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Iron supplement
Iron supplement
Iron supplement
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Iron supplement
Iron supplement from the late 19th and early 20th century
Clinical data
Trade namesFeosol, Feostat, Feratab, others
Other namesIron pills, iron salts, ferrous salts, ferric salts
AHFS/Drugs.com
License data
Pregnancy
category
  • AU: B3
Routes of
administration		By mouth, intravenous, intramuscular
ATC code
Legal status
Legal status
Identifiers
CAS Number
ChemSpider
  • None

Iron supplements, also known as iron salts and iron pills, are a number of iron formulations used to treat and prevent iron deficiency including iron-deficiency anemia.[11][12] For prevention they are only recommended in those with poor absorption, heavy menstrual periods, pregnancy, hemodialysis, or a diet low in iron.[12][13] Prevention may also be used in low birth weight babies.[12] They are taken by mouth, injection into a vein, or injection into a muscle.[12] While benefits may be seen in days, up to two months may be required until iron levels return to normal.[14]

Common side effects include constipation, abdominal pain, dark stools, and diarrhea.[14] Other side effects, which may occur with excessive use, include iron overload and iron toxicity.[11][13] Ferrous salts used as supplements by mouth include ferrous fumarate, ferrous gluconate, ferrous succinate, and ferrous sulfate.[13] Injectable forms include iron dextran and iron sucrose.[13] They work by providing the iron needed for making red blood cells.[14]

Iron pills have been used medically since at least 1681, with an easy-to-use formulation being created in 1832 using chicken liver extracts and the majority from plants.[15] Ferrous salt is on the World Health Organization's List of Essential Medicines.[16] Ferrous salts are available as a generic medication and over the counter.[11] Slow-release formulations, while available, are not recommended.[12] In 2021, ferrous sulfate was the 105th most commonly prescribed medication in the United States, with more than 6 million prescriptions.[17][18]

Medical uses

[edit]

Iron supplements are used to treat or prevent iron deficiency and iron-deficiency anemia;[8] parenteral irons can also be used to treat functional iron deficiency, where requirements for iron are greater than the body's ability to supply iron such as in inflammatory states. The main criterion is that other causes of anemia have also been investigated, such as vitamin B12 or folate deficiency, drug induced or due to other poisons such as lead, as often the anemia has more than one underlying cause.[19]

Iron deficiency anemia is classically a microcytic, hypochromic anemia. Generally, in the UK oral preparations are trialled before using parenteral delivery,[20] unless there is a requirement for a rapid response, previous intolerance to oral iron, or likely failure to respond. Intravenous iron may decrease the need for blood transfusions however it increases the risk of infections when compared to oral iron.[21] Daily oral supplementation of iron during pregnancy reduces the risk of maternal anemia, and the effects on infant and other maternal outcomes are not clear.[22] Another review found tentative evidence that intermittent iron supplements by mouth for mothers and babies are similar to daily supplementation with fewer side effects.[23] Supplements by mouth should be taken on an empty stomach, optionally with a small amount of food to reduce discomfort.[24]

Athletes

[edit]

Athletes may be at elevated risk of iron deficiency and so benefit from supplementation, but the circumstances vary between individuals, and dosage should be based on tested ferritin levels, since in some cases supplementation may be harmful.[25]

Frequent blood donors

[edit]
Main article: Blood donation

Frequent blood donors may be advised to take iron supplements. Canadian Blood Services recommends discussing "taking iron supplements with your doctor or pharmacist" as "the amount of iron in most multivitamins may not meet your needs and iron supplements may be necessary".[26] The American Red Cross recommends "taking a multivitamin with 18 mg of iron or an iron supplement with 18–38 mg of elemental iron for 60 days after each blood donation, for 120 days after each power red donation or after frequent platelet donations".[27] A 2014 Cochrane Review found that blood donors were less likely to be deferred for low hemoglobin levels if they were taking oral iron supplements, although 29% of those who took them experienced side effects in contrast to the 17% who took a placebo. It is unknown what the long-term effects of iron supplementation for blood donors may be.[28]

Side effects

[edit]

Side effects of therapy with oral iron include diarrhea, constipation, or epigastric abdominal discomfort. Taken after a meal, side effects decrease, but there is an increased risk of interaction with other substances. Side effects are dose-dependent, and the dose may be adjusted.

The patient may notice that their stools become black. This is completely harmless, but patients must be warned about this to avoid unnecessary concern. When iron supplements are given in a liquid form, teeth may reversibly discolor (this can be avoided through the use of a straw). Intramuscular injection can be painful, and brown discoloration may be noticed.

Treatments with iron(II) sulfate have higher incidence of adverse events than iron(III)-hydroxide polymaltose complex (IPC)[29][30][31] or iron bis-glycinate chelate.[32][33]

Iron overdose has been one of the leading causes of death caused by toxicological agents in children younger than six years.[34]

Iron poisoning may result in mortality or short-term and long-term morbidity.[35]

Infection risk

[edit]

Because one of the functions of elevated ferritin (an acute phase reaction protein) in acute infections is thought to be to sequester iron from bacteria, it is generally thought that iron supplementation (which circumvents this mechanism) should be avoided in patients who have active bacterial infections. Replacement of iron stores is seldom such an emergency that it cannot wait for any such acute infection to be treated.

Some studies have found that iron supplementation can lead to an increase in infectious disease morbidity in areas where bacterial infections are common. For example, children receiving iron-enriched foods have demonstrated an increased rate in diarrhea overall and enteropathogen shedding. Iron deficiency protects against infection by creating an unfavorable environment for bacterial growth. Nevertheless, while iron deficiency might lessen infections by certain pathogenic diseases, it also leads to a reduction in resistance to other strains of viral or bacterial infections, such as Salmonella typhimurium or Entamoeba histolytica. Overall, it is sometimes difficult to decide whether iron supplementation will be beneficial or harmful to an individual in an environment that is prone to many infectious diseases; however this is a different question than the question of supplementation in individuals who are already ill with a bacterial infection.[36]

Children living in areas prone to malaria infections are also at risk of developing anemia. It was thought that iron supplementation given to such children could increase the risk of malaria infection in them. A Cochrane systematic review published in 2016 found high-quality evidence that iron supplementation does not increase the risk of clinical malaria in children.[37]

Contraindications

[edit]

Contraindications often depend on the substance in question. Documented hypersensitivity to any ingredients and anemias without proper work-up (i.e., documentation of iron deficiency) is true of all preparations. Some can be used in iron deficiency, others require iron deficiency anaemia to be present. Some are also contraindicated in rheumatoid arthritis.[7]

Hemochromatosis

[edit]

Individuals may be genetically predisposed to excessive iron absorption, as is the case with those with HFE hereditary hemochromatosis. Within the general population, 1 out of 400 people has the homozygous form of this genetic trait, and 1 out of every 10 people has its heterozygous form.[38] Neither individuals with the homozygous nor heterozygous form should take iron supplements.[38]

Interactions

[edit]

Non-heme iron forms an insoluble complex with several other drugs, resulting in decreased absorption of both iron and the other drug. Examples include tetracycline, penicillamine, methyldopa, levodopa, bisphosphonates, and quinolones. The same can occur with elements in food, such as calcium, which impacts both heme and non-heme iron absorption.[39] Absorption of iron is better at a low pH (i.e. an acidic environment), and absorption is decreased if there is a simultaneous intake of antacids.

Many other substances decrease the rate of non-heme iron absorption. One example is tannins from foods such as tea[40] and phytic acid.[41] Because iron from plant sources is less easily absorbed than the heme-bound iron of animal sources, vegetarians and vegans should have a somewhat higher total daily iron intake than those who eat meat, fish or poultry.[42][43]

Taken after a meal, there are fewer side effects, but there is also less absorption because of interaction and pH alteration. Generally, an interval of 2–3 hours between the iron intake and that of other drugs seems advisable, but is less convenient for patients and can impact compliance.

History

[edit]

The first pills were commonly known as Blaud's pills,[44] which were named after P. Blaud of Beaucaire, the French physician who introduced and started the use of these medications as a treatment for patients with anemia.[45]

Administration

[edit]

By mouth

[edit]
"Proferrin" redirects here. For the pupil dilator, see Prefrin.

Iron can be supplemented by mouth using various forms, such as iron(II) sulfate. This is the most common and well-studied soluble iron salt sold under brand names such as Feratab, Fer-Iron, and Slow-FE. It is in complex with gluconate, dextran, carbonyl iron, and other salts. Ascorbic acid, vitamin C, increases the absorption of non-heme sources of iron, but not to a clinically significant degree.[46]

Heme iron polypeptide (HIP) (e.g., Proferrin ES and Proferrin Forte) can be used when regular iron supplements such as ferrous sulfate or ferrous fumarate are not tolerated or absorbed. A clinical study demonstrated that HIP increased serum iron levels 23 times greater than ferrous fumarate on a milligram-per-milligram basis.[47]

Another alternative is ferrous glycine sulfate or ferroglycine sulfate, which has fewer gastrointestinal side effects than standard preparations such as iron fumarate.[48] [better source needed] It is unusual among oral preparations of iron supplements in that the iron in this preparation has very high oral bioavailability, especially in the liquid formulation. This option should be evaluated before resorting to parenteral therapy. It is especially useful in iron deficiency anemia associated with autoimmune gastritis and Helicobacter pylori gastritis, where it generally has a satisfactory effect.[49]

Since iron stores in the body are generally depleted, and there is a limit to what the body can process (about 2–6 mg/kg of body mass per day; i.e. for a 100 kg/220 lb man this is equal to a maximum dose of 200–600 mg/per day) without iron poisoning, this is a chronic therapy which may take 3–6 months.[50]

Due to the frequent intolerance of oral iron and the slow improvement, parenteral iron is recommended in many indications.[51][52]

Food fortification

[edit]

Fortified foods with iron such as breakfast cereals and wheat flour are effective in increasing hemoglobin levels and lowering prevalence of anemia and iron deficiency.[53][54][55] A 2021 Cochrane Review found that wheat flour fortified with iron may reduce anemia by 27%.[56] Fortified rice may increase haemoglobin concentrations and reduce iron deficiency in the general population but has not been found to reduce anemia.[57] In 2023, the World Health Organization recommended fortification of rice with iron as a public health strategy to improve the iron status of populations in regions where rice is a staple food.[58]

By injection

[edit]

Iron therapy (intravenously or intramuscular) is given when therapy by mouth has failed (not tolerated), oral absorption is seriously compromised (by illnesses, or when the person cannot swallow), benefit from oral therapy cannot be expected, or fast improvement is required (for example, prior to elective surgery).[59] Parenteral therapy is more expensive than oral iron preparations and is not suitable during the first trimester of pregnancy.[8]

There are cases where parenteral iron is preferable over oral iron. These are cases where oral iron is not tolerated, where the haemoglobin needs to be increased quickly (e.g. postpartum, postoperatively, post-transfusion), where there is an underlying inflammatory condition (e.g. inflammatory bowel disease) or renal patients, the benefits of parenteral iron far outweigh the risks.

Low-certainty evidence suggests that IBD-related anemia treatment with intravenous (IV) iron infusion may be more effective than oral iron therapy, with fewer people needing to stop treatment early due to adverse effects.[60] The type of iron preparation may be an important determinant of clinical benefit. Moderate-certainty evidence suggests response to treatment may be higher when IV ferric carboxymaltose, rather than IV iron sucrose preparation is used, despite very-low certainty evidence of increased adverse effects, including bleeding, in those receiving ferric carboxymaltose treatment.[60]

In many cases, use of intravenous iron such as ferric carboxymaltose has lower risks of adverse events than a blood transfusion and, as long as the person is stable, is a better alternative.[61] Ultimately this always remains a clinical decision based on local guidelines, although national guidelines are increasingly stipulating IV iron in certain groups of patients.[62][63]

A Cochrane Review of controlled trials comparing intravenous (IV) iron therapy with oral iron supplements in people with chronic kidney disease, found low-certainty evidence that people receiving IV-iron treatment were 1.71 times as likely to reach their target hemoglobin levels.[64] Overall, hemoglobin was 0.71g/dl higher than those treated with oral iron supplements. Iron stores in the liver, estimated by serum ferritin, were also 224.84 μg/L higher in those receiving IV-iron.[64] However, there was also low-certainty evidence that allergic reactions were more likely following IV-iron therapy. It was unclear whether the type of iron therapy administration affects the risk of death from any cause, including cardiovascular, or whether it may alter the number of people who may require a blood transfusion or dialysis.[64]

Soluble iron salts have a significant risk of adverse effects and can cause toxicity due to damage to cellular macromolecules. Delivering iron parenterally has utilised various molecules to limit this.[65] This has included dextrans, sucrose, carboxymaltose, ferumoxytol, derisomaltose and Isomaltoside 1000.[66]

One formulation of parenteral iron is iron dextran which covers the old high molecular weight (brand name Dexferrum) and the much safer low molecular iron dextrans (brand names including Cosmofer and Infed).[67]

Iron sucrose has an occurrence of allergic reactions of less than 1 in 1000.[68] A common side effect is taste changes, especially a metallic taste, occurring in between 1 in 10 and 1 in 100 treated patients.[68] It has a maximum dose of 200 mg on each occasion according to the SPC, but it has been given in doses of 500 mg. Doses can be given up to three times a week.[69]

Iron carboxymaltose is marketed as Ferinject,[8] Injectafer,[9][70] and Iroprem in various countries.[71] The most common side effects are headaches which occur in 3.3%, and hypophosphatemia, which occurs in more than 35%.[8][9]

Iron isomaltoside 1000 (brand name Monofer) is a formulation of parenteral iron that has a matrix structure that results in very low levels of free iron and labile iron. It can be given at high doses – 20 mg/kg in a single visit – with no upper dose limit. This formulation has the benefit of giving a full iron correction in a single visit.[72][71]

Ferric maltol, marketed as Accrufer[10] and Ferracru, is available in oral and intravenous preparations. When used as a treatment for IBD-related anemia, very low certainty evidence suggests a marked benefit with oral ferric maltol compared with placebo. However, it was unclear whether the IV preparation was more effective than oral ferric maltol.[60]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Iron supplement

View on Grokipedia
from Grokipedia
Iron supplements are dietary products containing elemental iron in various chemical forms, such as ferrous sulfate, ferrous gluconate, or ferrous fumarate, designed to prevent or treat and associated conditions like . Iron, an essential , plays a critical role in the production of protein in cells that transports oxygen throughout the body—and , which supports oxygen storage in muscles. These supplements are particularly recommended for populations at higher risk of deficiency, including pregnant women, menstruating individuals, infants, vegetarians, and those with issues or chronic loss. Available in oral forms like tablets, capsules, chewables, and liquids, iron supplements provide a concentrated source of the when dietary intake from foods such as , fortified cereals, beans, and leafy greens is insufficient. Recommended daily allowances vary by age, sex, and life stage—for instance, 8 mg for men, 18 mg for women aged 19–50, and 27 mg for pregnant women—with upper intake limits set at 45 mg per day for adults to avoid . Absorption is enhanced by and inhibited by calcium, fiber, or certain medications like antacids and inhibitors, so they are best taken on an empty with juice. Intravenous formulations exist for cases of poor oral tolerance or severe deficiency, such as in patients. Recent advancements as of 2025 include novel oral formulations, such as those combining iron with and prebiotics to enhance absorption and minimize gastrointestinal side effects, and new compounds that double . While effective in replenishing iron stores—often normalizing counts within two months and fully restoring reserves in six to twelve months—iron supplements commonly cause gastrointestinal side effects such as , , , and dark stools (due to unabsorbed iron), but do not cause skin pigmentation changes such as tanning, darkening, or hyperpigmentation. Skin darkening is associated with iron overload conditions like hemochromatosis, not with standard supplementation for iron deficiency. Overdose, especially in children, poses serious risks including organ damage and requires immediate attention. Monitoring through tests for , , and is essential, particularly for those with conditions like hemochromatosis, where is contraindicated. However, the use of iron supplements remains controversial in some settings, such as , due to potential risks including increased susceptibility to infections.

Overview

Definition and Types

Iron supplements are medicinal preparations containing iron or iron salts, formulated as oral or injectable products to address iron deficiencies. These supplements provide bioavailable iron to support essential physiological functions, such as oxygen transport via . The primary types of iron supplements are distinguished by their chemical form, particularly (divalent Fe²⁺) and ferric (trivalent Fe³⁺) irons. iron is directly absorbable in the , whereas ferric iron must undergo reduction to the state before absorption, potentially affecting . Among ferrous salts, ferrous sulfate is the most commonly prescribed, containing approximately 20% elemental iron by weight. gluconate, with about 12% elemental iron, is often preferred for its gentler effect on the due to lower iron content. Ferrous fumarate offers higher potency at around 33% elemental iron, allowing for smaller doses while delivering comparable iron amounts. Ferric forms include complexes like , a non-ionic preparation that is generally associated with reduced gastrointestinal upset compared to traditional salts. Other ferric options, such as ferric citrate, provide alternative profiles for those intolerant to compounds. These supplements are manufactured in diverse formats to enhance tolerability and convenience, including tablets, capsules, liquids, chewables, and extended-release versions that aim to reduce common side effects like .

Role of Iron in the Body

Iron is an essential trace mineral in the , playing critical roles in oxygen transport, energy production, and cellular protection. It serves as a central component of , the protein in red blood cells responsible for binding and transporting oxygen from the lungs to tissues throughout the body, and , which stores oxygen in muscle cells to support metabolic processes during . Beyond oxygen handling, iron functions as a cofactor in numerous enzymes vital for metabolic and defensive processes. In the , iron within facilitates the final step of , enabling efficient ATP production in mitochondria. Additionally, iron is integral to antioxidant enzymes such as and , which decompose and other to prevent oxidative damage to cells and tissues. The adult contains approximately 3–4 grams of iron, with about 60–70% incorporated into in circulating erythrocytes and 20–30% stored primarily as and in the liver, , and for release during times of increased demand. Daily iron requirements vary by age, sex, and physiological state to maintain these levels, with recommended dietary allowances of 8 mg per day for adult men and postmenopausal women, 18 mg per day for premenopausal women due to menstrual losses, and 27 mg per day during to support fetal development and maternal expansion. Iron is tightly regulated to prevent deficiency or excess, primarily through the liver-produced , which controls intestinal iron absorption and the release of iron from storage sites and macrophages by binding to and degrading , the sole cellular iron exporter.

Indications

Treatment of

(IDA) is characterized by insufficient iron availability for , leading to reduced production and impaired oxygen delivery. It is typically diagnosed through laboratory confirmation, including low serum ferritin levels below 30 ng/mL, decreased concentration (generally <13 g/dL in adult men and <12 g/dL in non-pregnant women), and transferrin saturation less than 16%. The primary treatment for IDA involves oral iron supplementation as the initial therapy for most patients with intact gastrointestinal absorption. Standard protocols recommend 100-200 mg of elemental iron per day, administered in divided doses (e.g., 60-100 mg two to three times daily) to optimize absorption and minimize side effects, preferably on an empty stomach with to enhance uptake. Response to therapy is monitored by an increase in reticulocyte count within 7-10 days, followed by a hemoglobin rise of approximately 1-2 g/dL every 3-4 weeks; full normalization of hemoglobin often occurs within 1-2 months, with continued treatment for 3-6 months to replenish iron stores. Oral iron therapy demonstrates high efficacy in uncomplicated IDA cases, when adherence is maintained and no underlying malabsorption or ongoing blood loss is present; however, complete repletion of iron stores may require additional months beyond hemoglobin normalization. In severe IDA, higher doses within the 100-200 mg elemental iron daily range may be used initially to accelerate recovery, but exceeding 200 mg per day is generally avoided to prevent potential toxicity and gastrointestinal intolerance.

Prevention in At-Risk Populations

Prophylactic iron supplementation is recommended for several high-risk populations to prevent iron deficiency and its consequences before anemia develops. Pregnant women are a primary group, as pregnancy increases iron demands due to expanded blood volume and fetal needs. The advises daily supplementation starting around the 12th week of gestation, providing 30–60 mg of elemental iron combined with 400 µg of folic acid to reduce the risk of maternal anemia. This approach is particularly crucial in regions with high anemia prevalence, where dietary iron intake may be insufficient. For vegetarians and vegans, who face elevated risks from the lower bioavailability of non-heme iron in plant-based foods, guidelines from the Institute of Medicine recommend increasing iron intake by 1.8 times the standard recommended dietary allowance to account for absorption differences, though routine supplementation is not universally mandated and monitoring is emphasized instead. Infants and young children in low-resource settings, especially those aged 6–23 months in areas where anemia prevalence is ≥40% or 24–59 months where prevalence is ≥20%, also benefit from preventive strategies. WHO guidelines endorse daily oral iron supplementation at doses of 10–12.5 mg elemental iron for infants 6–23 months and 30 mg for preschoolers 24–59 months, often for 3 months periodically, to address gaps in iron-rich complementary foods. These lower prophylactic doses, compared to therapeutic levels, aim to maintain iron stores without excess. In malaria-endemic areas, iron supplementation should be accompanied by malaria prevention and treatment measures. Niche groups such as athletes and frequent blood donors may require targeted monitoring and occasional supplementation due to heightened iron losses, though evidence is less robust for routine use. Evidence from systematic reviews supports these preventive measures. A Cochrane review of daily iron supplementation in pregnancy found it reduces the risk of maternal anemia by approximately 50% (RR 0.50, 95% CI 0.42–0.59) and low birth weight by approximately 16% (RR 0.84, 95% CI 0.75–0.94) compared to no supplementation or placebo. In children, supplementation has been shown to improve cognitive function, with studies indicating enhancements in intelligence test scores and development in iron-deficient populations, potentially averting long-term delays. Globally, anemia affects about 1.92 billion people, with 40% of children aged 6–59 months, 37% of pregnant women, and 30% of women aged 15–49 years impacted, underscoring the need for prevention. Public health programs in developing countries integrate prophylactic iron through national fortification initiatives and targeted supplementation to combat this burden. For instance, fortification of staple foods like flour and cereals with iron has been implemented in over 80 countries, often supported by organizations like the Food Fortification Initiative, leading to measurable declines in anemia rates among women and children. These efforts, combined with periodic supplementation campaigns, focus on vulnerable groups and have proven cost-effective in resource-limited areas.

Formulations and Administration

Oral Forms

Oral iron supplements are primarily delivered through non-invasive methods, including tablets, capsules, liquids, and effervescent forms, designed for ease of use and varying patient needs. Common preparations include ferrous sulfate tablets or capsules, where a standard 325 mg dose delivers 65 mg of elemental iron, making it a widely prescribed option for treating deficiency. Liquid formulations, such as those providing 15 mg of elemental iron per mL, are particularly suitable for pediatric patients to ensure accurate dosing and better tolerability. Effervescent tablets, often containing ferrous gluconate or similar salts, dissolve in water for consumption and appeal to individuals who struggle with swallowing solids. Dosing guidelines for adults typically involve 60-120 mg of elemental iron per day, divided into 1-3 administrations, preferably in the morning on an empty stomach to support uptake, with total daily intake tailored to deficiency severity. Co-administration with vitamin C, such as 250 mg of ascorbic acid or through sources like lemon juice, enhances iron uptake by reducing it to a more absorbable form. Strategies to improve patient compliance focus on minimizing side effects while maintaining efficacy. Recent randomized studies demonstrate that alternate-day dosing, such as 60-120 mg of elemental iron every other day, results in better gastrointestinal tolerance and higher fractional iron absorption compared to daily regimens, potentially increasing adherence. Extended-release formulations of ferrous sulfate or gluconate reduce peak concentrations in the gut, thereby lowering the incidence of nausea and constipation. Food fortification complements direct supplementation by incorporating iron into staple products like cereals and flour. Iron-fortified cereals often use electrolytic iron powder for stability during processing, while flours may employ sodium iron EDTA (NaFeEDTA), which offers 2-4 times higher bioavailability than ferrous sulfate in high-phytate meals, aiding absorption in populations with dietary inhibitors. For individuals with poor response or intolerance to oral forms, parenteral administration may be considered as an alternative.

Parenteral Forms

Parenteral iron formulations are indicated for the treatment of iron deficiency anemia in patients with malabsorption syndromes, such as inflammatory bowel disease (IBD) or post-bariatric surgery, where oral iron absorption is impaired. They are also used in cases of non-compliance with oral therapy, intolerance to oral iron, or severe anemia requiring rapid correction to avoid delays in hemoglobin restoration. While oral iron remains the first-line approach for most patients, parenteral administration is reserved for these specific scenarios under medical supervision. Several types of parenteral iron preparations are available, primarily administered intravenously (IV), with intramuscular (IM) options limited due to pain and inconsistent absorption. Key formulations include iron dextran, which is a high-molecular-weight complex associated with a risk of anaphylaxis; iron sucrose, a safer alternative with a concentration of 20 mg/mL; ferric carboxymaltose, allowing higher single doses up to 1000 mg for efficient repletion; ferumoxytol, which is compatible with magnetic resonance imaging (MRI) procedures due to its use as an off-label contrast agent; and , which permits high single doses up to 1000 mg with a low risk of hypersensitivity. The choice of formulation depends on patient factors, such as allergy history and need for rapid dosing, with non-dextran options generally preferred for lower hypersensitivity risks.
FormulationTrade NameConcentrationMax Single DoseKey Characteristics and Risks
Iron DextranINFeDVaries100 mgHigh-molecular-weight; risk of anaphylaxis; requires test dose.
Iron SucroseVenofer20 mg/mL400 mgSafer profile; lower anaphylaxis risk; suitable for chronic kidney disease.
Ferric CarboxymaltoseInjectaferVaries1000 mgAllows large single doses; minimal hypersensitivity.
FerumoxytolFerahemeUndiluted510 mgRapid administration; MRI-compatible; no test dose needed.
Ferric DerisomaltoseMonoferric100 mg/mL1000 mgHigh single-dose infusion (≥20 min for ≥50 kg); low hypersensitivity; no test dose.
Administration occurs via IV infusion, preferred for its reliability, or IM injection in select cases, with total iron dose calculated using the Ganzoni formula: total deficit (mg) = body weight (kg) × (target hemoglobin [g/dL] - actual hemoglobin [g/dL]) × 2.4 + 500 mg for iron stores (for patients >35 kg). IV infusions are typically diluted and given over 15 minutes to several hours, depending on the formulation and dose, to minimize infusion-related reactions. Protocols emphasize safety: a test dose is required for iron dextran to screen for , administered as 0.5 mL IV followed by observation. For all IV administrations, patients should be monitored for , especially during the first few minutes of infusion, with checked periodically and resuscitation equipment available. Post-administration, and iron studies are reassessed after 2-4 weeks to evaluate response.

Absorption and Bioavailability

Mechanisms of Absorption

Iron absorption from supplements predominantly occurs in the and proximal , where enterocytes facilitate the uptake of non-heme iron, the primary form found in these preparations. Supplemental iron is typically administered in the (Fe²⁺) form, which is directly transported into enterocytes through the divalent metal transporter 1 (DMT1). Ferric iron (Fe³⁺) formulations, if present, require reduction to the more soluble form at the apical of duodenal enterocytes. This reduction is catalyzed by the ferric reductase duodenal cytochrome B (Dcytb), enabling subsequent transport into the cell. The ferrous iron then enters the enterocytes through the divalent metal transporter 1 (DMT1), a proton-coupled located on the apical that facilitates iron uptake alongside ions. Once inside the , iron can either be stored as or exported across the basolateral via , the sole known iron exporter in mammals. Export is coupled with oxidation back to Fe³⁺ by the ferroxidase , allowing binding to plasma for systemic circulation. Absorption is tightly regulated by , a liver-derived that binds to , inducing its internalization and degradation, thereby inhibiting iron export from enterocytes and macrophages. In states of , hepcidin levels decrease, enhancing ferroportin activity and allowing greater iron absorption, which can reach up to 20-25% of the ingested dose from non-heme sources. Circulating ferric iron binds to in the plasma, forming diferric transferrin, which is transported to tissues with high iron demand, such as the . There, it is internalized by erythroid precursors via transferrin receptor 1 (TfR1)-mediated , where iron is released in acidic endosomes for synthesis. Iron supplements provide non-heme iron, which is absorbed with an efficiency of approximately 10-15% under typical conditions, though this increases in deficiency; in contrast, heme iron from animal sources like meat is absorbed more efficiently at 15-35%.

Factors Influencing Efficacy

The efficacy of iron supplements is significantly influenced by dietary enhancers, such as , which facilitates non-heme iron absorption by reducing ferric iron (Fe³⁺) to (Fe²⁺) and forming soluble chelates that remain stable across varying pH levels in the . Studies have shown that consuming approximately 25-100 mg of with a can approximately double the percentage of non-heme iron absorbed compared to iron taken alone. This enhancement is particularly beneficial for overcoming certain dietary inhibitors when vitamin C is ingested simultaneously with the supplement. In contrast, several inhibitors can substantially reduce iron bioavailability, including phytates found in grains and , polyphenols present in and , and calcium from products, which form insoluble complexes with iron in the gut. For instance, co-ingestion of or with iron-containing meals can decrease non-heme iron absorption by more than 50%, while high-phytate diets may inhibit absorption by up to 60-90% depending on the dose and meal composition. To maximize efficacy, it is recommended to avoid consuming these inhibitors concurrently with iron supplements, allowing at least a one-hour separation. Physiological factors also play a critical role; during , elevated levels—a liver-derived —suppress intestinal iron absorption by degrading , the primary iron exporter on enterocytes, often reducing fractional absorption to less than 5-10% even in iron-deficient states. Additionally, adequate gastric acidity is essential for iron solubilization and reduction, and its impairment by inhibitors (PPIs) can decrease absorption by altering duodenal and indirectly upregulating . Long-term PPI use has been associated with lower levels and increased risk of deficiency. Patient compliance and dosing regimen further determine therapeutic outcomes, as poor adherence—often due to gastrointestinal side effects—can substantially reduce overall in real-world settings. Recent studies from the indicate that intermittent dosing (e.g., alternate-day administration of 60 mg elemental iron) achieves comparable improvements in serum levels to daily dosing while potentially enhancing absorption by minimizing elevation from frequent intake. This approach may improve long-term adherence and in treating . The physical form of oral iron supplements (tablets versus liquids) generally has a limited impact on absorption rates and bioavailability, with similar overall effectiveness observed for both. Differences are primarily determined by the specific iron compound (e.g., ferrous sulfate, gluconate, or bisglycinate) and formulation characteristics rather than the physical form itself. Conventional-release ferrous sulfate tablets often demonstrate high absorption in studies, whereas some liquid forms (such as certain syrups) may exhibit lower bioavailability, potentially due to excipients or inhibitors in specific products. Newer formulations, such as liposomal and sucrosomial iron, have demonstrated enhanced exceeding 80-90% in clinical studies as of 2025, potentially offering improved and reduced side effects compared to traditional iron salts.

Adverse Effects

Common Gastrointestinal Issues

Oral iron supplements commonly cause gastrointestinal side effects, affecting 30% to 70% of users and often leading to reduced treatment compliance. These effects include (reported in about 11% of cases), (around 12%), (approximately 8%), , dark stools, and a metallic in the . Both tablet and liquid forms of oral iron supplements can cause similar gastrointestinal side effects, including constipation, nausea, stomach cramps, and dark stools, though some individuals tolerate liquid forms better, especially if they have sensitive stomachs or difficulty swallowing pills. Standard oral iron supplements do not cause skin tanning, darkening, hyperpigmentation, or other pigmentation changes; these effects are associated with chronic iron overload conditions (e.g., hemochromatosis), not typical therapeutic supplementation for iron deficiency. Dark stools are common due to unabsorbed iron but do not involve skin color changes. The primary cause of these issues is direct of the gastrointestinal mucosa by unabsorbed iron, which remains in the gut lumen and can lead to local . This is dose-dependent, with higher doses increasing the risk and severity of symptoms such as and abdominal discomfort. To manage these side effects, taking iron supplements with can improve tolerance, although it may slightly reduce absorption. Lower doses or administration on alternate days may also minimize while maintaining . Switching to ferrous bisglycinate, a chelated form of iron, is often better tolerated due to reduced gastrointestinal upset compared to traditional salts. For constipation specifically, mitigation strategies include using stool softeners such as sodium, increasing hydration to at least 8 ounces of fluid per dose, and incorporating fiber-rich foods into the diet to soften stools and promote regularity.

Serious Risks and Overdose

Excess iron from supplementation can promote by providing a essential for proliferation, particularly in the gut following or at intravenous sites. Observational studies have linked iron supplementation to increased rates, including higher susceptibility to bacterial infections such as in children receiving oral iron and elevated risks of infections in hospitalized patients treated with intravenous iron. Acute iron overdose, typically from ingestion exceeding 60 mg/kg of elemental iron, can lead to severe manifesting as gastrointestinal hemorrhage, , and . The estimated lethal dose (LD50) for elemental iron is approximately 200-250 mg/kg, though systemic effects may occur at lower thresholds around 60-120 mg/kg. Treatment involves gastrointestinal decontamination, supportive care, and with to bind and excrete excess iron. Chronic iron overload from prolonged supplementation can induce oxidative stress through the generation of reactive oxygen species, contributing to long-term risks such as via endothelial damage and promotion of . Additionally, excess iron has been associated with increased cancer risk, particularly in states of hepatic iron accumulation, due to oxidative damage and inflammatory pathways. Skin darkening or bronze pigmentation is a characteristic feature of chronic iron overload in hereditary hemochromatosis and similar conditions, but is not a consequence of typical therapeutic doses of iron supplements used to treat iron deficiency. Intravenous iron formulations carry specific risks, including rare with an incidence estimated at less than 1 in 250,000 administrations for iron sucrose, potentially mediated by immune complex formation or complement activation. may also occur during infusion, often self-limited but requiring monitoring to distinguish from reactions.

Contraindications and Precautions

Iron supplementation is absolutely contraindicated in hereditary hemochromatosis, a genetic disorder characterized by excessive intestinal iron absorption due to mutations in the HFE gene, most commonly the C282Y homozygote or C282Y/H63D compound heterozygote variants. These mutations impair hepcidin regulation, leading to progressive iron accumulation in parenchymal tissues, particularly the liver, where it exacerbates fibrosis, cirrhosis, and hepatocellular carcinoma risk. Additionally, iron overload in hemochromatosis contributes to arthropathy, with deposition in synovial tissues causing joint pain, stiffness, and degeneration resembling osteoarthritis, often affecting the metacarpophalangeal joints. Screening for hemochromatosis typically involves measuring serum ferritin levels, with values exceeding 1000 ng/mL indicating significant overload and warranting avoidance of iron supplements to prevent further organ damage. Patients with this condition should strictly avoid iron-containing multivitamins or supplements, as they accelerate iron loading and clinical complications. Other rare genetic conditions also prohibit iron supplementation due to inherent risks of overload. , prevalent in sub-Saharan African populations, involves a distinct pattern of iron accumulation influenced by genetic factors and environmental exposures like traditional consumption, leading to hepatic without typical HFE mutations; supplemental iron would intensify parenchymal deposition and associated morbidity. Hypotransferrinemia, caused by mutations in the TF gene resulting in deficient or dysfunctional , similarly predisposes individuals to severe from birth, with unrestricted absorption causing paradoxically alongside tissue deposition; iron therapy is contraindicated as it worsens hepatic and cardiac iron burden without addressing the underlying transport defect. Disease-related contraindications extend to conditions where supplemental iron could promote harm. In active bacterial infections, iron acts as a for pathogens, enhancing and by supporting replication and production; supplementation should generally be avoided to reduce the risk of exacerbating or , though clinical judgment is required. For major, a requiring frequent transfusions, patients already face transfusion-related , with elevated levels reflecting secondary hemochromatosis; oral or parenteral iron is contraindicated in most cases to prevent further accumulation that heightens risks of endocrinopathies, , and . As a general rule, iron supplementation should be absolutely avoided in individuals without confirmed deficiency if serum exceeds 300 ng/mL in men or 200 ng/mL in women, as these thresholds signal potential overload and contraindicate further iron intake to mitigate risks of and organ injury.

Monitoring and Precautions

Before initiating iron supplementation, clinicians should obtain baseline assessments including a (CBC), serum , and (TSAT) to confirm and establish a reference for treatment response. Follow-up testing, typically involving repeat CBC, , and TSAT, is recommended 4-8 weeks after starting therapy to evaluate efficacy, with an expected hemoglobin increase of at least 1 g/dL if is present. Supplementation should be discontinued if there is no hematologic response after this period or if levels exceed 150-200 ng/mL in women, indicating replete iron stores and a risk of overload. Special precautions are necessary for certain populations to minimize risks during iron therapy. In elderly patients, lower doses are advised due to heightened vulnerability to and adverse effects from standard regimens, necessitating closer monitoring of iron parameters. For individuals with (IBD), due to mucosal and elevated may reduce oral iron efficacy, often requiring dose adjustments, alternative formulations, or a shift to intravenous administration. Iron supplements should generally be avoided during the first trimester of unless deficiency is confirmed, as they may exacerbate and . Patient education is essential for safe use and early recognition of issues. Black or dark stools are a common and harmless side effect of oral iron due to unabsorbed portions, but patients should promptly report severe gastrointestinal symptoms such as persistent vomiting, abdominal pain, or tarry black stools, which may signal complications. To prevent accidental overdose—a leading cause of poisoning in children—iron supplements must be stored securely out of reach, as even small amounts can be toxic. Current guidelines from the (AAFP), aligning with U.S. Preventive Services Task Force recommendations, advise against routine screening for in asymptomatic adults, emphasizing targeted testing for those with risk factors instead.

Interactions

Drug Interactions

Iron supplements can interact with various medications, primarily by altering absorption through changes in gastrointestinal pH or , thereby reducing the efficacy of either the iron or the co-administered drug. Medications that reduce gastric acidity, such as antacids, inhibitors (PPIs), and H2-receptor blockers, impair iron solubilization and absorption by decreasing levels necessary for iron to remain in a bioavailable form. To minimize this interaction, iron supplements should be taken at least 2 hours before or after these acid-reducing agents. Certain antibiotics, including tetracyclines and quinolones, form chelates with iron, which significantly reduces the absorption of both the antibiotic and the iron supplement. For example, co-administration with can decrease its by more than 50%. Dosing separation of 2 to 4 hours is recommended to avoid these effects. Iron supplements may also decrease the absorption of other drugs such as levodopa, methyldopa, and by forming complexes that hinder their uptake in the . Spacing administration by at least 2 hours can help mitigate reduced efficacy of these medications.

Dietary Interactions

Certain dietary components can significantly inhibit the absorption of iron from supplements, particularly non-heme iron, which is the form found in most oral supplements. Calcium, present in products such as and cheese, binds to iron in the , forming insoluble complexes that reduce . Zinc, when taken simultaneously as a supplement, can compete with iron for absorption sites in the intestine, potentially reducing the bioavailability of both minerals. Polyphenols like in and are potent inhibitors; for instance, consuming a cup of coffee with a meal can decrease iron absorption by approximately 60%, while may reduce it by up to 80%. Similarly, phytates found in high-fiber foods such as whole grains, , and cereals chelate iron, limiting its uptake, especially in plant-based diets. In contrast, specific foods can enhance iron absorption when consumed alongside supplements. , abundant in fruits like , acts as a and chelator, increasing non-heme iron absorption by up to fourfold in a dose-dependent manner. The , , and (MFP) factor, consisting of certain peptides and in animal proteins, also promotes non-heme iron uptake by counteracting inhibitors and facilitating in the gut. To optimize absorption, timing of iron supplements relative to meals is crucial. Supplements should ideally be taken on an empty or at least 1-2 hours before or after consuming foods high in inhibitors like , , , or high-fiber items to minimize interference. Individuals following vegetarian diets, which lack iron and contain more inhibitors, require approximately 1.8 times the recommended iron intake to compensate for lower .

History and Guidelines

Historical Development

The use of iron in medicinal contexts dates back to ancient civilizations, where it was employed to address symptoms resembling anemia. Around 1500 BCE, ancient Egyptians therapeutically administered iron preparations, including iron salts and powders, to treat conditions characterized by pallor, weakness, and fatigue indicative of iron deficiency. This early recognition of iron's role in vitality laid foundational groundwork for later therapeutic applications, though mechanisms were not understood at the time. In the 17th through 19th centuries, iron supplementation gained prominence in European medicine, particularly for treating —a condition affecting adolescent girls, now recognized as (IDA). French physician Blaud introduced "Blaud's pills" in 1832, consisting of ferrous sulfate combined with , which proved effective in restoring levels within weeks to months for chlorosis patients. These oral formulations marked a significant advancement, becoming a standard treatment for and remaining in use for nearly two centuries due to their efficacy and accessibility. By the mid-19th century, iron therapy had shifted chlorosis from a vaguely defined "hysterical" disorder to a nutritional deficiency, supported by clinical observations of improved blood coloration and energy. The saw innovations in iron delivery methods, driven by wartime needs and advances in understanding risks. Intravenous (IV) iron dextran was developed in the early 1950s, initially to address severe and in post-World War II recovery efforts, offering a bypass for gastrointestinal absorption issues. Concurrently, in the 1930s, clinicians began recognizing the dangers of excessive iron accumulation, identifying hemochromatosis as a linked to , which prompted cautious dosing protocols to prevent hepatic and cardiac complications. More recent developments have focused on safer and more efficient IV formulations. Ferric carboxymaltose received approval in in 2007, enabling higher-dose infusions with reduced hypersensitivity risks compared to earlier dextran products, facilitating rapid correction of IDA in patients intolerant to oral iron. In the , studies demonstrated the benefits of evidence-based intermittent dosing regimens, such as alternate-day oral supplementation, which enhanced fractional iron absorption by minimizing elevation and gastrointestinal side effects relative to daily dosing.

Current Recommendations

The (WHO) recommends universal daily iron supplementation of 30-60 mg elemental iron for pregnant women to prevent maternal and support fetal development, regardless of levels. Similarly, the Centers for Disease Control and Prevention (CDC) endorses routine screening in children at ages 9-12 months and again at 15-18 months, particularly in high-risk groups, to identify early and initiate supplementation as needed. For populations with prevalence exceeding 20% in children or pregnant women, WHO guidelines advocate iron of staple foods or home with multiple powders to address widespread deficiencies at a level. The U.S. Preventive Services Task Force (USPSTF) issued an I statement in 2006, concluding that the current evidence is insufficient to assess the balance of benefits and harms of screening for in pregnant women and in children aged 6 to 12 months; this applies to asymptomatic pregnant women but does not specifically address non-pregnant adults, for whom no dedicated USPSTF recommendation exists, with no major updates by 2023. In pediatric care, the (AAP) recommends 3-6 mg/kg/day of elemental iron for treating (IDA) in infants and young children, divided into 1-3 doses, while advising against routine supplementation in low-risk, formula-fed infants beyond fortified sources to avoid unnecessary exposure. Recent guidelines emphasize oral iron as the first-line for most cases of due to its efficacy, low cost, and non-invasive nature, reserving intravenous (IV) iron for refractory cases, intolerance to oral forms, or conditions impairing absorption, such as . In 2024 updates, including those from the American Gastroenterological Association (AGA) and the November 2024 public review draft of the Kidney Disease: Improving Global Outcomes (KDIGO) guideline on in , there is heightened focus on monitoring for through serial and assessments during long-term supplementation, particularly in patients with inflammation, where hepcidin-mediated absorption issues may complicate dosing and increase overload risks if not vigilantly tracked. As of November 2025, the final KDIGO guideline remains pending publication.

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