Elevated serum transferrin receptor concentration in children with juvenile chronic arthritis as evidence of iron deficiency

Kivivuori, S. M.; Pelkonen, P.; Ylijoki, Heikki; Verronen, P; Ma, Siimes

doi:10.1093/rheumatology/39.2.193

Cited by 14 publications

(10 citation statements)

References 26 publications

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“…There have been some reports that s-TfR levels are correlated with serum cytokine levels increased at the active stage of joint inflammation in RA patients [25], or that s-TfR level is related to iron status in adult and juvenile RA patients [26][27][28][29][30]. We also found that s-TfR levels were correlated with markers of anaemia but not of inflammation, as shown in Table 1, consistent with the results of previous studies.…”

Section: Discussionsupporting

confidence: 91%

“…They might have had IDA and ACD at the same time, although this should be confirmed by iron supplementation, as described above. It was necessary to resolve whether s-TfR level reflects erythropoiesis or inflammation in RA [25][26][27][28][29][30]. The results of the present study showed that s-TfR level was correlated with indicators of anaemia but not of inflammation, consistent with the results of previous studies [27,28].…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Serum Transferrin Receptor Levels in Patients with Rheumatoid Arthritis are Correlated with Indicators for Anaemia

Chijiwa¹,

Nishiya²,

Hashimoto³

2001

Clin Rheumatol

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To measure serum soluble transferrin receptor (s-TfR) levels in patients with rheumatoid arthritis (RA), sera were obtained from 50 Japanese RA patients and 20 healthy subjects. Both s-TfR and serum erythropoietin (EPO) levels were measured by enzyme-linked immunosorbent assay (ELISA). Routine laboratory tests were also performed, including peripheral blood analysis and determination of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF), serum iron levels, total iron-binding capacity (TIBC) and serum ferritin levels. The s-TfR levels in the 50 RA patients (mean +/- SD, 1,801 +/- 512 ng/ml) were significantly higher than those in the 20 control subjects (1,316 +/- 345 ng/ml). There were no differences in the values of s-TfR between men and women in either group, or between RA patients over and under 50 years old. Serum EPO levels in 47 RA patients were as low as 14.0 +/- 10.1 mlU/ml (mean +/- SD), ranging from 3.9 to 58.7 mIU/ml (normal range 2.8-17.2 mlU/ml), unrelated to low haemoglobin concentration. The s-TfR levels in RA patients showed negative correlations with red blood cell count, serum iron level and haemoglobin concentration, and positive correlations with ESR and serum EPO levels. However, there were no correlations between s-TfR level and markers of inflammation such as CRP, platelet count or RF titre. In conclusion, s-TfR level in RA patients could be a marker of erythropoiesis rather than of joint inflammation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 89%

Serum Transferrin Receptor Levels in Patients with Rheumatoid Arthritis are Correlated with Indicators for Anaemia

Chijiwa¹,

Nishiya²,

Hashimoto³

2001

Clin Rheumatol

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“…This has also been proven with the use of automated analyzers that measure the transferring receptors in the serum [78]. Moreover, since the serum-transferring receptor concentration is not altered in inflammatory states, it may be a more useful test than serum ferritin in assessing the iron stores in AOSD [79]. The defective release of iron from ferritin could be secondary to the presence of a mutant form of ferritin, which could also explain the defect in ferritin glucosylation seen in AOSD.…”

Section: Resultsmentioning

confidence: 99%

Ferritin in Adult-Onset Still’s Disease: Just a Useful Innocent Bystander?

Mehta

Efthimiou

2012

International Journal of Inflammation

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Background. Adult-Onset Still’s Disease (AOSD) is an immune-mediated systemic disease with quotidian-spiking fever, rash, and inflammatory arthritis. Hyperferritinemia is a prominent feature, often used for screening.Methods. The key terms “ferritin” and “hyperferritinemia” were used to search PubMed and Medline and were cross-referenced with “Still’s Disease.”Results. Hyperferritinemia, although nonspecific, is particularly prevalent in AOSD. While most clinicians associate ferritin with iron metabolism, this is mostly true for the H isoform and not for the L isoform that tends to increase dramatically in hyperferritenemia. In these situations, hyperferritinemia is not associated with iron metabolism and may even mask an underlying iron deficiency. We review, in systematic fashion, the current basic science and clinical literature regarding the regulation of ferritin and its use in the diagnosis and management of AOSD.Conclusion. Serum hyperferritinemia in AOSD has been described for 2 decades, although its mechanism has not yet been completely elucidated. Regulation by proinflammatory cytokines such as interleukin (IL)-1b, IL-6, IL-18, MCSF, and INF-α provides a link to the disease pathogenesis and may explain rapid resolution of hyperferritinemia after targeted treatment and inhibition of key cytokines.

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“…Iron (Fe) deficiency (ID) can increase brain Mn levels (Heilig et al, 2005), as it is associated with high concentrations of serum transferrin receptors (TfR) (Kivivuori et al, 2000; Punnonen et al, 1994), which are transporters present at the blood-brain barrier (BBB) that mediate brain influx of both Fe and Mn (Aschner and Aschner, 1991; Erikson et al, 2002). …”

Section: Modulating Factors Of Mn Induced Neurotoxicitymentioning

confidence: 99%

Manganese in human parenteral nutrition: Considerations for toxicity and biomonitoring

et al. 2014

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The iatrogenic risks associated with excessive Mn administration in parenteral nutrition (PN) patients are well documented. Hypermanganesemia and neurotoxicity are associated with the duration of Mn supplementation, Mn dosage, as well as pathological conditions, such as anemia or cholestasis. Recent PN guidelines recommend the biomonitoring of patients if they receive Mn in their PN longer than 30 days. The data in the literature are conflicting about the method for assessing Mn stores in humans as a definitive biomarker of Mn exposure or induced-neurotoxicity has yet to be identified. The biomonitoring of Mn relies on the analysis of whole blood Mn (WB Mn) levels, which are highly variable among human population and are not strictly correlated with Mn-induced neurotoxicity. Alterations in dopaminergic (DAergic) and catecholaminergic metabolism have been studied as predictive biomarkers of Mn-induced neurotoxicity. Given these limitations, this review addresses various approaches for biomonitoring Mn exposure and neurotoxic risk.

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Elevated serum transferrin receptor concentration in children with juvenile chronic arthritis as evidence of iron deficiency

Cited by 14 publications

References 26 publications

Serum Transferrin Receptor Levels in Patients with Rheumatoid Arthritis are Correlated with Indicators for Anaemia

Serum Transferrin Receptor Levels in Patients with Rheumatoid Arthritis are Correlated with Indicators for Anaemia

Ferritin in Adult-Onset Still’s Disease: Just a Useful Innocent Bystander?

Manganese in human parenteral nutrition: Considerations for toxicity and biomonitoring

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