Role of some inflammatory markers in recent ischemic stroke

ABSTRACT

The onset of cerebral ischemia triggers a cascade of pro-inflammatory molecular and cellular events. Clinical studies suggest that the strength of this acute response is important in early and late clinical outcomes, early clinical worsening, and extent of brain damage. The aim of this work was to estimate the. role of some inflammatory markers in recent ischemic stroke, and to correlate these inflammatory markers with the short term outcome. Twenty sex patients presented with recent history of hemiplegia within 24 hours were included. The patient group was planned to contain 13 patients with the age between 20 and <40years and 13 patients with the age between 40 and 60 years. 15 subjects, [age and sex matched to the patients] were included in the study as control Neurological deficits were rated by Scandinavian Stroke Scale. Clinical assessments and serum levels of the inflammatory markers, Neopterin C -Reactive Protein [CRP], Tumor Necrosis Factor-alpha [TNF-alpha], Complement 4 [C-4], Interleukin-8 [IL-8], and Neopterin, were done at the time of admission, day 3, and day 7 from the stroke onset. Serum levels of neopterin started to increase from the 3 rd day and remained high to the end of the first week from the onset of the stroke. The increase was more obvious in the young aged patients. Serum levels of IL-8, raised rapidly in the acute phase of the stroke and then gradually decreased through the first wee and but still higher than the base line of the total patients and control. Serum levels of TNF-alpha and CRP had rapid significant increase from the first day to reach maximum levels in the 3 rd day and still significantly high till the end of the first week Serum CRP levels were higher in the old age group while serum C4 levels decreased from the 1 st day then gradually increased to reach maximum levels in the 7 th day, but still significantly lower than the control group. Also, there were statistically positive correlations between serum levels of neopterin and C-4 in the 3 rd sample with the Scandinavian scale in the 3 rd assessment. Brain ischemia induced an inflammatory cascade by the increase in serum levels of neopterin, IL-8, TNF-alpha, CRP and decrease in C4. This inflammatory response continued through the first week by the increase in the levels of complement -4. The inflammatory response was more obvious in the young aged patients. There were positive correlations between serum levels of neopterin, and C-4 with the short-term outcome of the stroke patients