Abstract
Patients with inflammatory conditions such as inflammatory bowel disease (IBD), chronic heart failure (CHF), and chronic kidney disease (CKD) have high rates of iron deficiency with adverse clinical consequences. Under normal circumstances, serum ferritin levels are a sensitive marker for iron status but ferritin is an acute-phase reactant that becomes elevated in response to inflammation, complicating the diagnosis. Proinflammatory cytokines also trigger an increase in hepcidin, which restricts uptake of dietary iron and promotes sequestration of iron by ferritin within storage sites. Patients with inflammatory conditions may thus have restricted availability of iron for erythropoiesis and other cell functions due to increased hepcidin expression, despite normal or high levels of serum ferritin. The standard threshold for iron deficiency (<30 μg/L) therefore does not apply and transferrin saturation (TSAT), a marker of iron availability, should also be assessed. A serum ferritin threshold of <100 μg/L or TSAT < 20% can be considered diagnostic for iron deficiency in CHF, CKD, and IBD. If serum ferritin is 100–300 μg/L, TSAT < 20% is required to confirm iron deficiency. Routine surveillance of serum ferritin and TSAT in these at-risk groups is advisable so that iron deficiency can be detected and managed.
Highlights
Patients with inflammatory conditions such as inflammatory bowel disease (IBD), chronic heart failure (CHF), and chronic kidney disease (CKD) have high rates of iron deficiency with adverse clinical consequences
A serum ferritin threshold of
In inflammatory conditions, where serum ferritin levels are raised as part of the acute-phase response, these thresholds do not apply and TSAT should be measured to avoid a misdiagnosis of iron overload
Summary
Iron deficiency is a major global health problem, representing one of the leading nonfatal disease conditions worldwide [1], and is frequently seen in everyday clinical practice [2]. Patients with chronic illnesses may have a poor appetite and inadequate dietary iron intake This can be exacerbated by impaired iron absorption from the intestinal lumen caused by medications such as proton pump inhibitors [7], histamine receptor antagonists [7], and calcium-based phosphate binders [8], while antiplatelet therapy can increase the risk of International Journal of Chronic Diseases. In addition to these patient-specific etiologies, CHF, CKD, and IBD share the common effect of an ongoing inflammatory stimulus In these chronic conditions, high hepcidin levels can restrict the uptake of dietary iron and, over time, lead to iron deficiency with reduced availability of iron for essential cellular functions [10] (see “The Effect of Inflammation on Iron Homeostasis” below). Understanding the nature of serum ferritin and, how levels of serum ferritin are influenced by inflammation is key to successful diagnosis in this context
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