临床消化病杂志
臨床消化病雜誌
림상소화병잡지
CHINESE JOURNAL OF CLINICAL GASTROENTEROLOGY
2001年
1期
15-16
,共2页
周立红%刘敏涓%董临江%刘泽霖%孙玉卫%张小蔓
週立紅%劉敏涓%董臨江%劉澤霖%孫玉衛%張小蔓
주립홍%류민연%동림강%류택림%손옥위%장소만
肝硬化%纤维蛋白原%纤维蛋白单体%聚合功能
肝硬化%纖維蛋白原%纖維蛋白單體%聚閤功能
간경화%섬유단백원%섬유단백단체%취합공능
目的:研究肝硬化患者血浆纤维蛋白原(Fbg)水平及去肽A后纤维蛋白单体(desA-Afibrinmonomer)的聚合功能。方法:以蕲蛇酶水解Fbg,用计算机自动检测系统测定患者血浆中纤维蛋白单体聚合反应速率(FMPS)、最大吸光度(Amax)、凝固性纤维蛋白原含量(FC)、反应延滞时间(DT)、功能指标(FI=FMPS/Amax)。结果:失代偿性肝硬化患者30例,其FMPS为0.326±0.06,Amax为0.178±0.028,FC为1.700±0.400g/L,DT为6±20s,FI为1.831。除DT外其它数据均较对照组为低。结论:失代偿性肝硬化患者因纤维蛋白原浓度下降致使纤维蛋白单体聚合功能降低,从而出现低凝状态,这可能是构成出血倾向的原因之一。
目的:研究肝硬化患者血漿纖維蛋白原(Fbg)水平及去肽A後纖維蛋白單體(desA-Afibrinmonomer)的聚閤功能。方法:以蘄蛇酶水解Fbg,用計算機自動檢測繫統測定患者血漿中纖維蛋白單體聚閤反應速率(FMPS)、最大吸光度(Amax)、凝固性纖維蛋白原含量(FC)、反應延滯時間(DT)、功能指標(FI=FMPS/Amax)。結果:失代償性肝硬化患者30例,其FMPS為0.326±0.06,Amax為0.178±0.028,FC為1.700±0.400g/L,DT為6±20s,FI為1.831。除DT外其它數據均較對照組為低。結論:失代償性肝硬化患者因纖維蛋白原濃度下降緻使纖維蛋白單體聚閤功能降低,從而齣現低凝狀態,這可能是構成齣血傾嚮的原因之一。
목적:연구간경화환자혈장섬유단백원(Fbg)수평급거태A후섬유단백단체(desA-Afibrinmonomer)적취합공능。방법:이기사매수해Fbg,용계산궤자동검측계통측정환자혈장중섬유단백단체취합반응속솔(FMPS)、최대흡광도(Amax)、응고성섬유단백원함량(FC)、반응연체시간(DT)、공능지표(FI=FMPS/Amax)。결과:실대상성간경화환자30례,기FMPS위0.326±0.06,Amax위0.178±0.028,FC위1.700±0.400g/L,DT위6±20s,FI위1.831。제DT외기타수거균교대조조위저。결론:실대상성간경화환자인섬유단백원농도하강치사섬유단백단체취합공능강저,종이출현저응상태,저가능시구성출혈경향적원인지일。
Purpose: Study of plasma fibrinogen level and fibrin monomer after des A peptide polymerize function. Method: Acutulase hydrolyzed fibrinogen, and calculator automatic detection system were used for: fibrin monomer polymerization reaction speed(FMPS), maximum attraction luminosity (Amax), fibrinogen concentration (FC), reaction delayed time (DT), and function index (FI = FMPS/Amax). Results: Decompensation hepatocirrhosis 30 cases, its detection value: FMPS was 0.326 ± 0.06, Amax was 0.178±0.028, FC was 1.700 ± 0.400 g/L, DT was 6 ± 20 s, FI was1.831, except for DT they were lower than normal control group. Conclusion: Plasma Fbg concentration and fibrin monomer polymerize function were decrease, showed that patients were low coagulation state and contributing to one cause of hemorrhage.