It may also be the result of increased synthesis and/or increased cellular secretion of ferritin upon various stimuli such as cytokines, oxidants, hypoxia, oncogenes, and growth factors. High ferritin, hyperferritinemia, may indicate increased iron stores, but is more commonly seen upon acute phase reactions and as a result of ferritin being released from damaged cells such as hepatocytes in liver disease. When concurrent inflammation is absent, ferritin has proven to be a highly specific and sensitive parameter for the diagnosis of iron deficiency. Ascribed to its proportionality to total body iron stores, ferritin function is an indirect marker of iron status. Finally, an algorithm for the diagnostic workup and management of hyperferritinemia is proposed, and general principles regarding the treatment of iron overload are discussed.įerritin is one of the most commonly requested laboratory tests in general and secondary care, and levels deviating from reference ranges are a frequent finding.
We address the biology, etiology, and epidemiology of hyperferritinemia. In this review, we have performed a review of a selection of the literature based on the authors’ own experiences and assessments in accordance with international recommendations and guidelines. Differentiation of the presence or absence of an associated iron overload upon hyperferritinemia is essential, although often proves to be complex. In routine medical practice, only 10% of cases are related to an iron overload, whilst the rest is seen as a result of acute phase reactions and reactive increases in ferritin due to underlying conditions. Hyperferritinemia is, however, a non-specific finding, which is frequently overlooked in general practice.
Serving as an indirect marker for total body iron stores, low ferritin is highly specific for iron deficiency.
Ferritin is one of the most frequently requested laboratory tests in primary and secondary care, and levels often deviate from reference ranges.
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