ABSTRACT
Objective To investigate the changes of platelet reactivity and its influencing factors after aspirin treatment in patients with ischemic stroke complicated with diabetes. Methods From September 2016to December 2017, patients with acute ischemic stroke admitted to the Department of Neurology, Weihai Municipal Hospital within 24 h of onset were enrolled. All patients took aspirin (100 mg/d) within 24 h ofadmission, and after taking the drug (7 ±2 d), the PL-11 platelet function analyzer was used to determine the maximum platelet aggregation ratio (MAR) induced by arachidonic acid (AA). The baseline data of the patients were documented. The factors affecting high platelet reactivity (HPR) were analyzed. Results A total of 398 patients with ischemic stroke were enrolled, including 137 in the diabetes group and 261 in the non-diabetes group. MARAA (43. 45％ ± 14. 11％ vs. 31. 55％ ± 19. 39％; t = 6. 996, P < 0. 001) and the incidence of HPR (34. 3％ vs. 19. 9％; χ2 = 9. 946, P = 0. 002) in the diabetes group were significantly higher than in those in the non-diabetes group. Of the 137 patients with ischemic stroke complicated with diabetes, 47 had HPR. The proportions of patients with hyperlipidemia, previous history of stroke or transient ischemic attack and baseline NIHSS score, HOMA-IR (homeostatis model assessment-insulin resistance),high-sensitivity C-reactive protein, fasting blood glucose, and glycosylated hemoglobin in the HPR group were significantly higher than those in the non-HPR group (all P < 0. 05). Multivariate logistic regression analysis showed that HOMA-IR (odds ratio [OR] 1. 153, 95％ confidence interval [CI] 1. 027-1. 295; P =0. 016), high-sensitivity C-reactive protein (OR 9. 416, 95％ CI 2. 271-39. 049; P = 0. 002), fasting blood glucose (OR 1. 125, 95％ CI 1. 025-1. 235; P = 0. 013), and glycosylated hemoglobin (OR 1. 458, 95％ CI 1. 170-1. 816; P = 0. 001) were the independent risk factors for HPR. Conclusion The platelet reactivity during aspirin therapy in patients with ischemic stroke complicated with diabetes mellitus was high, and platelet activity was associated with multiple mechanisms, such as inflammation, insulin resistance, and hyperglycemia.
ABSTRACT
Objective To observe the changes of spleen volume in patients with acute cerebral infarction, and to explore the relationship between the spleen volume and platelet reactivity , inflammatory factors'lymphocyte subsets.Methods This is a case control study.Thirty patients with acute cerebral infarction from January 2017 to June 2017 in Department of Neurology , Weihai Municipal Hospital were included.The spleen volume, arachidonic acid-induced maximum platelet aggregation ratio ( AA-MAR), interferon gamma (IFN-γ) and lymphocyte subsets of patients were monitored in 24 hours of stroke, at 48 hours of stroke, at four days of stroke and at seven days of stroke.Twenty patients without acute cerebral infarction with the same baseline data were selected as the control group , to determine the baseline of spleen volume, AA-MAR, IFN-γand lymphocyte subsets.A t test was used to describe the changes of spleen volume, AA-MAR, IFN-γand lymphocyte subsets at different time points , and Pearson's correlation analysis was used to estimate the relationship between the spleen volume and these variables .Results Compared with the control group ((120.12 ±10.28) cm3), the patients with acute cerebral infarction in 24 hours of stroke ((117.48 ±7.93) cm3) and at 48 hours of stroke ((111.61 ±9.21) cm3) had smaller spleen volume (t＝-2.142, P＜0.05; t＝-2.790, P＜0.01), whereas at four days ((121.31 ±8.16) cm3) and seven days of stroke ((126.11 ±10.31) cm3) had bigger spleen volume (t＝2.242, P＜0.05;t＝2.762, P＜0.01), with the spleen volume decreased first and increased later.Compared with the control group, the patients with acute cerebral infarction had more AA-MAR (control group:20.97%±8.21%;24 h:31.86%±9.54%,t＝3.165,P＜0.01;48 h:41.38%±8.55%,t＝3.254,P＜0.01;4 d:35.34%± 8.15%, t＝3.203,P＜0.01;7 d:29.38% ±10.46%,t＝2.494,P＜0.05) and IFN-γ(pg/L, control group:15.21 ±5.21;24 h:29.75 ±4.57,t＝3.262,P＜0.01;48 h:43.37 ±12.15,t＝3.304,P＜0.01;4 d:40.44 ±9.86, t＝3.291,P＜0.01;7 d:20.93 ±5.51, t＝2.417,P＜0.05) at different time points, with the most AA-MAR at 48 hours of onset, and the most IFN-γat four days of stroke.Compared with the control group, the patients with acute cerebral infarction had more T 4, B lymphocytes and natural killer lymphocytes at the four time points , while the level of T8lymphocytes did not show statistically significant difference even though also increased at the four time points.The correlation analysis results showed that in patients with acute cerebral infarction , the level of AA-MAR (r＝-0.397, P＜0.05; r＝-0.515, P＜0.01; r＝-0.382, P＜0.05) and IFN-γ(r＝-0.408, P＜0.05; r＝-0.479, P＜0.01; r＝-0.378, P＜0.05) was negatively corelated with the spleen volume in 24 hours of onset, at 48 hours of stroke and at four days of stroke; the level of T4, B and natural killer lymphocytes were negatively corelated with the spleen volume in 24 hours of stroke and at 48 hours of stroke.Conclusion After the acute cerebral infarction onset, the spleen volume tends to reduce and then increases , the levels of platelet reactivity , inflammatory factors and lymphocyte subsets are correlated with the spleen volume , and the spleen may aggravate the brain injury by releasing platelets inflammatory factors and lymphocyte subsets.
ABSTRACT
Secondary immune response is an important endogenous mechanism of neurological injury after ischemic stroke.Spleen and interferon-γγplay an important role in it.Monitoring the spleen size and the level of interferon-γγhave an important reference significance for the severity of stroke and outcome assessment.
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Minocycline is the second generation semisynthetic tetracycline antibiotics.A variety of animal models and clinical trials have shown that it has neuroprotective effect.Its mechanism is associated with inhibiting apoptosis, alleviating inflammatory reaction, reducing infarct volume, and alleviating vascular injury.This article reviews the neuroprotective effect of minocycline in preclinical phase and early clinical trials of acute ischemic stroke.
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Prediabetes is a glucose metabolism status between normal glucose metabolism and diabetes.It can not only increase the risks of occurrence and recurrence of stroke, but also affect stroke outcomes.Prediabetes causes ischemic stroke mainly through the insulin resistance and blood-brain barrier damage.Non-drug or drug intervention in patients with prediabetes can delay progression from prediabetes to diabetes and reduce the risks of occurrence and recurrence of stroke.
ABSTRACT
Diabetes mellitus is an independent predictor of high platelet reactivity after antiplatelet therapy in patients with ischemic stroke,and the latter is closely related to the increased risk of recurrence of stroke.The mechanisms of high platelet reactivity in patients with diabetes or insulin resistance are associated with a variety of factors.Some circulating molecules can be used as markers for predicting the reactivity of platelets.Monitoring of platelet reactivity after treatment with new antiplatelet agents may provide basis for individualized antithrombotic therapy in ischemic stroke patients with diabetes or insulin resistance.