Limitations of Serum Ferritin in Diagnosing Iron Deficiency in Inflammatory Conditions

Author:

Dignass Axel12ORCID,Farrag Karima23,Stein Jürgen23ORCID

Affiliation:

1. Department of Medicine 1, Agaplesion Markus Hospital, Goethe University, 60431 Frankfurt am Main, Germany

2. Interdisciplinary Crohn Colitis Center Rhein-Main, 60594 Frankfurt am Main, Germany

3. Department of Gastroenterology and Clinical Nutrition, DGD Clinics Sachsenhausen, 60594 Frankfurt am Main, Germany

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.

Funder

Vifor Pharma

Publisher

Hindawi Limited

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