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Anemia Medication

  • Author: Joseph E Maakaron, MD; Chief Editor: Emmanuel C Besa, MD  more...
Updated: Jul 22, 2016

Medication Summary

Therapeutic approaches to anemia include the use of blood and blood products, immunotherapies, hormonal/nutritional therapies, and adjunctive therapies. The goal of therapy in acute anemia is to restore the hemodynamics of the vascular systems and to replace lost red blood cells. To achieve this, the practitioner may use mineral and vitamin supplements, blood transfusions, vasopressors, histamine (H2) antagonists, and glucocorticosteroids.

Documentation of the etiology of anemia is essential in the selection of therapy. Not all microcytic anemias are caused by iron deficiency; some are iron-overloading disorders. Similarly, not all megaloblastic anemias are associated with either vitamin B-12 deficiency or folic acid deficiency. Hereditary hemolytic disorders do not improve with corticosteroid therapy.


Blood and Blood Products

Class Summary

Correction of acute anemia often requires blood and/or blood products. With significant ongoing hemorrhage or hemolysis, transfusion of blood alone is insufficient. Nonetheless, providing timely transfusion to restore hemoglobin to safe levels can prevent major complications of acute anemia.

Packed red blood cells


Packed red blood cells (PRBCs) are used preferentially to whole blood, since they limit volume, immune, and storage complications. PRBCs have 80% less plasma, are less immunogenic, and can be stored about 40 days (versus 35 d for whole blood). PRBCs are obtained after centrifugation of whole blood. Leukocyte-poor PRBCs are used in patients who are transplant candidates/recipients and in those with prior febrile transfusion reactions. Washed or frozen PRBCs are used in individuals with hypersensitivity transfusion reactions.

Fresh frozen plasma


Fresh frozen plasma (FFP) contains coagulation factors, as well as protein C and protein S. Its uses include the treatment of coagulopathies and thrombotic thrombocytopenic purpura (TTP) and the reversal of warfarin. FFP does not transmit infections.



This agent is used for the treatment of Von Willebrand disease. It contains fibrinogen, factor VIII, and von Willebrand factor and can be used in lieu of factor VIII concentrate if the latter is unavailable.



Patients who are thrombocytopenic and have clinical evidence of bleeding should receive a platelet transfusion. Patients with platelet counts of less than 10,000/mcL are at risk for spontaneous cerebral hemorrhage and require a prophylactic transfusion.

The preferred treatment for TTP and hemolytic-uremic syndrome is large-volume plasmapheresis with FFP replacement. Immune thrombocytopenic purpura (ITP) is rarely treated with transfusion, as the transfused platelets are destroyed rapidly. In stable patients, initial treatment is with prednisone. High-dose immunoglobulin and splenectomy are very effective treatments.

Factor IX (BeneFix, Mononine)


Hemophilia B is treated with factor IX concentrate. Recombinant factor IX currently is undergoing clinical trials (the current treatment is FFP or prothrombin-rich plasma concentrate).

Recombinant factor VIII (Advate, Helixate FS, Xyntha)


This is used to treat hemophilia A.


Iron Products

Class Summary

Iron salts are used to provide adequate iron for hemoglobin synthesis and to replenish body stores of iron. Iron is administered prophylactically during pregnancy because of the anticipated requirements of the fetus and the losses that occur during delivery.

Ferrous sulfate (MyKidz Iron 10, Fer-Iron, Slow-FE)


Mineral supplements are used to provide adequate iron for hemoglobin synthesis and to replenish body stores of iron. Iron is administered prophylactically during pregnancy because of the anticipated requirements of the fetus and the losses that occur during delivery.

Carbonyl iron (Feosol, Iron Chews, Icar)


Carbonyl iron is used as a substitute for ferrous sulfate. It has a slower release of iron and is more expensive than ferrous sulfate. The slower release affords the agent greater safety if ingested by children. On a milligram-for-milligram basis, it is 70% as efficacious as ferrous sulfate. Claims are made that there is less gastrointestinal (GI) toxicity, prompting use when ferrous salts are producing intestinal symptoms and in patients with peptic ulcers and gastritis. Tablets are available containing 45 mg and 60 mg of iron.

Iron dextran complex (INFeD, Dexferrum)


Iron dextran complex replenishes depleted iron stores in the bone marrow, where it is incorporated into hemoglobin. Parenteral use of iron-carbohydrate complexes has caused anaphylactic reactions, and its use should be restricted to patients with an established diagnosis of iron deficiency anemia whose anemia is not corrected with oral therapy.

The required dose can be calculated (3.5 mg iron/g of hemoglobin) or obtained from tables in the prescribing information. For IV use, this agent may be diluted in sterile 0.9% NaCl. Do not add to solutions containing medications or parenteral nutrition solutions.

Ferric carboxymaltose (Injectafer)


Ferric carboxymaltose is a nondextran IV colloidal iron hydroxide in complex with carboxymaltose, a carbohydrate polymer that releases iron. It is indicated for iron deficiency anemia (IDA) in adults who have intolerance or an unsatisfactory response to oral iron. It is also indicated for IDA in adults with non-dialysis-dependent chronic kidney disease.



Class Summary

Vitamins are used to meet necessary dietary requirements and are used in metabolic pathways, as well as DNA and protein synthesis.

Cyanocobalamin (vitamin B12) and folic acid are used to treat megaloblastic and macrocytic anemias secondary to deficiency. Both vitamin B12 and folic acid are required for synthesis of purine nucleotides and metabolism of some amino acids. Each is essential for normal growth and replication. Deficiency of either cyanocobalamin or folic acid results in defective DNA synthesis and cellular maturation abnormalities. Consequences of deficiency are most evident in tissues with high cell turnover rates (eg, hematopoietic system).

Vitamin K deficiency causes elevation of prothrombin time and is commonly seen in patients with liver disease.

Cyanocobalamin ( Calo-Mist, Ener-B, Nascobal)


Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B12 in humans. Microbes synthesize vitamin B12, but humans and plants do not. Vitamin B12 deficiency may result from intrinsic factor (IF) deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum.

Folic acid (Folvite)


Folic acid is an essential cofactor for enzymes used in the production of red blood cells (RBCs).

Vitamin K


A decrease in levels of vitamin K–dependent factors (II, VII, IX, X, protein C, protein S) can lead to bleeding. Vitamin K is also used to treat hemorrhagic disease of the newborn, warfarin-induced bleeding, and hypothrombinemia from other causes (eg, antibiotic, aspirin).


Electrolyte Supplements

Class Summary

Serum potassium levels can fall during therapy for severe cobalamin or folate deficiency and can lead to sudden death. Therefore, potassium supplements may be indicated.

Potassium Chloride (K-Tab, Klor-Con, microK, Epiklor)


Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion, through GI loss or because of low intake.

Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, if associated with vomiting, or inadequate replacement during prolonged parenteral nutrition.

Potassium depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of about 100 to 200 mEq of potassium from the total body store.



Class Summary

These drugs decrease portal circulation pressure by diminishing blood flow due to vasoconstriction. The major indication is variceal bleeding.

Vasopressin (Pitressin)


Vasopressin causes vasoconstriction of vascular smooth muscles and increases water permeability and reabsorption in the collecting tubules. It decreases portal pressure in patients with portal hypertension.

Somatostatin (Zecnil)


Somatostatin diminishes blood flow to the portal system due to vasoconstriction, thus decreasing variceal bleeding. It has similar effects to vasopressin but does not cause coronary vasoconstriction. No longer marketed in the United States.


Histamine (H2) Antagonists

Class Summary

These agents produce a blockade of H2 receptors.

Cimetidine (Tagamet)


The primary indication is to reduce symptoms and accelerate healing of gastric ulcers. In the acutely bleeding patient, it has limited benefit.

Ranitidine (Zantac)


Ranitidine inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)


Famotidine competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Nizatidine (Axid)


Nizatidine competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.



Class Summary

These agents are used to treat idiopathic and acquired autoimmune hemolytic anemias.



Glucocorticoids inhibit phagocytosis of antibody-covered platelets. Treatment of ITP during pregnancy is conservative unless the condition is severe. For severe cases, use the lowest dose of glucocorticoids. In neonates, if the platelet count drops below 50,000-75,000 platelets/µL, consider prednisone and exchange transfusions and immunoglobulin.

Contributor Information and Disclosures

Joseph E Maakaron, MD Research Fellow, Department of Internal Medicine, Division of Hematology/Oncology, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.


Ali T Taher, MD, PhD, FRCP Professor of Medicine, Associate Chair of Research, Department of Internal Medicine, Division of Hematology/Oncology, Director of Research, NK Basile Cancer Center, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Marcel E Conrad, MD Distinguished Professor of Medicine (Retired), University of South Alabama College of Medicine

Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, SWOG

Disclosure: Partner received none from No financial interests for none.

Chief Editor

Emmanuel C Besa, MD Professor Emeritus, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American Society of Clinical Oncology, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, New York Academy of Sciences

Disclosure: Nothing to disclose.


Jose A Perez Jr, MD, MBA, MSEd Consulting Staff, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez Jr, MD, MBA, MSEd is a member of the following medical societies: American College of Physician Executives, American College of Physicians, Society of General Internal Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Ronald A Sacher, MB, BCh, MD, FRCPC Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Anemia. Decreased production of red blood cells is suggested in certain patients with anemia. Bone marrow biopsy specimen allows categorization of patients with anemia without evidence of blood loss or hemolysis into 3 groups: aplastic or hypoplastic disorder, hyperplastic disorder, or infiltration disorder. Each category and its associated causes are listed in this image.
Microcytic anemia.
Peripheral smear showing classic spherocytes with loss of central pallor in the erythrocytes.
Bone marrow aspirate containing increased numbers of plasma cells.
Bone marrow aspirate showing erythroid hyperplasia and many binucleated erythroid precursors.
Table 1. Microcytic Hypochromic Anemia (MCV < 83; MCHC < 31)
Condition Serum Iron Total Iron-Binding Capacity (TIBC) Bone Marrow Iron Comment
Iron deficiency 0 Responsive to iron therapy
Chronic inflammation ++ Unresponsive to iron therapy
Thalassemia major N ++++ Reticulocytosis and indirect bilirubinemia
Thalassemia minor N N - ↓ ++ Elevation of fetal hemoglobin and Hb A2, target cells, and poikilocytosis
Lead poisoning N N ++ Basophilic stippling of RBCs
Sideroblastic N ++++ Ring sideroblasts in marrow
Hemoglobin N N ++ Hemoglobin electrophoresis
↓ = decreased; ↑ = increased; 0 = absent; +'s indicate the amount of stainable iron in bone marrow specimens, on a scale of 0-4; N = normal.
Table 2. Macrocytic Anemia (MCV >95)
Megaloblastic bone marrow Deficiency of vitamin B-12
Deficiency of folic acid
Drugs affecting deoxyribonucleic acid (DNA) synthesis
Inherited disorders of DNA synthesis
Nonmegaloblastic bone marrow Liver disease
Hypothyroidism and hypopituitarism
Accelerated erythropoiesis (reticulocytes)
Hypoplastic and aplastic anemia
Infiltrated bone marrow
Table 3. Various Forms of RBCs
Macrocyte Larger than normal (>8.5 µm diameter). See Table 2.
Microcyte Smaller than normal (< 7 µm diameter). See Table 1.
Hypochromic Less hemoglobin in cell. Enlarged area of central pallor. See Table 1.
Spherocyte Loss of central pallor, stains more densely, often microcytic. Hereditary spherocytosis and certain acquired hemolytic anemias
Target cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D, and postsplenectomy
Leptocyte Hypochromic cell with a normal diameter and decreased MCV. Thalassemia
Elliptocyte Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly vitamin B-12 and folate deficiency)
Schistocyte Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia, artificial heart valves, uremia, and malignant hypertension
Stomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies, hereditary stomatocytosis, and artifact
Tear-shaped RBCs Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow with tumor. Thalassemia
Acanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of RBCs
Echinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact
Sickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l
Table 4. Classification of the Hemolytic Disorders
  Hereditary Acquired
Intracorpuscular defect Hereditary spherocytosis

Hereditary elliptocytosis



Congenital dyserythropoietic anemias

Hereditary RBC enzymatic deficiencies

Rarer hereditary abnormalities

Vitamin B-12 and folic acid deficiency

Paroxysmal nocturnal hemoglobinuria

Severe iron deficiency

Extracorpuscular defect   Physical agents: Burns, cold exposure

Traumatic: Prosthetic heart valves, march hemoglobinuria, disseminated intravascular coagulation (DIC), graft rejection

Chemicals: Drugs and venoms

Infectious agents: Malaria, toxoplasmosis, mononucleosis, hepatitis, primary atypical pneumonia, clostridial infections, bartonellosis, leishmaniasis

Hepatic and renal disease

Collagen vascular disease

Malignancies: Particularly hematologic neoplasia

Transfusion of incompatible blood

Hemolytic disease of the newborn

Cold hemagglutinin


Autoimmune hemolytic anemia Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS)

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