Iron therapy and infection

To the Editor: In their article, “Is iron therapy for anemia harmful in the setting of infection?” in the March 2011 issue, Daoud et al¹ illustrated an interesting aspect we often encounter, especially in nephrology practice. However, I believe several points should be clarified in this context.

First, “iron therapy” and “iron stores” are quite different things when we talk about infection. As Daoud et al state, human studies involving iron therapy and infection are conflicting in their results. The explanation is likely that iron therapy per se does not always translate to increased iron stores, while iron stores do correlate with increased risk of infection and death, whether in hemodialysis patients² or in the general population.³ Intravenous iron therapy mostly gains the association with risk of infection when dosed greater than a certain amount or for an extended duration. In addition, Pieracci et al⁴ showed that oral iron therapy for anemia does not boost the infection rate during critical illness when equivalent iron markers are achieved.

This mounting evidence solidifies the view that iron stores underlie the infection susceptibility. But to prove this concept, a randomized controlled study consisting of achieving similar iron stores by component therapy or intravenous iron supplementation would be the best option.

Second, I wish to add a category of infection omitted in their article, ie, fungal infection (mucormycosis). Mucormycosis, a rare but life-threatening disease, is caused by fungi of the class Zygomycetes that spread systemically in immunocompromised hosts, with a high death rate. Iron overload, whether or not accompanied by the use of deferoxamine (Desferal), is an established risk factor for mucormycosis. These fungi possess a high-affinity iron permease and produce siderophores, both of which facilitate the uptake of iron.⁵ An abundant host iron pool further enhances their scavenging process, resulting in devastating proliferation and tissue damage. This disease category should be borne in mind when dealing with immunocompromised patients undergoing iron therapy.

To the Editor: In their article, “Is iron therapy for anemia harmful in the setting of infection?” in the March 2011 issue, Daoud et al¹ illustrated an interesting aspect we often encounter, especially in nephrology practice. However, I believe several points should be clarified in this context.

First, “iron therapy” and “iron stores” are quite different things when we talk about infection. As Daoud et al state, human studies involving iron therapy and infection are conflicting in their results. The explanation is likely that iron therapy per se does not always translate to increased iron stores, while iron stores do correlate with increased risk of infection and death, whether in hemodialysis patients² or in the general population.³ Intravenous iron therapy mostly gains the association with risk of infection when dosed greater than a certain amount or for an extended duration. In addition, Pieracci et al⁴ showed that oral iron therapy for anemia does not boost the infection rate during critical illness when equivalent iron markers are achieved.

This mounting evidence solidifies the view that iron stores underlie the infection susceptibility. But to prove this concept, a randomized controlled study consisting of achieving similar iron stores by component therapy or intravenous iron supplementation would be the best option.

Second, I wish to add a category of infection omitted in their article, ie, fungal infection (mucormycosis). Mucormycosis, a rare but life-threatening disease, is caused by fungi of the class Zygomycetes that spread systemically in immunocompromised hosts, with a high death rate. Iron overload, whether or not accompanied by the use of deferoxamine (Desferal), is an established risk factor for mucormycosis. These fungi possess a high-affinity iron permease and produce siderophores, both of which facilitate the uptake of iron.⁵ An abundant host iron pool further enhances their scavenging process, resulting in devastating proliferation and tissue damage. This disease category should be borne in mind when dealing with immunocompromised patients undergoing iron therapy.

To the Editor: In their article, “Is iron therapy for anemia harmful in the setting of infection?” in the March 2011 issue, Daoud et al¹ illustrated an interesting aspect we often encounter, especially in nephrology practice. However, I believe several points should be clarified in this context.

First, “iron therapy” and “iron stores” are quite different things when we talk about infection. As Daoud et al state, human studies involving iron therapy and infection are conflicting in their results. The explanation is likely that iron therapy per se does not always translate to increased iron stores, while iron stores do correlate with increased risk of infection and death, whether in hemodialysis patients² or in the general population.³ Intravenous iron therapy mostly gains the association with risk of infection when dosed greater than a certain amount or for an extended duration. In addition, Pieracci et al⁴ showed that oral iron therapy for anemia does not boost the infection rate during critical illness when equivalent iron markers are achieved.

This mounting evidence solidifies the view that iron stores underlie the infection susceptibility. But to prove this concept, a randomized controlled study consisting of achieving similar iron stores by component therapy or intravenous iron supplementation would be the best option.

Second, I wish to add a category of infection omitted in their article, ie, fungal infection (mucormycosis). Mucormycosis, a rare but life-threatening disease, is caused by fungi of the class Zygomycetes that spread systemically in immunocompromised hosts, with a high death rate. Iron overload, whether or not accompanied by the use of deferoxamine (Desferal), is an established risk factor for mucormycosis. These fungi possess a high-affinity iron permease and produce siderophores, both of which facilitate the uptake of iron.⁵ An abundant host iron pool further enhances their scavenging process, resulting in devastating proliferation and tissue damage. This disease category should be borne in mind when dealing with immunocompromised patients undergoing iron therapy.