Iron Deficiency Anemia in Adult Onset Still's Disease with a Serum Ferritin of 26,387 μg/L

Sheetal Patel,Seyed Monemian,Harvey Dosik,Ayesha Khalid

doi:10.1155/2011/184748

Sheetal Patel, Seyed Monemian + Show 2 more

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https://doi.org/10.1155/2011/184748

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Abstract

Serum ferritin rises in the anemia of chronic inflammation reflecting increased iron storage and other changes mediated by inflammation. When iron deficiency coexists, the ferritin may not always decline into the subnormal range. We describe the rare interaction of iron deficiency with the extreme hyperferritinemia characteristic of adult onset Still's disease. The combination has clinical relevance and allows deductions about the presence of serum ferritin at 26,387 μg/L despite obvious iron depletion. The diagnosis of iron deficiency anemia was delayed and became fully obvious when her Still's disease remitted and serum ferritin decreased to 6.5 μg/L. The coexistence of iron deficiency should be considered when evaluating a patient with anemia of chronic inflammation even when the ferritin level is elevated several hundredfold. Further insights on ferritin metabolism in Still's disease are suggested by the likelihood that the patient's massive hyperferritinemia in the acute phase of Still's disease was almost entirely of the iron-free apoferritin form.

Highlights

In the anemia of chronic inflammation, iron metabolism is disturbed and the serum ferritin usually rises moderately, achieving mean levels such as 300–400 μg/L [1]
We describe an extreme manifestation of this situation in a patient with the massive hyperferritinemia of adult onset Still’s disease
Anemia of chronic inflammation features a network of intracellular absorptive and plasma iron changes that are mediated by hepcidin

Summary

Case Report

Iron Deficiency Anemia in Adult Onset Still’s Disease with a Serum Ferritin of 26,387 μg/L. The ferritin may not always decline into the subnormal range. We describe the rare interaction of iron deficiency with the extreme hyperferritinemia characteristic of adult onset Still’s disease. The combination has clinical relevance and allows deductions about the presence of serum ferritin at 26,387 μg/L despite obvious iron depletion. The diagnosis of iron deficiency anemia was delayed and became fully obvious when her Still’s disease remitted and serum ferritin decreased to 6.5 μg/L. The coexistence of iron deficiency should be considered when evaluating a patient with anemia of chronic inflammation even when the ferritin level is elevated several hundredfold. Further insights on ferritin metabolism in Still’s disease are suggested by the likelihood that the patient’s massive hyperferritinemia in the acute phase of Still’s disease was almost entirely of the iron-free apoferritin form

Introduction

Findings

Discussion