| Background:Acute cerebral infarction has become an endanger disease in human health and life,with these characteristics of high morbidity,high disability and high mortality.Although there have been significant progress in the diagnosis and treatment of cerebral infarction,the mortality and disability rate of cerebral infarction are still high.Glucose-6-phosphate dehydrogenase deficiency(G6PD deficiency)had a higher incidence in our country,especially in the south of our country.It is inevitable to meet cerebral infarction with G6PD deficiency.Studies have shown that G6PD has a significant impact on the development of cardiovascular diseases,diabetes,hypertension,and tumors.However,G6PD deficiency whether affect the development and prognosis of cerebral infarction or not,which is a question worth exploring.Research finding thatG6PDdeficientindividuals showedanhigher platelet-derived microparticles(MPs)concentrations as compared with G6PD-normal individuals,MPs are procoagulant and in some cases also contain tissue factor,can activate the coagulation cascade,thereby promoting the coagulation process and can lead to hypercoagulation in patients with cerebral infarction.Currently,routine coagulation tests can not detect the slight changes in blood coagulation in patients due to G6PD deficient.Thrombelastography(TEG)was tested with whole blood,can reflect the patient's coagulation function with more real and more accurately.In addition,Previous clinical studies have found that the G6PD deficiency were independent risk factors for abnormally high cerebral velocities in patients with sickle cell anemia(SCA),suggesting that G6PD deficiency can accelerate the blood flow rate of cerebrovascular and increase the risk of cerebrovascular disease,but there were also studies suggest they had no correlation.Animal experiments have confirmed that in the early stage of ischemia/reperfusion in rat hippocampal CA1 region,G6PD deficiency weakened the neuron damage,however,in the later stage of ischemia/reperfusion in rat hippocampal CA1 region,G6PD deficiency exacerbated the neuron damage,suggesting that G6PD has important effect on the pathological process of neuronal damage in rats with ischemia reperfusion injury.Therefore,the study on the effect of G6PD deficiency on neuronal injury of ischemic cerebrovascular disease is of great significance in clinical practice.However,currently,the correlation between G6PD deficiency and ischemic cerebrovascular disease are mostly limited to animal experiments.Although there are clinical reports on the correlation between G6PD deficiency and cerebrovascular disease,but most mergers have sickle cell anemia(SCA),lack the general population data about G6PD deficiency associated with cerebral infarction.The secondary prevention of cerebrovascular disease should take long-term antiplatelet drugs,and aspirin is the most commonly used,but G6PD deficiency can induce acute hemolysis.Therefore,it is not known whether long-term aspirin use is safe in cerebral infarction with G6PD deficiency or not.Objective:To explore the effect of G6PD deficiency on coagulation function in patients with acute cerebral infarction,and the effects on the degree of neurological impairment and the recovery process in patients with acute cerebral infarction.To investigate the effect of coagulation function change on the degree of neurological deficit and the neurological recovery process in patients with cerebral infarction caused by G6PD deficiency,and to investigate the safety of long-term aspirin use in cerebral infarction with G6PD deficiency.Methods:A prospective review of acute cerebral infarction with G6PD deficiency admitted to The First Affiliated Hospital of Guangxi Medical University from November 2015 to December 2017 was recruited as the experimental group.At the same time,recruited age and gender Matched acute cerebral infarction with G6PD activity normal as the control group.All patients who be admitted to the hospital within 24 hours underwent G6PD activity detection,blood routine,urine routine,liver function,kidney function,blood lipid and coagulation,etc.All patients underwent thrombelastography on admission(before treatment),and obtain parameter,such as R values?K values?a values?MA values.All patients underwent CTA,MRI and DWI during the hospital stay.Recorded the stenosis of the lesion vessels showed by CTA and the infarct volume displayed by DWI.All patients were evaluated with NIHSS and before the onset of mRS on admission,and all patients were evaluated with mRS and BI to assess the prognosis and ability of daily life at the onset of 90 days.The use of antiplatelet agents was observed in the experimental group and the control group at the onset of 90 days,G6PD deficiency in patients with cerebral infarction use antiplatelet drugs(aspirin and clopidogrel,etc.)need to review routine blood,liver function to assess whether Long-term aspirin is safe in G6PD deficiency with cerebral infarction or not.The hemolysis of the experimental group was recorded during the period of hospitalization and the onset of 90 days,such as lumbago,anemia,jaundice,soy sauce color urine,etc.The hemorrhage of the two groups was recorded during the period of hospitalization and the onset of 90 days,including intracranial hemorrhage,gastrointestinal bleeding,gingival bleeding,urinary system bleeding,etc.The clinical scores and thrombelastography parameter were compared of the two groups by SPSS 18.0,and correlation analysis was used to assess thrombelastography parameter and loss of neuron function.P<0.05 considered statistical significance.Results:A total of 50 patients in the experimental group with G6PD deficiency combined with acute cerebral infarction were collected..The average age was(58.74±11.40)years,42 were male,8 were female.The control group also collected 50 cases of acute cerebral infarction patients with normal G6PD,there was no significant difference in age and gender between the two groups due to the selective results.Compared to control group,experimental group had a higher NIHSS score on admission(6.80±2.77 vs 4.90±3.28,P=0.002),longer hospital days(12.88±4.61 vs 11.16±3.95,P=0.048),larger volume of cerebral infarction(3.07±1.70 vs 2.22±1.34,P=0.006),higher incidence of anterior cerebral artery stenosis(2.5%vs 0.7%,P=0.017),higher incidence of middle cerebral artery stenosis(5.6%vs 3.1%,P=0.039),higher rate of moderate cerebral artery stenosis(x~2=10.818,P=0.001),and the worse prognosis of the onset of 90 days.No hemolytic symptoms or signs were found in the experimental group during hospitalization and the onset of 90 days.The experimental group and the control group patients had no bleeding events during hospitalization.The total incidence of hemorrhage was not statistically significant in the experimental group and the control group at the onset of 90days,and neither group showed intracranial hemorrhage.Compared to control groups,experimental groups had a lower R values(4.43±1.62 vs 5.27±1.53 min,P<0.05),higher MA values(62.83±5.84vs 60.07±7.36mm.P<0.05).Further statistical analysis found that MA value was positively correlated with NIHSS(r=0.342,P<0.05),infarction volume(r=0.532,P<0.05),and moderate cerebral artery stenosis(r=0.414,P<0.05).Conclusion:1.G6PDdeficiencyinpatientswithcerebralinfarctionhave hypercoagulation.2.G6PD deficiency may accelerate the process of cerebral artery stenosis,aggravate the nerve damage in patients with cerebral infarction,and has adverse effects on the prognosis of cerebral infarction patients.3.G6PD deficiency may lead to the aggravation of cerebral artery stenosis,the larger cerebral infarction volume and the serious degree of neurological deficit in patients with cerebral infarction,which may be related to the patients'high coagulation state.4.Long-term(3 months)aspirin is safe in cerebral infarction with G6PD deficiency. |
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