IRON DEFICIENCY ANEMIA (IDA) RECOMMENDATIONS, Lecture notes of Decision Making

Download IRON DEFICIENCY ANEMIA (IDA) RECOMMENDATIONS and more Lecture notes Decision Making in PDF only on Docsity! IRON DEFICIENCY ANEMIA (IDA) Clinical Practice Guideline | March 2018 These recommendations are systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances. They should be used as an adjunct to sound clinical decision making. OBJECTIVE Alberta clinicians (specifically primary care and emergency department physicians) will be able to diagnose iron deficiency anemia (IDA), treat using oral and parenteral iron supplementation and provide ongoing management; will understand why red blood cell transfusion (RBC) may be harmful and is only occasionally required for the treatment of IDA. TARGET POPULATION Patients >5 years of age, hemodynamically stable, seen in emergency departments and primary care settings EXCLUSIONS Patients <5 years of age, all patients who are hemodynamically unstable, chronic kidney disease, rare genetic causes of and treatment of IDA, other types of iron deficiency, and the pre-latent stage of iron deficiency RECOMMENDATIONS ASSESSMENT INVESTIGATION FOR IDA  Identify patients at risk for iron deficiency anemia Table 1: Possible Features, Signs and Symptoms of IDA ADULTS AND ADOLESCENTS  Anticipated ongoing bleeding (e.g., menstruation, gastrointestinal)  Head and neck manifestations including pallor (e.g., facial, conjunctival or palmar), blue sclerae, atrophic glossitis or loss of tongue papillae, angular cheilitis, alopecia  Koilonychia (spoon nails)  Restless leg syndrome  Fatigue, shortness of breath, chest pain, lightheaded, syncope weakness, headache  Irritability and/or depression  Pica (craving/consumption of non-food substances e.g., dirt, clay, chalk) and pagophagia (ice craving)  Decreased exercise tolerance  Regular blood donors, particularly females donating more than twice a year and males donating more than three or four times a year SCHOOL-AGED CHILDREN (e.g., >5 to <18 years old)  Tiredness, restlessness, irritability  Pica and pagophagia  Growth retardation  Cognitive and intellectual impairment  Signs of attention-deficit/hyperactivity disorder (ADHD)  Breath-holding spells Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 2 of 21 Recommendations PRACTICE POINT Investigating the underlying cause of IDA is as important as treating the IDA. Table 2: Common and/or Possible Causes of IDA INCREASED REQUIREMENT DECREASED INTAKE Rapid growth (infants and adolescents) Menstruation Pregnancy (second and third trimesters) Lactation Low SES, malnutrition Diet (e.g., vegetarian, vegan, iron poor) Elderly Alcoholism INCREASED LOSS DECREASED ABSORPTION Gastrointestinal  Esophagitis  Erosive gastritis  Peptic ulcer  Inflammatory bowel disease (IBD) e.g., ulcerative colitis, Crohn’s disease*  Benign tumors  Intestinal/stomach cancer  Angiodysplasia  Hemorrhoids  Hookworm infestation  Occult blood loss secondary to cow’s milk protein-induced colitis  Chronic or high dose use of salicylates or NSAIDs Genitourinary  Menorrhagia  Chronic hematuria Hemolysis  Intravascular hemolysis Other  Regular blood donors  Frequent epistaxis  Hemorrhagic telangiectasia (rare) Dietary factors (carbonated drinks, coffee, etc.) Gastrointestinal  Gastrectomy  Duodenal bypass  Bariatric surgery  Helicobacter pylori  Celiac disease  Atrophic gastritis  Pediatric short bowel syndrome  Inflammatory bowel disease (IBD) e.g., ulcerative colitis, Crohn’s disease*  Chronic kidney disease *Inflammatory conditions may be associated with iron deficiency due to poor iron absorption and anemia of chronic inflammation. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 5 of 21 Recommendations MANAGEMENT TREATMENT  Treat all IDA patients that are hemodynamically stable, regardless of the presence of symptoms, with oral and/or intravenous iron supplementation and provide general information regarding an iron-rich diet refer to https://myhealth.alberta.ca/health/pages/conditions.aspx?hwid=ue4500&4500-sec.  See treatment algorithm (Appendix A).  See Table 8 (Appendix B) for a review of considerations when selecting an oral iron product.  See Table 9 (Appendix C) for a review of considerations when selecting an IV iron product. MONITORING  Order a CBC and reticulocytes at two to four weeks to see if the patient is responding to replacement regimen. See Optimizing Oral Iron Dosage (Appendix B).  Indicators of response to (i.e., targets for) iron therapy include: o Reticulocytosis in four days o Increasing hemoglobin >10g/L in four weeks  Correction of IDA should be observed within two to four months if appropriate iron dosages are administered and underlying cause of iron deficiency is addressed. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 6 of 21 Recommendations Table 5: Monitoring Algorithm IF PATIENT IS RESPONDING TO THERAPY IF PATIENT IS NOT RESPONDING TO THERAPY:  Continue to monitor hemoglobin and Ferritin monthly/bimonthly to ensure levels remain within the normal range.  For school-aged children, treat for 3-4 months then stop as long as all parameters have normalized (CBC, ferritin and iron studies).  Reassess iron dosage, and ensure underlying cause has been addressed.  Continue with iron supplementation for an additional 4-6 months (all patients) until Hgb/MCV and Ferritin normalize and to replenish iron stores.  If prescribed oral iron, rule out cause of poor response. If the cause is non- adherence and hemoglobin is not lower than 90g/L, try another oral formulation that may be better tolerated (see Appendix B). Note: Non-adherence is the most common cause of oral iron failure.  Once IDA has resolved and iron stores normalize, a low dose of oral iron may be necessary for maintenance if there is an ongoing need for additional iron (e.g., growth spurt, menstruation, dietary habits). Note: women with menses and ongoing IDA should be evaluated for a bleeding disorder.  If iron supplementation is discontinued consider repeating CBC, iron studies and ferritin in 4-6 months.  If there is not an adequate response to an appropriate oral treatment dose for a three-month period, OR  If the patient has not tolerated a trial of two different oral agents, OR  If hemoglobin continues to decline (e.g., <90 g/L)  Adults: Initiate IV iron therapy (as per Appendix A algorithm).  Pediatrics (<18 years old): refer to Pediatric Hematology  Consider referral for dietary advice if IDA is primarily diet related.  Refer to hematology if no response to IV iron and another cause for the anemia is suspected. ONGOING MANAGEMENT  Once the cause of IDA has been identified, ongoing need for iron supplementation and/or management of the condition will be determined accordingly and is beyond the scope of this clinical practice guideline. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 7 of 21 Background HIGHER RISK  In addition to specific conditions, patient populations that may/will require ongoing monitoring for IDA, and possibly further iron supplementation include but are not limited to: o Pregnancy o Elderly o Patients with underlying conditions predisposing to IDA, e.g., GI malabsorption, celiac disease, hereditary hemorrhagic telangiectasia, hemolysis and dysfunctional uterine bleeding BACKGROUND Iron is crucial to biologic functions, including respiration, energy production, DNA synthesis, and cell proliferation.1 Iron is biologically conserved in several ways including recycling after the degradation of red cells and iron retention in the absence of an excretion mechanism. Because excess iron levels can be toxic, absorption is limited to one to two mg daily, and most of the iron required daily (approximately 25 mg per day) is provided through recycling by macrophages that phagocytose senescent erythrocytes.2 The latter two mechanisms are controlled by hepcidin, a hormone that maintains total-body iron within normal ranges, avoiding both iron deficiency and excess.2 The degree of iron store repletion is determined by the rapidity with which iron deficiency develops in the context of blood loss or a substantial reduction in iron absorption. Hepatocytes are thought to be a long-term reservoir for iron and release it more slowly than macrophages. Iron deficiency is defined as the reduction of iron stores that precedes overt iron-deficiency anemia (IDA) or may persist but not progress to IDA. IDA is a serious condition whereby low levels of iron are associated with anemia and the presence of microcytic hypochromic red cells. 2 A recent systematic review of 29 guidelines was published in 2015.3 These guidelines were developed by professional associations throughout the world including the United States (n = 8), Europe (n = 6), Britain (n = 4), Canada (n = 3), other international organizations (n = 2), France (n = 2), Poland (n = 1), Australia (n = 1), Mexico (n = 1), and Japan (n = 1). Findings from this guideline summary reveal that, for the most part, Iron Deficiency (ID) guideline recommendations are somewhat heterogenous largely because different patient populations were addressed. Recommendations in this guideline were informed by available evidence located as well as the guideline development committees’ expertise, experience and consensus. SCREENING To our knowledge, there is no evidence to routinely screen for (i.e., order iron studies) for iron deficiency anemia (IDA) in patients >5 years of age in the absence of signs, symptoms or risk factors for IDA. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 10 of 21 Background Table 6: Sequence of events that occur with gradual depletion of iron stores in the body (in the absence of chronic inflammatory disease).9 Reproduced with permission from Medscape9 LABORATORY MEASURES AND RESULTS A complete blood count (CBC) demonstrates a microcytic, hypochromic anemia with a normal or reduced red blood cell (RBC) count.10 These laboratory findings may be present before the onset of clinical symptoms of anemia thus iron deficiency should be suspected. It should be noted that early stage iron deficiency can exist before any hematological changes occur with the exception of a low serum ferritin result which would indicate iron deficiency.10 Serum ferritin concentration is the most commonly recommended indicator for determining iron deficiency and IDA and considered a gold standard.3 A low serum ferritin concentration does indeed reflect a state of iron depletion however, there is considerable variation in serum ferritin cut-offs recommended by different expert groups to diagnose iron deficiency and IDA. The diagnosis of iron- deficiency anemia in the context of inflammation requires significantly higher threshold levels for ferritin to define iron-deficiency anemia. Table 7 shows the variation in ferritin cut-off values among different guidelines addressing different patient populations. There are very few studies that demonstrate appropriate serum ferritin concentrations to detect iron deficiency in otherwise healthy individuals or populations. The commonly reported threshold of 15 μg/L is likely specific but can be expected to miss as many as half the cases of iron deficiency .10 While a serum ferritin concentration cut-off of 30 μg /L is more sensitive, it will generate many false- positive diagnoses. Therefore, the evidence available to support any recommended serum ferritin cut-off for diagnosis of iron deficiency is at best-limited and is one of several tests that can be used to detect iron deficiency.11 Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 11 of 21 Background Table 7: Varying ferritin threshold values for IDA reported for various patient populations from various guidelines throughout the world.3 NUMBER OF GUIDELINES FERRITIN PATIENT POPULATION ADDRESSED 10 12-15 µg/L General (men, women children, CKD, digestive diseases 9 25-30 µg/L General (with chronic disease or peri-op bleed), inactive IBD, CKD, on chemotherapy, peri-gestational 3 45-50 µg/L General- “iron deficiency probable”, digestive disease 12 100 µg /L Mainly CKD, general- “iron deficiency possible”, heart disease, active IBD, for anesthesia 2 200 µg/L CKD hemodialysis and receiving hemodialysis According to Thomas et al 2013, moderate quality evidence suggests that mean cell volume (MCV) and mean cell haemoglobin (MCH) values are useful at diagnosis and trends from ongoing assessment over weeks or months but they have no utility for assessing acute changes in iron availability secondary to therapy with erythropoiesis-stimulating agents (ESAs).8 The percentage of hypochromic red cells (%HRC) is the best-established variable for the identification of functional iron deficiency and thus has the greatest level of evidence. Reticulocyte haemoglobin content (CHr) is the next most established option. But both tests have limitations e.g., sample stability or equipment availability. Other parameters may be as good but there is no evidence that they are any better, and generally there is less evidence for newer red cell and reticulocyte parameters.8 Red cell indices can provide a sensitive indication of iron deficiency in the absence of chronic disease or haemoglobinopathy.4 One-half of guidelines reviewed by Peyrin-Biroulet et al. proposed transferrin saturation (TSAT) be considered as an alternative or complementary diagnostic test to serum ferritin.3 Other biochemical assessment tests (transferrin saturation, and soluble transferrin receptor [sTfR], as well as erythrocyte protoporphyrin) can be used to determine iron status but also present challenges in interpretation. While sTfR concentration is an indicator of functional iron deficiency and is not an acute-phase reactant, it lacks assay standardization, common reference ranges, and common cut-offs.12 This clinical practice guideline has purposefully recommended a more simplified approach to lab testing for IDA based on review and evaluation of current evidence and the committee’s expertise and opinion regarding detection of IDA in the general patient population i.e., those without inflammatory conditions. TREATMENT To treat iron deficiency, the guidelines reviewed by Peyrin-Biroulet et al.2015, varied in their recommendations as to treatment approach primarily because of the heterogenous patient populations addressed among the guidelines reviewed. For this guideline, the management of iron Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 12 of 21 Background deficiency includes two concurrent components: 1. correcting the iron deficiency diagnosis and 2. treating the underlying disorder leading to the iron deficiency. The treatment of iron deficiency may involve some or all of the following: dietary advice; oral iron supplements; intravenous iron infusion; and less commonly, blood transfusion. Once replacement has been achieved, many patients require dietary advice to ensure deficiency does not recur. The goal of treatment should be to restore haemoglobin levels and red cell indices to normal levels and to replenish body stores with iron supplementation.13 Some guidelines do recommend specific treatment targets for Hb and/or Serum ferritin and/or TSAT % at specific intervals of time but these targets vary and are typically condition-specific guidelines e.g., CKD.3 ORAL IRON INTAKE DIET AND ORAL IRON SUPPLEMENTS Regardless of the source, all patients should receive iron supplementation both to correct anemia and replenish body stores.14 Guidelines differ in their recommendations for daily dosage and the type of iron salt supplement recommended. This guideline suggests the type and dosages that have been best tolerated based on patient experience, but tolerance will be patient specific and may require trial of different iron salt formulations and/or dosages. Once oral iron corrects the IDA, it should be continued for at least three months to replenish iron stores.4 Limited information on efficacy when comparing one to another, so most decisions are based on tolerability, adherence and cost. Typical adult treatment dose is 100 to 200 mg elemental iron per day. The Nutrition and Gastroenterology Committee of the Canadian Paediatric Society recommends that assuming 10% of the iron in a mixed diet is absorbed, the required elemental iron intake is approximately 8 mg/day for children aged four to 12 years. Children with IDA should also receive iron supplementation. The recommended therapeutic dose of oral iron is 3 to 6 mg/kg/day of elemental iron, for three to four months with adequate follow-up.15 Starting doses vary depending on patient tolerance and potential benefit of starting low and increasing slowly in less acute situations. Oral iron at treatment doses should be tried for three months before considering other routes of iron supplementation. Three to six months of treatment are required for repletion of iron stores.2 Adding a source of vitamin C (e.g., 125ml orange juice or if not tolerated, a 250-500mg ascorbic acid supplement) may enhance the absorption of dietary or oral iron.16,17 A 250-500 mg ascorbic acid supplement can be taken up to twice daily with an iron supplement to enhance absorption, but there is no evidence for its effectiveness in treating IDA.4 Oral iron should be avoided after bariatric surgery and in inflammatory bowel disease and when blood loss exceeds absorption (e.g. heavy uterine bleeding and hereditary hemorrhagic telangiesctasia).18 INTRAVENOUS IRON THERAPY In the past, hypersensitive reactions to high-molecular-weight iron dextran resulted in limited administration of IV iron. However, with the availability of safer iron formulations such as iron sucrose and ferric gluconate, use of I.V iron is common and generally well tolerated by most patients. Mild side effects can be observed in about 35% of patients with symptoms such as abdominal pain, Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 15 of 21 References REFERENCES 1. Hentze M, Muckenthaler M, Galy B, Camaschella C. Two to tango: regulation of mammalian iron metabolism. Cell. 2010;142:24-38. 2. Camaschella C. Iron deficiency anemia. N Engl J Med. 2015 May;372:1832-43. 3. Peyrin-Biroulet L, et al. Guidelines on the diagnosis and treatment of iron deficiency anemia. Am J Clin Nutr. 2015 Dec;102:1585-94. 4. Goddard A, James M, McIntyre A, Scott B, on behalf of the British Society of Gastroenterology. Guidelines for the management of iron deficiency anemia. Gut. 2011;60:1309-16. 5. Tovey F, Godfrey J, Lewin M. A gastrectomy population: 25-30 years on. Postgrad Med J. 1990;66:450e6. 6. Hershko C, Camaschella C. How I treat unexplained refractory iron deficiency anemia. Blood. 2014;123:326-33. 7. De Falco L, Sanchez M, Silvestri L, et al. Iron refractory iron deficiency anemia. Haematologica. 2013;98:845-53. 8. Thomas D, Hinchliffe R, Briggs C, Macdougall I, Littlewood T, Cavill I, et al. Guideline for the laboratory diagnosis of functional iron deficiency. Br J Haematol. 2013 Jun;161(5):639-48. 9. Harper J, Conrad M. Iron deficiency anemia. Medscape. 2017 [cited 2018 Jan 29]. Available from: https://emedicine.medscape.com/article/202333-overview 10. Kuruvilla P, Wozniak M. Guidelines for the use of serum tests for iron deficiency. Ontario, Canada: Ontario Association of Medical Laboratories; 1995. 11. Daru J, et al. Serum ferritin as an indicator of iron status: what do we need to know? Am J Clin Nutr. 2017 Oct;106:17035-17125. 12. Pfeiffer C. Laboratory methodologies for indicators of iron status: strengths, limitations, and analytical challenges. Am J Clin Nutr. 2017 Dec;106(Suppl 6):1606S-1614S. 13. Pasricha S, Drakesmith H, Black J, Hipgrave D, Biggs B. Control of iron deficiency anemia in low- and middle- income countries. Blood. 2013;121:2607-17. 14. Smith A. Prescribing iron. Prescribers’ J. 1997;37:82-7. 15. Abdullah K, Zlotkin S, Parkin P, Grenier D. Iron-deficiency anemia in children. Canadian Pediatric Surveillance Program (CPSP). The Hospital for Sick Children. Toronto 2011. 16. Crosby W. The rationale for treating iron deficiency anemia. Arch Intern Med. 1984;144:471. 17. Alleyne M, Horne M, Miller J. Individualized treatment for iron-deficiency anemia in adults. Am J Med. 2008;121:943. 18. Auerbach M, Ballard H, Glaspy J. Clinical update: intravenous iron for anemia. SO Lancet. 2007;369(9572):1502. 19. Fishbane S. Safety in iron management. Am J Kidney Dis. 2003;6(Suppl 5):S18-26. 20. Silverstein S, Rodgers G. Parenteral iron therapy options. Am J Hematol 2004;76:74-8. 21. Johnson-Wimbley T, Graham D. Diagnosis and management of iron deficiency anemia in the 21st century. Therapeutic Advances in Gastroenterology. 2011;4(3):177-84. doi:10.1177/1756283X11398736. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 16 of 21 References 22. Macdougall I, Bock A, Carrera F, et al. FIND-CKD: a randomized trial of intravenous ferric carboxymaltose versus oral iron in patients with chronic kidney disease and iron deficiency anemia. Nephrol Dial Transplant. 2014;29:2075-84. 23. Onken J, Bregman D, Harrington R, et al. A multicenter, randomized, active-controlled study to investigate the efficacy and safety of intravenous ferric carboxymaltose in patients with iron deficiency anemia. Transfusion. 2014;54:306-15. 24. Vadhan-Raj S, Strauss W, Ford D, et al. Efficacy and safety of IV ferumoxytol for adults with iron deficiency anemia previously unresponsive to or unable to tolerate oral iron. Am J Hematol. 2014;89:7-12 25. Carson J, Grossman B, Kleinman S, et al. Red blood cell transfusion: a clinical practice guideline from the AABB. Ann Intern Med. Jul 3 2012;157(1):49-58. 26. Bager P, Dahlerup JF. The health care cost of intravenous iron treatment in IBD patients depends on the economic evaluation perspective. J Crohns Colitis. 2010;4:427-30. 27. Reinisch W, Chowers Y, Danese S, et al. The management of iron deficiency in inflammatory bowel disease — an online tool developed by the RAND/UCLA appropriateness method. Aliment Pharmacol Ther. 2013;38:1109-18. 28. Solomons N, Schumann K. Intramuscular administration of iron dextran is inappropriate for treatment of moderate pregnancy anemia, both in intervention research on underprivileged women and in routine prenatal care provided by public health services. Am J Clin Nutr. 2004;79:1-3. 29. Grasso P. Sarcoma after intramuscular iron injection. Br Med J. 1973 Jun;2(5867):667. 30. Greenberg G. Sarcoma after intramuscular iron injection. Br Med J. 1976 Jun;1(6024):1508- 9. 31. Murphy M, Wallington T, Kelsey P, et al. British Committee for Standards in Haematology. Guidelines for the clinical use of red cell transfusions. Br J Haematol. 2001;113:24-31. 32. Carson J, Guyatt G, Heddle N, Grossman, et al. Clinical Practice Guidelines From the AABB: Red blood cell transfusion thresholds and storage. JAMA. 2016 Nov;15;316(19):2025-35. 33. Bothwell T. Iron requirements in pregnancy and strategies to meet them. Am J Clin Nutr. July 2000;72(1):257-64. 34. Reveiz L, Gyte GM, Cuervo LG, Casasbuenas A. Treatments for iron-deficiency anaemia in pregnancy. Cochrane Database Syst Rev. 2011;(10):CD003094. 35. Pavord S, Myers B, Robinson S, Allard S, Strong J, Oppenheimer C, et al. UK guidelines on the management of iron deficiency in pregnancy. Br J Haematol. 2012 Mar;156(5):588–600. 36. Guralnik J, Eisenstaedt R, Ferrucci L, Klein H, Woodman R. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104(8):2263-8. Epub 2004 Jul 6. 37. Den Elzen W, Willems J, Westendorp R, de Craen A, Assendelft W, Gussekloo J. Effect of anemia and comorbidity on functional status and mortality in old age: results from the Leiden 85-plus study. CMAJ. 2009;181(3-4):151-7. Epub 2009 Jul 27. 38. Ioannou G, Rockey D, Bryson C, Weiss N. Iron deficiency and gastrointestinal malignancy: a population-based cohort study. Am J Med. 2002;113(4):276-80. 39. Linebald et al. Alberta College of Family Physicians. Tools for Practice. Canadian Family Physician. 2015 Feb;(61):159. Iron Deficiency Anemia (IDA) | March 2018 Clinical Practice Guideline Page 17 of 21 References 40. Guidelines and Protocols and Advisory Committee 2010. Iron deficiency - investigation and management. BC Guidelines. Available at: https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc- guidelines/iron-deficiency 41. Auerbach M. How we diagnose and treat iron deficiency anemia. Am J Hematol 2016;91:31- 38. 42. Lopez A. Iron deficiency anemia. Lancet. 2016;387:907-16. 43. Clinical Resource, Comparison of Oral Iron Supplements. Pharmacist’s Letter/Prescriber’s Letter. March 2017. CPS. Ottawa (ON): Canadian Pharmacists Association; c2016. Iron Preparations: Oral [product monograph]. Available from http://www.myrxtx.ca (accessed March 2017). 44. RxFiles Drug Comparison Charts - 10th Edition. Saskatoon, SK: Saskatoon Health Region; 2014. Available from www.RxFiles.ca (accessed March 2017). 45. Powers et al., Effect of low dose ferrous sulfate vs iron polysaccharide complex in young children with nutritional deficiency anemia- a RCT. JAMA. 2017;317(22)2297-2304. 46. Stoffel N, et al. Iron absorption from oral iron supplements given on consecutive days vs alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women. Lancet Hematol. 2017;4:524-33. 47. Kroot J, Hendriks J, Laarakkers C, et al. (Pre)analytical imprecision, between-subject variability, and daily variations in serum and urine hepcidin: implications for clinical studies. Anal Biochem. 2009;389:124-9. 48. Iron Sucrose (Venofer©). In: Lexicomp Online Database [database on the Internet]. Hudson (OH): Lexicomp Inc.: publication year [updated 5 March 2018; cited 21 March 2018]. Available from: http://online.lexi. 49. Ferric Gluconate (Ferrlecit©). In: Lexicomp Online Database [database on the Internet]. Hudson (OH): Lexicomp Inc.: publication year [updated 26 Feb 2018; cited 21 March 2018]. Available from: http://online.lexi. 50. Iron Dextran (Dexiron©). In: Lexicomp Online Database [database on the Internet]. Hudson (OH): Lexicomp Inc.: publication year [updated 5 March 2018; cited 21 March 2018]. Available from: http://online.lexi. SUGGESTED CITATION Toward Optimized Practice Iron Deficiency Anemia Committee. 2018 March. Iron deficiency anemia clinical practice guideline. Edmonton, AB: Toward Optimized Practice. Available from: http://www.topalbertadoctors.org This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 2.5 Canada License with the exception of external content reproduced with permission for use by TOP. For more information see www.topalbertadoctors.org GUIDELINE COMMITTEE The committee consisted of representatives of anatomical pathology, emergency medicine, hematological pathology, internal medicine and primary care. March 2018 Iron Deficiency Anemia (IDA) | March 2018 These recommendations are systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances. They should be used as an adjunct to sound clinical decision making. Clinical Practice Guideline Page 20 of 21 Appendix B IRON TYPE FORMULATION (elemental iron) USUAL MAXIMUM ADULT DOSE COST ESTIMATE PER MONTH OF MAX DOSE (* indicates generic) CONSIDERATIONS Note: Retail pricing is accurate as of the date this guideline was written (2017). Pricing is provided based on a quote from an Alberta retail pharmacy and reflects one example of monthly costs. Pricing for oral supplements will vary depending on the amount prescribed and the specific pharmacy where the product is purchased. TIPS FOR OPTIMIZING ORAL IRON THERAPY  Calculation of dosage should always consider elemental iron content of product.  To maximize absorption, iron supplements should: o Be taken on an empty stomach with full glass of water or fruit juice, if appropriate (e.g., one hour before or two hours after meals). o Be taken in the morning or earlier in the day. (Iron absorption is decreased when Hepcidin levels are highest. Hepcidin peaks in the evening hours.)47 o Be taken with a supplement or dietary source of Vitamin C (e.g., fruit juice, oranges, tomatoes). o NOT be taken with Calcium products (e.g.: supplements, certain antacids) or foods (e.g., dairy products such as milk, cheese, yogurt). o NOT be taken with high-oxalate foods (e.g., coffee, tea, spinach, kale, broccoli).  Oral iron can cause nausea, vomiting, dyspepsia, constipation, diarrhea, metallic taste or dark stools. If your patient is experiencing GI based adverse effects, consider the following: o Start at a lower dose (e.g., one tablet once daily) and titrate up slowly (i.e., every four to five days). o Switch to liquid form for smaller dose titrations. o Switch to another preparation with less elemental iron. o Recommend taking iron with small snack or with meals (however food will decrease iron absorption by 40%). o Take at bedtime (however, iron absorption is lowest in evening when Hepcidin hormone levels are highest). o Could consider polysaccharide iron complex as an option however, it is more expensive and its effectiveness is no better than other iron salts.  For patient information on dietary sources of iron see: https://myhealth.alberta.ca/health/pages/condtions.aspx?hwid=ue4500&#ue4500-sec Iron Deficiency Anemia (IDA) | March 2018 These recommendations are systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances. They should be used as an adjunct to sound clinical decision making. Clinical Practice Guideline Page 21 of 21 Appendix C APPENDIX C IV IRON PREPARATIONS FOR ADULTS >18 YEARS (NOTE: CHILDREN <18 YEARS REFER TO PEDIATRIC HEMATOLOGY FOR IV IRON ASSESSMENT AND TREATMENT) Table 9: IV Iron Preparations Available in Alberta IRON TYPE USUAL DOSE  Calculate ‘Iron Deficit’ (total dose needed) using hemoglobin deficit equation.  Divide ‘Iron Deficit’ into appropriate individual doses.  Administer doses 1-2 times weekly until total dose complete (interval varies by product, check product monograph). COST ESTIMATE for 1000 mg (Note: drug cost only – not administration cost) CONSIDERATIONS Iron Sucrose (Venofer®) Ex: Total Iron Deficit 1000mg, consider: 200 mg IV x 5 doses48 $393.80  CAUTION: Dosages >300 mg are associated with increased risk adverse reaction due to iron overload. Ferric Gluconate Complex (Ferrlecit®) Ex: Total Iron Deficit 1000 mg, consider: 125 mg IV x 8 doses49 $453.60 Iron Dextran (Dexiron®) Ex: Total Iron Deficit 1000 mg, consider: 100 mg IV x 10 doses50 $297.69  REQUIRED: TEST DOSE (25 mg) and one hour observation before proceeding with first dose.  Only IV iron covered Alberta Health Drug Benefit List (AHDBL). Disclaimer: Above are general dosing examples. Consult product monograph for specific indicators, dosing and administration or when used in Alberta Health Services (AHS), refer to local protocols and parenteral monograph for more information. Parenteral iron should only be used by professionals familiar with dosing, administration and appropriate monitoring.