SERUM HEPCIDIN-25 IN COMPARISON WITH BIOCHEMICAL MARKERS AND HAEMATOLOGICAL INDICES FOR THE DIFFERENTIATION OF ANAEMIA STATES AND CORRELATION WITH RESPONSE TO ORAL IRON
(Abstract release date: 05/19/16)
EHA Library. Cowley A. 06/09/16; 133038; E1489
Dr. Anna Cowley
Contributions
Contributions
Abstract
Abstract: E1489
Type: Eposter Presentation
Background
Hepcidin is a key regulator of iron metabolism and may be a useful analyte in the differentiation of iron states in anaemia. Hepcidin is down regulated in the presence of iron deficiency to promote iron absorption and is up regulated when iron stores are in excess or in the setting of inflammation via IL-6. In combination with hypochromia indices and other markers of iron deficiency such as reticulocyte haemoglobin (Ret-He), a raised hepcidin level may provide evidence of both reduced iron absorption and iron restricted erythropoiesis. Conversely, a low or normal hepcidin level may be suggestive of true iron deficiency. In recent years immunoassays have become more readily available, allowing hepcidin to complement existing routine biochemical indices to differentiate anaemia states.
Aims
The primary aim of this study was to assess whether there was a correlation between hepcidin and markers of iron status in patients referred via the iron deficiency clinic at Plymouth Hospitals NHS Trust. The second objective was to investigate the association of baseline hepcidin-25 with response to oral iron.
Methods
Patients referred to the iron deficiency anaemia clinic by their GP were prospectively recruited. A clinical history, examination, blood tests including haematological indices and biochemical markers, appropriate investigations and oral iron supplementation were prescribed where appropriate. To determine the response to oral iron, the full blood count was repeated at 1 and 3 months. For the measurement of hepcidin-25, serum was frozen at -70C and then determined by batch analysis using a commercial ELISA kit (DRG Instruments, Marburg, Germany). Patients were classified as having iron deficiency anaemia (IDA), anaemia of chronic disease (ACD) or the combined state of iron restricted erythropoiesis (IRE) with ACD (ACD/IRE) using clinical findings and standard biochemical markers and haematological indices.
Results
The Hepcidin-25 immunoassay performed well, with a low within- and between- assay coefficient of variation. The table shows the numbers and characteristics of the patients allocated to the 3 types of anaemia. Numbers given as median and interquartile range.
Hepcidin concentrations correlated significantly with ferritin concentrations. Serum hepcidin was less than 1 ng/mL in 80 of 85 patients with IDA. This is consistent with previous data. There were no linear associations seen between hepcidin and other indices of anaemia (Total Hb, MCV, MCH, Ret-He, Transferrin, Transferrin saturation, Iron and CRP). 96 patients had a trial of oral iron, with 65 responding (increase of >10g/l by 12 weeks) and 31 failing to achieve an adequate rise in haemoglobin. There was no correlation between response to oral iron and hepcidin.
Conclusion
A positive correlation exists between Hepcidin-25 and serum ferritin. The majority of patients in this study had iron deficiency anaemia and correspondingly low hepcidin concentrations. A low hepcidin did not correlate with subsequent response to oral iron therapy. Further investigation, however, of hepcidin in anaemic patients with normal to high ferritin levels is warranted to further evaluate the role of this hormone in the management of these patients.
Session topic: E-poster
Keyword(s): Anemia, Hepcidin, Iron deficiency anemia
Type: Eposter Presentation
Background
Hepcidin is a key regulator of iron metabolism and may be a useful analyte in the differentiation of iron states in anaemia. Hepcidin is down regulated in the presence of iron deficiency to promote iron absorption and is up regulated when iron stores are in excess or in the setting of inflammation via IL-6. In combination with hypochromia indices and other markers of iron deficiency such as reticulocyte haemoglobin (Ret-He), a raised hepcidin level may provide evidence of both reduced iron absorption and iron restricted erythropoiesis. Conversely, a low or normal hepcidin level may be suggestive of true iron deficiency. In recent years immunoassays have become more readily available, allowing hepcidin to complement existing routine biochemical indices to differentiate anaemia states.
Aims
The primary aim of this study was to assess whether there was a correlation between hepcidin and markers of iron status in patients referred via the iron deficiency clinic at Plymouth Hospitals NHS Trust. The second objective was to investigate the association of baseline hepcidin-25 with response to oral iron.
Methods
Patients referred to the iron deficiency anaemia clinic by their GP were prospectively recruited. A clinical history, examination, blood tests including haematological indices and biochemical markers, appropriate investigations and oral iron supplementation were prescribed where appropriate. To determine the response to oral iron, the full blood count was repeated at 1 and 3 months. For the measurement of hepcidin-25, serum was frozen at -70C and then determined by batch analysis using a commercial ELISA kit (DRG Instruments, Marburg, Germany). Patients were classified as having iron deficiency anaemia (IDA), anaemia of chronic disease (ACD) or the combined state of iron restricted erythropoiesis (IRE) with ACD (ACD/IRE) using clinical findings and standard biochemical markers and haematological indices.
Results
The Hepcidin-25 immunoassay performed well, with a low within- and between- assay coefficient of variation. The table shows the numbers and characteristics of the patients allocated to the 3 types of anaemia. Numbers given as median and interquartile range.
| Variables | IDA | ACD | ACD/IRE |
| Number | 85 | 30 | 15 |
| Age | 72 (61-80) | 76 (65-79) | 79 (64-79) |
| Haemoglobin (g/L) | 109 (99-120) | 112 (98-121) | 111 (106-117) |
| MCV (fL) | 80.4 (76.2-84.9) | 86.7 (83.8-90.7) | 82.5 (77.5-83.8) |
| MCH (pg) | 25.1 (23.6-27.1) | 28.1 (26.6-29.8) | 26.1 (24.7-27.7) |
| Ferritin (ug/L) | 12 (9-16) | 119 (63-256) | 40 (34-72) |
| CRP (mg/L) | 2 (1-5) | 9 (2-56) | 4 (2-14) |
| Transferrin saturation (%) | 7.29 (5.67-11.13) | 16.45 (9.87-21.93) | 13.72 (11.41-18.51) |
| Ret-He (pg) | 27.6 (24.9-30.5) | 31.9 (28.5- 35.6) | 31.6 (30.1-32.9) |
| Hepcidin (ng/mL) | 0 (0 - 0) | 5.4 (0 - 75.4) | 0 (0 - 1.268) |
Conclusion
A positive correlation exists between Hepcidin-25 and serum ferritin. The majority of patients in this study had iron deficiency anaemia and correspondingly low hepcidin concentrations. A low hepcidin did not correlate with subsequent response to oral iron therapy. Further investigation, however, of hepcidin in anaemic patients with normal to high ferritin levels is warranted to further evaluate the role of this hormone in the management of these patients.
Session topic: E-poster
Keyword(s): Anemia, Hepcidin, Iron deficiency anemia
Abstract: E1489
Type: Eposter Presentation
Background
Hepcidin is a key regulator of iron metabolism and may be a useful analyte in the differentiation of iron states in anaemia. Hepcidin is down regulated in the presence of iron deficiency to promote iron absorption and is up regulated when iron stores are in excess or in the setting of inflammation via IL-6. In combination with hypochromia indices and other markers of iron deficiency such as reticulocyte haemoglobin (Ret-He), a raised hepcidin level may provide evidence of both reduced iron absorption and iron restricted erythropoiesis. Conversely, a low or normal hepcidin level may be suggestive of true iron deficiency. In recent years immunoassays have become more readily available, allowing hepcidin to complement existing routine biochemical indices to differentiate anaemia states.
Aims
The primary aim of this study was to assess whether there was a correlation between hepcidin and markers of iron status in patients referred via the iron deficiency clinic at Plymouth Hospitals NHS Trust. The second objective was to investigate the association of baseline hepcidin-25 with response to oral iron.
Methods
Patients referred to the iron deficiency anaemia clinic by their GP were prospectively recruited. A clinical history, examination, blood tests including haematological indices and biochemical markers, appropriate investigations and oral iron supplementation were prescribed where appropriate. To determine the response to oral iron, the full blood count was repeated at 1 and 3 months. For the measurement of hepcidin-25, serum was frozen at -70C and then determined by batch analysis using a commercial ELISA kit (DRG Instruments, Marburg, Germany). Patients were classified as having iron deficiency anaemia (IDA), anaemia of chronic disease (ACD) or the combined state of iron restricted erythropoiesis (IRE) with ACD (ACD/IRE) using clinical findings and standard biochemical markers and haematological indices.
Results
The Hepcidin-25 immunoassay performed well, with a low within- and between- assay coefficient of variation. The table shows the numbers and characteristics of the patients allocated to the 3 types of anaemia. Numbers given as median and interquartile range.
Hepcidin concentrations correlated significantly with ferritin concentrations. Serum hepcidin was less than 1 ng/mL in 80 of 85 patients with IDA. This is consistent with previous data. There were no linear associations seen between hepcidin and other indices of anaemia (Total Hb, MCV, MCH, Ret-He, Transferrin, Transferrin saturation, Iron and CRP). 96 patients had a trial of oral iron, with 65 responding (increase of >10g/l by 12 weeks) and 31 failing to achieve an adequate rise in haemoglobin. There was no correlation between response to oral iron and hepcidin.
Conclusion
A positive correlation exists between Hepcidin-25 and serum ferritin. The majority of patients in this study had iron deficiency anaemia and correspondingly low hepcidin concentrations. A low hepcidin did not correlate with subsequent response to oral iron therapy. Further investigation, however, of hepcidin in anaemic patients with normal to high ferritin levels is warranted to further evaluate the role of this hormone in the management of these patients.
Session topic: E-poster
Keyword(s): Anemia, Hepcidin, Iron deficiency anemia
Type: Eposter Presentation
Background
Hepcidin is a key regulator of iron metabolism and may be a useful analyte in the differentiation of iron states in anaemia. Hepcidin is down regulated in the presence of iron deficiency to promote iron absorption and is up regulated when iron stores are in excess or in the setting of inflammation via IL-6. In combination with hypochromia indices and other markers of iron deficiency such as reticulocyte haemoglobin (Ret-He), a raised hepcidin level may provide evidence of both reduced iron absorption and iron restricted erythropoiesis. Conversely, a low or normal hepcidin level may be suggestive of true iron deficiency. In recent years immunoassays have become more readily available, allowing hepcidin to complement existing routine biochemical indices to differentiate anaemia states.
Aims
The primary aim of this study was to assess whether there was a correlation between hepcidin and markers of iron status in patients referred via the iron deficiency clinic at Plymouth Hospitals NHS Trust. The second objective was to investigate the association of baseline hepcidin-25 with response to oral iron.
Methods
Patients referred to the iron deficiency anaemia clinic by their GP were prospectively recruited. A clinical history, examination, blood tests including haematological indices and biochemical markers, appropriate investigations and oral iron supplementation were prescribed where appropriate. To determine the response to oral iron, the full blood count was repeated at 1 and 3 months. For the measurement of hepcidin-25, serum was frozen at -70C and then determined by batch analysis using a commercial ELISA kit (DRG Instruments, Marburg, Germany). Patients were classified as having iron deficiency anaemia (IDA), anaemia of chronic disease (ACD) or the combined state of iron restricted erythropoiesis (IRE) with ACD (ACD/IRE) using clinical findings and standard biochemical markers and haematological indices.
Results
The Hepcidin-25 immunoassay performed well, with a low within- and between- assay coefficient of variation. The table shows the numbers and characteristics of the patients allocated to the 3 types of anaemia. Numbers given as median and interquartile range.
| Variables | IDA | ACD | ACD/IRE |
| Number | 85 | 30 | 15 |
| Age | 72 (61-80) | 76 (65-79) | 79 (64-79) |
| Haemoglobin (g/L) | 109 (99-120) | 112 (98-121) | 111 (106-117) |
| MCV (fL) | 80.4 (76.2-84.9) | 86.7 (83.8-90.7) | 82.5 (77.5-83.8) |
| MCH (pg) | 25.1 (23.6-27.1) | 28.1 (26.6-29.8) | 26.1 (24.7-27.7) |
| Ferritin (ug/L) | 12 (9-16) | 119 (63-256) | 40 (34-72) |
| CRP (mg/L) | 2 (1-5) | 9 (2-56) | 4 (2-14) |
| Transferrin saturation (%) | 7.29 (5.67-11.13) | 16.45 (9.87-21.93) | 13.72 (11.41-18.51) |
| Ret-He (pg) | 27.6 (24.9-30.5) | 31.9 (28.5- 35.6) | 31.6 (30.1-32.9) |
| Hepcidin (ng/mL) | 0 (0 - 0) | 5.4 (0 - 75.4) | 0 (0 - 1.268) |
Conclusion
A positive correlation exists between Hepcidin-25 and serum ferritin. The majority of patients in this study had iron deficiency anaemia and correspondingly low hepcidin concentrations. A low hepcidin did not correlate with subsequent response to oral iron therapy. Further investigation, however, of hepcidin in anaemic patients with normal to high ferritin levels is warranted to further evaluate the role of this hormone in the management of these patients.
Session topic: E-poster
Keyword(s): Anemia, Hepcidin, Iron deficiency anemia
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