒlɪsɪs/),[1] also known byseveral other names, is the rupturing (lysis) ofred blood cells (erythrocytes) and the release of their contents (cytoplasm) into surrounding fluid (e.g.blood plasma). Hemolysis may occurin vivo orin vitro.
One cause of hemolysis is the action ofhemolysins, toxins that are produced by certainpathogenic bacteria orfungi. Another cause is intense physical exercise.[2]Hemolysins damage the red blood cell'scytoplasmic membrane, causing lysis and eventually cell death.[3]
From hemo- + -lysis, fromAncient Greekαἷμα (haîma, 'blood') +λύσιςlúsis, 'loosening').
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-inducedhemolytic anemia,atypical hemolytic uremic syndrome (aHUS)[4]),[5] some genetic disorders (e.g.,Sickle-cell disease orG6PD deficiency), or blood with too low a solute concentration (hypotonic to cells).[6]
Hemolysis can lead tohemoglobinemia due tohemoglobin released into theblood plasma, which plays a significant role in thepathogenesis ofsepsis[7] and can lead to increased risk of infection due to its inhibitory effects on theinnate immune system.[7]
Because the feeding process of thePlasmodium parasites damages red blood cells,malaria is sometimes called "parasitic hemolysis" in medical literature.[citation needed]
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.[8]
Becausein vivo hemolysis destroys red blood cells, in uncontrolled, chronic or severe cases it can lead tohemolytic anemia.
A hemolytic crisis, or hyperhemolytic crisis, is characterized by an accelerated rate of red blood cell destruction leading toanemia,jaundice, andreticulocytosis.[9] Hemolytic crises are a major concern withsickle-cell disease andG6PD deficiency.
Paxillus involutus ingestion can cause hemolysis.
Spaceflight can cause hemolysis.[10]
Hemolysis may result from intrinsic defects in the red blood cell itself:[11][12]
Extrinsic hemolysis is caused by the red blood cell's environment:[5][6]
Intravascular hemolysis describes hemolysis that happens mainly inside thevasculature.[16] As a result, the contents of the red blood cell are released into the general circulation, leading tohemoglobinemia[17] and increasing the risk of ensuinghyperbilirubinemia.[18]
Intravascular hemolysis may occur when red blood cells are targeted byautoantibodies, leading tocomplement fixation, or by damage by parasites such asBabesia.[19] Additionally, thrombotic microangiopathy (TMA) can result in hemolysis of red blood cells.[20] TMA is frequently observed inaHUS 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.[21]
Extravascular hemolysis refers to hemolysis taking place in theliver,spleen,bone marrow, andlymph nodes.[16] In this case little hemoglobin escapes intoblood plasma.[18] Themacrophages of thereticuloendothelial system in these organsengulf and destroy structurally-defective red blood cells, or those with antibodies attached, and release unconjugated bilirubin into the blood plasma circulation.[22][23] Typically, the spleen destroys mildly abnormal red blood cells or those coated withIgG-type antibodies,[24][25] while severely abnormal red blood cells or those coated withIgM-type antibodies are destroyed in the circulation or in the liver.[24]
If extravascular hemolysis is extensive,hemosiderin can be deposited in the spleen, bone marrow, kidney, liver, and other organs, resulting inhemosiderosis.[18]
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.
Most causes ofin 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.[27]
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 ofpotassium 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.
In some surgical procedures (especially some heart operations) where substantial blood loss is expected, machinery is used forintraoperative blood salvage. A centrifuge process takes blood from the patient, washes the red blood cells withnormal 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 preventhypotension,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.[28]
Visualizing the physical appearance of hemolysis in cultured blood samples may be used as a tool to determine the species of variousGram-positive bacteria infections (e.g.,Streptococcus).
Hemolysis is sometimes calledhematolysis,erythrolysis, orerythrocytolysis. The wordshemolysis (/hiːˈmɒlɪsɪs/)[1] andhematolysis (/ˌhiːməˈtɒlɪsɪs/)[29] both usecombining forms conveying the idea of "lysis of blood" (hemo- orhemato- +-lysis). The wordserythrolysis (/ˌɛrəˈθrɒlɪsɪs/)[30] anderythrocytolysis (/əˌrɪθroʊsaɪˈtɒlɪsɪs/)[31] both use combining forms conveying the idea of "lysis of erythrocytes" (erythro- ±cyto- +-lysis).
Red blood cells (erythrocytes) have a short lifespan (approximately 120 days), and old (senescent) cells are constantly removed and replaced with new ones viaerythropoiesis. 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 ispathological.
Pulmonary hypertension has been gaining recognition as a complication of chronic hereditary and acquired hemolysis.[32][33][34] Free hemoglobin released during hemolysis inactivates thevasodilator nitric oxide (NO).[32] Hemolysis also releasesarginase that depletesL-arginine, the substrate needed for NO synthesis.[32][34] This reduces NO-dependent vasodilation[32] and inducesplatelet activation,thrombin generation,procoagulant factors andtissue factor activation,[32] contributing to the formation ofthrombosis.[32] This can lead toesophageal spasm anddysphagia,abdominal pain,erectile dysfunction,systemic hypertension,decreased organ perfusion, promotion ofinflammation andcoagulation, andthrombosis.[35]
Chronic hemolysis may also lead toendothelial dysfunction, heightenedendothelin-1-mediated responses andvasculopathy.[32][36] The release ofheme leads to the production ofbilirubin and depletion of plasma proteins, such asalbumin,haptoglobin, andhemopexin, which may lead tojaundice.[37][38] It may also lead to increased levels of the heme breakdown productstercobilin in the stool.[24]
Splenectomy of those with hemolytic disorders appears to increase risk of developingpulmonary thrombosis.[32]
Complications may also arise from the increased workload for the kidney as it secreteserythropoietin to stimulate thebone marrow to produce morereticulocytes (red blood cell precursors) to compensate for the loss of red blood cells due to hemolysis.[24]
{{cite journal}}:Cite journal requires|journal= (help)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
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