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A Review of Treatment Recommendations for Iron Deficiency Anemia in Inflammatory Bowel Disease


Crohn's disease (CD) and ulcerative colitis (UC) are the 2 chronic inflammatory conditions of the gastrointestinal (GI) tract that comprise inflammatory bowel disease (IBD). Each has distinct characteristics, but both CD and UC have strong negative impacts on quality of life. IBD has a bimodal age of onset: diagnosis most commonly occurs between the ages of 15 and 30 years or 60 and 80 years.1 Globally, IBD occurs most frequently in developed countries in North America and Western Europe; the highest incidences occur in the United States (U.S.), Canada, Europe, and the United Kingdom. Interestingly, IBD is more common in northern climates than southern climates and in urban areas than rural areas.1,2,3

In the U.S., IBD affects approximately 1 to 1.3 million people.4 While the majority of symptoms and complications are related directly to the disease affecting the GI tract, extraintestinal complications also occur, with anemia being one of the most prevalent. Iron deficiency is one of the leading causes of anemia for patients with IBD.5,6 This article will discuss the prevalence and risk factors of iron deficiency anemia (IDA) among patients with IBD, highlight the goals and current recommendations for the treatment of IDA, discuss key factors in selecting intravenous (IV) iron regimens, review monitoring parameters for iron supplementation, and discuss patient-related barriers and the pharmacist's role in the management of IDA for patients with IBD.

The prevalence of anemia is consistently reported to be greater than 50% in patients with IBD5; however, the exact prevalence is difficult to estimate because of variations in patient characteristics. For example, anemia is more common for patients with CD and/or active disease than for those with UC and/or inactive disease. Therefore, anemia is more frequently reported in the hospital setting than in the outpatient setting.5,6 For this reason, anemia prevalence rates have been reported to be as low as 6% and as high as 78%, depending on the patient population studied. Anemia is a complex, multifactorial morbidity of IBD that is, in large part, caused by iron deficiency followed by anemia of chronic disease. Additionally, adverse reactions related to IBD treatments, such as sulfasalazine and thiopurines, hemolysis, and myelodysplastic syndrome can also contribute to anemia for patients with IBD.7Sulfasalazine can lead to hemolytic anemia, especially for patients with glucose-6-phosphate dehydrogenase deficiency. Thiopurines such as azathioprine and 6-mercaptopurine can cause profound myelosuppression, especially for patients with thiopurine methyltransferase deficiency.8 Additional causes of anemia that are particularly relevant for patients with CD include decreased folate and vitamin B12 absorption and extensive bowel resection. Furthermore, many of these factors often overlap, complicating the clinical scenario for patients with IBD and anemia.7

IDA is the most common type of anemia in patients with IBD. Some studies report that iron deficiency is the cause of 30% of the cases of anemia in patients with IBD, but other studies report that iron deficiency causes as many as 90% of cases.5 This variation may be partially attributable to complications involving anemia for those with chronic disease, which often occurs concurrently with iron deficiency in patients with IBD.

Patients with IBD and IDA frequently report chronic fatigue, leading to decreased work capacity and poor quality of life.5,9 Patients also report other symptoms, such as decreased functional capacity, headaches, vertigo, tachycardia, exertional dyspnea, and dyspnea at rest.10 Moreover, IDA has been linked to IBD complications and even death.5

Iron deficiency is caused by an inadequate supply of iron to the bone marrow when iron stores are depleted.11 In IBD, this can occur as a result of continuous blood loss from the ulcerated bowel, malnutrition with reduced iron intake, or impaired iron absorption across the duodeno-jejunal mucosa.12 IDA is diagnosed when there is biochemical evidence of iron deficiency in the setting of low hemoglobin. IDA is typically diagnosed in IBD patients who are either hospitalized from complications associated with their disease and/or with increased inflammation occurring with active disease.

Despite knowing the high prevalence of risk factors and complications IDA can cause for patients with IBD, historically, many clinicians have ignored anemia treatment because they viewed anemia as an inevitable complication of IBD.7 This view may have been supported by the challenging side effects associated with oral iron administration, as well as the safety challenges associated with the older IV iron formulations. With the appropriate use of iron supplementation, IDA in patients with IBD can be treated and, hopefully, result in improved outcomes and improved quality of life.


Understanding general concepts in iron physiology, transport, and storage in the human body aids in understanding how IDA is assessed in clinical practice. The body stores about 3500 mg of iron: approximately 2300 mg is stored in hemoglobin—a protein inside red blood cells. Other storage sites include the macrophages (500 mg), muscle fibers (350 mg), the liver (200 mg), and bone marrow (150 mg). The body loses 1 to 2 mg of iron each day, and GI absorption in the duodenum is the only way the body maintains iron homeostasis.10 The average daily diet contains roughly 15 to 20 mg of elemental iron.9 Once absorbed, iron is stored inside the mucosal cells by ferritin, the intracellular iron storage protein. Iron is then transported out of the cells and bound to transferrin, the iron plasma binding protein, in order to be delivered to other cells for storage or to the bone marrow where erythropoiesis occurs. Ferritin concentrations are directly correlated with iron content inside the mucosal cells and, therefore, reduced ferritin levels represent iron deficiency. Transferrin saturation represents the iron content of circulating transferrin and, therefore, low saturation levels represent a decreased amount of iron for erythropoiesis.10

Diagnosing iron deficiency and anemia

Iron deficiency (ID) is diagnosed when the transferrin saturation is less than 16% and the serum ferritin concentration is less than 30 μg/L (without evidence of inflammation) or less than 100 μg/L (with evidence of inflammation). Anemia is defined as a hemoglobin level less than 11 g/dL in pregnant women, less than 12 g/dL in nonpregnant women, and less than 13 g/dL in men. IDA is diagnosed when ID is present along with anemia.12 Once IDA is diagnosed, treatment largely depends on the severity of the anemia, yet certain patient factors are also considered when deciding which administration route to use for iron supplementation. Diagnosis and management of IDA for patients with IBD was largely unaddressed until the early 2000s, with the first consensus guidelines being published in 2007 and updated in 2015.12


Iron supplementation regimens may include oral or IV forms of iron. The choice of route of administration and dosage regimen depends on myriad factors, including patient characteristics, disease severity, tolerability, and cost.

Oral iron supplementation

The selection and dose of oral iron has been debated within the literature because oral iron replacement is associated with GI intolerance; it can also have poor bioavailability, especially in the setting of inflammation, and it can exacerbate IBD.13 However, there does seem to be a consensus among experts and primary researchers regarding patient characteristics amenable to oral iron supplementation, especially since oral iron is easier to administer and has significant cost savings compared with IV iron supplementation.5 Oral iron can be used by patients with mild anemia (hemoglobin ≥ 10 g/dL) and inactive IBD. The recommended dose is based on elemental iron and ranges from 50 to 120 mg by mouth daily,5,6,14 which is lower than previous recommendations of 200 mg/day.5 This recommendation is based largely on similar efficacy with fewer side effects, since side effects are dose related. Tolerability is one of the greatest drawbacks to oral iron supplementation. Only 10% to 20% of an oral dose is absorbed in the duodenum each day, and the amount absorbed can be even lower in times of inflammation. The remaining unabsorbed iron can lead to abdominal pain, diarrhea, and constipation or even exacerbate IBD symptoms. Also, animal models have shown unabsorbed iron salts to be toxic to the intestinal tract.5

Three oral iron supplement products are commonly used today and each delivers a different amount of elemental iron: ferrous fumarate, ferrous sulfate, and ferrous gluconate provide 33%, 20%, and 12%, respectively, of the dose as elemental iron.15 Therefore, pharmacists must remember that, even though all 3 oral formulations are available as 325-mg tablets, each iron salt has varying degrees of elemental iron: 100 mg in ferrous fumarate, 65 mg in ferrous sulfate, and 38 mg in ferrous gluconate. No particular regimen is recommended over another, so there are many ways for patients to achieve the goal intake of 50 to 120 mg of elemental iron each day (Table 1). Most medical literature recommends higher doses, but lower-dose regimens can decrease the pill burden to 1 or 2 tablets once or twice daily, depending on the formulation.5,6,14

The regular-release formulations of all oral products are preferred because absorption occurs in the duodenum. Enteric-coated or delayed-release formulations are better tolerated but have less absorption than regular-release products because a portion of the iron can be released distal to the duodenum. If a patient is initiated on oral iron, pharmacists should counsel them to take the medication with either water or, preferably, orange juice because the acidic environment promotes iron absorption and the ascorbic acid (vitamin C) supports the iron oxidative state that is best for absorption. Alternatively, vitamin C supplements taken concomitantly with the iron or as a combined product can also be recommended.5 Furthermore, patients should avoid taking iron supplements with tea or coffee or with medications that can decrease iron absorption such as proton pump inhibitors, antacids, tetracyclines, or cholestyramine.16 Patients should remain aware of the strong potential for GI side effects and, if oral therapy is not well tolerated, they can be switched to IV iron therapy.14

Table 1. Low-dose Recommendations for Oral Iron Supplementation Regimens*5,6,14


Ferrous fumarate

Ferrous sulfate

Ferrous gluconate

Elemental Fe (%)




Tablet size (mg)

150 - 325


240 - 325

Elemental Fe/tab (mg)

50 - 100


27 - 38

Possible regimens

150-mg tablet: 1 tablet by mouth 1 - 2 times daily

325-mg tablet: 1 tablet by mouth daily

1 - 2 tablets by mouth daily

1 tablet by mouth 1 - 2 times daily

2 tablets by mouth daily

1 tablet by mouth 1 - 2 times daily

*Regimens are designed from low-dose recommendations of 50 to 120 mg elemental iron/day.

IV iron supplementation

IV iron supplementation should be initiated when a patient has moderate-to-severe anemia (hemoglobin < 10 g/dL), has active IBD, is intolerant to oral iron, or has an inadequate response to oral iron.12 Additionally, IV iron can be used when a quick response is needed; for example, when a procedure is scheduled in the near future. Once initiated, IV iron has a response rate of 70% to 80%.11 For patients who do not respond to IV iron, it is important to rule out other causes of anemia and to ensure that IBD flare-ups are adequately treated. Once this is done, the addition of erythropoietin therapy can be considered. The main patient populations requiring IV iron plus erythropoietin are patients with IBD unresponsive to IV iron, patients with low erythropoietin levels, or those who have not responded to aggressive IBD treatment.5,14 It is important to note that patients receiving erythropoietin should always receive IV iron concomitantly.5,6,11,14

The total cumulative dose of IV iron needed to effectively treat IDA in patients with IBD is difficult to estimate and, presently, there are 2 methods for calculating iron doses. The Ganzoni formula determines the cumulative iron dose with the following calculation: cumulative total dose (mg) = [actual body weight (kg) × (target hemoglobin – actual hemoglobin) × 2.4] + 500, with the target hemoglobin being that recommended based on gender and pregnancy status.5 For example, a man weighs 60 kg; he has an actual hemoglobin of 9 g/dL and a target of 13 g/dL: he requires a cumulative total dose of 1076 mg. A more recent, simplified dosing strategy was studied with ferric carboxymaltose, and it has been applied clinically with the other IV iron products.12 The simplified strategy identifies if the baseline hemoglobin is above or below 10 g/dL and if the patient's weight is above or below 70 kg (Table 2). Based on these factors, a patient can receive 1000 mg, 1500 mg, or 2000 mg as the total cumulative dose.6

Table 2. Dosing Strategy for Intravenous Iron Products6,12


Actual body weight


< 70 kg

≥ 70 kg

≥ 10 g/dL

1000 mg

1500 mg

< 10 g/dL

1500 mg

2000 mg

Currently, 7 IV iron formulations are available: high molecular weight (HMW) and low molecular weight (LMW) iron dextran, ferric gluconate, iron sucrose, ferumoxytol, ferric carboxymaltose, and iron isomaltoside (Table 3). The U.S. has approved all except the newest formulation, iron isomaltoside. IV iron has a long and evolving history of safety issues, including severe toxicity and hypersensitivity reactions, including fatal anaphylaxis, and burdensome administration schedules involving multiple infusions to complete a cumulative iron dose. Thus, the differentiating characteristics of available IV iron products include anaphylaxis and hypersensitivity risk and the amount of iron that can be administered in 1 infusion (i.e., the number of infusions needed to complete the cumulative iron dose). Also, the newer agents are costly, so pharmacoeconomics must be evaluated when selecting an agent.

It is important to recognize the considerable toxicity that existed with the original IV iron formulations in order to appreciate the newer formulations. One of the first iron formulations in the 1930s was administered as an oxyhydroxide complex and was toxic because of the release of the bioactive free iron.6,17 In the mid-1950s, HMW iron dextran was released. While the dextran molecule covered the iron core, which prevented the toxic bioactivity, there was a very high incidence of severe anaphylaxis caused by patients developing or having already formed antibodies to the HMW dextran molecule.17 It was not until the 1990s that a safer, LMW iron dextran was released; although patients still experienced anaphylaxis, it was not as frequent of an occurrence.6 Even so, LMW iron dextran requires a test dose prior to the full dose to decrease the risk for hypersensitivity reactions. Furthermore, the HMW iron dextran is often avoided because the risk for adverse events is significantly higher than with more modern formulations. The first dextran-free IV iron formulations, ferric gluconate and iron sucrose, were released around 2000 and had substantially less anaphylaxis risk than the dextran-containing formulations. Currently, neither ferric gluconate nor iron sucrose require a test dose to assess hypersensitivity. Interestingly, the original ferric gluconate package label required a test dose, but these instructions were removed in 2001.18

LMW iron dextran can be administered in multiple 100-mg doses or as a diluted total dose infusion (TDI) in which the total cumulative dose is given as a single infusion. Ferric gluconate and iron sucrose require multiple doses (e.g., ranging from 5 to 8) to achieve the total cumulative dose. Ferumoxytol, ferric carboxymaltose, and iron isomaltoside are the newest formulations designed to give the total cumulative dose in 1 to 2 infusions (ferumoxytol) or as a TDI (ferric carboxymaltose, iron isomaltoside).6,8,17 These agents have had fewer adverse events related to hypersensitivity or anaphylaxis than older products. However, ferumoxytol labeling still contains warnings for products released in the U.S. and in Canada: the U.S. boxed warning describes fatal and serious hypersensitivity reactions, including anaphylaxis, and the warning applies to patients who have tolerated previous doses.8 The Health Products and Food Branch of the Canadian government (similar to the U.S. Food and Drug Administration) published an alert on ferumoxytol in July and November 2014 regarding concerns of the increased risks of these adverse events. The alert warns that post-marketing data showed patients with allergies to other IV iron formulations or patients with 2 or more drug allergies were more likely to have serious hypersensitivity reactions to ferumoxytol. Because of this, the manufacturer extended the risk to patients with any known drug allergies, and it is now contraindicated in these patients.19

All IV iron agents still have risks for hypersensitivity and other adverse events. Therefore, all formulations require monitoring for hypersensitivity during and at least 30 minutes following a dose. LMW iron dextran requires monitoring for 1 hour after the test dose and before completing the remainder of the infusion because fatal reactions have occurred following the test dose, even when the test dose is tolerated. Because of this, the newer agents are generally selected instead of LMW iron dextran, even though it is still used infrequently today. If frequent infusions pose significant burdens to patients, a TDI formulation could be selected, with safer, newer agents being first-line choices. Of note, the LMW iron dextran TDI dosing recommendations are used off-label in the U.S., and, as such, it might not be widely used to treat IDA in patients with IBD nor reimbursed by insurance companies in the U.S.6,8

Table 3. Intravenous Iron Products 6,8,12


(brand name), year approved

Test dose required?

Number of infusions needed

Average dose

Availability (mg/vial), (Cost)a

Total cost of treatment (U.S.D.)

LMW iron dextran

(INFeD), 1991



20 mg/kg

100 mg/vial, ($30)

Total: $300

Ferric gluconate

(Ferrlecit), 1999



125 mg

62.5 mg/vial, ($38)

Total: $304

Iron sucrose

(Venofer), 2000



200 mg

100 mg/vial, ($60)

Total: $600


(Feraheme), 2009



510 mg

510 mg/vial (single use), ($876)

Total: $1230

Ferric carboxymaltose

(Injectafer), 2013



15 mg/kg

up to 1000 mg

750 mg/vial (single use), ($1136)

Total: $2272

Iron isomaltoside

(Monofer), 2009 (Available in Europe only)



Up to 20 mg/kg

Product unavailable in the United States, so no pricing is available for comparison

Abbreviations: LMW = low molecular weight; U.S.D. = United States Dollars.

aPricing from Lexi-comp database; cost rounded to nearest whole dollar. Total cost based on total iron requirements of 1000 mg; cost for entire vial used regardless of amount needed to complete dose if specified as single-use vial.

Monitoring response to iron supplementation

The goal of iron supplementation therapy is to normalize hemoglobin concentration, relieve symptoms related to anemia, and improve quality of life. Monitoring includes hemoglobin, transferrin saturation, and serum ferritin concentrations at least 4 weeks after starting therapy. Response to therapy includes increases in hemoglobin of at least 2 g/dL, restoration of transferrin saturation above 30%, and ferritin concentrations above 100 μg/L.6,12,20 Responses to IV iron can be seen as quickly as 2 to 4 weeks, but 4 to 8 weeks may be required for hemoglobin concentrations to normalize with oral iron regimens.6,12,14

Iron supplementation comes with risks, and transferrin saturations above 50% and ferritin concentrations above 800 μg/L are considered toxic.20 Additionally, there is evidence to support that IDA recurs in as many as 50% of patients treated with IV iron and erythropoietin within 10 months after discontinuing iron replacement therapy. Patients should be monitored for recurrence and, in some patients, continuing less-frequent IV iron maintenance therapy or switching to low dose oral iron may be considered.21

Safety and tolerability of iron supplementation

The decision to use oral or IV iron replacement remains a source of debate. A cross-sectional survey of gastroenterologists treating IDA in patients with IBD in 9 European countries was published in 2013 to compare the prescribing habits with current guideline recommendations. The authors reported that 78% of the gastroenterologists practiced solely in the hospital setting. Most of the patients (88%) had hemoglobin levels measured and, of these, 56% percent of the patients had hemoglobin levels less than 10 g/dL, qualifying them for IV iron replacement. However, 67% (range, 24% - 83%) of the patients received oral iron replacement, while 28% (range, 16% - 72%) received IV iron replacement. Physicians stated that they selected oral iron because it was familiar, easy to use, and convenient; physicians who selected IV iron did so to achieve a faster response. Additionally, 23% of patients had the administration route of iron changed during therapy: 47% of the changes were from oral to IV administration.13

Consensus guidelines recommend basing the choice of IV versus oral iron on laboratory findings and patient characteristics, but there have been few prospective, randomized, controlled trials addressing this decision. In January 2016, Bonovas and colleagues published a systematic review and meta-analysis of trials conducted in adult patients with IDA and IBD being treated with either IV or oral iron products to correct anemia.22 The authors screened 437 articles and found 26 to review for further eligibility. Of the 26, only 5 met the eligibility criteria of being a randomized, controlled trial with either a parallel or crossover design in the specified patient population. All 5 studies were conducted in Europe and they were published between 2005 and 2013. The primary efficacy outcome was hemoglobin response to therapy, defined as the percentage of patients whose hemoglobin increased at least 2 g/dL at the end of the study follow-up. The secondary outcomes included safety issues such as rates of discontinuation due to adverse events, GI adverse events, or incidence of serious adverse events.22

The number of patients enrolled in each study ranged from 19 to 338, and follow-up time for the studies ranged from 2 to 20 weeks. While each individual study found a numerically higher response rate for patients on IV iron compared to oral iron, none of the different responses rates were significantly different. Pooling the sample size for the meta-analysis allowed a total of 713 study patients: 448 received IV iron and 265 received oral iron. The meta-analysis showed that 65.6% of patients responded to IV iron, and only 52.1% responded to oral iron, with odds ratios of 1.59 (95% confidence interval [CI] 1.15 - 2.20) in the fixed effect model and 1.57 (95% CI 1.13 - 2.18) in the random effects model. The authors also performed a "leave-one-out" sensitivity analysis to identify any studies that weighed the overall results of the analysis, and they found similar robustness to their results when they analyzed the data each time a study was omitted.22 The meta-analysis did not report each study's inclusion and exclusion criteria, and many of the individual trials included patients whose baseline hemoglobin was less than 10 g/dL, which would warrant consideration of IV iron therapy according to current guidelines. As such, the efficacy results reported in the meta-analysis may be misinterpreted, since IV iron is known to be more effective in patients with lower baseline hemoglobin concentrations. Additionally, there was a large range of follow-up time in the included studies; 2 of the 5 included studies had follow-up times of 2 and 6 weeks, all of which are shorter response times than what might be needed to achieve response to oral therapy. This could also weigh in favor of IV iron, as a faster response would be seen compared to oral iron.

In terms of safety, the authors reported that there was less treatment discontinuation due to adverse events and fewer GI adverse events in the IV iron group compared to the oral iron group. However, there were more serious adverse events in the IV iron group than in the oral iron group. Of note, the serious adverse events were all ruled to be unrelated to the study drug, 22 so the impact of this data remains inconclusive.

The authors concluded that all 5 included studies had a high risk of bias according to Cochrane Collaboration's tool due to the unblinded nature of the trials, possibly biasing interpretation of adverse events or intolerance, and differential drop-outs of patients. However, using Begg's and Egger's tests, the authors found no evidence of publication bias related to efficacy and safety outcomes. Overall, the authors concluded that IV iron is more effective and has fewer GI side effects than oral iron.22 This is in agreement with current guidelines that recommend IV iron in patients with lower baseline hemoglobin, patients with active IBD, and patients who cannot tolerate oral iron formulations. 

New options for iron supplementation

Tolerability continues to be a major limitation to the use of oral iron, even in patients with quiescent disease or baseline hemoglobin above 10 g/dL. Interestingly, a recent study evaluated a new formulation of oral iron, which is already available in Europe, to assess its efficacy and safety in IBD patients with IDA. Gasche and colleagues conducted a randomized, double-blind, placebo-controlled trial assessing the efficacy and tolerability of ferric maltol in IBD patients with IDA who had failed previous oral iron therapy.23 Adult patients with IBD and mild-to-moderate IDA were included in the study; IDA was defined as a baseline serum ferritin less than 30 µg/L and a hemoglobin ranging between 9.5 and 12 g/dL in females and 9.5 and 13 g/dL in males. IBD was required to be in remission or have mild-to-moderate disease activity. Additionally, the patients were to have failed previous oral ferrous iron therapy. Failure of previous therapy was defined as discontinuation due to adverse drug events, deterioration of IBD that was caused by the therapy, lack of efficacy, and other signs of failure that were documented.23

Patients were randomized to receive ferric maltol 231.5 mg (30 mg elemental iron) by mouth twice daily or placebo for 12 weeks. Hemoglobin levels were monitored at baseline and 4, 8, and 12 weeks after initiation. The primary outcome was change in hemoglobin from baseline to week 12. Secondary efficacy outcomes included change in hemoglobin from baseline to weeks 4 and 8, serum ferritin and transferrin saturation, and percentage of patients deemed as 'responders,' which was defined as those who achieved either an increase in hemoglobin of at least 1 g/dL or total hemoglobin of at least 12 g/dL for females and an increase in hemoglobin of at least 2 g/dL or total hemoglobin of at least 13 g/dL for males at week 12. Additional secondary outcomes included safety and tolerability, as well as quality of life assessment.23

A total of 128 patients were included: 64 in the ferric maltol group and 64 in the placebo group. A total of 55 (86%) patients in the ferric maltol group and 53 (83%) in the placebo group completed the 12 week, double-blind therapy; 5 patients in the ferric maltol group and 4 in the placebo group withdrew due to adverse events. The other withdrawals were due to patient withdrawal, physician decision, or protocol violation. For the primary efficacy endpoint, there was a statistically significant increase in hemoglobin in patients receiving ferric maltol compared to those receiving placebo at week 12. Hemoglobin increased from a mean baseline of 11 g/dL to 13.2 g/dL in the ferric maltol group and from a baseline of 11.1 g/dL to 11.2 g/dL in the placebo group (p < 0.0001). The hemoglobin levels in the ferric maltol group improved from baseline to 12.05 g/dL at week 4 and to 12.8 g/dL at week 8; however, the median time to normalization of hemoglobin concentration was 57 days.23

Treatment adverse events were reported in 35 (58%) patients receiving ferric maltol and 43 (72%) receiving placebo. GI adverse events were reported in 23 (38%) patients receiving ferric maltol and 24 (40%) receiving placebo. The investigators attributed adverse events to the study drug in 15 (25%) patients receiving ferric maltol and 7 (12%) patients receiving placebo. The most common treatment-related GI events in the ferric maltol group—abdominal pain, constipation, and flatulence—occurred in 4 (6.7%) patients; in the placebo group, abdominal pain occurred in 5% of patients, constipation in 1.7%, and flatulence in 0%. Additionally, there was no difference in quality of life in the ferric maltol group compared to the placebo group. The authors concluded that the novel, oral ferric maltol product was safe and effective in this patient population, and they further hypothesized that oral ferric maltol may be an alternative to IV iron, as it showed a meaningful response at 4 and 8 weeks and a hemoglobin response rate of at least 2 g/dL.23

This is the first phase III trial reported with ferric maltol, and the drug is only available in Europe, but it has promising GI tolerability results for patients with IBD and IDA that fall within the guideline recommendations for patients requiring oral iron replacement. Future studies need to address the efficacy and safety of ferric maltol compared to oral ferrous iron products to clarify how oral agents should be selected. Moreover, studies comparing oral ferric maltol to IV iron could be warranted, since it would provide an oral option for patients with more severe IDA.


IV iron appears to have faster and better response rates in patients with more severe IDA or active IBD, while oral iron can be reserved for patients with less severe IDA or quiescent disease. GI intolerance is a major limiting factor to most currently available oral iron products; however, the use of a newer oral iron formulation, ferric maltol, may provide a safer alternative for iron replacement. The last 2 published consensus guidelines recommend IV instead of oral iron replacement on the basis of severity of anemia, active versus quiescent disease, and tolerability of oral formulations. However, these recommendations are based on a limited number of randomized, controlled trials, which reinforces the need for future studies to direct therapy. As such, physician preference and comfort level drive most treatment decisions.

Role of the pharmacist

Similar to their responsibilities in the management of countless disease states in both the inpatient and outpatient settings, pharmacists can assist with the management of IDA for patients with IBD in many ways. Pharmacists can be involved with formulary decisions, weighing the benefits and risks of the different IV iron formulations, including safety concerns and direct and indirect costs. They should also be involved with direct patient care by identifying the most appropriate therapy—oral versus IV—according to available lab findings and patient characteristics. Moreover, pharmacists can educate patients about their disease states and medications to promote adherence to prescribed regimens. Counseling patients to separate or avoid, if feasible, medications such as proton-pump inhibitors, antacids, tetracyclines, or cholestyramine can help improve iron absorption and, therefore, response to oral iron supplements.16 Lastly, pharmacists should be involved with monitoring treatment to identify patients who cannot tolerate oral iron or who have inadequate response to either oral or IV iron in order to optimize care and improve patient outcomes.


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