Of the various iron salts available, ferrous sulfate is the one most commonly used. Although the traditional dosage of ferrous sulfate is mg 65 mg of elemental iron orally three times a day, lower doses eg, mg of elemental iron daily may be as effective and cause fewer side effects. To promote absorption, patients should avoid tea and coffee and may take vitamin C units with the iron pill once daily. However, a study by Moretti et al suggests that the standard dosing of iron supplements may be counterproductive.
Their research focuses on the role of hepcidin, which regulates systemic iron balance, partly in response to plasma iron levels. They found that when a large oral dose of iron is taken in the morning, the resulting increase in the plasma iron level stimulates an increase in hepcidin, which in turn will interfere with the absorption of an iron dose taken later in the day; indeed, suppression of iron absorption could last as long as 48 hours. With increasing doses, study subjects showed an increase in the absolute amount of iron absorbed, but a decrease in the fraction of the dose that was absorbed.
A six-fold increase in iron dose from 40 mg to mg resulted in only a three-fold increase in iron absorbed. In another part of the study, total iron absorbed from a morning and an afternoon dose on one day plus a morning dose the next day was not significantly greater than absorption from two consecutive morning doses. Moretti et al concluded that providing lower dosages and avoiding twice-daily dosing will maximize fractional iron absorption. They note that although the short-term effects observed in their study will require confirmation in longer-term studies, their results support supplementation with mg of iron taken every other day.
A possible additional benefit of this schedule may be that improving absorption will reduce gastrointestinal exposure to unabsorbed iron and thereby reduce adverse effects from supplements. Stoffel et al also concluded that alternate-day dosing of oral iron supplements may be preferable because it sharply increases fractional iron absorption. Claims are made that other iron salts eg, ferrous gluconate are absorbed better than ferrous sulfate and have less morbidity. Generally, the toxicity is proportional to the amount of iron available for absorption. If the quantity of iron in the test dose is decreased, the percentage of the test dose absorbed is increased, but the quantity of iron absorbed is diminished.
Each tablet of ferric citrate 1 gram is equivalent to mg of ferric iron. Approval was based on results from a week placebo-controlled phase 3 clinical trial in adults with stage non—dialysis-dependent CKD. Trial participants had hemoglobin levels of The starting dose in the study was 3 tablets daily with meals; the mean dose was 5 tablets per day.
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Importantly, during the study, patients were not allowed to receive any intravenous or oral iron, or erythropoiesis-stimulating agents ESAs. Decreased gastric toxicity is claimed but not clearly demonstrated in human trials. In July , the FDA approved ferric maltol Accrufer for treatment of iron deficiency anemia in adults. Under the brand name Feraccru, ferric maltol is approved in the European Union for treatment in adults and in Switzerland for treatment in adults with inflammatory bowel disease IBD.
Ferric maltol improved Hb from baseline by 2. Further analysis and peer review of this study are in progress as of July Ferric maltol is an alternative to IV iron for patients that cannot tolerate salt-based oral iron therapies and wish to avoid parenteral treatment.
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The authors suggest that, "Day Hb may be a useful tool for clinicians in determining whether and when to transition patients from oral to IV iron. Reserve parenteral iron for patients who are either unable to absorb oral iron or who have increasing anemia despite adequate doses of oral iron. It is expensive and has greater morbidity than iron preparations taken orally. In July , the FDA approved ferric carboxymaltose injection Injectafer for the intravenous treatment of iron deficiency anemia in adults who either cannot tolerate or have not responded well to oral iron.
The drug is also indicated for the treatment of iron deficiency anemia in adults with non—dialysis-dependent CKD. A review of the safety of IV iron preparations, particularly in patients with CKD, by Kalra and Bhandari concluded that high molecular weight iron dextrans are associated with increased risks, so their use for IV therapy should be avoided. The second- and third-generation IV irons are considered equally efficacious in treating iron deficiency in equivalent doses, but iron isomaltoside seems to have a lower frequency of serious and severe hypersensitivity reactions.
Feraheme ferumoxytol injection , a hematinic, was initially approved by the FDA in to treat iron deficiency anemia in adults with CK. Ferumoxytol injection consists of a superparamagnetic iron oxide that is coated with a carbohydrate shell, which helps isolate the bioactive iron from plasma components until the iron-carbohydrate complex enters the reticuloendothelial system macrophages of the liver, spleen, and bone.
The released iron then either enters the intracellular storage iron pool eg, ferritin or is transferred to plasma transferrin for transport to erythroid precursor cells for incorporation into hemoglobin. In January , the FDA expanded the indication for ferumoxytol injection to include all eligible adults with iron deficiency anemia who have intolerance or unsatisfactory response to oral iron. Expanded approval was based on data from two phase 3 trials comparing ferumoxytol and iron sucrose, as well as data from a phase 3 trial comparing ferumoxytol with ferric carboxymaltose injection.
Ferumoxytol was effective and well tolerated in patients with iron deficiency anemia of any underlying cause in whom oral iron was ineffective or could not be used. Surgical treatment consists of stopping hemorrhage and correcting the underlying defect so that it does not recur. This may involve surgery for treatment of either neoplastic or nonneoplastic disease of the gastrointestinal GI tract, the genitourinary GU tract, the uterus, and the lungs.
On a worldwide basis, diet is the major cause of iron deficiency. However, to suggest that iron-deficient populations correct the problem by the addition of significant quantities of meat to their diet is unrealistic. The addition of nonheme iron to national diets has been initiated in some areas of the world. Problems encountered in these enterprises include changes in taste and appearance of food after the addition of iron and the need to supplement foodstuffs that are consumed by most of the population in predictable quantities.
In addition, many dietary staples, such as bread, contain iron chelators that markedly diminish the absorption of the iron supplement phosphates, phytates, carbonates, oxalates, tannates. In North America and Europe, persons on an iron-poor diet need to be identified and counseled on an individual basis.
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Patients who have diet-related iron deficiency due to pica need to be identified and counseled to stop their consumption of clay and laundry starch. Patients with moderately severe iron deficiency anemia and significant cardiopulmonary disease should limit their activities until the anemia is corrected with iron therapy. If these patients become hypoxic or develop evidence of coronary insufficiency, they should be hospitalized and placed on bed rest until improvement of their anemia can be accomplished by transfusion of packed RBCs.
Obviously, such decisions must be made on an individual basis and will depend on the severity of the anemia and the comorbid conditions. March hemoglobinuria can produce iron deficiency, and its treatment requires modification of activity. Cessation of jogging or wearing sneakers while running usually diminishes the hemoglobinuria. Certain populations are at sufficiently high risk for iron deficiency to warrant consideration for prophylactic iron therapy. These include pregnant women, women with menorrhagia, [ 34 ] consumers of a strict vegetarian diet, infants, [ 35 ] adolescent girls, and regular blood donors.
Pregnant women have been given supplemental iron since World War II, often in the form of all-purpose capsules containing vitamins, calcium, and iron. The practice of routinely administering iron to pregnant females in affluent societies has been challenged. Nevertheless, providing prophylactic iron therapy during the last half of pregnancy continues to be advisable, except in settings where careful follow-up for anemia and methods for measurement of serum iron and ferritin are readily available.
Iron supplementation of the diet of infants is advocated. Premature infants require more iron supplementation than term infants. Infants weaned early and fed bovine milk require more iron because the higher concentration of calcium in cow milk inhibits absorption of iron. Usually, infants receive iron from fortified cereal. Additional iron is present in commercial milk formulas. Iron supplementation in populations living on a largely vegetarian diet is advisable because of the lower bioavailability of inorganic iron than heme iron.
The addition of iron to basic foodstuffs in affluent nations where meat is an important part of the diet is of questionable value and may be harmful. Excess body iron is postulated to be important in the etiology of coronary artery disease, strokes, certain carcinomas, and neurodegenerative disorders because iron is important in free radical formation. Surgical consultation often is needed for the control of hemorrhage and treatment of the underlying disorder. In the investigation of a source of bleeding, consultation with certain medical specialties may be useful to identify the source of bleeding and to provide control.
Among the medical specialties, gastroenterology is the most frequently sought consultation.
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Endoscopy has become a highly effective tool in identifying and controlling GI bleeding. If bleeding is brisk, angiographic techniques may be useful in identifying the bleeding site and controlling the hemorrhage. Radioactive technetium labeling of autologous erythrocytes also is used to identify the site of bleeding. Monitor patients with iron deficiency anemia on an outpatient basis to ensure that there is an adequate response to iron therapy and that iron therapy is continued until after correction of the anemia to replenish body iron stores.
Follow-up also may be important to treat any underlying cause of the iron deficiency. Response to iron therapy can be documented by an increase in reticulocytes days after the initiation of iron therapy. These responses are blunted in the presence of sustained blood loss or coexistent factors that impair hemoglobin synthesis. Med Clin North Am. JAMA Cardiol. Iron deficiency, anemia, and mortality in renal transplant recipients. Transpl Int.
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Treatment of primary defective iron-reutilization syndrome: revisited. Ann Hematol. Besa EC.
Hematologic effects of androgens revisited: an alternative therapy in various hematologic conditions. Semin Hematol. Epidemiology of iron deficiency anaemia in four European countries: a population-based study in primary care. Eur J Haematol. Pan Afr Med J. Brooks M. Medscape Medical News. Accessed: July 2, Association between psychiatric disorders and iron deficiency anemia among children and adolescents: a nationwide population-based study.