Iron-related damage in acute ischemic stroke.

Abstract

Although iron-mediated mechanisms are important in experimental brain injury after carotid occlusion, their clinical role in acute ischemic stroke has not been determined. We evaluated the influence of iron stores, measured as serum ferritin, on the outcome of acute cerebral infarct. Admission and fasting glycemia, glycosylated hemoglobin, serum cortisol, serum ferritin, and 24-hour urinary free cortisol levels were measured on the first day of hospitalization in 67 patients admitted with an acute ischemic stroke of less than 24 hours' duration. Patients were classified into two groups according to their Canadian Stroke Scale (CSS) score on day 30: good outcome group (alive and CSS score > 7 points) and poor outcome group (dead or CSS score < or = 7 points). Thirty-three patients (49%) had good outcome and 34 (51%) poor outcome. Fasting glycemia (P = .001), serum cortisol (P < .001), and urinary free cortisol (P = .001) but not admission glycemia and glycosylated hemoglobin had higher levels in patients with poor outcome. Serum ferritin values were greater in the poor outcome group (218 +/- 156 micrograms/L versus 133 +/- 125 micrograms/L; P = .004), and a correlation between ferritin values and degree of worsening or improvement of the CSS score on day 30 was found (P = .002). Serum cortisol (odds ratio [OR], 6.7; 95% confidence interval [CI], 1.7 to 26), fasting glycemia (OR, 5.4; 95% CI, 1.2 to 24), and serum ferritin (OR, 4.6; 95% CI, 1.1 to 19) were independently related to poor outcome in a logistic regression analysis. High serum ferritin levels within the first 24 hours of hospitalization for an acute ischemic stroke are related to a poor prognosis, independent of the stress response. More research is needed to determine the origin of increased serum ferritin levels and the therapeutic implications.