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Hemolytic Anemia
Article Last Updated: Jan 29, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Paul Schick, MD, Emeritus Professor, Department of Internal Medicine, Thomas Jefferson University Medical College; Research Professor, Department of Internal Medicine, Drexel University College of Medicine
Paul Schick is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences
Editors: Rodger L Bick, MD, PhD, FACP, Clinical Professor of Medicine, University of Texas Southwestern Medical Center; Director, Dallas & Pacific Thrombosis Hemostasis Vascular Medicine Clinical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Ronald A Sacher, MB, BCh, MD, FRCPC, Director of the Hoxworth Blood Center, Professor, Departments of Internal Medicine and Pathology, University of Cincinnati Medical Center; Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems; Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Thomas Jefferson University
Author and Editor Disclosure
Synonyms and related keywords:
hemolysis, premature erythrocyte destruction, hereditary hemoglobin abnormalities, glucose-6-phosphate dehydrogenase deficiency, G6PD deficiency, G-6-PD deficiency, hereditary spherocytosis, sickle cell anemia, sickle cell trait, sickle cell disease, AIHA, autoimmune hemolytic anemia, microangiopathic anemia, disseminated intravascular coagulation, DIC, hemolytic uremic syndrome, HUS, hemolytic-uremic syndrome, TTP, thrombotic thrombocytopenic purpura, defective prosthetic cardiac valves, parvovirus B19 infection, anemia
Background
Hemolysis is the premature destruction of erythrocytes, and it leads to hemolytic anemia when bone marrow activity cannot compensate for the erythrocyte loss. Clinical presentation depends on whether the onset of hemolysis is gradual or abrupt and on the severity of erythrocyte destruction. A patient with mild hemolysis may be asymptomatic. In more serious cases, the anemia can be life threatening, and patients can present with angina and cardiopulmonary decompensation. Clinical presentation also reflects the underlying cause for hemolysis. For example, sickle cell anemia is associated with a painful occlusive crisis.
Pathophysiology
Hemolysis is the final event triggered by a large number of hereditary and acquired disorders. The etiology of premature erythrocyte destruction is diverse and can be due to conditions such as intrinsic membrane defects, abnormal hemoglobins, erythrocyte enzymatic defects, immune destruction of erythrocytes, mechanical injury, and hypersplenism. Hemolysis is associated with a release of hemoglobin and lactic acid dehydrogenase (LDH). An increase in indirect bilirubin and urobilinogen is derived from released hemoglobin. A patient with mild hemolysis may have normal hemoglobin levels if increased production matches the rate of erythrocyte destruction.
Marked anemia may occur in patients with mild hemolysis if bone marrow erythrocyte production is transiently shut off by viral (parvovirus B19) or other infections due to uncompensated destruction of erythrocytes (aplastic hemolytic crisis). Skull and skeletal deformities can occur with a marked increase in hematopoiesis, expansion of bone in infancy, and early childhood disorders such as sickle cell anemia or thalassemia.
Frequency
International
Hemolytic anemia represents approximately 5% of all anemias.
Mortality/Morbidity
The overall incidence of death is low. However, older patients and patients with cardiovascular impairment are at an increased risk. Morbidity is dependent on the etiology of hemolysis and the underlying disorder such as sickle cell anemia or malaria.
- Tachycardia and dyspnea symptoms occur when the onset of hemolysis is abrupt and the anemia is severe.
- Angina and heart failure symptoms can occur in patients with underlying cardiovascular disease and severe uncompensated hemolysis.
- Hemosiderosis, leg ulcers, folate deficiency, and gallstones can also occur.
Race
Most of the disorders that lead to hemolysis are not specific to any race.
- Sickle cell disorders are found primarily in Africans, African Americans, some Arabic peoples, and Aborigines in southern India.
- Several variants of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency exist. The A variant generally is found in West Africans and African Americans. Approximately 10% of African Americans have at least 1 gene for this variant. The Mediterranean variant occurs in individuals of Mediterranean descent and in some Asians.
Sex
- Most cases of hemolytic anemia are not sex specific.
- Autoimmune hemolytic anemia (AIHA) is slightly more likely to occur in females than in males.
- G-6-PD deficiency is an X-linked recessive disorder. Males are usually affected, and females are carriers.
Age
- Hemolytic anemia can occur in persons of any age.
- Hereditary disorders are usually evident early in life.
- Autoimmune hemolytic anemia is more likely to occur in middle-aged and older individuals.
History
Symptoms are diverse and are due to anemia, the extent of compensation, previous treatment, and the underlying disorder.
- Patients with minimal or long-standing hemolytic anemia can be asymptomatic, so hemolysis is often found incidentally during routine laboratory testing.
- In intravascular hemolysis, iron deficiency due to chronic hemoglobinuria can exacerbate anemia and weakness.
- Tachycardia, dyspnea, angina, and weakness occur in patients with severe anemia. Cardiac function is sensitive to anoxia. Angina and evidence of cardiac decompensation occurs if anemia is severe or if the onset is rapid.
- Gallstones may cause abdominal pain. Bilirubin stones can develop in patients with persistent hemolysis.
- Bronze skin color and diabetes result from hemochromatosis due to multiple transfusions or erroneously administered iron therapy.
- Hemoglobinuria produces dark urine. It can occur in patients with intravascular hemolysis and has similar results to a transfusion of ABO-incompatible blood.
- Patients with thrombotic thrombocytopenic purpura (TTP) may reveal fever, neurological signs, renal failure, petechiae, and hemolysis because of the widespread occlusion of small vessels.
- Sickle cell anemia and other hemolytic disorders can be associated with leg ulcers caused by decreased red cell deformity and endothelial changes.
- Penicillin, quinine, quinidine, L-dopa, and other agents may cause immune hemolysis (see Medical Care).
- Oxidant drugs (see Diet) and stress from infections can trigger hemolysis in patients with G-6-PD deficiency.
- Fava beans can induce hemolysis in susceptible individuals with the Mediterranean variant of G-6-PD deficiency.
- A patient who needs a transfusion but does not show evidence of blood loss or bone marrow suppression may have hemolytic anemia.
Physical
The physical examination can reveal signs of anemia, erythrocyte destruction, complications of hemolysis, and evidence of an underlying disease.
- General pallor and pale conjunctivae and fingernails indicate anemia but are not specific for hemolytic anemias.
- Tachycardia, tachypnea, and hypotension due to anoxia and decreased vascular volume usually occur in severe anemias but are not specific for hemolytic anemias.
- Jaundice may occur because of a modest increase in indirect bilirubin in hemolysis. The rise is not specific for hemolytic disorders and may occur in liver disease, biliary obstruction, and hereditary liver disorders. Bilirubin levels rarely are greater than 4 mg/dL in hemolysis unless complicated by hepatic disease or cholelithiasis.
- Splenomegaly
- Splenomegaly occurs in hereditary spherocytosis and other hemolytic anemias but is not present in other hemolytic disorders such as G-6-PD deficiency.
- It suggests underlying disorders such as chronic lymphocytic leukemia (CLL), some lymphomas, and systemic lupus erythematosus (SLE).
- Leg ulcers
- Right upper abdominal quadrant tenderness may indicate gallbladder disease.
- Bleeding and petechiae indicate thrombocytopenia due to Evans syndrome or thrombotic thrombocytopenic purpura if neurological signs are also present.
- Butterfly malar rash and arthritis suggest systemic lupus erythematosus.
- Lymphadenopathy with splenomegaly may indicate an underlying chronic lymphocytic leukemia.
Causes
More than 200 causes for hemolysis exist. Only the main categories and some examples of hemolytic disorders are considered in this article.
- Hereditary disorders include erythrocyte membrane and enzymatic defects and hemoglobin abnormalities. Some hereditary disorders include the following:
- G-6-PD deficiency
- Hereditary spherocytosis
- Sickle cell anemia
- Acquired hemolytic conditions can be due to immune disorders, toxic chemicals and drugs, antiviral agents (eg, ribavirin), physical damage, and infections. They can include the following:
- Autoimmune hemolytic anemia (AIHA)
- Microangiopathic anemia is found in patients with disseminated intravascular coagulation (DIC) or hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura. Fragmented erythrocytes (schistocytes) also occur with defective prosthetic cardiac valves.
- Autoimmune hemolytic anemia and hereditary spherocytosis are classified as examples of extravascular hemolysis because the RBCs are destroyed in the spleen and other reticuloendothelial organs.
- Intravascular hemolysis occurs in hemolytic anemia due to prosthetic cardiac valves, G-6-PD deficiency, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, and paroxysmal nocturnal hemoglobinuria (PNH).
Disseminated Intravascular Coagulation
Systemic Lupus Erythematosus
Thrombotic Thrombocytopenic Purpura
Other Problems to be Considered
Other causes for fatigue, tachycardia, and dyspnea
Other causes for anemia
Lab Studies
- CBC count
- The test documents anemia, leukocyte counts, and differential counts.
- Platelet counts help to exclude an underlying infection or hematological malignancy. The platelet count is within the reference range in most hemolytic anemias.
- Thrombocytopenia can occur in systemic lupus erythematosus (SLE), chronic lymphocytic leukemia (CLL), and microangiopathic hemolytic anemia (defective prosthetic cardiac valves, thrombotic thrombocytopenic purpura [TTP], hemolytic uremic syndrome [HUS], and disseminated intravascular coagulation [DIC]). Thrombocytopenia associated with a positive direct Coombs test result is known as Evans syndrome.
- Peripheral smear and morphological examination
- Identifies polychromasia, indicating RBC immaturity reticulocytosis (see Image 1)
- Demonstrates spherocytes, suggesting congenital spherocytosis or autoimmune hemolytic anemia (AIHA, see Image 2)
- Can identify schistocytes (fragmented RBCs), suggesting thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, or mechanical damage (see Image 3)
- Can help diagnose a concomitant underlying hematological malignancy associated with hemolysis (ie, chronic lymphocytic leukemia)
- RBC indices
- They are performed when a CBC count is requested.
- A low mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) are consistent with a microcytic hypochromic anemia, which may occur in chronic intravascular hemolysis, eg, paroxysmal nocturnal hemoglobinuria (PNH).
- A high MCV is consistent with a macrocytic anemia. Macrocytosis usually is due to megaloblastic anemias but can occur in liver disease. A high number of reticulocytes also may cause a high MCH.
- A high MCH and mean corpuscular hemoglobin concentration (MCHC) suggest spherocytosis.
- Increased red blood cell distribution width (RDW) study
- This is usually performed when a CBC count is requested.
- An increased RDW is a measure of anisocytosis, which is likely in hemolytic anemia.
- Reticulocyte count
- An increased reticulocyte count is a criterion for hemolysis but is not specific for hemolysis.
- An increase may be caused by blood loss or a bone marrow response to iron, vitamin B-12, or folate deficiencies.
- The reticulocyte count may be normal or low in patients with bone marrow suppression despite ongoing severe hemolysis.
- Lactic acid dehydrogenase
- Serum LDH is a criterion for hemolysis. LDH is not specific because it is ubiquitous and can be released from the neoplastic cells of the liver or other damaged organs.
- Although an increase in LDH isozyme 1 and 2 is more specific for RBC destruction, these enzymes are also increased in patients with myocardial infarction.
- Serum haptoglobin
- A low serum haptoglobin is a criterion for moderate-to-severe hemolysis.
- A decrease is more likely in intravascular hemolysis than in extravascular hemolysis, but it is an acute phase reactant.
- The presence of concomitant infection, other reactive states, or chronic hemolysis may mask the diagnosis by raising haptoglobin levels.
- Indirect bilirubin
- Unconjugated bilirubin is a criterion for hemolysis, but it is not specific because an elevated bilirubin also may indicate Gilbert disease.
- With hemolysis, the level of indirect bilirubin usually is less than 4 mg/dL.
- Higher levels of indirect bilirubin indicate compromised hepatic function or cholelithiasis and hemolysis.
- Changes in the LDH and serum haptoglobin levels are the most sensitive general tests because the indirect bilirubin is not always increased.
- Specific studies directed by history, physical examination, peripheral smear, and other laboratory findings
- The direct antiglobulin test (DAT) result is usually positive in autoimmune hemolytic anemia, but it may be occasionally negative in this disorder. DAT-negative autoimmune hemolytic anemias have been reviewed. From 5-10% of all autoimmune hemolytic anemias are DAT negative. The Polybrene test can detect DAT-negative autoimmune hemolytic anemia (Garratty, 2005).
- The urine-free hemoglobin test reveals hemoglobinuria, which occurs with intravascular hemolysis when the amount of free hemoglobin exceeds the available haptoglobin. Urine may be dark due to hemoglobinuria, but myoglobinuria, porphyria, and other conditions can also cause dark urine.
- Urine hemosiderin may suggest intravascular hemolysis because an iron stain in sloughed renal epithelial cells in spun urinary sediment detects hemosiderin.
- RBC survival (chromium Cr 51 survival) is rarely used, but it can definitively demonstrate a shortened RBC survival (hemolysis). It is ordered when the clinical history and laboratory studies cannot establish a diagnosis of hemolysis.
- Cold agglutinin titer shows that a high titer of anti-I antibody may be found in mycoplasmal infections and a high titer of anti-i antibody may be found in hemolysis associated with infectious mononucleosis. An anti-P cold agglutinin may be seen in paroxysmal cold hemoglobinuria.
- A G-6-PD screen can detect an enzyme deficiency, but results are normal if the reticulocyte count is elevated (reticulocytes contain a considerable amount of G-6-PD). A Heinz body preparation also detects G-6-PD deficiency.
- Screen for sickle cell syndrome by demonstrating sickling under reduced conditions (sickle cell preparations) and testing for hemoglobin solubility. Hemoglobin electrophoresis confirms the presence of abnormal hemoglobin.
- Other tests depend on the possibility of sickle cell anemia, hereditary spherocytosis, systemic lupus erythematosus, a hematological malignancy, and types of hemolytic anemias that are more rare.
Imaging Studies
- Use ultrasound to estimate spleen size. The physical examination occasionally does not detect significant splenomegaly.
- Chest radiograph is used to evaluate cardiopulmonary status.
Other Tests
- ECG and other studies are used to evaluate cardiopulmonary status.
Medical Care
More than 200 types of hemolytic anemia exist, and each type requires specific treatment. Therefore, only the aspects of medical care relevant to most cases of hemolytic anemia are discussed.
- Transfusion therapy
- Avoid transfusions unless absolutely necessary, but they may be essential for patients with angina or severely compromised cardiopulmonary status.
- Administer packed RBCs slowly to avoid cardiac stress.
- In autoimmune hemolytic anemia (AIHA), type matching and crossmatching may be difficult. Use the least incompatible blood if transfusions are indicated. The risk of acute hemolysis of transfused blood is high, but the degree is dependent on the rate of infusion. Slowly transfuse by administering half units of packed red cells to prevent rapid destruction of transfused blood.
- Discontinuing medications
- Discontinue penicillin and other agents that can cause immune hemolysis and oxidant medication such as sulfa drugs (see Diet).
- Medications that can cause immune hemolysis include the following (see Bibliography for more complete lists):
- Penicillin
- Cephalothin
- Ampicillin
- Methicillin
- Quinine
- Quinidine
- Fava beans can cause hemolysis in patients with a G-6-PD deficiency and should be discontinued.
- Administer folic acid because active hemolysis may consume folate and cause megaloblastosis.
- Corticosteroids are indicated in autoimmune hemolytic anemia.
- IV immunoglobulin G (IVIG) has been used for patients with autoimmune hemolytic anemia, but only a few patients have responded, and the response has been transient.
- Iron therapy
- This is indicated for patients with severe intravascular hemolysis in which persistent hemoglobinuria has caused substantial iron loss.
- Before iron is administered, document the iron deficiency by serum iron studies and, possibly, by assessing iron stores in bone marrow aspirates.
- Because iron stores increase in hemolysis, iron administration is generally contraindicated in hemolytic disorders, particularly those that require chronic transfusion support.
Surgical Care
- Splenectomy may be the first choice of treatment in some types of hemolytic anemia such as hereditary spherocytosis.
- In other cases, such as in autoimmune hemolytic anemia, it is recommended when other measures have failed.
- Splenectomy is usually not recommended in hemolytic disorders such as cold agglutinin hemolytic anemia.
- Immunize against infections with encapsulated organisms, such as Haemophilus influenzae and Streptococcus pneumoniae, as far in advance of the procedure as possible.
Consultations
- Hematology consultation helps select appropriate diagnostic approaches and laboratory tests and assists in planning and monitoring therapy. Perform tests to identify hemolysis in an experienced laboratory that is selected by a hematologist.
- Consult a general surgeon if considering splenectomy.
Diet
- Fava beans can cause severe hemolysis in certain populations with the Mediterranean G-6-PD isoenzyme variant. These patients should avoid eating dishes with fava beans.
- Medications and chemicals that should be avoided in G-6-PD deficiency include the following (see Bibliography for more complete lists):
- Acetanilid
- Furazolidone
- Isobutyl nitrite
- Nalidixic acid
- Naphthalene
- Niridazole
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Drug Category: Vitamins
These agents are essential for normal DNA synthesis and formation of a number of coenzymes in many metabolic systems.
| Drug Name | Folic acid (Folvite) |
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| Description | Cofactor for enzymes involved in production of red blood cells. Replenishes depleted folate stores consumed during chronic hemolysis. |
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| Adult Dose | In patients with folic acid deficiency: 50 mcg/d PO/IV for 2 d, followed by 2 mg PO twice a wk or 0.5-1 mg/d
In patients with chronic hemolysis:
Administer folic acid indefinitely |
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| Pediatric Dose | <12 years: Not established
>12 years: 1 mg PO/IM/SC qd |
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| Contraindications | Documented hypersensitivity; folic acid administration may cause neuropathy in patients with latent or overt pernicious anemia if these patients are not receiving vitamin B-12 |
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| Interactions | Increase in seizure frequency and a decrease in subtherapeutic levels of phenytoin reported when used concurrently |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
|
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| Precautions | Benzyl alcohol is preservative in some products and is associated with fatal gasping syndrome in premature infants; resistance to treatment may occur in patients with alcoholism and deficiencies of other vitamins |
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Drug Category: Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the immune response of the body to diverse stimuli.
Glucocorticoids, such as prednisone, are usually the first line of treatment in autoimmune hemolytic anemia (AIHA). Consult a hematologist to individualize therapy and determine whether other forms of therapy are indicated in the treatment of AIHA. Taper glucocorticoids very gradually to avoid a relapse of hemolysis.
| Drug Name | Prednisone (Deltasone, Orasone, Sterapred) |
|---|
| Description | Inhibits phagocytosis of antibody-covered red blood cells. Indicated in some hemolytic disorders such as AIHA. |
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| Adult Dose | 1-1.5 mg/kg/d PO maintained for as many as 3-4 wk, or until response seen; if no response, consider other form of treatment |
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| Pediatric Dose | Individualize pediatric dose because corticosteroids may affect growth; consult a pediatric hematologist to establish dose of corticosteroids and determine whether other forms of therapy are needed |
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| Contraindications | Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease |
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| Interactions | Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
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| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
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Further Inpatient Care
- Monitor hemoglobin level, reticulocyte count, indirect bilirubin, LDH, and haptoglobin to determine the response to therapy.
- Monitor urine hemoglobin and hemosiderin to evaluate the response of intravascular hemolysis therapy.
- Avoid transfusions unless evidence of angina, cardiopulmonary decompensation, or other severe organ impairment due to anemia is present.
- Continue to administer folic acid.
- Administer oral iron to patients who have become iron deficient due to intravascular hemolysis.
- Taper corticosteroids.
- Treat the underlying cause of hemolysis.
Further Outpatient Care
- Initially, monitor hemoglobin, reticulocyte count, and other parameters of hemolysis closely. After the initial period, monitor these limits as indicated.
- Treat the underlying disorder.
- Continue folic acid because a patient with ongoing hemolysis consumes this vitamin for the accelerated production of erythrocytes.
- Taper corticosteroids. However, if indicated, patients may have to continue low-dose steroids if no contraindications exist for prolonged corticosteroid therapy.
Deterrence/Prevention
- Avoid medications that can induce immune hemolysis in susceptible individuals or oxidant medications that can cause hemolysis in patients with G-6-PD deficiency.
Prognosis
- Depends upon the underlying cause for hemolysis
Patient Education
- The patient must be able to identify symptoms and signs of hemolysis recurrence and seek prompt medical attention if they occur.
- For excellent patient education resources, visit eMedicine's Blood and Lymphatic System Center. Also, see eMedicine's patient education article Anemia.
Medical/Legal Pitfalls
- Failure to diagnose and treat correctly
| Media file 2:
Spherocytes. One arrow points to a spherocyte; the other, to a normal RBC with a central pallor. |
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Media type: Photo
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| Media file 3:
Schistocytes (thrombotic thrombocytopenic purpura). |
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Media type: Photo
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Hemolytic Anemia excerpt Article Last Updated: Jan 29, 2007
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