Reversible atransferrinemia in a patient with chronic enteropathy: is transferrin mandatory for iron transport?

Abstract

Herein, we report the case of a 42-year-old woman, hospitalized in a French tertiary hospital for a relapse of a chronic enteropathy, who was found on admission to have no detectable serum transferrin. Surprisingly, she only exhibited mild anaemia. This atransferrinemia persisted for two months throughout her hospitalization, during which her haemoglobin concentration remained broadly stable. Based on her clinical history and evolution, we concluded to an acquired atransferrinemia secondary to chronic undernutrition, inflammation and liver failure. We discuss the investigations performed in this patient, and hypotheses regarding the relative stability of her haemoglobin concentration despite the absence of detectable transferrin.

Keywords: enteritis; inflammation; iron; transferrin.

Figure 1

A. Evolution of serum markers during the course of the patient’s hospitalization. For each parameter, the laboratory reference interval is indicated between parentheses. B. Capillary zone electrophoresis of serum transferrin (Tf) glycoforms (5, 4 and 3-sialotransferrin). Overlay of Tf patterns after admission (black) and before discharge (white). RBC - red blood cells. Tf - transferrin. ALT - alanine aminotransferase. AST - aspartate aminotransferase. CRP - C-reactive protein.

Figure 2

Iron uptake pathways in erythroid precursors. Physiologically, the transferrin/transferrin receptor 1 (Tf/TfR1) pathway supplies the iron required for haemoglobin synthesis. Possible minor pathways, which could play a significant role when the Tf/TfR1 pathway is affected, could include ferritin delivery mediated by TIM-1, SCARA5, TfR1 or CXCR4, or non-transferrin-bound iron (NTBI) delivery by ZIP14 or CD44. TfR1 - transferrin receptor 1. TBI - transferrin-bound iron. NTBI - non-transferrin-bound iron. Original figure designed by Raynor et al.