Elevated transferrin concentration in cerebral spinal fluid after subarachnoid hemorrhage

Takenaka, Katsunobu; Sakai, Noboru; Murase, Shinobu; Kuroda, Taira; Okumura, Ayumi; Sawada, Michio

doi:10.1080/01616412.2000.11740755

Cited by 11 publications

(7 citation statements)

References 27 publications

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“…Moreover, significantly elevated CSF levels have been recently described in patients who developed this condition. 28, 29 We could not replicate these findings and CSF Tf, while elevated in SAH patients, trended down over time and no significant difference by DCI status was observed. It is important to note that we measured Tf levels at an earlier time frame and that may at least partially account for this discrepancy.…”

Section: Discussionmentioning

confidence: 73%

Brain Iron Metabolism and Brain Injury Following Subarachnoid Hemorrhage: iCeFISH-Pilot (CSF Iron in SAH)

et al. 2014

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Objectives To explore the relationship between levels of non-protein bound iron in cerebrospinal fluid and the development of early brain injury in patients with aneurysmal SAH. Design Prospective observational cohort pilot study. Setting Neurointensive care unit of an academic, tertiary medical center Patients Patients admitted with aneurysmal subarachnoid hemorrhage Hunt and Hess grades 2 to 4 requiring ventriculostomy insertion as part of their clinical management. Interventions None. Measurements and main results Samples of cerebrospinal fluid (CSF) were obtained on days 1, 3, and 5. A fluorometric assay that relies on an oxidation sensitive probe was used to measure unbound iron, and levels of iron-handling proteins were measured by means of enzyme-linked immunosorbent assays. We prospectively collected and recorded demographic, clinical, and radiological data. A total of 12 patients were included in this analysis. Median Hunt and Hess score on admission was 3.5 (IQR: 1) and median modified Fisher scale score was 4 (IQR: 1). Seven of 12 patients (58%) developed delayed cerebral ischemia (DCI). Day 5 non-transferrin bound iron (NTBI) (7.88±1 vs. 3.58± 0.8, p= 0.02) and mean NTBI (7.39± 0.4 vs. 3.34±0.4 p= 0.03) were significantly higher in patients who developed DCI. Mean and day 3 levels of redox-active iron correlated with development of angiographic vasospasm in logistic regression analysis (p= 0.02); while mean redox-active iron and lower levels of ceruloplasmin on days 3, 5 and peak were correlated with development of deep cerebral infarcts. Conclusions our preliminary data indicate a causal relationship between unbound iron and brain injury following SAH and suggest a possible protective role for ceruloplasmin in this setting, particularly in the prevention of cerebral ischemia. Further studies are needed to validate these findings and to probe their clinical significance.

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Section: Discussionmentioning

confidence: 73%

Brain Iron Metabolism and Brain Injury Following Subarachnoid Hemorrhage: iCeFISH-Pilot (CSF Iron in SAH)

et al. 2014

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“…Tf is unique in chelating iron with very high affinity. It has been reported that Tf concentration is significantly increased in cerebral spinal fluid after subarachnoid hemorrhage 20 . It has also been demonstrated that Tf could protect neurons from an iron-dependent injury in an established cell culture model of hemoglobin neurotoxicity 21 .…”

Section: Discussionmentioning

confidence: 94%

A combination of serum iron, ferritin and transferrin predicts outcome in patients with intracerebral hemorrhage

Yang

Zhang

et al. 2016

Sci Rep

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Association of a high-serum ferritin with poor outcome showed that iron might play a detrimental role in the brain after intracerebral hemorrhage (ICH). Here, we investigated changes in serum iron, ferritin, transferrin (Tf) and ceruloplasmin (CP) in patients with ICH (n = 100) at day 1 (admission), 3, 7, 14 and 21 and those in control subjects (n = 75). The hematoma and edema volumes were also determined in ICH-patients on admission and at day 3. The Modified Rankin Scale (mRS) of 59 patients was ≥3 (poor outcome) and 41 < 3 (good outcome) at day 90. Serum ferritin was significantly higher and serum iron and Tf markedly lower in patients with poor-outcome than the corresponding values in patients with good-outcome at day 1 to 7 and those in the controls. There was a significant positive correlation between serum ferritin and relative edema volume or ratio at day 1 and 3 and hematoma volume at day 1 (n = 28), and a negative correlation between serum iron or Tf and hematoma volume at day 1 (n = 100). We concluded that not only increased serum ferritin but also reduced serum iron and Tf are associated with outcome as well as hematoma volume.

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“…Transferrin also up-regulated chemokine synthesis in human proximal tubular epithelial cells [4] and induced a dose-dependent increase in iNOS mRNA and nitrite accumulation in rat aortic smooth muscle cells [5]. In chickens, ovatransferrin is a key modulator of cellular activation measured by its ability to induce the production of IL-6, matrix metalloproteinases and respiratory burst in activated chicken macrophages [6,7].…”

Section: Introductionmentioning

confidence: 98%

Recombinant transferrin induces nitric oxide response in goldfish and murine macrophages

Stafford

Wilson

Belosevic

2004

Fish & Shellfish Immunology

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Elevated transferrin concentration in cerebral spinal fluid after subarachnoid hemorrhage

Cited by 11 publications

References 27 publications

Brain Iron Metabolism and Brain Injury Following Subarachnoid Hemorrhage: iCeFISH-Pilot (CSF Iron in SAH)

Brain Iron Metabolism and Brain Injury Following Subarachnoid Hemorrhage: iCeFISH-Pilot (CSF Iron in SAH)

A combination of serum iron, ferritin and transferrin predicts outcome in patients with intracerebral hemorrhage

Recombinant transferrin induces nitric oxide response in goldfish and murine macrophages

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