DOCSLIB.ORG

Continuing Education for Pharmacists Volume XXXI, No

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Continuing Education for Pharmacists Volume XXXI, No continuing education for pharmacists Volume XXXI, No. 6 Anemia: Disease Basics, Treatment and Appropriate Use of ESAs Mona T. Thompson, R.Ph., PharmD Dr. Mona T. Thompson has no relevant considered a public health concern have an increased demand for iron. financial relationships to disclose. that affects both developed and In the United States, the preva- developing countries. Estimates lence of iron-deficiency anemia in the Americas and Europe were among children declined during the The goal of this lesson is Goal. lower than in other regions such as 1970s in association with increased to provide a basic background on Africa and Eastern Mediterranean. iron intake during infancy. It is anemia to include pathophysiol- Anemia is the result of one estimated that 4 percent of women ogy, epidemiology, and associated or more of the three independent in the United States between the laboratory studies in the diagnosis mechanisms that occur secondary ages of 20 to 49 years have iron of anemia; common types of anemia to various deficiencies and disor- deficiency anemia. According to and their causes; and treatment ders: (1) decreased red blood cell the WHO definition, more than 10 options in adults. (RBC) production, (2) increased percent of persons older than 65 RBC destruction, and (3) blood loss. years are anemic. The prevalence At the completion of Objectives. Decreased RBC production is the increases with age, and one study this activity, the participant will be result of nutrient deficiencies such found that it approaches 50 percent able to: as iron, vitamin B12, and folate; in chronically ill patients living in 1. demonstrate an understand- bone marrow suppression (drugs, nursing homes. ing of the epidemiology, pathophys- chemotherapy, radiation); bone Table 1 lists the normal red iology, and associated laboratory marrow disorders (aplastic anemia, blood cell parameters in adults. studies in the diagnosis of anemia; myelodysplasia, tumor infiltration); Several studies have demonstrated 2. recognize the general charac- low levels of erythropoietin (EPO); that anemia is an independent risk teristics and causes for select types chronic kidney disease; and other factor for increased morbidity and of anemia; chronic diseases. Iron deficiency is mortality, and decreases quality of 3. identify the general adult the cause in approximately 30 to 50 life in older persons living indepen- treatment options for anemia percent of anemia cases. Hemolyt- dently. Functional deterioration types, as well as key prescribing ic anemias are caused by RBC de- increases with decreased hemoglo- and counseling points for the enti- struction. Examples include sickle bin concentration in an inverse and ties discussed; and cell disease and thalassemias. In linear fashion. 4. demonstrate an understand- some cases, the cause of anemia is ing of the current recommenda- unexplained. Red Blood Cells Life Cycle tions for the use of erythropoietin The WHO defines anemia as a and Function of stimulating agents (ESAs). hemoglobin (Hb) level less than 13 Erythropoietin grams per dL in men, and less than RBCs, also known as erythrocytes, Background 12 grams per dL in women. Other are produced through the process Anemia is one of the most com- authors have proposed different of erythropoiesis which occurs in mon hematologic problems in ranges and lower limits of normal the bone marrow. While the pro- both adults and children. In a that vary based on age, sex, and cess is dependent on various fac- prevalence study conducted us- race. Patients living at high alti- tors, erythropoietin (EPO) plays an ing data from 1993 to 2005, the tude and athletes may also have integral role. EPO is an endocrine World Health Organization (WHO) different normal values. hormone produced in the kidney reported that globally, anemia Anemia occurs at all stages by cells that sense inadequate affected 1.62 billion people, cor- of life but most often in pregnant tissue oxygenation. Once hypoxia relating to almost 25 percent of women and preschool-aged chil- is sensed, EPO is produced and the population. Therefore, it is dren, which are populations that travels to the bone marrow where microcytic anemias are iron defi- Table 1 ciency, thalassemia, and anemia of Normal Red Blood Cell Parameters for Adults chronic inflammation. Macrocytic anemias are often due to alcohol- Red Cell Parameter Men Women ism, liver disease, folic acid and Hemoglobin, g/dL 15.7 +/- 1.7 13.8 +/- 1.5 vitamin B12 deficiency. Ferritin Hematocrit, percent 46 +/- 4.0 40.0 +/- 4.0 serum levels, which measure iron RBC count, 5.2 +/- 0.7 4.6 +/- 0.5 million/µL storage in the body (but not the Reticulocytes, percent 1.6 +/- 0.5 1.4 +/- 0.5 iron contained in heme or hemo- Mean corpuscular 88.0 +/- 8.0 88.0 +/- 8.0 globin), may also be obtained with volume, fL vitamin B12 and folate levels. Peripheral blood smears entail examining a single layer of blood it augments and differentiates of breath, dizziness, coldness in microscopically, in order to study two erythroid progenitors – burst hands and feet, and chest pain are the content of the cell. A reticu- forming units-erythroid (BFU-E) common, yet nonspecific, symptoms locyte count is a blood test that and colony forming units-erythroid that are often experienced. These measures how fast red blood cells (CFU-E) – into normoblasts. Once symptoms occur due to the lack are made by the bone marrow and the normoblast loses its nucleus, it of oxygen delivery to tissue and/ released into the blood. Reticulo- is termed a reticulocyte or imma- or acute, marked bleeding caus- cyte counts usually rise secondary ture red blood cell. The reticulo- ing hypovolemia. Clinicians are to blood loss or in cases of hemolyt- cyte spends about three days in the encouraged to complete a thorough ic anemia. Additionally, a low total bone marrow, and an additional and systematic approach so as white blood cell (WBC) count in a day in peripheral blood before it is not to overlook underlying causes. patient with anemia would lead fully matured. The mature RBC Angular cheilitis (cracking at the to consideration of bone marrow circulates in the body, deliver- edges of the lips) and koilonychias suppression, whereas a high total ing oxygen linked to hemoglobin (spooning of the nails) may ac- WBC may correlate with infection, from the lungs to tissue capillar- company iron deficiency anemia. inflammation, or a hematologic ies. After 110 to 120 days, the Neurological manifestations can malignancy. RBC is removed from circulation accompany or predate anemia asso- by macrophages sensing that the ciated with vitamin B12 deficiency. cell is aged. Under steady state The patient’s past medical history Treatment of Select conditions, the rate of RBC produc- can be helpful, as can a review of Anemias The remainder of this lesson will tion equals the rate of RBC loss, pharmacologic agents since certain review iron deficiency anemia and the reticulocyte count repre- medications, especially chemother- (IDA), anemia of chronic disease sents about 1 percent (normal for apy, may be associated with bone (ACD), and anemia associated with adults is 0.5 to 2 percent) of the marrow suppression. In addition, chronic kidney disease (CKD) as total circulating RBC. The normal some medications such as NSAIDs these types of anemia are often RBC count is five million µL (5 x and anticoagulants can increase encountered in the community set- 1012/L). Therefore, the bone mar- the risk of bleeding resulting in ting. Various oral and intravenous row must produce approximately anemia secondary to blood loss. iron agents as well as erythropoi- 50,000 reticulocytes/µL of whole etin stimulating agents (ESAs) are blood each day in order to main- Laboratory Studies for prescribed for their treatment. tain stable RBC mass. Persistent Diagnosing Anemia reduced rates of production lead to This section will briefly review the anemia. The rate of red blood cell laboratory studies that a clinician Iron Deficiency Anemia Iron deficiency is the most common production greatly increases under may utilize to not only confirm a di- nutritional deficiency worldwide. the influence of high levels of EPO. agnosis of anemia, but classify the Iron metabolism is controlled by In fact, normal bone marrow can type and determine the treatment absorption rather than excretion, increase erythropoiesis in response approach. Upon confirmation of and iron is only lost through blood to EPO approximately fivefold in anemia (Hb <13g/dL in men; <12g/ loss or in RBCs as they slough. adults. dL in women according to WHO), Men and non-menstruating women a complete blood count is generally lose approximately 1mg of iron Signs and Symptoms of obtained. The mean corpuscular each day, while menstruating Anemia volume (MCV) or red blood cell size women lose 0.6 to 2.5 percent more. The signs and symptoms of anemia is used to distinguish microcytic Pregnancy requires about 700mg are dependent on the degree of ane- (MCV <80fL), normocytic (MCV 80 of iron; a complete blood donation mia, the rate at which it evolved, to 100fL), and macrocytic (>100fL) of 500mL contains 250mg of iron. and the oxygen demands of the anemias. Iron absorption occurs mostly in patient. Fatigue, pallor, shortness The most commonly seen Dietary Reference Intake (DRI) for disease, diabetes, trauma, etc. Table 2 iron is 8mg per day for healthy, ACD is generally mild, normo- Causes and Examples of non-menstruating adults, 18mg per cytic and normochromic (concen- Iron Deficiency in Adults day for menstruating women, and tration of Hb in RBC is normal). 16mg per day for vegetarians (due However, it can become microcytic Increased iron loss to the difference in absorption of and hypochromic in long-standing Acute hemorrhage non-heme iron). cases, and can be severe. Labora- Chronic or occult hemorrhage IDA is usually a microcytic tory findings usually reveal a low Menstruation Inflammation anemia.
Load more

Recommended publications
  • New Brunswick Drug Plans Formulary
    New Brunswick Drug Plans Formulary August 2019 Administered by Medavie Blue Cross on Behalf of the Government of New Brunswick TABLE OF CONTENTS Page Introduction.............................................................................................................................................I New Brunswick Drug Plans....................................................................................................................II Exclusions............................................................................................................................................IV Legend..................................................................................................................................................V Anatomical Therapeutic Chemical (ATC) Classification of Drugs A Alimentary Tract and Metabolism 1 B Blood and Blood Forming Organs 23 C Cardiovascular System 31 D Dermatologicals 81 G Genito Urinary System and Sex Hormones 89 H Systemic Hormonal Preparations excluding Sex Hormones 100 J Antiinfectives for Systemic Use 107 L Antineoplastic and Immunomodulating Agents 129 M Musculo-Skeletal System 147 N Nervous System 156 P Antiparasitic Products, Insecticides and Repellants 223 R Respiratory System 225 S Sensory Organs 234 V Various 240 Appendices I-A Abbreviations of Dosage forms.....................................................................A - 1 I-B Abbreviations of Routes................................................................................A - 4 I-C Abbreviations of Units...................................................................................A
    [Show full text]
  • How Do We Treat Life-Threatening Anemia in a Jehovah's Witness
    HOW DO I...? How do we treat life-threatening anemia in a Jehovah’s Witness patient? Joseph A. Posluszny Jr and Lena M. Napolitano he management of Jehovah’s Witness (JW) The refusal of allogeneic human blood and blood prod- patients with anemia and bleeding presents a ucts by Jehovah’s Witness (JW) patients complicates clinical dilemma as they do not accept alloge- the treatment of life-threatening anemia. For JW neic human blood or blood product transfu- patients, when hemoglobin (Hb) levels decrease Tsions.1,2 With increased understanding of the JW patient beyond traditional transfusion thresholds (<7 g/dL), beliefs and blood product limitations, the medical com- alternative methods to allogeneic blood transfusion can munity can better prepare for optimal treatment of severe be utilized to augment erythropoiesis and restore life-threatening anemia in JW patients. endogenous Hb levels. The use of erythropoietin- Lower hemoglobin (Hb) is associated with increased stimulating agents and intravenous iron has been mortality risk in JW patients. In a study of 300 patients shown to restore red blood cell and Hb levels in JW who refused blood transfusion, for every 1 g/dL decrease patients, although these effects may be significantly in Hb below 8 g/dL, the odds of death increased 2.5-fold delayed. When JW patients have evidence of life- (Fig. 1).3 A more recent single-center update of JW threatening anemia (Hb <5 g/dL), oxygen-carrying patients (n = 293) who declined blood transfusion capacity can be supplemented with the administration reported an overall mortality rate of 8.2%, with a twofold of Hb-based oxygen carriers (HBOCs).
    [Show full text]
  • Intravenous Iron Replacement Therapy (Feraheme®, Injectafer®, & Monoferric®)
    UnitedHealthcare® Commercial Medical Benefit Drug Policy Intravenous Iron Replacement Therapy (Feraheme®, Injectafer®, & Monoferric®) Policy Number: 2021D0088F Effective Date: July 1, 2021 Instructions for Use Table of Contents Page Community Plan Policy Coverage Rationale ....................................................................... 1 • Intravenous Iron Replacement Therapy (Feraheme®, Definitions ...................................................................................... 3 Injectafer®, & Monoferric®) Applicable Codes .......................................................................... 3 Background.................................................................................... 4 Benefit Considerations .................................................................. 4 Clinical Evidence ........................................................................... 5 U.S. Food and Drug Administration ............................................. 7 Centers for Medicare and Medicaid Services ............................. 8 References ..................................................................................... 8 Policy History/Revision Information ............................................. 9 Instructions for Use ....................................................................... 9 Coverage Rationale See Benefit Considerations This policy refers to the following intravenous iron replacements: Feraheme® (ferumoxytol) Injectafer® (ferric carboxymaltose) Monoferric® (ferric derisomaltose)* The following
    [Show full text]
  • Venofer ® (Iron Sucrose Injection, USP)
    NDA 21-135/S-017 Page 3 Venofer ® (iron sucrose injection, USP) Rx Only DESCRIPTION Venofer® (iron sucrose injection, USP) is a brown, sterile, aqueous, complex of polynuclear iron (III)- hydroxide in sucrose for intravenous use. Iron sucrose injection has a molecular weight of approximately 34,000 – 60,000 daltons and a proposed structural formula: [Na2Fe5O8(OH) ⋅3(H2O)]n ⋅m(C12H22O11) where: n is the degree of iron polymerization and m is the number of sucrose molecules associated with the iron (III)-hydroxide. Each mL contains 20 mg elemental iron as iron sucrose in water for injection. Venofer® is available in 5 mL single dose vials (100 mg elemental iron per 5 mL) and 10 mL single dose vials (200 mg elemental iron per 10 mL). The drug product contains approximately 30% sucrose w/v (300 mg/mL) and has a pH of 10.5- 11.1. The product contains no preservatives. The osmolarity of the injection is 1,250 mOsmol/L. Therapeutic class: Hematinic CLINICAL PHARMACOLOGY Pharmacodynamics: Following intravenous administration of Venofer®, iron sucrose is dissociated by the reticuloendothelial system into iron and sucrose. In 22 hemodialysis patients on erythropoietin (recombinant human erythropoietin) therapy treated with iron sucrose containing 100 mg of iron, three times weekly for three weeks, significant increases in serum iron and serum ferritin and significant decreases in total iron binding capacity occurred four weeks from the initiation of iron sucrose treatment. Pharmacokinetics: In healthy adults treated with intravenous doses of Venofer®, its iron component exhibits first order kinetics with an elimination half-life of 6 h, total clearance of 1.2 L/h, non-steady state apparent volume of distribution of 10.0 L and steady state apparent volume of distribution of 7.9 L.
    [Show full text]
  • Ferric Maltol 30Mg Hard Capsules (Feraccru®) SMC No
    ferric maltol 30mg hard capsules (Feraccru®) SMC No. (1202/16) Shield TX UK Limited 04 November 2016 The Scottish Medicines Consortium (SMC) has completed its assessment of the above product and advises NHS Boards and Area Drug and Therapeutic Committees (ADTCs) on its use in Scotland. The advice is summarised as follows: ADVICE: following a full submission ferric maltol (Feraccru®) is not recommended for use within NHS Scotland. Indication under review: in adults for the treatment of iron deficiency anaemia (IDA) in patients with inflammatory bowel disease (IBD). In a pooled analysis of two phase III studies in IBD patients with IDA who had failed previous treatment with oral ferrous products, there was a significantly greater increase in haemoglobin concentrations after 12 weeks of ferric maltol treatment compared with placebo. The submitting company did not present sufficiently robust clinical and economic analyses to gain acceptance by SMC. Overleaf is the detailed advice on this product. Chairman, Scottish Medicines Consortium Published 12 December 2016 1 Indication In adults for the treatment of iron deficiency anaemia (IDA) in patients with inflammatory bowel disease (IBD). Dosing Information One capsule twice daily, morning and evening, on an empty stomach. Treatment duration will depend on severity of iron deficiency but generally at least 12 weeks treatment is required. The treatment should be continued as long as necessary to replenish the body iron stores according to blood tests. Ferric maltol capsules should be taken whole on an empty stomach (with half a glass of water) as the absorption of iron is reduced when it is taken with food.
    [Show full text]
  • A Randomized Controlled Trial of Repeated Doses of Ferumoxytol Or Iron Sucrose in Patients on Hemodialysis: Background and Rationale Iain C
    Macdougall et al. BMC Nephrology (2017) 18:117 DOI 10.1186/s12882-017-0523-8 STUDY PROTOCOL Open Access The Ferumoxytol for Anemia of CKD Trial (FACT)—a randomized controlled trial of repeated doses of ferumoxytol or iron sucrose in patients on hemodialysis: background and rationale Iain C. Macdougall1, Naomi V. Dahl2, Kristine Bernard2, Zhu Li2, Alka Batycky2 and William E. Strauss2* Abstract Background: Iron deficiency anemia (IDA) is a common manifestation of chronic kidney disease (CKD), affecting most patients on hemodialysis and imposing a substantial clinical burden. Treatment with iron supplementation increases hemoglobin levels and can reduce the severity of anemia in patients with CKD. While correcting anemia in these patients is an important therapeutic goal, there is a lack of long-term trials directly comparing intravenous iron therapies in patients with CKD receiving hemodialysis. Methods/Design: The Ferumoxytol for Anemia of CKD Trial (FACT) is a 13-month, open-label, randomized, multicenter, international, prospective study with 2 substudies. Entry criteria for the main study include adults with IDA (defined as hemoglobin <11.5 g/dL [<115.0 g/L] and a transferrin saturation <30%), serum ferritin <800 ng/mL (<1798 pmol/L), and receiving hemodialysis for ≥3 months. Patients are randomized to receive ferumoxytol (1.02 g over 2 doses) or iron sucrose (1.0 g over 10 doses) during the initial 5-week treatment period. Those with persistent/recurrent IDA over the 11-month observation period will receive additional 5-week treatment periods, as appropriate. The primary efficacy endpoint of the main study is the mean change in hemoglobin from Baseline to Week 5 for each treatment period.
    [Show full text]
  • Anemia Landmark Trials Chart
    ANEMIA OF CKD: Hemoglobin Control – Landmark Trials Summary Z Dumont BSP, P Ricci, L Gross, B Lang, A Wiebe © www.RxFiles.ca May 2021 Trials Intervention Population Key Baseline Indices Results Comments Mean follow-up, n CKD stage, age, etc. (e.g. Iron Studies) 1 Charytan et al. Oral vs IV iron for ND-CKD ND-CKD; Age mean ~61; mostly ♀, Hgb (g/L): 97 oral vs 98 IV Hgb (g/L): +7 oral vs +10 IV; NS Iron therapy: 43 days; n=96; FeSO4 325mg po TID x 29 days vs (71% oral, 60% IV); multi-racial Ferritin (ng/mL): 103 oral vs 125 IV Ferritin (ng/mL): -5.1 oral vs 288 IV; p<0.0001 Should be guided by iron status tests, Hgb Iron sucrose 200mg IV weekly x 5 doses; Included: CrCl(C-G)≤40ml/min, RCT, OL TSAT (%): 15.6 oral vs 16.6 IV Change in TSAT (%): day 36=2.1 oral vs 5.1 IV | day 43=0.5 oral vs 4.5 IV; sig levels, ESA dose, & pt status CSN 2008 Guidelines assessments made up to 14 days after last Hgb<105g/L, TSAT<25%, increase for IV, but not oral dose ferritin<300ug/L | Excluded: iron tx # of pts achieved Hgb >110g/L: 31.3% vs 54.2% IV (p=0.028) Iron Therapy in Non-hemodialysis CKD pts or blood transfusion w/in last month, AE: similar between groups, most common is GI in oral group, & taste- (ND-CKD) disturbances more common in IV group apparent GI bleed, Alb<30g/L Route of admin has been shown to have no 2 Van Wyck et al.
    [Show full text]
  • Iron Sucrose, Folic Acid, Cyanocobalamin Capsule MARTIN EKWEALOR PHARMACEUTICALS, INC
    MYFERON 150 FORTE - iron sucrose, folic acid, cyanocobalamin capsule MARTIN EKWEALOR PHARMACEUTICALS, INC. Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. For further information about unapproved drugs, click here. ---------- DESCRIPTION: Myferon 150 Forte capsules are highly water soluble low molecular weight polysaccharide iron complex and vitaminns. Each capsule contains: Elemental Iron .......... 150 mg (as Polysaccharide Iron Complex) Folic Acid .................. 1 mg Vitamin B 12 ............... 25 mcg. (Cyanocobalamin) Other ingredients: Microcrystalline Cellulose, Gelatin, Dicalcium, Phosphate, Stearic Acid, Pharmaceutical Glaze, Magnesium Stearate, Iron Oxides, Titanium Dioxide, FD and C Red #40 Lake and FD and C Blue #1 Lake. CLINICAL PHARMACOLOGY: Iron is an essential component in the formation of hemoglobin. Adequate amounts of iron are necessary for effective erythropoiesis. Iron also serves as a cofactor of several enzymes, including cytochromes that are involved in electron transport. Folic acid is required for nucleoprotein synthesis and the maintenance of normal erythropoiesis. Folic acid is converted in the liver and plasma to its metabolically active form, tetrahydrofolic acid by dihydrofolate reductase. Vitamin B 12 is required for the maintenance of normal erythhropoiesis, nucleoprotein and myelin synthesis, cell reproduction and normal growth. Intrinsic factor, a glycoprotein secreted by the gastric mucosa, is required for active absorption of Vitamin B 12 from the gastric tract. INDICATIONS AND USAGE: Myferon 150 Forte is indicated for the prevention and treatment of iron deficiency anemia and/or nutritional megaloblastic anemias. CONTRAINDICATIONS: Myferon 150 Forte is contraindicated in patients with a known hypersensitivity to any of the components of this product.
    [Show full text]
  • Treatment of Anemia of Chronic Disease with True Iron Deficiency in Pregnancy
    1 Treatment of anemia of chronic disease with true iron deficiency in pregnancy Gabriela AMSTAD BENCAIOVA, Alexander KRAFFT, Roland ZIMMERMANN, Tilo BURKHARDT Department of Obstetrics and Gynecology University Hospital of Zurich Frauenklinikstrasse 10 CH-8091 Zurich SWITZERLAND Phone: +41 44 255 51 92 Email: [email protected] Treatment of anemia of chronic disease with true iron deficiency in pregnancy 31.10.2017 2 Study population and criteria Fifty anemic pregnant women with moderate anemia were prospectively observed and treated in the Anemia clinic at the Department of Obstetrics, University Hospital Zurich. All patients had singleton pregnancies. All pregnant women fulfilled criteria of moderate iron deficiency anemia defined as hemoglobin between 8.0 and 9.9 g/dl and serum ferritin <15 µg/l. In all women, the analyses of a blood count, iron status, erythropoietin, cross reactive protein (CRP), folic acid and vitamin B12 were conducted. Primary endpoint was the assessment and comparison of the efficacy of anemia treatment in pregnant women with iron deficiency anemia and anemia of chronic disease with true iron deficiency. Secondary endpoint was the target hemoglobin ≥10.5 g/dl. Exclusion criteria were anemia of other etiology (i.e. vitamin B12 deficiency, folic acid deficiency, hemoglobinopathy etc.), liver or kidney disease, and multiples. Women with mean corpuscular hemoglobin (MCH) ≤25 pg, mean corpuscular volume (MCV) ≤75 fl; and percentage of microcytic erythrocytes (MRC) ≥3% were tested for hemoglobinopathies. Flow cytometry was used to determine the total iron demand of erythropoiesis by measuring HRC, CHr, and RDW. Iron deficiency anemia is defined as anemia with depleted iron stores and with elevated levels of HRC >2.5%, decreased CHr <28 pg and elevated RDW >15%.
    [Show full text]
  • Chronic Anemia and the Role of the Infusion Therapy Nurse
    VOLUME 38 | NUMBER 5 | SEPTEMBER/OCTOBER 2015 The Art and Science of Infusion Nursing Jeffrey Betcher, RPh, BCOP Velvet Van Ryan, BSN, RN, OCN® Joseph Mikhael, MD Chronic Anemia and the Role of the Infusion Therapy Nurse destruction of erythrocytes. They encompass a broad ABSTRACT range of anemias that develop acutely or chronically Chronic anemia develops over a course of weeks and may persist for several months if left untreated. to months and is usually mild to moderate in Formally, anemia of chronic disease is a specific catego- nature. It is important to understand the etiology ry of anemia associated with underlying infection, of the reduced number of circulating red blood inflammation, or malignancy. For the purpose of this cells to treat the anemia appropriately. Diagnosis publication, the term chronic anemia will be used to is dependent on patient history and laboratory encompass anemia of chronic disease; anemia of chron- findings, such as complete blood counts, iron ic kidney disease (CKD); anemia of cancer; and vitamin studies, a peripheral smear, and occasionally, a B12, folate, and iron deficiency anemias. On diagnosis, the infusion therapy nurse may be involved with treat- bone marrow biopsy. Treatment modalities fre- ment strategies ranging from treatment of an underlying quently administered by infusion therapy nurses chronic disease, replacement of deficiencies (iron, vita- include treatment of the underlying chronic dis- min B12, folate, or erythropoietin), or transfusion of ease, replacement of deficiencies (iron, vitamin red blood cells (RBCs) in symptomatic patients or those B12, folate, or erythropoietin), or transfusion of with cardiovascular instability. Normal erythropoiesis, red blood cells.
    [Show full text]
  • How I Treat Cancer Anemia
    American Society of Hematology 2021 L Street NW, Suite 900, Washington, DC 20036 Phone: 202-776-0544 | Fax 202-776-0545 [email protected] How I treat Cancer Anemia Downloaded from https://ashpublications.org/blood/article-pdf/doi/10.1182/blood.2019004017/1745373/blood.2019004017.pdf by IMPERIAL COLLEGE LONDON user on 19 June 2020 Tracking no: BLD-2019-004017-CR1 Jeffrey Gilreath (Huntsman Cancer Institute, United States) George Rodgers (University of Utah Huntsman Cancer Institute, United States) Abstract: Despite increasing use of targeted therapies to treat cancer, anemia remains a common complication of cancer therapy. Physician concerns about the safety of intravenous (IV) iron products and erythropoiesis-stimulating agents (ESAs) have resulted in many patients with cancer receiving no or suboptimal anemia therapy. In this article, we present four patient cases illustrating both common and complex clinical scenarios. We first present a review of erythropoiesis, then describe our approach to cancer anemia by identifying contributing causes before selecting specific treatments. We summarize clinical trial data affirming the safety and efficacy of currently-available IV iron products used to treat cancer anemia, and illustrate how we use commonly-available laboratory tests to assess iron status during routine patient management. We compare adverse event rates associated with IV iron versus red cell transfusion and discuss using front-line IV iron monotherapy to treat anemic patients with cancer, decreasing the need for ESAs. A possible mechanism behind ESA-induced tumor progression is discussed. Finally, we review the potential of novel therapies such as ascorbic acid, prolyl hydroxylase inhibitors, activin traps, hepcidin and bone morphogenetic protein antagonists, in treating cancer anemia.
    [Show full text]
  • Intravenous Iron in Chemotherapy and Cancer-Related Anemia Michael Auerbach, MD,1 April S
    Review Intravenous iron in chemotherapy and cancer-related anemia Michael Auerbach, MD,1 April S. Liang,2 and John Glaspy, MD3 1 Private practice, Baltimore, Maryland; Georgetown University, Washington, DC; 2 Princeton University, Princeton, New Jersey; 3 University of California, Los Angeles Recent guidance from the Centers for Medicare and Medicaid Services restricting erythropoiesis-stimulating agents (ESAs) in chemotherapy and cancer-related anemias has resulted in an increase in transfusions. Nine studies, without published contradictory evidence, have shown optimization of the response to ESAs by intravenous (IV) iron when the iron was added to the treatment of chemotherapy-induced anemia. The synergy observed, although greater in iron deficiency, was independent of pretreatment iron parameters. Three studies demonstrated decreased transfusions when IV iron is administered without ESAs. Discordant recommendations regarding IV iron currently exist among the American Society of Hematology/American Society of Clinical Oncology guidelines, the National Comprehensive Cancer Network, and the European Society of Medical Oncology. This discordance is at least partly the result of misconceptions about the clinical nature and incidence of adverse effects with IV iron. Other reasons for this discordance are presented in this review. Based on thousands of studied patients, we conclude that IV iron is safe and probably safer than most physicians realize. Education is needed relating to the interpretation of minor, subclinical infusion reactions that resolve without therapy. IV iron without ESAs may be an effective treatment for chemotherapy- induced anemia and warrants further study. We present evidence supporting the conclusion that baseline serum hepcidin levels may predict responses to IV iron, and we examine the published evidence supporting the conclusion that IV iron should be a standard addition to the management of chemotherapy and cancer-related anemia.
    [Show full text]