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Published on: January 31, 2022
Serum hepcidin concentrations in relation to iron status in children with type 1 diabetes
Mirjam Vreugdenhil1, Marjolijn D Akkermans1, Rachel P L van Swelm2
1Department of Pediatrics, Juliana Children's Hospital/Haga Teaching Hospital, The Hague, The Netherlands.
Insights
In type 1 diabetes (T1D) children, hepcidin levels were similar in functional iron deficiency (FID) and normal iron status groups. Single hepcidin measurements are not sufficient for assessing FID in T1D.
Area of Science:
- Pediatric Endocrinology
- Hematology
- Metabolic Disorders
Background:
- Chronic low-grade inflammation in type 1 diabetes (T1D) may elevate hepcidin, potentially causing functional iron deficiency (FID).
- Understanding iron status in T1D is crucial for managing potential complications.
Purpose of the Study:
- To investigate hepcidin concentrations in T1D children with FID compared to those with normal iron status and absolute iron deficiency (AID).
- To assess the utility of hepcidin in identifying FID in pediatric T1D patients.
Main Methods:
- Cross-sectional study of 215 T1D children (median age 13.7 years).
- FID defined by elevated zinc protoporphyrin/heme ratio and/or red blood cell distribution width; AID by low serum ferritin.
- Serum hepcidin measured by mass-spectrometry; post-hoc analyses used transferrin saturation and reticulocyte hemoglobin content.
Main Results:
- Hepcidin concentrations were significantly higher in FID patients than in AID patients (p < 0.001).
- Hepcidin levels did not differ between FID patients and those with normal iron status, regardless of FID definition.
- Median hepcidin: 1.8 nmol/L (normal), 0.4 nmol/L (AID), 1.6 nmol/L (FID).
Conclusions:
- Single hepcidin measurements appear insufficient for assessing FID in children with T1D.
- Variability in hepcidin influenced by multiple factors may explain findings.
- Future studies with longitudinal hepcidin measurements might offer better insights into FID in T1D.
Abstract:
Chronic low-grade inflammation in type 1 diabetes (T1D) might increase hepcidin synthesis, possibly resulting in functional iron deficiency (FID). We hypothesized that in T1D children with FID, hepcidin concentrations are increased compared to those with normal iron status and those with absolute iron deficiency (AID). We evaluated hepcidin concentrations in T1D children in relation to iron status, and investigated whether hepcidin is useful in assessing FID. A cross-sectional study was conducted. FID was defined as elevated zinc protoporphyrin/heme ratio and/or red blood cell distribution width, and AID as low serum ferritin concentration. Post-hoc analyses with different definitions of FID were performed, using transferrin saturation and reticulocyte hemoglobin content. Serum hepcidin concentrations were measured using mass-spectrometry. The IRODIAB-study is registered at www.trialregister.nl (NTR4642). This study included 215 T1D children with a median age of 13.7 years (Q1-Q3: 10.1-16.3). The median (Q1-Q3) hepcidin concentration in patients with normal iron status was 1.8 nmol/l (0.9-3.3), in AID-patients, 0.4 nmol/l (0.4-0.4) and in FID-patients, 1.6 nmol/l (0.7-3.5). Hepcidin concentrations in FID-patients were significantly higher than in AID-patients (p < 0.001). Irrespective of FID-definition used, hepcidin concentrations did not differ between FID-patients and patients with normal iron status. This might be explained by the influence of various factors on hepcidin concentrations, and/or by differences in response of iron parameters over time. Single hepcidin measurements do not seem useful in assessing FID in T1D children. Multiple hepcidin measurements over time in future studies, however, might prove to be more useful in assessing FID in children with T1D.
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