Serum C-reactive protein and lipid hydroperoxides in predicting short-term clinical outcome after spontaneous intracerebral hemorrhage.

There is no effective treatment for spontaneous intracerebral hemorrhage (sICH). We examined 46 patients with sICH within 48 hours after onset of symptoms, aiming to assess the predictive value of C-reactive protein (CRP) and lipid hydroperoxides (ROOH) on "first-week mortality" and "clinical outcome at discharge" by binary logistic regression. We found that serum CRP and hematoma volume were predictors of short-term mortality. Although serum ROOH level was positively correlated with mortality, it did not predict early lethal outcome. Serum ROOH concentration, however, was a predictor of poor clinical outcome in sICH survivors. After confirmation of the results obtained through observing a larger group of patients, an oxidative stress marker could be used as an additional criterion for patient stratification, especially when severe disability is expected and supplementary therapeutic approaches are urgent.

Oxidative stress in the chronic phase after stroke.

The spontaneous and the stimulated extracellular generation of reactive oxygen species (ROS) by peripheral phagocytes, the blood antioxidant capacity and the degree of oxidative damage were evaluated in patients with severe ischemic and hemorrhagic stroke in the chronic phase of disease. It was found in patients compared to the control group that: (i) the spontaneous phagocyte oxidative activity was enhanced independently of the type of stroke and the time elapsed after stroke onset; (ii) there was no difference in the extracellular ROS generation stimulated by opsonin-dependent and independent receptor mechanisms; (iii) there was no change in the indices of blood antioxidant capacity; (iv) the concentration of plasma lipid peroxides was enhanced regardless of the type of stroke, but it significantly increased over time; and (v) the concentration of blood thiobarbituric acid-reactive material was also enhanced. It was independent of the type of stroke and remained elevated during the whole period studied. We have demonstrated an enhanced spontaneous phagocyte oxidative activity and oxidative damage to lipids in patients in the chronic phase after stroke. The elimination of generated ROS and products of lipid peroxidation from the circulation could prevent the aggravation of chronic vascular injury in patients and could reduce the possibility of a subsequent stroke. This suggests the need for complex therapy, including antioxidant treatment directed to exclude the effects of free radicals, after the oxidative stress of stroke.