Hemolytic Anemia

Updated: May 26, 2016

Author: Paul Schick, MD; Chief Editor: Emmanuel C Besa, MD more...

Background
Hemolysis is the premature destruction of erythrocytes. A hemolytic anemia will develop if bone
marrow activity cannot compensate for the erythrocyte loss. The severity of the anemia depends
on whether the onset of hemolysis is gradual or abrupt and on the extent of erythrocyte
destruction. Mild hemolysis can be asymptomatic while the anemia in severe hemolysis can be
life threatening and cause angina and cardiopulmonary decompensation.

The clinical presentation also reflects the underlying cause for hemolysis. For example, sickle
cell anemia (see the image below) is associated with painful occlusive crises. (See Presentation.)

Peripheral blood smear with sickled cells at 1000X

magnification. Image courtesy of Ulrich Woermann, MD.
View Media Gallery

Hemolytic anemia has multiple causes, and the clinical presentation can differ depending on the
etiology. An array of laboratory tests are available for detecting hemolysis, and specialized tests
may be indicated to diagnose the cause for hemolysis (see Workup). There are differences in the
management of various types of hemolytic anemias (see Treatment).

Go to Anemia, Iron Deficiency Anemia, and Chronic Anemia for complete information on these
topics.

Pathophysiology
Hemolysis can be due to 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 may be an extravascular or an intravascular phenomenon. Autoimmune hemolytic

anemia and hereditary spherocytosis are examples of extravascular hemolysis because the red
blood cells are destroyed in the spleen and other reticuloendothelial tissues. [1] Intravascular
hemolysis occurs in hemolytic anemia due to the following:

Prosthetic cardiac valves

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Thrombotic thrombocytopenic purpura

Disseminated intravascular coagulation

Transfusion of ABO incompatible blood

Paroxysmal nocturnal hemoglobinuria (PNH)

Hemolysis may also be intramedullary, when fragile red blood cell (RBC) precursors are
destroyed in the bone marrow prior to release into the circulation. Intramedullary hemolysis
occurs in pernicious anemia and thalassemia major.

Hemolysis is associated with a release of RBC lactate dehydrogenase (LDH). Hemoglobin

released from damaged RBCs leads to an increase in indirect bilirubin and urobilinogen levels.

A patient with mild hemolysis may have normal hemoglobin levels if increased RBC production
matches the rate of RBC destruction. However, patients with mild hemolysis may develop
marked anemia if their bone marrow erythrocyte production is transiently shut off by viral
(parvovirus B-19) or other infections. This scenario would be an aplastic crisis since the bone
marrow can no longer compensate for ongoing hemolysis.

Skull and skeletal deformities can occur in childhood due to a marked increase in hematopoiesis
and resultant bone marrow expansion in disorders such as thalassemia.

Etiology
A wide range of causes of hemolytic anemia have been documented. [2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12] Only the
more commonly encountered hemolytic disorders are discussed in this article.

Recent articles have noted that intravenous immunoglobulin G (IVIG) therapy given during
pregnancy, [13] the contrast medium iomeprol, [14] and mitral valve replacement [15] can cause
hemolysis.
Hereditary disorders may cause hemolysis as a result of erythrocyte membrane abnormalities,
enzymatic defects, and hemoglobin abnormalities. Hereditary disorders include the following:

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Hereditary spherocytosis

Sickle cell anemia

Acquired causes of hemolysis include the following:

Immune disorders

Toxic chemicals and drugs [3, 16]

Antiviral agents (eg, ribavirin [17] )

Physical damage

Infections [18]

Autoimmune hemolytic anemia (AIHA) can be due to warm or cold autoantibody types and,
rarely, mixed types. [12, 19, 20] Most warm autoantibodies belong to the immunoglobulin IgG class.
These antibodies can be detected by a direct Coombs test, which also is known as a direct
antiglobulin test (DAT). AIHA may occur after allogeneic hematopoietic stem cell
transplantation. The 3-year cumulative incidence in this population has been reported at 4.44%.
[21]

Microangiopathic hemolytic anemia, which results in the production of fragmented erythrocytes

(schistocytes), may be caused by any of the following [22, 23] :

Defective prosthetic cardiac valves

Disseminated intravascular coagulation (DIC)

Hemolytic uremic syndrome (HUS)

Thrombotic thrombocytopenic purpura (TTP)

In paroxysmal nocturnal hemoglobinuria, hemolysis is due to intravascular complement-

mediated destruction of erythrocytes.

Epidemiology
Hemolytic anemia represents approximately 5% of all anemias. Acute AIHA is relatively rare,
with an incidence of one to three cases per 100,000 population per year. [24]

Hemolytic anemias are not specific to any race. However, sickle cell disorders are found
primarily in Africans, African Americans, some Arabic peoples, and Aborigines in southern
India.

Several variants of G6PD deficiency exist. The A(-) variant is found in West Africans and
African Americans. Approximately 10% of African Americans carry at least 1 copy of the gene
for this variant. The Mediterranean variant occurs in individuals of Mediterranean descent and in
some Asians.

Most cases of hemolytic anemia are not sex specific. However, AIHA is slightly more likely to
occur in females than in males. G6PD deficiency is an X-linked recessive disorder. Therefore,
males are usually affected, and females are carriers.

Although hemolytic anemia can occur in persons of any age, hereditary disorders are usually
evident early in life. AIHA is more likely to occur in middle-aged and older individuals.

Prognosis
The prognosis for patients with hemolytic anemia depends on the underlying cause.

Overall, mortality rates are low in hemolytic anemias. However, the risk is greater in older
patients and patients with cardiovascular impairment.

Morbidity depends on the etiology of the hemolysis and the underlying disorder, such as sickle
cell anemia or malaria.

History
Signs and symptoms of hemolytic anemia 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 may be asymptomatic, and hemolysis is often found incidentally
during routine laboratory testing. Clinical manifestations may include the following:

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, as
cardiac function is sensitive to anoxia

Persistent hemolysis may result in the development of bilirubin gallstones; these patients
may present with abdominal pain
 Bronze skin color and diabetes occur in hematosiderosis; iron overload may occur in
patients who have received multiple transfusions or those who have been administered
iron therapy erroneously

Dark urine may be due to hemoglobinuria

In addition to hemolysis, patients with thrombotic thrombocytopenic purpura (TTP) may

experience fever, neurologic signs, renal failure, and thrombocytopenia

Leg ulcers may develop in patients with sickle cell anemia and other hemolytic disorders,
as a result of decreased red blood cell (RBC) deformability and endothelial changes

Patients may report recent use of medications that can cause immune hemolysis. These include
penicillin, quinine, quinidine, and L-dopa.

In patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency, hemolysis can be

triggered by oxidant drugs and stress from infections. Fava beans can induce hemolysis in
susceptible individuals with the Mediterranean variant of G6PD deficiency.

Physical Examination
The physical examination in an individual with hemolytic anemia can reveal signs of anemia,
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 can 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 and biliary obstruction.
Bilirubin levels are rarely greater than 3 mg/dL in hemolysis, unless complicated by hepatic
disease or cholelithiasis.

Splenomegaly occurs in hereditary spherocytosis and other hemolytic anemias, but it is not
present in all hemolytic disorders. For example, splenomegaly usually is not present in G6PD
deficiency. The presence of splenomegaly could suggest an underlying disorder such as chronic
lymphocytic leukemia (CLL), some lymphomas, or systemic lupus erythematosus (SLE).
Butterfly malar rash and arthritis also suggest SLE. Lymphadenopathy along with splenomegaly
is consistent with CLL.

Splenomegaly sometimes is not evident on physical examination, and ultrasonic imaging or CT

scanning may be necessary to define spleen size. When evaluating spleen size, it is important to
avoid unnecessary pressure in order to avoid splenic rupture.

Leg ulcers may be present.

Right upper abdominal quadrant tenderness may indicate cholelithiasis (bilirubin gallstones) and
gallbladder disease.

Tachycardia and dyspnea may be evident 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.

In patients with chronic hemolytic anemia, increased folate consumption may lead to folate
deficiency. Clinical manifestations may include patchy hyperpigmentation, sore tongue, and
gastrointestinal symptoms.

Diagnostic Considerations
Other causes for fatigue, tachycardia, and dyspnea should be considered. Other causes for
anemia should be ruled out. A transfusion requirement in the absence of blood loss or bone
marrow aplasia would suggest hemolysis.

Go to Anemia, Iron Deficiency Anemia, and Chronic Anemia for complete information on these
topics.

Differential Diagnoses
Disseminated Intravascular Coagulation

Physical Medicine and Rehabilitation for Systemic Lupus Erythematosus

Thrombotic Thrombocytopenic Purpura (TTP)

Approach Considerations
Standard blood studies for the workup of suspected hemolytic anemia include the following:

Complete blood cell count

Peripheral blood smear

Serum lactate dehydrogenase (LDH) study

Serum haptoglobin

Indirect bilirubin

Changes in the LDH and serum haptoglobin levels are the most sensitive general tests because
the indirect bilirubin is not always increased.
Other laboratory studies may be directed by history, physical examination, peripheral smear, and
other laboratory findings. Ultrasonography is used to estimate the spleen size, since the physical
examination occasionally does not detect significant splenomegaly. Chest radiography,
electrocardiography (ECG), and other studies are used to evaluate cardiopulmonary status.

Complete Blood Cell Count

This test can detect an anemia, pancytopenia, and infections. Along with the differential count, a
CBC count can help diagnose hematologic malignancies and other hematological disorders. The
platelet count usually is normal in most hemolytic anemias.

Thrombocytopenia can occur in systemic lupus erythematosus (SLE), chronic lymphocytic

leukemia (CLL), and microangiopathic hemolytic anemias (eg, patients with 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 occurs in the Evans syndrome. [25]

Red blood cell indices

These studies 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 due to iron deficiency that may occur in chronic intravascular hemolysis.

A high MCV is consistent with a macrocytic anemia. Folate consumed during chronic hemolysis
may lead to megaloblastosis and a high MCV. However, the MCV also may be elevated in
patients with high reticulocyte counts since these cells are larger than mature RBCs. A high
MCH and mean corpuscular hemoglobin concentration (MCHC) would suggest spherocytosis.

Red blood cell distribution width study

The red blood cell distribution width (RDW) study is usually performed when a CBC count is
requested. An increased RDW is a measure of anisocytosis that can occur in hemolytic anemias.

Reticulocyte count

An increased reticulocyte count represents increased RBC production and is a criterion for
hemolysis but is not specific for hemolysis. In addition to hemolysis, increased reticulocytes may
be a response to blood loss or the treatment of 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 (aplastic crisis).
Peripheral Blood Smear
Peripheral smear findings can help in the diagnosis of a concomitant underlying hematologic
malignancy associated with hemolysis. For example, smears in CLL are characterized by an
abundance of small lymphocytes and smudge cells (ruptured CLL cells).

The following are examples of the value of evaluating peripheral blood smears.

Polychromasia indicates RBC immaturity (see the image below).

 Polychromasia.

A peripheral smear may demonstrate spherocytes, suggesting congenital spherocytosis or

autoimmune hemolytic anemia (AIHA); see the image below.

Spherocytes. One arrow points to a

spherocyte; the other, to a normal RBC with central pallor.

View Media Gallery

The presence of schistocytes (fragmented red blood cells) suggests TTP, HUS, or mechanical
damage (see the image below).
 Schistocytes (thrombotic
thrombocytopenic purpura).

Lactate Dehydrogenase Study

Serum LDH elevation is a criterion for hemolysis.

LDH elevation is sensitive for hemolysis, but is not specific since LDH is ubiquitous and can be
released from neoplastic cells, the liver, or from other damaged organs.

Although an increase in LDH isozymes 1 and 2 is more specific for red blood cell destruction,
these enzymes are also increased in patients with myocardial infarction.

Serum Haptoglobin
A low serum haptoglobin level is a criterion for moderate-to-severe hemolysis.

A decrease in serum haptoglobin is more likely in intravascular hemolysis than in extravascular

hemolysis.

However, it is an acute phase reactant. Therefore, haptoglobin levels can be normal or elevated
despite significant hemolysis in patients with infections and in other reactive states.

Indirect Bilirubin
Unconjugated bilirubin is a criterion for hemolysis, but it is not specific because an elevated
indirect bilirubin level also occurs in Gilbert disease.

With hemolysis, the level of indirect bilirubin usually is less than 3 mg/dL. Higher levels of
indirect bilirubin indicate compromised hepatic function or cholelithiasis.
Other Laboratory Studies
The following specific studies may be indicated:

Direct antiglobulin test (DAT)

Urine free hemoglobin test

Urine hemosiderin test

Red blood cell survival test

Cold agglutinin titer

Glucose-6-phosphate dehydrogenase (G6PD) screen

Sickle cell screen

The DAT result is usually positive in autoimmune hemolytic anemia (AIHA), but it may
occasionally be negative in this disorder. DAT-negative AIHAs have been reviewed. [26] From 5-
10% of all AIHAs are DAT negative. The polybrene test can detect DAT-negative AIHA. [26] In
addition, the immunoradiometric assay (IRMA) for red blood cellbound IgG can be used to
diagnose AIHA in patients whose autoantibody levels are too low to be detected by conventional
DAT. [27] DAT-negative AIHA has a better prognosis than DAT-positive AIHA. [28]

MicroRNA analysis has been found to be helpful in the diagnosis of AIHA in patients with
chronic lymphocytic leukemia. [29]

In addition to hemoglobinuria, either myoglobinuria or porphyria may result in dark urine. To

rule out these possibilities, the urine should be tested for free hemoglobin. Hemoglobinuria
occurs when the amount of free hemoglobin released during hemolysis exceeds available
haptoglobin.

Urine hemosiderin may suggest severe or intravascular hemolysis. Hemosiderin is detected in

iron-stained urinary sediment in sloughed renal epithelial cells. The source of urinary
hemosiderin is hemoglobinuria that occurs in severe and intravascular hemolysis. When urinary
hemoglobin is reabsorbed by renal tubular cells, it is processed to hemosiderin. Therefore,
urinary hemosiderin reflects hemoglobinuria and suggests severe or intravascular hemolysis.

Red blood cell survival (chromium-51 [51 Cr] survival) is rarely used, but it can definitively
demonstrate shortened red blood cell survival (hemolysis). If available, this test can be helpful
when the clinical history and laboratory studies cannot establish a diagnosis of hemolysis.

The cold agglutinin titer will be elevated in cold agglutinin disease, with the specific IgM
antibody varying according to the underlying disorder. For example, a high titer of anti-I
antibody (ie, antibody directed against the I antigen found on normal adult RBCs) occurs in
mycoplasmal infections. High titers of anti-i antibody (antibody directed against the i antigen
found on fetal cord blood RBCs) have been reported in infectious mononucleosis. An anti-P cold
agglutinin may be seen in paroxysmal cold hemoglobinuria.

A G6PD screening can usually detect deficiency of this enzyme, but results can be normal if the
reticulocyte count is elevated (reticulocytes contain a considerable amount of G6PD). A positive
Heinz body preparation can suggest denatured hemoglobin and thus G6PD deficiency (see the
image below).

Supra vital stain in hemoglobin H

disease that reveals Heinz bodies (golf ball appearance).
View Media Gallery

Screening for sickle cell syndrome is performed by demonstrating sickling under reduced
conditions (sickle cell preparations) and testing for hemoglobin solubility (see the image below).
Hemoglobin electrophoresis confirms the presence of abnormal hemoglobin.
 Peripheral blood smear with sickled
cells at 1000X magnification. Image courtesy of Ulrich Woermann, MD.
View Media Gallery

Other tests may be indicated to diagnose hereditary spherocytosis, hematologic malignancy, and
rarer types of hemolytic anemias.

Approach Considerations
There are numerous types of hemolytic anemia, and treatment may differ depending on the type
of hemolysis. [2, 3, 4, 30, 31] Only the general care of hemolytic anemias and the management of the
most commonly encountered hemolytic anemias are discussed. The diagnosis and treatment of
cold agglutinin hemolytic anemia has been reviewed. [32]

Folic acid, corticosteroids, rituximab, and IVIG

Prophylactic folic acid is indicated because active hemolysis can consume folate and cause
megaloblastosis.

Corticosteroids are indicated in autoimmune hemolytic anemia (AIHA).

Increasing evidence supports the use of rituximab in AIHA, particularly warm antibody AIHA. [33,
33]
Results of a phase III trial in 64 patients support its use as first-line therapy for warm AIHA, in
combination with corticosteroids. Birgens et al reported that after 12 months, a satisfactory
response was observed in 75% of the patients treated with rituximab and prednisolone, but in
36% of those given prednisolone alone (P = 0.003). After 36 months, about 70% of the patients
who had received rituximab and prednisolone were still in remission, compared with about 45%
of those in the prednisolone group. [31]

Intravenous immunoglobulin G (IVIG) has been used for patients with AIHA, but only a few
patients have responded to this treatment, and the responses have been transient.
Transfusion Therapy
One should avoid transfusions unless absolutely necessary. However, transfusions may be
essential for patients with angina or a severely compromised cardiopulmonary status. It is best to
administer packed red blood cells slowly to avoid cardiac stress.

In autoimmune hemolytic anemia (AIHA), typing and cross-matching may be difficult. One
should use the least incompatible blood if transfusions are indicated. The risk of destruction of
transfused blood is high, but the degree of the hemolysis depends on the rate of infusion.
Therefore, one should slowly transfuse half units of packed red blood cells to prevent rapid
destruction of transfused blood.

Iron overload due to multiple transfusions for chronic anemia (eg, thalassemia or sickle cell
disorder) can be treated with chelation therapy. A systematic review that compared the oral iron
chelator deferasirox with the oral chelator deferiprone and the traditional parenteral agent
deferoxamine found little clinical difference between the 3 chelation agents in terms of removing
iron from the blood and liver. [34]

Erythropoietin Therapy
Erythropoietin (EPO) has been used to try to reduce transfusion requirements, with variable
outcomes. Settings in which EPO therapy has reduced transfusion requirements include the
following:

Children with chronic renal failure [35]

Autoimmune hemolytic anemia associated with reticulocytopenia [36]

A patient with sickle cell disease undergoing hemodialysis for renal failure [37]

Jehovahs Witnesses [38]

Infants with hereditary spherocytosis [39, 40]

However, the ability of EPO to reduce transfusion requirement has been questioned in newborns
with hereditary spherocytosis [41] and in post-diarrheal hemolytic uremic syndrome. [42]

There is a general impression that additional studies should be carried out to establish the role
and indications for EPO in hemolytic disorders. EPO therapy costs more than transfusions. The
potential for EPO-induced cardiovascular complications needs to be considered. EPO has
pleiotropic effects and might inhibit macrophages in Salmonella infections. [43] EPO was reported
to be helpful in treating cerebral malaria due to itspleiotropic effect and not its hematopoietic
action. [44] Hence, EPO should be used judiciously.
Discontinuing Medications
Penicillin and other agents that can cause immune hemolysis should be discontinued in patients
who develop hemolysis. The following is a partial list of medications that can cause immune
hemolysis:

Penicillin

Cephalothin

Ampicillin

Methicillin

Quinine

Quinidine

One should discontinue oxidant medications such as sulfa drugs in patients with G-6-PD
deficiency or those who have unstable hemoglobins. The following is a partial list of medications
and chemicals that should be avoided in G6PD deficiency:

Acetanilide

Furazolidone

Isobutyl nitrite

Nalidixic acid

Naphthalene

Niridazole

Iron Therapy
Iron therapy is contraindicated in most cases of hemolytic anemia. The reason is that iron
released from RBCs in most hemolytic anemias is reused and iron stores are not reduced.

However, iron therapy is indicated for patients with severe or intravascular hemolysis in which
persistent hemoglobinuria has caused substantial iron loss. Before starting iron therapy, one
should document iron deficiency by serum iron studies and, possibly, by assessing iron stores in
bone marrow aspirates.
Splenectomy
Splenectomy may be the first choice of treatment in some types of hemolytic anemia, such as
hereditary spherocytosis. [45] In other cases, such as in AIHA, splenectomy is recommended when
other measures have failed. Splenectomy is usually not recommended in hemolytic disorders
such as cold agglutinin hemolytic anemia in which hemolysis is intravascular.

Overwhelming postsplenectomy sepsis is a rare but a potentially fatal event, especially during
the first 2 years after splenectomy. One should immunize against infections with encapsulated
organisms, such as Haemophilus influenzae and Streptococcus pneumoniae, in advance of the
procedure. Immunization can be performed post splenectomy.

Deterrence/Prevention of Hemolytic Anemia

The following is a partial list of medications and chemicals that individuals with glucose-6-
phosphate dehydrogenase (G6PD) deficiency should avoid:

Acetanilid

Furazolidone

Isobutyl nitrite

Nalidixic acid

Naphthalene

Niridazole

Sulfa drugs

The G6PD Deficiency Association has a more comprehensive online list of medications that
people with G6PD deficiency should avoid.

Fava beans can cause severe hemolysis in certain populations with the Mediterranean G6PD
isoenzyme variant. These patients should avoid eating dishes with fava beans.

Patients should know to avoid medications that caused them to have immune hemolysis. The
following is a partial list of medications that can cause immune hemolysis:

Penicillin

Cephalothin

Ampicillin
 Methicillin

Quinine

Quinidine

Long-Term Monitoring
One should monitor the hemoglobin level, reticulocyte count, indirect bilirubin value, LDH
level, and haptoglobin value in patients with hemolytic anemia to determine the response to
therapy. Urine hemoglobin and hemosiderin should be monitored to evaluate recovery in patients
with severe or intravascular hemolysis.

Other treatments are as follows:

Folic acid should be recommended for patients with ongoing hemolysis.

Administer oral iron to patients who have become iron deficient due to intravascular
hemolysis.

One should taper corticosteroids. Occasionally, patients may have to continue low-dose
steroids.

Avoid transfusions unless there is evidence of angina, cardiopulmonary decompensation,

or other severe organ impairment.

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients
with hemolytic anemia. Treatment is specific to the type of hemolytic anemia. For example,
corticosteroids are usually the first line of treatment in autoimmune hemolytic anemia (AIHA)
but are seldom effective in pediatric cold agglutinin disease. Rituximab has been used and can be
effective in steroid-resistant AIHA. [33, 46]

Vitamins
Class Summary

Vitamins are essential for normal DNA synthesis and the formation of a number of coenzymes in
many metabolic systems.

Folic acid (Folacin-800)

View full drug information

Folic acid is a cofactor for enzymes involved in production of red blood cells. Administered folic
acid replenishes depleted folate stores consumed during chronic hemolysis.

Corticosteroids
Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic
effects. These agents 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.

Prednisone

View full drug information

Prednisone inhibits phagocytosis of antibody-covered red blood cells. This agent is indicated in
some hemolytic disorders such as AIHA.

Iron Salts
Class Summary

Iron therapy is contraindicated in most hemolytic anemias. However, iron therapy is indicated for
patients with severe intravascular hemolysis in which persistent hemoglobinuria has caused
substantial iron loss.

Ferrous sulfate (Feosol, Fer-In-Sol, MyKidz iron 10)

View full drug information

Ferrous sulfate is the most common and inexpensive form of iron used. Tablets contain 50-60 mg
of iron salt. Other ferrous salts are used and may cause less intestinal discomfort because they
contain a smaller dose of iron (25-50 mg). Oral solutions of ferrous iron salts are available for
use in pediatric populations.

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