Plasma myeloperoxidase levels in patients with acute ischemic stroke.

Myeloperoxidase (MPO) is a glycoprotein released by activated polymorphonuclear neutrophils, which takes part in the defence of the organism through production of hypochlorous acid (HOCl), a potent oxidant. MPO has a role in pathogenesis of atherosclerosis. The aim of the study was to evaluate the time course of MPO plasma levels in the early stage of ischemic stroke. The study included 78 patients with acute ischemic stroke, 46 females and 32 males, mean age 74.3 +/- 6.8 years. Blood samples for MPO measurement were taken within 24 hours after the onset of ischemic stroke. Seventy-two patients served as matched controls 43 females and 29 males, mean age 71.3 +/- 6.4 years. MPO was measured in plasma using the Abbott Architect platform (Abbott Diagnostics Inc., Abbott Parck IL). Comparisons between patients and controls and patients group were expressed as relative risk with its 95% confidence interval (RR [95% CI]), where a lower limit > 1.0 was considered significant. All p values were determined by Fischer's exact test. A value of p < 0.05 was considered statistically significant. Mean plasma MPO level was in patients with acute ischemic stroke 583 +/- 48 pmol/L. Seventy-one patients out of seventy-eight patients with ischemic stroke presented mean plasma MPO levels greater than the upper of normal (425 +/- 36 pmol/L, p < 0.0001, (RR 8.188, [95% CI 4.038 to 16.600]). Twelve controls presented mean plasma MPO level greater than the upper of normal. In conclusion, plasma MPO levels were statistically significantly higher in patients after ischemic stroke as compared to controls. MPO has been associated with acute ischemic stroke but its direct role in its pathogenesis has not been established. MPO could be proposed as a potential prognostic marker of such lesions rather than a marker of diagnosis. MPO is a new biomarker and a possible future therapeutic target.

Detection of serum of IgG anti-neuronal antibodies in systemic lupus erythematosus patients with central nervous system manifestations.

The objective of the study was to assess the frequence of serum IgG anti-neuronal antibodies (NA) in SLE patints with CNS manifestations. Serum anti-NA antibodies were measured in 47 patients with SLE with CNS manifestations (CNS-SLE), age 33-52 years, mean age 38.6 years, 18 men and 29 women, as compared to 31 patients with SLE without CNS manifestations, age 28-56 years, mean age 41.2 years, 13 men and 18 women and 56 healthy subjects. Serum IgG antineuronal antibodies were measured by indirect immunofluorescent assay. Thirty-five of out 47 CNS-SLE patients presented anti-NA (74.6%). Anti-NA were observed in 15 out of 15 patients with acute confusional state (100%), in 8 of 8 patients with cerebrovascular disease (100%), in 5 out of 7 patients with seizure disorder (76.3%), and in 4 out of 5 patients in intractable headache (86.8%). Out of 31 nonCNS-SLE patients 1 patient presented anti-NA (3.9%). Serum anti-NA were more frequently observed in CNS-SLE patients as compared to controls (p < 0.000001). The frequence of serum anti-NA was significantly higher in CNS-SLE patients as compared to non CNS-SLE patients (p < 0.00001). In conclusion, serum anti-neuronal antibodies are associated with CNS-SLE. These antibodies are more frequent in CNS-SLE than in nonCNS-SLE patients, demonstrating a strong association between serum anti-NA and CNS involvement of SLE. The presence of serum anti-NA could be a useful diagnostic tool for CNS-SLE, the test could help to distinguish SLE from other diseases with similar symptoms. Further studies are needed to evaluate the predictive value of anti-NA in SLE.