hemolytic anemia

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Hemolytic Anemia



Red blood cells have a normal life span of approximately 90-120 days, at which time the old cells are destroyed and replaced by the body's natural processes. Hemolytic anemia is a disorder in which the red blood cells are destroyed prematurely. The cells are broken down at a faster rate than the bone marrow can produce new cells. Hemoglobin, the component of red blood cells that carries oxygen, is released when these cells are destroyed.


As a group, anemias (conditions in which the number of red blood cells or the amount of hemoglobin in them is below normal) are the most common blood disorders. Hemolytic anemias, which result from the increased destruction of red blood cells, are less common than anemias caused by excessive blood loss or by decreased hemoglobin or red cell production.
Since a number of factors can increase red blood cell destruction, hemolytic anemias are generally identified by the disorder that brings about the premature destruction. Those disorders are classified as either inherited or acquired. Inherited hemolytic anemias are caused by inborn defects in components of the red blood cells—the cell membrane, the enzymes, or the hemoglobin. Acquired hemolytic anemias are those that result from various other causes. With this type, red cells are produced normally, but are prematurely destroyed because of damage that occurs to them in the circulation.

Causes and symptoms

Inherited hemolytic anemias involve conditions that interfere with normal red blood cell production. Disorders that affect the red blood cell membrane include hereditary spherocytosis, in which the normally disk-shaped red cells become spherical, and hereditary elliptocytosis, in which the cells are oval, rather than disk-shaped. Other hereditary conditions that cause hemolytic anemia include disorders of the hemoglobin, such as sickle cell anemia and thalassemia, and red blood cell enzyme deficiencies, such as G6PD deficiency.
The causes of acquired hemolytic anemias vary, but the most common are responses to certain medications and infections. Medications may cause the body to develop antibodies that bind to the red blood cells and cause their destruction in the spleen. Immune hemolytic anemia most commonly involves antibodies that react against the red blood cells at body temperature (warm-antibody hemolytic anemia), which can cause premature destruction of the cells. About 20% of hemolytic anemias caused by warm antibodies come from diseases such as lymphocytic leukemia, 10% from an autoimmune disease, and others are drug-induced. Cold-antibody hemolytic anemia is a condition in which the antibodies react with the red blood cells at a temperature below that of normal body temperature. Red blood cells can also receive mechanical damage as they circulate through the blood vessels. Aneurysms, artificial heart valves, or very high blood pressure can cause the red cells to break up and release their contents. In addition, hemolytic anemia may be caused by a condition called hypersplenism, in which a large, overactive spleen rapidly destroys red blood cells.
Major symptoms of hemolytic anemias are similar to those for all anemias, including shortness of breath; noticeable increase in heart rate, especially with exertion; fatigue; pale appearance; and dark urine. A yellow tint, or jaundice, may be seen in the skin or eyes of hemolytic anemia patients. Examination may also show an enlarged spleen. A more emergent symptom of hemolytic anemia is pain in the upper abdomen. Severe anemia is indicated if there are signs of heart failure or an enlarged liver.


In order to differentiate hemolytic anemia from others, physicians will examine the blood for the number of young red blood cells, since the number of young cells is increased in hemolytic anemia. The physician will also examine the abdominal area to check for spleen or liver enlargement. If the physician knows the duration of hemolysis, it may also help differentiate between types of anemia. There are a number of other indications that can be obtained from blood samples that will help a physician screen for hemolytic anemia. An antiglobulin (Coomb's) test may be performed as the initial screening exam after determining hemolysis. In the case of immune hemolytic anemia, a direct Coomb's test is almost always positive.


Treatment will depend on the cause of the anemia, and may involve treatment of the underlying cause. If the hemolytic anemia was brought on by hereditary spherocytosis, the spleen may be removed. Corticosteroid medications, or adrenal steroids, may be effective, especially in hemolytic anemia due to antibodies. If the cause of the disorder is a medication, the medication should be stopped. When anemia is severe in conditions such as sickle cell anemia and thalassemia, blood transfusions may be indicated.


Hemolytic anemias are seldom fatal. However, if left untreated, hemolytic anemia can lead to heart failure or liver complications.


Hemolytic anemia due to inherited disorders can not be prevented. Acquired hemolytic anemia may be prevented if the underlying disorder is managed properly.



American Autoimmune Related Diseases Association, Inc. Focus: A quarterly newsletter of the AARDA. Detroit, MI. (313) 371-8600. http://www.aarda.org.
The American Society of Hematology. 1200 19th Street NW, Suite 300, Washington, DC 20036-2422. (202) 857-1118. http://www.hematology.org.
National Heart, Lung and Blood Institute. PO Box 30105, Bethesda, MD 20824-0105. (301) 251-1222. http://www.nhlbi.nih.gov.

Key terms

Antibody — Antibodies are parts of the immune system which counteract or eliminate foreign substances or antigens.
Erythrocyte — The name for red blood cells or red blood corpuscles. These components of the blood are responsible for carrying oxygen to tissues and removing carbon dioxide from tissues.
Hemolysis — The process of breaking down of red blood cells. As the cells are destroyed, hemoglobin, the component of red blood cells which carries the oxygen, is liberated.
Thalassemia — One of a group of inherited blood disorders characterized by a defect in the metabolism of hemoglobin, or the portion of the red blood cells that transports oxygen throughout the blood stream.


a condition in which there is reduced delivery of oxygen to the tissues; it is not actually a disease but rather a symptom of any of numerous different disorders and other conditions. The World Health Organization has defined anemia as a hemoglobin concentration below 7.5 mmol/L (12 g/dL) in women and below 8.1 mmol/L (13 g/dL) in men.
 Peripheral blood smears from a patient with megaloblastic anemia (left) and from a normal subject (right), both at the same magnification. The smear from the patient shows variation in the size and shape of erythrocytes and the presence of macro-ovalocytes. From Goldman and Bennett, 2000.

Some types of anemia are named for the factors causing them: poor diet (nutritional anemia), excessive blood loss (hemorrhagic anemia), congenital defects of hemoglobin (hypochromic anemia), exposure to industrial poisons, diseases of the bone marrow (aplastic anemia and hypoplastic anemia), or any other disorder that upsets the balance between blood loss through bleeding or destruction of blood cells and production of blood cells. Anemias can also be classified according to the morphologic characteristics of the erythrocytes, such as size (microcytic, macrocytic, and normocytic anemias) and color or hemoglobin concentration (hypochromic anemia). A type called hypochromic microcytic anemia is characterized by very small erythrocytes that have low hemoglobin concentration and hence poor coloration. Data used to identify anemia types include the erythrocyte indices: (1) mean corpuscular volume (MCV), the average erythrocyte volume; (2) mean corpuscular hemoglobin (MCH), the average amount of hemoglobin per erythrocyte; and (3) mean corpuscular hemoglobin concentration (MCHC), the average concentration of hemoglobin in erythrocytes. adj., adj ane´mic.
Symptoms. Mild degrees of anemia often cause only slight and vague symptoms, perhaps nothing more than easy fatigue or a lack of energy. As the condition progresses, more severe symptoms may be experienced, such as shortness of breath, pounding of the heart, and a rapid pulse; these are caused by the inability of anemic blood to supply the body tissues with enough oxygen. Pallor, particularly in the palms of the hands, the fingernails, and the conjunctiva (the lining of the eyelids), may also indicate anemia. In very advanced cases, swelling of the ankles and other evidence of heart failure may appear.
Common Causes of Anemia. Loss of Blood (Hemorrhagic Anemia): If there is massive bleeding from a wound or other lesion, the body may lose enough blood to cause severe and acute anemia, which is often accompanied by shock. Immediate transfusions are generally required to replace the lost blood. Chronic blood loss, such as excessive menstrual flow, or slow loss of blood from an ulcer or cancer of the gastrointestinal tract, may also lead to anemia. These anemias disappear when the cause has been found and corrected. To help the blood replenish itself, the health care provider may prescribe medicines containing iron, which is necessary to build hemoglobin, and foods with high iron content, such as kidney and navy beans, liver, spinach, and whole wheat bread.

Dietary Deficiencies and Abnormalities of Red Blood Cell Production (Nutritional Anemia, Aplastic Anemia, and Hypoplastic Anemia): Anemia may develop if the diet does not provide enough iron, protein, vitamin B12, and other vitamins and minerals needed in the production of hemoglobin and the formation of erythrocytes. The combination of poor diet and chronic loss of blood makes for particular susceptibility to severe anemia. Anemias associated with folic acid deficiency are very common.

Excessive Destruction of Red Blood Cells (hemolytic anemia): Anemia may also develop related to hemolysis due to trauma, chemical agents or medications (toxic hemolytic anemia), infectious disease, isoimmune hemolytic reactions, autoimmune disorders, and the paroxysmal hemoglobinurias.
Patient Care. Assessment of patients with some form of anemia will depend to some extent on the specific type of blood dyscrasia presented. In general, these patients do share some common problems requiring special assessment skills and interventions. Anemia can affect many different body systems
(see table). Although pallor of the skin is a sign of anemia, it is not the most reliable sign; many other factors can affect complexion and skin color. Jaundice of the skin and sclera can occur as a result of hemolysis and the release of bilirubin into the blood stream, where it eventually finds its way into the skin and mucous membranes. (See also jaundice.) Bleeding under the skin and bruises in response to the slightest trauma often are present in anemic and leukemic patients. A bluish tint to the skin (cyanosis) can indicate hypoxia due to inadequate numbers of oxygen-bearing erythrocytes.

Activity intolerance is a common problem for patients with anemia. Physical activity increases demand for oxygen, but if there are not enough circulating erythrocytes to provide sufficient oxygen, patients become physically weak and unable to engage in normal physical activity without experiencing profound fatigue. This can result in some degree of self-care deficit as the fatigue interferes with the patient's ability to carry on regular or enjoyable activities.
acute posthemorrhagic anemia hemorrhagic anemia.
aplastic anemia see aplastic anemia.
autoimmune hemolytic anemia (AIHA) an acquired disorder characterized by hemolysis due to the production of autoantibodies against one's own red blood cell antigens.
Blackfan-Diamond anemia congenital hypoplastic anemia (def. 1).
congenital hypoplastic anemia
idiopathic progressive anemia occurring in the first year of life, without leukopenia and thrombocytopenia; it is due to an isolated defect in erythropoiesis and is unresponsive to hematinics, requiring multiple blood transfusions to sustain life. For those responding to steroid therapy the prognosis is good. Called also Blackfan-Diamond anemia or syndrome, Diamond-Blackfan anemia or syndrome, and erythrogenesis imperfecta.
Cooley's anemia tthalassemia major.
deficiency anemia nutritional anemia.
Diamond-Blackfan anemia congenital hypoplastic anemia (def. 1).
drug-induced hemolytic anemia (drug-induced immune hemolytic anemia) a form of immune hemolytic anemia induced by the taking of drugs, involving one of four different mechanisms:

Immune complex problems: Ingestion of any of a large number of drugs is followed by immunization and the formation of a soluble drug–anti-drug complex that adsorbs nonspecifically to the erythrocyte surface.

Drug absorption: Drugs bind firmly to erythrocyte membrane proteins, inducing the formation of specific antibodies; the drug most commonly associated with this mechanism is penicillin.

Membrane modification: A nonimmunologic mechanism whereby the drug involved is able to modify erythrocytes so that plasma proteins can bind to the membrane.

Autoantibody formation: Methyldopa (Aldomet) induces the production of autoantibodies that recognize erythrocyte antigens and are serologically indistinguishable from those seen in patients with warm autoimmune hemolytic anemia.
Fanconi's anemia (Fanconi's hypoplastic anemia) Fanconi's syndrome (def. 1).
hemolytic anemia see hemolytic anemia.
hemorrhagic anemia anemia caused by the sudden and acute loss of blood; called also acute posthemorrhagic anemia.
hypochromic anemia anemia in which the decrease in hemoglobin is proportionately much greater than the decrease in number of erythrocytes.
hypochromic microcytic anemia any anemia with microcytes that are hypochromic (reduced in size and in hemoglobin content); the most common type is iron deficiency anemia.
hypoplastic anemia anemia due to incapacity of blood-forming organs.
immune hemolytic anemia an acquired hemolytic anemia in which a hemolytic response is caused by isoantibodies or autoantibodies produced on exposure to drugs, toxins, or other antigens. See also autoimmune hemolytic anemia, drug-induced immune hemolytic anemia, and erythroblastosis fetalis.
iron deficiency anemia a type of hypochromic microcytic anemia that results from the presence of greater demands on stored iron than can be met, usually because of chronic blood loss, dietary deficiency, or defective absorption; it is characterized by low or absent iron stores, low serum iron concentration, low transferrin saturation, elevated transferrin (total iron-binding capacity), and low hemoglobin concentration or hematocrit. Iron deficiency anemia is the most common nutritional disorder in the United States.
macrocytic anemia anemia characterized by macrocytes (erythrocytes much larger than normal).
Mediterranean anemia thalassemia major.
megaloblastic anemia any of various anemias characterized by the presence of megaloblasts in the bone marrow or blood; the most common type is pernicious anemia.
microangiopathic hemolytic anemia thrombotic thrombocytopenic purpura.
microcytic anemia anemia characterized by microcytes (erythrocytes smaller than normal); see also hypochromic microcytic anemia and microcythemia.
myelopathic anemia (myelophthisic anemia) leukoerythroblastosis.
normochromic anemia that in which the hemoglobin content of the red blood cells is in the normal range.
normocytic anemia anemia characterized by proportionate decrease in hemoglobin, packed red cell volume, and number of erythrocytes per cubic millimeter of blood.
nutritional anemia anemia due to a deficiency of an essential substance in the diet, which may be caused by poor dietary intake or by malabsorption; called also deficiency anemia.
pernicious anemia see pernicious anemia.
sickle cell anemia see sickle cell anemia.
sideroachrestic anemia (sideroblastic anemia) any of a heterogenous group of acquired and hereditary anemias with diverse clinical manifestations, commonly characterized by large numbers of sideroblasts in the bone marrow, ineffective erythropoiesis, variable proportions of hypochromic erythrocytes in the peripheral blood, and usually increased levels of tissue iron.
spur cell anemia anemia in which the erythrocytes are acanthocytes (spur cells) and are destroyed prematurely, primarily in the spleen; it is an acquired form occurring in severe liver disease in which there is increased serum cholesterol and increased uptake of cholesterol into the erythrocyte membrane, causing the abnormal shape.


pertaining to, characterized by, or producing hemolysis.
hemolytic anemia anemia caused by the increased destruction of erythrocytes. A frequently fatal type occurs in infants as a result of Rh incompatibility with the mother's blood (see Rh factor and erythroblastosis fetalis). Other types result from mismatched blood transfusions; from industrial poisons such as benzene, trinitrotoluene (TNT), or aniline; and from hypersensitivity to certain antibiotics and tranquilizers (drug-induced hemolytic anemia). Another important cause is mechanical obstruction caused by microvascular or valvular abnormalities. In addition, it sometimes occurs as a result of a disorder of the immune response in which B-cell–produced antibodies fail to recognize the body's own erythrocytes and directly attack and destroy them (autoimmune hemolytic anemia). Finally, some types of hemolytic anemia appear in the course of other diseases such as leukemia, hodgkin's disease, other types of cancer, acute alcoholism, and liver diseases. Along with the usual symptoms of anemia, the patient may exhibit jaundice. If the cause of the condition can be determined, and if it can be successfully treated, there is a good chance of recovery. steroids and transfusion therapy are used to treat some types. In other cases, surgical removal of the spleen may bring about great improvement.
hemolytic disease of newborn erythroblastosis fetalis.
hemolytic jaundice a rare, chronic, and generally hereditary disease characterized by periods of excessive hemolysis due to abnormal fragility of the erythrocytes, which are small and spheroidal. It is accompanied by enlargement of the spleen and by jaundice. The hereditary form is also known as familial acholuric jaundice; there is also a rare acquired form. See also hyperbilirubinemia.
hemolytic uremic syndrome a form of thrombotic microangiopathy with renal failure, hemolytic anemia, and severe thrombocytopenia and purpura, usually seen in children but occurring at any age. Some authorities consider it identical to thrombotic thrombocytopenic purpura.

he·mo·lyt·ic a·ne·mi·a

any anemia resulting from an increased rate of erythrocyte destruction.

hemolytic anemia

Anemia resulting from the lysis of red blood cells, as in response to certain toxic or infectious agents and in certain inherited blood disorders.

hemolytic anemia

Etymology: Gk, haima + lysis + a, without, + haima, blood
a disorder characterized by acute or chronic premature destruction of red blood cells. Anemia may be partially compensated by bone marrow production. The condition may be associated with some infectious diseases, certain inherited red cell disorders, or neoplastic diseases. It may be a response to drugs or other toxic agents. Also spelled haemolytic anemia. Compare aplastic anemia, congenital nonspherocytic hemolytic anemia, iron deficiency anemia, myelophthisic anemia. See also anemia, hemolysis, spherocytosis.

hemolytic anemia

Hematology Anemia which occurs when more RBCs are lysed than are produced; HA may be immune-mediated or non-immune, due to intrinsic or extrinsic RBC defects. See Nonimmune hemolytic anemia Immunology Immune hemolysis is alloimmune, autoimmune, and drug-induced, and may be intravascular or extravascular Microbiology Hemolysis is characteristic of certain strains of streptococci and is divided into α- and β-hemolysis; γ 'hemolysis' is a complete misnomer. See Gamma-hemolysis, Innocent bystander hemolysis.

he·mo·lyt·ic a·ne·mi·a

(hē'mō-lit'ik ă-nē'mē-ă)
Any anemia resulting from an increased rate of erythrocyte destruction.
Synonym(s): haemolytic anaemia.

he·mo·lyt·ic a·ne·mi·a

(hē'mō-lit'ik ă-nē'mē-ă)
Anemia due to increased rate of erythrocyte destruction.
Synonym(s): haemolytic anemia.


a reduction below normal in the number or volume of erythrocytes or in the quantity of hemoglobin in the blood. Clinically it is manifested by weakness, exercise intolerance, hyperpnea which is only moderate, pallor of mucosae, tachycardia and a large increase in the intensity of the heart sounds. There are often accompanying signs related to the site of blood or hemoglobin loss.

aplastic anemia
a form of anemia generally unresponsive to specific antianemia therapy. It is often chronic, accompanied by granulocytopenia and thrombocytopenia, in which the bone marrow is usually acellular or hypoplastic. It may, however, be rapidly fatal. The term is actually all-inclusive and most probably encompasses several clinical syndromes. See pure red cell aplasia.
autoimmune hemolytic anemia
immune-mediated hemolytic anemia, which occurs in many species, particularly dogs, in which autoantibodies directed against red blood cells are produced. Different classes of immunoglobulins may be involved giving rise to differing clinical syndromes. Signs include pallor, lethargy, splenomegaly, and sometimes icterus, bilirubinuria and hemoglobinuria. There may also be an accompanying thrombocytopenia with bleeding tendencies. Diagnosis is based on a positive Coombs test.
avian infectious anemia
see chicken anemia.
blood loss anemia
see hemorrhagic anemia (below).
anemia of chronic disease
see anemia of inflammatory disease (below).
cold antibody anemia
an immune-mediated hemolytic anemia in which the antibody is maximally active at temperatures below 98.6°F (37°C). See also cold agglutinin disease.
cold (or cold water) anemia
a disease of cattle, especially calves, housed in warm barns and given near freezing water to drink. Dyspnea and the passage of red urine occur several hours after a large drink.
Coombs-positive anemia
immunoglobulin-mediated anemia that gives a positive reaction to Coombs tests, indicating the presence of immunoglobulins on the red cell surface. See also autoimmune hemolytic anemia (above), alloimmune hemolytic anemia of the newborn.
deficiency anemia
nutritional anemia.
drug-induced hemolytic anemia
some drugs such as quinine, quinidine, para-aminosalicylic acid, phenacetin, penicillin, insecticides, chlorpromazine, sulfonamides and dipyrone may be directly injurious to red cells or act to initiate an immune response in which red cells are destroyed.
familial nonspherocytic anemia of Basenji dogs
an inherited pyruvate kinase deficiency causes a hemolytic anemia with shortened red cell life span. In early stages, the disease is characterized by very active erythropoiesis but eventually, usually by the second or third year of life, a terminal myelofibrosis and osteosclerosis develops. The disease is inherited as an autosomal recessive trait.
feline infectious anemia
see feline infectious anemia.
fragmentation anemia
see microangiopathic anemia (below).
Heinz body anemia
hemolytic anemia resulting from oxidation of globin and formation of Heinz bodies, which are seen in blood smears as dark refractile intracytoplasmic bodies and stain with new methylene blue. Some common causes are ingestion of onions and plants in the Brassicaeae family, phenazopyridine, methylene blue and acetaminophen (paracetamol). Cats are particularly susceptible to Heinz body formation.
hemolytic anemia
see hemolytic anemia.
hemorrhagic anemia
is caused by loss of whole blood. If this is very rapid hypovolemic shock develops. At a slower rate there is anemic anoxia and the animal is suffering from anemia. Called also blood loss anemia.
hypochromic anemia
anemia in which the decrease in hemoglobin is proportionately much greater than the decrease in number of erythrocytes.
hypoplastic anemia
anemia due to incapacity of blood-forming organs, i.e. inactivity of the bone marrow. See also aplastic anemia (above).
idiopathic immune anemia
see autoimmune hemolytic anemia (above).
infectious equine anemia
see equine infectious anemia.
anemia of inflammatory disease
a nonregenerative, usually mild, anemia that occurs in association with malignancy or chronic infection. Although other causes of anemia such as hemolysis and blood loss may also occur with these conditions, there is altered iron metabolism with decreased serum iron and iron-binding capacity but with increased iron storage that results in decreased erythropoiesis.
iron-deficiency anemia
a form characterized by low or absent iron stores, low serum iron concentration, low transferrin saturation, elevated transferrin (iron-binding capacity), low hemoglobin concentration or hematocrit, and hypochromic, microcytic red blood corpuscles, and thrombocytosis. See also iron.
isoimmune hemolytic anemia
see alloimmune hemolytic anemia of the newborn.
lizard viral anemia
produces inclusion bodies in erythrocytes, commonly mistaken for protozoan parasites.
macrocytic anemia
anemia in which the erythrocytes are much larger than normal. The MCV (mean corpuscular volume) and MCH (mean corpuscular hemoglobin) are increased and the MCHC (mean corpuscular hemoglobin concentration) is normal.
megaloblastic anemia
anemia characterized by the presence of megaloblasts in the bone marrow and macrocytic erythrocytes. It occurs in vitamin B12, cobalt and folic acid deficiencies and in some myeloproliferative disorders in cats.
microangiopathic anemia
anemia due to fragmentation of erythrocytes in blood vessels whose endothelium has been badly damaged, usually by an infectious disease such as septicemias, disseminated intravascular coagulation and salmonellosis. Called also fragmentation anemia.
microcytic anemia
anemia characterized by decrease in size of the erythrocytes.
myelopathic anemia, myelophthisic anemia
anemia due to destruction or crowding out of hematopoietic tissues by space-occupying lesions, neoplasms and fibrosis.
nonregenerative anemia
one occurring without an appropriate erythropoietic response by the bone marrow.
normochromic anemia
that in which the hemoglobin content of the red cells as measured by the MCHC and MCH is within the normal range.
normocytic anemia
the anemia in which the red blood cells are normal in size.
nutritional anemia
anemia due to a deficiency of an essential substance in the diet, which may be caused by poor dietary intake or by malabsorption; called also deficiency anemia. See also pyridoxine, vitamin b12, folic acid, copper, iron.
parasitic anemia
hemorrhagic anemia due to blood loss caused by blood-sucking parasites such as fleas, hookworms and Haemonchus contortus.
pernicious anemia
see pernicious anemia.
physiological anemia
the anemia which occurs as part of a natural event, e.g. in neonates.
piglet anemia
see iron nutritional deficiency.
primary immune anemia
see autoimmune hemolytic anemia (above).
regenerative anemia, responsive anemia
associated with active erythropoiesis with increased numbers of reticulocytes, nucleated red blood cells, anisocytosis and polychromasia in the peripheral blood.
spur-cell anemia
anemia in which the red cells have a bizarre spiculated shape and are destroyed prematurely, primarily in the spleen; it is an acquired form occurring in severe liver disease, and represents an abnormality in the cholesterol content of the red cell membrane.
unresponsive anemia
see nonregenerative anemia (above).


pertaining to, characterized by, or producing hemolysis.

hemolytic anemia
anemia caused by the increased destruction of erythrocytes which may occur in the vascular system—intravascular hemolysis, or due to phagocytosis by the monocyte-macrophage system—extravascular or intracellular hemolysis. It may result from incompatibility (see alloimmune hemolytic anemia of the newborn), from mismatched blood transfusions, from poisons such as copper, organic agents in plants such as kale, from nutritional deficiencies such as phosphorus and from protozoan infections such as babesiosis. Hemolytic anemia may also occur as a result of a disorder of the immune response in which B cell-produced antibodies fail to recognize erythrocytes that are 'self' and directly attack and destroy them. In addition to the usual signs of anemia, the patient may also exhibit jaundice.
hemolytic component
a degree of extravascular hemolysis in association with other types of anemia.
hemolytic disease of the newborn
see alloimmune hemolytic anemia of the newborn.
hemolytic enterotoxemia
a little reported disease recorded mostly in Australia in sheep, cattle and foals; a highly fatal hemolytic anemia associated with a heavy population of Clostridium perfringens type A in the intestines.
hemolytic plaque assay
see plaque assay.
hemolytic-uremic syndrome
a microangiopathic hemolytic anemia with thrombocytopenia and severe involvement of renal vasculature which leads to acute renal failure. In humans associated with verocytoxin-producing bacteria such as Escherichia coli, Shigella and some Salmonella; usually associated with the ingestion of poorly cooked meat. A similar clinical syndrome has been reported in cows, horses and dogs.
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