Serum Ferritin Concentrations Are Not Modified in the Acute Phase of Ischemic Stroke

103

Background and Purpose-Preclinical evidence indicates that iron plays a key role in mediating neuronal injury and edema formation after intracerebral hemorrhage (ICH). However, the clinical role of iron in patients with ICH has not been well studied. We undertook this exploratory study to investigate the association of serum ferritin, as an indicator of body iron load, with perihematoma edema after ICH. Methods-We retrospectively reviewed prospectively-collected clinical and laboratory data from 23 consecutive patients with acute spontaneous ICH who had a CT scan and serum ferritin checked on admission, and a follow-up CT scan 3 to 4 days afterward. We measured hematoma and edema volumes on admission and follow-up scans, and calculated the relative edema volume to correct for hematoma volume. We used Spearman correlation coefficient to determine the association of various variables with relative perihematoma edema volume. Results-Whereas the median hematoma volume increased by approximately 28% from baseline to day 3 to 4, the relative edema volume almost doubled during this time period. We observed a significant positive correlation between serum ferritin and relative perihematoma edema volume on day 3 to 4 (rϭ0.78; Pϭ0.002), but not at baseline; and little correlation between the changes in hematoma volumes and corresponding relative edema volumes (rϭ0.14). There was a trend for a positive correlation between body temperature and relative edema volumes. Conclusions-Our findings support the notion that delayed iron toxicity plays a role in causing brain injury and edema formation after ICH. These findings are preliminary and need to be further investigated in future studies.

Section: Discussionsupporting

confidence: 49%

Association Between Serum Ferritin Level and Perihematoma Edema Volume in Patients With Spontaneous Intracerebral Hemorrhage

Mehdiratta

Kumar

Hackney

et al. 2008

103

“…Because of this, it is difficult to disentangle whether the increased serum ferritin concentrations reflect high body iron stores or were merely due to the acute-phase response. 25 This limitation highlights the need for prospective studies that measure serum ferritin before the onset of disease, like the present one, and that study its effect on stroke fatality.…”

Section: Van Der a Et Al Serum Ferritin And Stroke Risk In Womenmentioning

confidence: 88%

Serum Ferritin Is a Risk Factor for Stroke in Postmenopausal Women

Der

Grobbee

Roest

et al. 2005

Background and Purpose-Iron is an essential element for the human body. It has, however, been suggested that excessive iron stores may increase the risk of vascular disease. So far, epidemiologic studies on stroke are sparse. Methods-We studied the association between iron status and stroke risk in a population-based cohort of 11 471 Dutch postmenopausal women between 49 and 70 years of age. Women were included between 1993 and 1997 and followed up until January 1, 2000, for cerebrovascular events. We conducted a case-cohort study by using all stroke cases (nϭ63) and a random sample of the baseline cohort (nϭ1134). Serum ferritin, serum iron, and transferrin saturation were measured as markers of iron status. A weighted Cox proportional-hazards model was used to estimate crude and multivariate-adjusted hazard ratios for tertiles of different iron parameters in relation to stroke. Results-In a multivariate model, the highest tertile of serum ferritin concentration was associated with an increased risk of stroke (hazard ratio [HR], 1.45; 95% confidence interval [CI], 0.87 to 2.42) compared with the lowest tertile. For ischemic stroke, the increase was more pronounced (HR, 2.23; 95% CI, 1.05 to 4.73) and reached statistical significance. Conclusions-Neither serum iron nor transferrin saturation was associated with an increased stroke risk. However, higher serum ferritin concentrations in postmenopausal women are associated with an increased risk of ischemic stroke.

“…In addition, previous studies have shown stability of serum ferritin levels during the first 48 hours after stroke onset and a lack of correlation between ferritin and acute-phase reactants in blood such as cortisol and C-reactive protein. 15,23 Iron Figure 1. Distribution of mRS scores at day 90 by serum ferritin levels categorized in quartiles.…”

Section: Discussionmentioning

confidence: 99%

Increased Body Iron Stores Are Associated With Poor Outcome After Thrombolytic Treatment in Acute Stroke

Millán

Sobrino²,

Castellanos³

et al. 2007

Self Cite

Background and Purpose-Iron overload has been associated with greater oxidative stress and brain injury in experimental cerebral ischemia and reperfusion. This study investigates whether high serum ferritin levels, as an index of increased cellular iron stores, are associated with poor outcome, hemorrhagic transformation, and brain edema after treatment with tissue plasminogen activator in patients with acute ischemic stroke. Methods-A total of 134 consecutive patients treated with intravenous tissue plasminogen activator were prospectively studied in four centers. Serum ferritin levels were determined at baseline, 24 and 72 hours after treatment. Cranial computed tomography was performed on admission and at 24 to 36 hours after tissue plasminogen activator infusion. Stroke severity and outcome were evaluated by using the National Institute of Health Stroke Scale and the modified Rankin Scale. Results-Computed