Serum soluble CD40 ligand levels after acute intracerebral hemorrhage.

BACKGROUND: Soluble CD40 ligand (sCD40L) is associated with inflammation. This study aimed to assess the prognostic value of sCD40L for clinical outcomes of acute intracerebral hemorrhage (ICH) patients. MATERIALS AND METHODS: The serum sCD40L levels of 110 patients and 110 age- and gender-matched healthy controls were measured using sandwich immunoassays. The relationships between serum sCD40L levels and 1-week mortality, 6-month mortality, 6-month overall survival, 6-month unfavorable outcome (modified Rankin Scale score >2), and ICH severity including hematoma volume and National Institutes of Health Stroke Scale (NIHSS) score were assessed using multivariate analysis. RESULTS: Compared with healthy controls, ICH patients had higher serum sCD40L levels. Serum sCD40L levels were correlated positively with hematoma volumes and NIHSS scores using a multivariate linear regression. Multivariate analysis results indicated that sCD40L was identified an independent predictor of 1-week mortality, 6-month mortality, 6-month unfavorable outcome and 6-month overall survival. sCD40L also showed high predictive performances for 1-week mortality, 6-month mortality and 6-month unfavorable outcome based on receiver operating characteristic curve. CONCLUSIONS: Elevated serum sCD40L levels are independently associated with ICH severity and clinical outcomes. And sCD40L has potential to be a good prognostic biomarker of ICH.

[Effect of xingnaojing injection combined with minimally invasive percutaneous drainage in treating brain edema and content of serum AQP4 in patients with moderate hypertensive basal ganglia hemorrhage].

OBJECTIVE: To observe the effect of Xingnaojing Injection combined with minimally invasive percutaneous drainage on brain edema and content of serum aquaporin-4 (AQP4) in patients with moderate hypertensive basal ganglia hemorrhage, and discuss the treatment mechanism of Xingnaojing injection combined with minimally invasive percutaneous drainage for cerebral hemorrhage. METHOD: Forty-two patients with moderate (25-50 mL) hypertensive basal ganglia hemorrhage (< 24 h) were selected and randomly divided into two groups: the observation group (n = 22) and the control group (n = 20). The neurological severity score were evaluated by the NIHSS (national institutes of health stroke scale), the volume of brain edemas were measured by head CT, the serum levels of AQP4 were determined by ELISA method on admission and 1 and 2 weeks after treatment. RESULT: On admission, there was no significant difference in the scores of NIHSS, the volume of brain edemas and the level of serum AQP4 between the observation group and the control group. At the end of the first week after the treatment, the score of NIHSS of the observation group were lower than that of the control group, with significant different (P < 0.05); the observation group showed reduced volume of brain edemas than that on admission (P < 0.05), whereas the control group the control group showed increased volume of brain edemas than that on admission; the control group displayed increased level of serum AQP4 than that on admission, but without significant difference; the observation group displayed decreased level of serum AQP4 than that on admission (P < 0.05). At the end of the second week after the treatment, the control group showed decreased score of NIHSS than that on admission and at the end of the first week after treatment (P < 0.05). Compared with the control group, the observation group showed a much lower score of NIHSS (P < 0.01), the control group displayed reduced volume of brain edemas than that on admission and at the end of the first week after treatment, but the observation group was even lower than the control group. Both of observation and control groups displayed significantly reduced level of AQP4 (P < 0.05), but the observation group showed a lower AQP4 level than that of the control group (P < 0.05). CONCLUSION: The therapy of Xingnaojing injection combined with minimally invasive percutaneous drainage could remarkably reduce brain edema, and promote neural functional recovery, thus could be selected as a therapeutic regimen for patients with moderate hypertensive basal ganglia hemorrhage.

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage.

We examined a possible relationship -420C>G SNP of the resistin gene with plasma resistin and C-reactive protein concentrations in intracerebral hemorrhage. Three hundred and forty-four Chinese Han patients with intracerebral hemorrhage and 344 age- and gender-matched healthy controls were included in our study. Plasma resistin and C-reactive concentrations were measured and SNP -420C>G was genotyped. The genotype frequencies in controls and patients were not significantly different (P = 0.672). Plasma resistin and C-reactive protein levels were significantly different between the SNP -420C>G genotypes, even after adjustment for age, gender and body mass index. The common homozygote (C-C) had the lowest resistin and C-reactive protein plasma concentrations; the plasma resistin and C-reactive protein concentrations in the heterozygote (C-G) and the rare allele homozygote (G-G) did not differ significantly. Plasma resistin levels were significantly associated with plasma C-reactive protein level. We conclude that SNP -420C>G of the resistin gene could be involved in the inflammatory component of intracerebral hemorrhage through enhanced production of resistin.

Time course of plasma microparticle concentrations after acute spontaneous basal ganglia hemorrhage.

OBJECTIVES: To examine the changes in plasma microparticle (MP) levels in patients after intracerebral hemorrhage (ICH) and assess their association with outcome along with biological markers of the acute phase response. MATERIALS AND METHODS: Thirty healthy controls and 86 patients with acute ICH were recruited. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7 after ICH. MPs with procoagulant potential were measured with a prothrombinase assay. RESULTS: Plasma MP levels in patients were substantially higher than those in healthy controls during the 7-day period. Plasma MP levels were strongly associated with outcome and with biological markers of the acute phase response. Multivariate analysis showed baseline plasma MP level was a good predictor of 1-week mortality (odds ratio, 1.930; 95% confidence interval, 1.229-3.031; P=0.004). A receiver operating characteristic curve identified the plasma MP cutoff level (8.4 nmol/l phosphatidylserine equivalent) that predicted 1-week mortality with high sensitivity (90.6%) and specificity (68.5.0%) (P<0.001). CONCLUSIONS: Increased membrane microparticle levels occur after ICH and may contribute to the subsequent brain injury, in association with a poor clinical outcome.

Utility of serum amyloid A as a potential prognostic biomarker of acute primary basal ganglia hemorrhage.

BACKGROUND: Intracerebral hemorrhage (ICH) can lead to inflammation. Serum amyloid A (SAA) is an acute phase protein, which might be implicated in acute brain injury. We ascertain relationship between serum SAA and inflammation, severity plus outcome after ICH. METHODS: In this prospective, observational study, serum SAA concentrations were quantified in 159 healthy volunteers and 159 acute primary basal ganglia hemorrhage patients admitted within 24 h after stroke symptom. Prognostic parameters included death and a poor outcome (modified Rankin Scale score > 2) at 90 days after stroke. RESULTS: Serum SAA concentrations were substantially higher in patients than in controls. Among patients, serum SAA concentrations were strongly correlated with serum C-reactive protein concentrations, hematoma volume and National Institutes of Health Stroke Scale scores. Serum SAA appeared to be an independent predictor for 90-day death, overall survival and poor outcome. Under receiver operating characteristic curve, this protein exhibited similar prognostic capability, as compared to hematoma volume and National Institutes of Health Stroke Scale scores. CONCLUSIONS: Rising serum SAA concentrations, in close correlation with inflammation and hemorrhagic severity, are independently related to mortality and poor outcome after ICH, indicating that serum SAA might serve as a potential prognostic biomarker for ICH.

Hemoglobin Concentration Affects Hypertensive Basal Ganglia Hemorrhage After Surgery: Correlation Analysis in a High-Altitude Region.

OBJECTIVE: Hypertensive cerebral hemorrhage leads to greater mortality and worse functional outcomes at high altitudes. Experimental studies have suggested that hemoglobin can lead to increased perihemorrhagic edema after intracerebral hemorrhage. METHODS: Patients were divided into a high-hemoglobin (H-H) group (>180 g/L) and a low-hemoglobin (L-H) group (≤180 g/L). The distance from the cortex to the midline was used to indicate the degree of edema. At 1, 7, 14, and 21 days, the patients' status was scored using the Glasgow coma scale, and survival was plotted using Kaplan-Meier survival curves. Pearson correlation analysis showed that the difference between the postoperative and preoperative Glasgow coma scale score correlated with the hemoglobin concentration. The Glasgow outcome scale was used to assess neurological recovery after 6 months. RESULTS: On days 7, 14, and 21, the edema of the H-H group was significantly greater than that of the L-H group (P < 0.01 and P < 0.001, respectively). The edema of the H-H group peaked at 14 and 21 days, but that of the L-H group peaked at 7 days. The hemoglobin concentration and postoperative neurological recovery had a linear relationship in the H-H group. The L-H group had greater survival compared with the H-H group (P < 0.05). The L-H group had higher Glasgow outcome scale scores compared with the H-H group (P < 0.05). CONCLUSION: The hemoglobin concentration affects the mortality and morbidity from hypertensive cerebral hemorrhage in high-altitude regions, and a linear relationship exists between hemoglobin concentration and neurological recovery in the H-H group.

A clinical study on the effects of recombinant human colony stimulating factor on the expression of Bcl-2 in serum of patients with basal ganglia hemorrhage and its clinical significance.

OBJECTIVE: We investigated the effects of the colony-stimulating factor (CSF-1) on Bcl-2 expression in serums of patients with basal ganglia hemorrhage and subsequently, its clinical significance. PATIENTS AND METHODS: The expression levels of Bcl-2 in serums of patients with basal ganglia hemorrhage were analyzed, and the effects of the CSF-1 on Bcl-2 expression were observed. Samples of peripheral blood were taken from 120 patients with basal ganglia hemorrhage admitted to the Neurology Department and 120 healthy people undergoing a physical examination at Xiangyang Central Hospital between May 2013 to December 2014. The detection of Bcl-2 levels in serums of patients was performed using the ELISA method, and patients were divided into two groups, the colony-stimulating factor (CSF-1) group and the control group. The CSF-1 group was treated with recombinant human granulocyte colony-stimulating factor after routine treatment, while the control group was treated only with routine treatment. The two groups of patients were followed up for observation of treatment effects. RESULTS: Before treatment, serum Bcl-2 levels in both the CSF-1 and control group showed no significant differences; however, their levels were significantly higher than those of the healthy cohort (p<0.05). After treatment, serum Bcl-2 levels of the CSF-1 group were significantly higher than those of the control group (p<0.05). However, compared to the healthy control group, the levels remained significantly higher and the differences were statistically significant (p<0.05). When compared to the recovering conditions of patients in the CSF-1 group and the control group, we found that the average hospitalization time and occurrences of complications in the CSF-1 group were significantly less than those in the control group (p<0.05). CONCLUSIONS: CSF-1 is clinically effective in improving the serum Bcl-2 levels after a basal ganglia hemorrhage, and it can be used as adjuvant therapy in the treatment of basal ganglia hemorrhage.

Differences in Neuropeptide Y Secretion Between Intracerebral Hemorrhage and Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Neuropeptide Y (NPY) is one of the most potent endogenous vasoconstrictors, and its contribution to the multifactorial cascade of cerebral vasospasm due to nontraumatic subarachnoid hemorrhage (SAH) is not yet fully understood. This experimental study compared the hemorrhage-specific course of NPY secretion into cerebrospinal fluid (CSF) and into plasma between 2 groups: patients with SAH and patients with basal ganglia hemorrhage (BGH) or cerebellar hemorrhage (CH) over the first 10 days after hemorrhage. MATERIALS AND METHODS: Seventy-nine patients were prospectively included: SAH patients (n=66) (historic population) and intracerebral hemorrhage patients (n=13). All patients received an external ventricular drain within 24 hours of the onset of bleeding. CSF and plasma were drawn daily from day 1 to day 10. The levels of NPY were determined by means of competitive enzyme immunoassay. The CSF samples of 29 patients (historic population) who had undergone spinal anesthesia due to orthopedic surgery served as the control group. RESULTS: NPY levels in CSF were significantly higher in the 2 hemorrhage groups than in the control group. However, the 2 hemorrhage groups showed significant differences in NPY levels in CSF (SAH mean, 0.842 ng/mL vs. BGH/CH mean, 0.250 ng/mL; P<0.001) as well as in the course of NPY secretion into CSF over the 10-day period. NPY levels in plasma did not differ significantly among SAH, BGH/CH, and controls. CONCLUSIONS: Our findings support the hypothesis that excessive release of NPY into CSF but not into plasma is specific to aneurysmal SAH in the acute period of 10 days after hemorrhage. In BGH/CH, CSF levels of NPY were also increased, but the range was much lower.

Expressions of serum inflammatory cytokines and their relationship with cerebral edema in patients with acute basal ganglia hemorrhage.

OBJECTIVE: The aim of the present study is to investigate expressions of inflammatory cytokines and their relationship with cerebral edema in the patients with acute basal ganglia hemorrhage. PATIENTS AND METHODS: Between January 2015 and March 2016, 94 patients with acute basal ganglia hemorrhage admitted to our institution were included in the present study. Serum levels of interleukin (IL)-4, IL-6, IL-8 and IL-10 were measured using enzyme-linked immunosorbent assay (ELISA), and conditions of cerebral edema were evaluated using head CT upon admission, 1d after admission and 3d after admission, respectively. RESULTS: Serum levels of IL-4, IL-6 and IL-8 peaked 1d after admission and decreased 3d after admission with statistical significance (p <0.05); the IL-10 level was continuously increased after admission and peaked 3 days after admission with statistical significance (p<0.05). Cerebral edema was not observed in any of these patients upon admission, while occurred with a maximal edema volume 1 day after admission and the volume decreased 3 days after admission with statistical significance (p <0.05). Correlation analysis showed that levels of IL-4, IL-6 and IL-8 were positively correlated with severity of cerebral edema (r=0.324, 0286, 0.305, p <0.05 respectively), whereas IL-10 level was negatively correlated with severity of cerebral edema (r=-0.336, p <0.05). CONCLUSIONS: Serum levels of IL-4, IL-6 and IL-10 are positively correlated while the IL-10 level is negatively correlated with the severity of the cerebral edema in patients with acute basal ganglia hemorrhage.

Plasma pituitary adenylate cyclase-activating polypeptide concentrations and mortality after acute spontaneous basal ganglia hemorrhage.

BACKGROUND: Plasma pituitary adenylate cyclase activating polypeptide (PACAP) concentrations are elevated after traumatic brain injury. We assessed the prognostic value of PACAP for short-term and long-term mortality of acute intracerebral hemorrhage (ICH) patients. METHODS: A total of 150 patients and 150 age- and gender- matched healthy controls were recruited. The plasma PACAP concentrations were measured using sandwich immunoassays. ICH severity was assessed using hematoma volume and National Institutes of Health Stroke Scale (NIHSS) score. The end points included 1-week mortality and 6-month mortality. The relationships between plasma PACAP concentrations and ICH severity and the end points were analyzed statistically. RESULTS: Plasma PACAP concentrations were statistically significantly higher in the ICH patients than in the healthy controls and were correlated positively with hematoma volumes and NIHSS scores using a multivariate linear regression. Multivariate analysis results indicated that plasma PACAP concentration was an independent predictor of 1-week mortality, 6-month mortality and 6-month overall survival. It also had high predictive value based on receiver operating characteristic curve. CONCLUSIONS: Plasma PACAP concentrations are increased and are highly associated with the severity of ICH; PACAP may be a good predictor of short-term and long-term mortality of ICH.

High concentrations of visfatin in the peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

Higher plasma visfatin concentration has been associated with clinical outcomes of traumatic brain injury. No published information exists to date about change in plasma visfatin after intracerebral hemorrhage. This study included one hundred and twenty-eight healthy controls and 128 patients with intracerebral hemorrhage. The unfavorable outcome was defined as modified Rankin Scale score >2 at 6 months. The patients had higher plasma visfatin measurements than control subjects. Plasma visfatin levels were highly correlated with National Institutes of Health Stroke Scale score and plasma C-reactive protein levels in the patients. A multivariate analysis identified plasma visfatin level as an independent predictor for 6-month mortality and unfavorable outcome. According to receiver operating characteristic curve analysis, the predictive value of the plasma visfatin concentration was similar to National Institutes of Health Stroke Scale score. In a combined logistic-regression model, visfatin improved the predictive value of National Institutes of Health Stroke Scale score for 6-month unfavorable outcome. Thus, increased plasma visfatin level is associated with 6-month clinical outcomes after intracerebral hemorrhage.

Plasma leptin level predicts hematoma growth and early neurological deterioration after acute intracerebral hemorrhage.

Higher plasma leptin levels have been associated with poor clinical outcomes after intracerebral hemorrhage. Nevertheless, their links with hematoma growth and early neurological deterioration are unknown. Therefore, we aimed to investigate the relationship between plasma leptin levels, hematoma growth, and early neurological deterioration in patients with acute intracerebral hemorrhage. We prospectively studied 102 consecutive patients with acute spontaneous basal ganglia hemorrhage presenting within 6h from symptoms onset. Significant hematoma growth was defined as hematoma enlargement >33% at 24h. Early neurological deterioration was defined as an increase of ≥4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. We measured plasma leptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma leptin level emerged as the independent predictor of hematoma growth (odds ratio, 1.182; 95% confidence interval, 1.061-2.598; P=0.008) and early neurological deterioration (odds ratio, 1.193; 95% confidence interval, 1.075-2.873; P=0.004). Using receiver operating characteristic curves, we calculated areas under the curve for hematoma growth (area under curve, 0.844; 95% confidence interval, 0.759-0.908) and early neurological deterioration (area under curve, 0.857; 95% confidence interval, 0.774-0.918). The predictive performance of leptin was similar to, but did not obviously improve that of hematoma volume. Thus, leptin may help in the prediction of hematoma growth and early neurological deterioration after intracerebral hemorrhage.

Admission plasma visfatin level strongly correlates with hematoma growth and early neurologic deterioration in patients with acute spontaneous basal ganglia hemorrhage.

BACKGROUND: Visfatin, a proinflammatory mediator, has been associated with poor clinical outcomes after acute brain injury. The present study is designed to investigate the potential association between plasma visfatin levels and the risk of hematoma growth (HG) and early neurologic deterioration (END) after intracerebral hemorrhage. METHODS: There were 85 patients as cases who presented with first-time hemorrhagic stroke that were assessed within 6h after the incident. The control group consisted of 85 healthy volunteers. HG was defined as hematoma enlargement >33% at 24h. END was defined as an increase of ≥ 4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. Plasma visfatin levels were determined using enzyme immunoassay. RESULTS: Plasma visfatin levels were significantly higher in patients compared to controls. Plasma visfatin level emerged as an independent predictor of HG [odds ratio (OR), 1.154; 95% confidence interval (CI), 1.046-3.108; P=0.009] and END (OR, 1.195; 95% CI, 1.073-3.516; P=0.005). For predicting HG, area under curve (AUC) of plasma visfatin level (0.814; 95% CI: 0.715-0.890) was similar to that of hematoma volume (0.839; 95% CI, 0.743-0.909) (P=0.703). For predicting END, AUC of plasma visfatin level (0.828; 95% CI: 0.730-0.901) was similar to that of hematoma volume (0.863; 95% CI, 0.771-0.928) (P=0.605). Visfatin did not improve AUC of hematoma volume for predicting HG and END (both P>0.05). CONCLUSION: Plasma visfatin level represents a novel biomarker for predicting HG and END.

Copeptin is associated with one-year mortality and functional outcome in patients with acute spontaneous basal ganglia hemorrhage.

High plasma copeptin levels have been found to be associated with short-term poor outcome after intracerebral hemorrhage (ICH). We furthermore evaluate the relation of plasma copeptin levels to long-term outcome and early neurological deterioration after ICH. Fifty healthy controls and 89 patients with acute spontaneous basal ganglia hemorrhage were recruited in this study. Plasma copeptin concentrations on admission measured by enzyme-linked immunosorbent assay were considerably high in patients than healthy controls. A multivariate analysis identified plasma copeptin level as an independent predictor for 1-year mortality, 1-year unfavorable outcome (modified Rankin Scale score>2) and early neurological deterioration. A receiver operating characteristic curve showed that the predictive value of plasma copeptin concentration was similar to that of National Institutes of Health Stroke Scale scores for long-term poor outcome and early neurological deterioration. However, copeptin did not obviously improve the predictive values of National Institutes of Health Stroke Scale scores. Thus, increased plasma copeptin level is an independent prognostic marker of 1-year mortality, 1-year unfavorable outcome and early neurological deterioration after ICH.

Association of interleukin-11 with mortality in patients with spontaneous basal ganglia haemorrhage.

This study evaluated interleukin (IL)-11 as an independent prognostic marker of mortality following intracerebral haemorrhage (ICH). Plasma IL-11 levels in patients with ICH were significantly higher than in healthy controls. Multivariate analysis indicated that plasma IL-11 level was an independent predictor for mortality within 1 week of ICH onset and was positively associated with haematoma volume. Receiver operating characteristic curve analysis identified that a baseline plasma IL-11 level > 20.9 pg/ml predicted mortality within 1 week of ICH onset with 81.2% sensitivity and 74.1% specificity. The area under the curve for IL-11 level was significantly smaller than that for the Glasgow Coma Scale score, but similar to that for haematoma volume. IL-11 did not, however, significantly improve the predictive value of the Glasgow Coma Scale or haematoma volume. Thus, IL-11 may be considered as a new independent prognostic marker of mortality and an additional valuable tool for risk stratification and decision-making in the acute phase of ICH.

Change in plasma copeptin level after acute spontaneous basal ganglia hemorrhage.

High plasma copeptin levels are associated with mortality after intracerebral hemorrhage (ICH). However, there is a paucity of data available on whether copeptin is an independent prognostic marker of mortality. Thus, we sought to furthermore evaluate this relation. Thirty healthy controls and 86 patients with acute ICH were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7 after ICH. Its concentration was measured by enzyme-linked immunosorbent assay. After ICH, plasma copeptin level in patients increased during the 6-h period immediately, peaked in 24h, decreased gradually thereafter, and was substantially higher than that in healthy controls during the 7-day period. A multivariate analysis showed plasma copeptin level was an independent predictor for 1-week mortality (odds ratio, 1.013; 95% confidence interval (CI), 1.003-1.023; P=0.009) and positively associated with hematoma volume (t=6.616, P<0.001). A receiver operating characteristic curve identified that a baseline plasma copeptin level >577.5pg/mL predicted 1-week mortality with 87.5% sensitivity and 72.2% specificity (area under curve (AUC), 0.873; 95% CI, 0.784-0.935). The AUC of the copeptin concentration was similar to those of Glasgow Coma Scale (GCS) scores and hematoma volumes (P=0.136 and 0.280). However, copeptin did not statistically significantly improve the AUCs of GCS scores and hematoma volumes (P=0.206 and 0.333). Hence, increased plasma copeptin level is associated with hematoma volume and an independent prognostic marker of mortality after ICH.

Change in plasma S100B level after acute spontaneous basal ganglia hemorrhage.

S100B has been described as a marker of brain injury. However, not much is known regarding change in plasma S100B and its relation with mortality after spontaneous intracerebral hemorrhage (ICH).Thus, we sought to investigate change in plasma S100B level after ICH and to evaluate its relation with disease outcome. Thirty healthy controls and 86 patients with acute ICH were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7 after ICH. Its concentration was measured by enzyme-linked immunosorbent assay. After ICH, plasma S100B level in patients increased during the 6-h period immediately, peaked in 24 h, plateaued at day 2, decreased gradually thereafter, and was substantially higher than that in healthy controls during the 7-day period. Plasma S100B levels were highly associated with Glasgow Coma Scale scores, ICH volumes, presences of intraventricular hemorrhage, and survival rates (all P < 0.05). Multivariate analysis showed baseline plasma S100B level as a good predictor for 1-week mortality (odds ratio, 1.046; 95%confidence interval, 1.014 - 1.078; P = 0.004). A receiver operating characteristic curve identified plasma S100B cutoff level (192.5 pg/mL) that predicted 1-week mortality with the high sensitivity (93.8%) and specificity (70.4%) values (P < 0.001). The differences between areas under curves of plasma S100B levels and those of Glasgow Coma Scale scores and ICH volumes were not statistically significant (both P > 0.05). Increased S100B level is found after ICH and may contribute to the inflammatory process of ICH, in association with a poor clinical outcome.

High concentrations of resistin in the peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

PURPOSE: Resistin increases in peripheral blood of patients with intracerebral hemorrhage (ICH). We sought to evaluate its relation with disease outcome. MATERIALS AND METHODS: Thirty healthy controls and 86 patients with acute ICH were included. Plasma samples were obtained on admission. Its concentration was measured by enzyme-linked immunosorbent assay. RESULTS: Thirty-two patients (37.2%) died from ICH in a week. The plasma resistin level (24.2 +/- 9.7 ng/mL) in patients was significantly higher than that (8.8 +/- 2.4 ng/mL) in healthy controls after adjustment by age, sex, hypertension, diabetes mellitus, hyperlipidemia, and body mass index using analysis of covariate (F = 9.507, P = .003).A univariate correlation analysis found Glasgow Coma Scale (GCS) score and ICH volume, but a multivariate linear regression only selected GCS score (t = -4.587, P < .001) to be related to plasma resistin level. On a multivariate logistic regression, plasma resistin level (odds ratio = 1.257, 95% confidence interval = 1.058-1.492, P = .009) was an independent variable predicting 1-week mortality. A receiver operating characteristic curve identified that a plasma resistin level greater than 26.3 ng/mL predicted 1-week mortality of patients with 81.2% sensitivity and 81.5% specificity (P < .001). Areas under curves of GCS score and ICH volume were not statistically significantly larger than that of plasma resistin level (P > .05). CONCLUSIONS: Increased resistin level is found after ICH, in association with a poor clinical outcome.

Time course of plasma leptin concentrations after acute spontaneous basal ganglia hemorrhage.

BACKGROUND: Brain cortex leptin messenger ribonucleic acid (mRNA) expression and serum leptin level are up-regulated in ischemic mouse brain, as well as in rat brain with traumatic brain injury. Elevated leptin plasma levels predict cerebral hemorrhagic stroke independently of traditional risk factors. The goal of this study was to investigate change in plasma leptin level after intracerebral hemorrhage (ICH) and to evaluate its relation with disease outcome. METHODS: Eighty-six patients admitted within 6 hrs after ICH and 30 healthy controls were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7 after ICH. Its concentration was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: After ICH, plasma leptin level in patients increased during the 6-hour period immediately, peaked in 24 hours, decreased gradually thereafter, and was substantially higher than that in healthy controls during the 7-day period. Plasma leptin levels were highly associated with initial Glasgow coma scores, ICH volumes, presence of intraventricular hemorrhage, and survival rates (all P < 0.05). A multivariate analysis selected plasma leptin level related to plasma C-reactive protein level (standardized coefficient, 0.293; P = 0.003). A multivariate analysis showed baseline plasma leptin level as a good predictor for 1-week mortality (odds ratio, 1.228; 95% confidence interval, 1.070-1.409; P = 0.003). A receiver operating characteristic curve identified that a baseline plasma leptin level greater than 34.1 ng/mL predicted 1-week mortality of patients with 75.0% sensitivity and 85.2% specificity (P < 0.001). Area under curve of GCS score was statistically significantly larger than that of plasma leptin level (P = 0.035), but ICH volume's area under curve not (P = 0.078). CONCLUSIONS: Increased plasma leptin level is found after ICH and may contribute to inflammatory process of ICH, in association with a poor clinical outcome.

High concentrations of procoagulant microparticles in the cerebrospinal fluid and peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

BACKGROUND: Apoptosis plays an important role in further brain injury after intracerebral hemorrhage (ICH). Procoagulant microparticles (MPs) are shed from the plasma membrane of apoptotic cells. The objective of this study was to determine plasma and cerebrospinal fluid (CSF) levels of MPs in patients with spontaneous ICH and to correlate MP levels with Glasgow Coma Scale (GCS) scores, ICH volumes, presence of intraventricular hemorrhage (IVH), and survival rate. METHODS: Ten patients with suspicion of subarachnoid hemorrhage and 36 patients with spontaneous basal ganglia hemorrhage were included. Plasma and CSF samples were collected. Circulating MPs were obtained by double centrifugation and captured with annexinV. Their procoagulant potential was measured with a prothrombinase assay. RESULTS: Plasma or CSF MP levels in the ICH group were significantly higher than those in the control group (8.2 +/- 3.0 vs 3.2 +/- 1.7 nmol/L phosphatidylserine [PS] equivalent; P < .001 or 9.8 +/- 3.7 vs 1.4 +/- 0.6 nmol/L PS equivalent; P < .001). The MP levels were highly associated with GCS scores, ICH volumes, presence of IVH, and survival rate (all P < .05) in ICH. A receiver operating characteristic curve identified CSF and plasma MP cutoff levels that predicted 1-week mortality of patients with the high sensitivity and specificity values. Areas under curves (AUCs) of GCS scores and ICH volumes were larger than those of CSF and plasma MP levels, but only the difference between AUC of GCS scores and that of plasma MPs levels reached statistical significance (P < .05). CONCLUSIONS: High levels of procoagulant MPs are present in the CSF and peripheral blood of patients with ICH and may contribute to the pathogenesis of ICH. The levels of CSF and plasma MPs after spontaneous onset of ICH seem to correlate with clinical outcome in these patients. Taking clinical complexity into account, only plasma MP levels can be served as useful clinical markers for evaluating the prognosis of ICH.