Reduced iron export associated with hepcidin resistance can explain the iron overload spectrum in ferroportin disease.

Although intracellular ferritin measurements showed an overall high variation and so differences did not reach statistical significance, comparing these results with iron release studies (Figure 1A ) a reciprocal relationship was found, which confirms a dose‐dependent hepcidin response of normal ferroportin, which is absent in mutant ferroportin.

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