Significance Of The Dynamic Monitoring Of Coagulation Molecular Marker TF,TFPI In Patients With Closed Craniocerebral Injury

Significance of the dynamic monitoring of coagulation molecular marker TF> TFPI in patients with closed craniocerebral injuryMedical School of Zhejiang UniversityEmergency MedicineGrade 98 Master's Degree CandidateWU XuehaiPostgraduate TutorJIANG GuanyuABSTRCATDisturbance of microcirculation suffered from hemorrhage of micro vessel and thrombosis was one of main reasons for secondary brain injury after acute craniocerbral injury. Coagulopathy has a strong correlation with the severity of brain injury and secondary brain damage.It's very important to study the law of coagulation after brain injury.But alteration of coagulation is very complicated after injury.Now besides the table of coagulation and fibrinolytic product, there were rare studies on alteration law of coagulation after brain injury. Tissue factor(TF),that is to say the factorlll, formed Wa/TF after combining and activatingthe factor VE to Wa. VHa/TF was the only starting factor during thephysiologic coagulation. Tissue factor pathway inhibitor (TFPI) can hold up the activity of Xa by formation of TFPI/Xa directly. But it mainlyinhibited Wa/TF by the formation of Xa/TFPI/V II a/TF with the help of Ca2+ and modulated the activity of TF. Now TFPI was the only inhibitor of Vfla/TF.TF and TFPI were very important during coagulation. So, weprobed the law of coagulation after brain injury by monitoring TF, TFPI and TFPI/TF dynamically,hoped to be helpful for clinical treatment.Aim1. To probe the alteration law of TF, TFPI and TFPI/TF after closed craniocerebral injury.2. To probe the relationship between expression of TF, TFPI and the severity of brain injury.3. To probe the alteration law of TF, TFPI, TFPI/TF in secondary brain injury patients, especially for those who developed delayed intracerebral hematoma or enlargement of previously small hematomas.Materials and Methods1. Patients and groupingThe study population was drawn from patients with closed craniocerebral injury admitted to the emergency department of the NO.2 Hospital of Zhejiang University during July to November in 2000.The patients with coronary heart disease, hepatopathy, hypertension, diabetes mellitus, hematologic disease and primary brain stem injury were excepted. Forty-two patients were qualified for the study, thirty-six men, eight women. Thirty healthy adult were included in normal control group, twenty-two men, eight women.2. MaterialsTF, TFPI test box came from ADI company in USA.3. Methods2 ml venous blood samples were collected on the first day, 24h, 72h and 7d after craniocerebral injury in patients and in control group heathy adults respectively. Blood samples were anticoagulated with sodium citrate,centrifugated within three hours and cold stored -70癈in refrigerator.Assay TF, TFPI after all blood samples were collected. Cranial CT scan, platelet count and Glasgow Coma Score were recorded at first day, 24h, 72h and 7d respectively.4. TF> TFPI detectionELISA method were used to determine the level o TF and TFPI.5. StatisticsAll data were managed with SPSS 10.0, presented with mean + standard deviation( x眘). Analysis of variance and linear regression were used, significant at P<0.05 and high significant at P<0.01.Results1. Tissue factor was elevated markedly the day craniocerebral injuried (significant at/><0.05) , got to the highest at 24h, then began to declineand still higher at 72h than normal control group.Tissue factor didn't drop to normal level until 7d.Tissue factor pathway inhibitor began to decline continuously after craniocerebral injury, and much lower than normalcontrol group at 7d (significant at/?<0.01) . TFPI/TF was much lower in craniocerebral injury patients than in normal control group all time withinseven days markedly (significant at/?<0.05 ) .2. Tissue facor was elevated markedly the first day, 24h and 72h after craniocerebral injury in GCS^S group (significant at/?<0.05) . But tissuefactor had significant e...