Interpreting raised serum ferritin levels

Koperdanova, Marianna; Cullis, Jonathan O.

doi:10.1136/bmj.h3692

Cited by 66 publications

(62 citation statements)

References 16 publications

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“…8 An approach to hyperferritinaemia has previously been discussed. 6 Specialist techniques for assessing iron overload include liver biopsy, magnetic resonance imaging, and superconducting quantum interference device susceptometry, a non-invasive technique that measures the amount of in vivo magnetisation caused by hepatic iron. 1 Indications for these tests can include marked hyperferritinaemia (>1000 μg/L) or further assessment when the diagnosis of iron overload is in doubt.…”

Section: Iron Overloadmentioning

confidence: 99%

Interpreting iron studies

Kelly

McSorley

Patel³

et al. 2017

BMJ

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A 63 year old woman visits her doctor with a three month history of fatigue and generalised joint pains. Her medical history is unremarkable and she reports no recent stress, infection, or weight loss. There are no abnormalities on clinical examination. Haemoglobin, creatinine, and electrolytes, liver enzymes, glucose, inflammatory markers, and thyroid function tests are normal. Ferritin, iron, transferrin, and transferrin saturation are also requested.This article discusses some situations in which ferritin and iron studies might be helpful and how to avoid common pitfalls in their interpretation. What are the next investigations?The doctor in this case requested iron studies to investigate the possibility of iron overload and to screen for haemochromatosis. Iron studies are also commonly indicated in clinical practice to investigate iron deficiency, or to monitor response to treatment for these conditions (box 1).Conventional laboratory tests of iron status are often referred to as "iron studies." They include tests for serum ferritin, iron, transferrin, or total iron binding capacity (TIBC), and transferrin saturation.Iron is a key component of haemoglobin in red blood cells, myoglobin in muscle, and many metalloproteins and enzymes. It is essential for uptake of oxygen and its delivery to tissues, utilisation of oxygen by muscle cells, and mitochondrial energy production. 3 Normal iron metabolism and regulation is outlined in Figure 1⇓. The adult male body contains 3-5 g of iron. Less than 0.1% of total body iron stores circulate in plasma. Dietary Fe 3+ is reduced to Fe 2+ and transported into the enterocyte by the divalent metal transporter DMT1. Iron is exported across the basolateral membrane via the iron export protein ferroportin 1 or stored as ferritin. Transferrin bound iron binds to transferrin receptor 1 (TFR1) and is taken up into the cell via receptor mediated endocytosis. Expression of TFR1 is regulated locally by the iron demands of the cell, via binding of iron regulatory proteins. Old or damaged erythrocytes are removed from the circulation by splenic macrophages. Iron is removed from haem by haem oxygenase 1, and either stored as ferritin or released into the circulation.Regulation of iron release at a systemic level is mediated by the peptide hormone hepcidin (produced predominantly by hepatocytes) and has an inhibitory effect on iron release from cells and dietary iron absorption. Expression is controlled by complex signalling pathways. 1 What is included in iron studies?Ferritin-is the intracellular storage form of iron. A very small amount is found in serum. In inflammation, liver disease, and malignancy, ferritin levels can rise because ferritin is an acute phase protein. 4 In these patients, ferritin can appear either falsely high or normal, when in reality stores are low.Serum iron-refers to ferric ions (Fe 3+ ) bound to serum transferrin. Serum iron concentration is highly variable and is affected by dietary iron intake, inflammation, and infection. 5Transferrin-is the principal iron...

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Section: Iron Overloadmentioning

confidence: 99%

Interpreting iron studies

Kelly

McSorley

Patel³

et al. 2017

BMJ

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“…No pancreatic biopsy data are available for the analysis of PIC and pancreas T2* correlations, so future studies are needed to verify our data. Although serum ferritin may correlate with IOL in some organs, it can be influenced by many factors in individual patients [23] and needs to be considered in combination with other measurements, particularly organ T2*. On the other hand, organ MRI T2* can reflect organ function, to some extent, as revealed by our findings that cardiac T2* correlates with LVEF [24] and liver T2* correlates with TBIL.…”

Section: Discussionmentioning

confidence: 65%

Observational Monitoring of Patients with Aplastic Anemia and Low/Intermediate-1 Risk of Myelodysplastic Syndromes Complicated with Iron Overload

Long

Chen

et al. 2017

Acta Haematol

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Background: This study focuses on the iron overload (IOL) of patients with transfused aplastic anemia (AA) or a low/intermediate-1 risk of myelodysplastic syndrome (MDS). Methods: Ninety-two AA or MDS patients with IOL were prospectively recruited. Clinical data were collected every 6 months, and organ magnetic resonance imaging T2* values were collected annually. Patients with IOL were chelated. Results: Serum ferritin was correlated with liver T2* and pancreatic T2* in the AA and MDS groups. Transfusion amounts were correlated with serum ferritin values, liver T2*, and pancreatic T2* in the AA group. At the 6-month and 1-year evaluations, patients with sufficient chelation experienced significant decreases in serum ferritin, and those with decreased serum ferritin experienced an obvious increase in hemoglobin. At their 1-year-follow-up, patients with adequate chelation showed significant increases in hepatic T2*, cardiac T2*, and left ventricular ejection fraction (LVEF). Patients with decreased serum ferritin (including those without chelation) experienced an increase in hemoglobin, hepatic T2*, cardiac T2*, and LVEF. Conclusion: The transfusion amount was more reliable at predicting IOL in patients with AA than in those with MDS. Adequate iron chelation can decrease serum ferritin levels and may improve hepatic T2*, cardiac T2*, and LVEF levels. A decrease in serum ferritin, even in the absence of chelation, may also benefit patients.

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“…(775–780)], present at ca. 1–2 g L −1 , with ferritin being an intracellular iron storage molecule, so one is led to wonder why there is even any serum ferritin at all (126, 781). The answer is almost certainly that it is a leakage molecule from damaged cells (126), and when in serum it is found to have lost its iron content (782–785).…”

Section: Proteomic and Similar Biomarkers – Circulating And Placentalmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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Interpreting raised serum ferritin levels

Cited by 66 publications

References 16 publications

Interpreting iron studies

Interpreting iron studies

Observational Monitoring of Patients with Aplastic Anemia and Low/Intermediate-1 Risk of Myelodysplastic Syndromes Complicated with Iron Overload

A Dormant Microbial Component in the Development of Preeclampsia

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