急性脑梗死诱发全身炎症反应综合征致多器官功能障碍综合征的机制探讨

目的探讨急性脑梗死（ACI）后诱发SIRS及导致多器官功能障碍综合征（MODS）的发病机制。方法收集急性脑梗死患者48例,分为三组,急性单纯脑梗死组（SACI）26例;急性脑梗死致全身炎症反应综合征组（SIRS组）22例;急性脑梗死致多器官功能障碍综合征组（MODS组）13倒;应用酶联免疫吸附法（ELISA法）分别测定不同组别患者血清中TNF-α、IL-6值,与对照组（20例同期健康体检者）比较。结果（1）48例ACI致SIRS的发生率为45．83％,ACI致MODS的发生率为27．08％,ACI致SIRS时诱发MODS的发生率为59．09％。（2）ACI致MODS时均已提前发生了SIRS。（3）SACI组、SIRS组及MODS组患者血清TNF-α、IL-6含量均明显高于正常对照组（P〈0．01）;且SIRS组明显高于SACI组（P〈0．01）;MODS组明显SIRS组（P〈0．01）,呈逐渐升高的趋势。（4）MODS不同积分组血清TNF-α、IL-6含量均明显高于SIRS组（P〈0．01）;且MODS组患者,严重者（积分≥9分）血清TNF-α、IL-6含量明显高于病情较轻者（积分〈9分）（P〈0．01）。（5）MODS组死亡患者血清TNF-α、IL-6含量明显高于存活者（P〈0．01）。结论（1）急性脑梗死（ACI）可以诱发全身炎症反应综合征（SIRS）,并且是脑梗死致多器官功能障碍综合征（MODS）的发病基础和前提。（2）ACI首先诱发SIRS,SIRS是致MODS的主要机制,动态监测急性脑梗死患者血清TNF-α、IL-6的变化对急性脑梗死是否导致SIRS及MODS的发生有很高的预警价值。（3）急性脑梗死患者血清TNF-α、IL-6含量可作为判断急性脑梗死致SIRS、急性脑梗死致MODS病变程度、预后及转归的指标,并对及时指导临床早期治疗有着重要意义,对SIRS向MODS过度的早期诊断有非常重要的参考价值。     

急性脑梗死诱发全身炎症反应综合征致多器官功能障碍综合征的临床研究

目的　探讨急性脑梗死 (ACI)诱发全身炎症反应综合征 (SIRS)致多器官功能障碍综合征(MODS)的发病机制 ,以及血清肿瘤坏死因子 (TNF α)、白细胞介素 (IL 1) β含量变化在ACI诱发SIRS发生、发展并向MODS转化的临床意义。方法　 6 8例ACI患者根据病情变化分为 3组 ,其中单纯性ACI(SACI组 ) 36例 ,ACI致SIRS(SIRS组 ) 32例 ,ACI致SIRS后发展为MODS(MODS组 ) 2 4例 ;应用酶联免疫吸附法 (ELISA法 )分别测定患者不同病程中血清TNF α、IL 1β值 ,并与对照组 (为 2 8名同期健康体检者 )比较。 结果　 (1) 6 8例ACI中 4 7.0 6 %发生SIRS;SIRS时 75 %发生MODS。 (2 )血清TNF α、IL 1β的含量MODS 组 >SIRS组 >SACI组 >对照组 ,各组间比较 ,差异具有极显著性 (均P <0 0 1)。MODS重症者 (积分≥ 9分 )血清TNF α、IL 1β含量高于轻症者 (积分 <9分 ) (均P <0 0 1) ;MODS死亡者血清TNF α、IL 1β含量高于存活者 (均 P <0 0 1)。结论　 (1)ACI后出现SIRS可导致MODS的发生。 (2 )患者血清TNF α、IL 1β水平异常变化可作为判断ACI致SIRS、MODS病情进展、预后及转归的一项指标     

急性脑梗死诱发SIRS及MODS时患者血清SOD含量变化研究

目的 探讨急性脑梗死(ACI)诱发全身炎症反应综合征(SIRS)及多器官功能障碍综合征(MODS)的发生率,以及血清中超氧化物岐化酶(SOD)含量变化在ACI诱发SIRS及MODS中的作用机制及临床意义. 方法 选取自2006年1月至2008年6月菏泽市立医院神经内科住院及门诊就诊的68例ACI患者.分为3组,其中急性单纯性脑梗死36例(SACI组),ACI诱发SIRS患者(SIRS组)32例,ACI诱发MODS患者(MODS组)24例,采用黄嘌呤氧化酶法测定血清SOD含量,另设28例到本院查体的健康人为正常对照组(NC组). 结果 (1)本组SACI诱发SIRS的发生率为88.9%,诱发MODS的发生率为66.7%;ACI诱发SIRS时MODS的发生率为75.0%.ACI诱发MODS时100%发生SIRS.(2)各组之间SOD含量比较差异有统计学意义(P<0.05),且血清SOD含量水平依次为MODS组相似文献   

急性脑出血诱发全身炎症反应综合征致多器官功能障碍综合征的临床研究

目的　探讨急性脑出血并发全身炎症反应综合征 ( SIRS)致多器官功能障碍综合征 ( MODS)的可能机制 ,揭示 TNF- α、IL- 6在脑出血并发 SIRS及向 MODS转化机制中的作用及病理生理意义。方法　观察 73例急性脑出血患者并发 SIRS及 MODS的发生率 ;并应用双抗体夹心 ( EL ISA)法测定其血清 TNF-α、IL - 6的动态变化 ,并以 2 0名健康人作为对照。结果　脑出血时并发 SIRS的发生率为 4 7.95 % ( 35 /73) ,其中 74 .2 9% ( 2 6 /35 )诱导发生了MODS。单纯脑出血组、脑出血致 SIRS组及脑出血致 MODS组患者血清 TNF- α、IL- 6含量均明显高于正常对照组( P<0 .0 1) ,呈逐渐升高的趋势 ;并与病情的严重程度相关。结论　脑出血并发 SIRS是导致 MODS的主要机制 ,TNF-α、IL - 6参与了脑出血并发 SIRS及导致 MODS发生发展的病理生理过程 ,并具有很高的预警价值     

C反应蛋白与急性脑梗死的预后及并发多脏器功能障碍综合征的相关性

目的探讨急性脑梗死(ACI)及并发多脏器功能障碍综合征(MODS)时C反应蛋白的变化,评估C反应蛋白在ACI的预后及并发MODS中的临床价值.方法采用免疫透射比浊法测定30例体检健康者(对照组)和82例ACI患者(ACI组)出现首发症状7天以内血清CRP的含量,其中腔隙性脑梗死20例(LCI)组,ACI并发MODS患者(MODS)组32例,急性脑梗死30例(SACI组,即非LCI并且未并发多脏器功能障碍综合征).结果 (1)30例健康者全部CRP＜10 mg/L,ACI组CRP＞10 mg/L的阳性率达97.5%;(2)SACI组及MODS组CRP水平与LCI组比较差异显著(P＜0.05),MODS组CRP水平较SACI组明显增高;(3)血清CRP＜30mg/L时,MODS的发生率为0,血清CRP水平＞30mg/L时,随着CRP水平的升高,ACI发生MODS的发生率逐渐增高.结论血清CRP水平与病情的严重程度和MODS的发生率呈正相关,CRP是判断ACI预后和并发MODS的一个有效实验指标.     

血浆内皮素-1水平变化在急性脑梗死诱发全身炎症反应综合征中的意义

目的:以目前外科领域及危重病领域公认的全身炎症反应综合征(SIRS)统一诊断标准,探讨血浆内皮素-1(ET-1)在急性脑梗死(ACl)诱发SIRS发生中的作用。方法:应用放射免疫法分别测定52例ACI致SIRS患者(SIRS组),50例急性单纯性脑梗死(SACl)及46例正常对照组血浆ET-1含量。结果:1血浆ET-1含量在SIRS组、SACI组与正常对照组比较,差异均具有极显著(均P<0.01)。SIRS组血浆ET-1水平又明显高于SACI组(P<0.01)。其血浆ET-1含量SIRS组>SACI组>正常对照组。2血浆ET-1含量随符合SIRS诊断标准数目的增多而升高。结论:急性脑梗死进展为SIRS后,血浆内皮素-1明显升高,血浆内皮素-1可作为判断急性脑梗死病情进展为SIRS的一项指标。     

Cys-C在急性脑梗死并发SIRS致MODS患者中的水平变化

目的观察胱抑素-C(Cystatin-C,Cys-C)在急性脑梗死(acute cerebral infarction,ACI)并发全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)致多器官功能障碍综合征(multiple organdysfunction syndrome,MODS)患者中的水平变化。方法 ACI患者278例根据其并发SIRS、MODS情况分为3组:SACI组166例、SIRS组47例、MODS组65例。同时,收集健康体检者50例作为正常对照组。采用免疫比浊法(PETIA)测定血清Cys-C水平,观察其与超敏C反应蛋白(hypersensitive C-reactive protein,hs-CRP)、脂蛋白a(Lipoprotein a,LPa)的相关性。结果与对照组比较,观察组各组血清Cys-C、LPa、hs-CRP水平均明显升高(P<0.01),组间比较,SIRS、MODS组患者升高更为明显,以MODS组更为突出(P<0.05或P<0.01)。相关性分析表明,血清Cys-C水平与hsCRP、LPa呈正相关。结论 Cys-C与炎症反应关系密切,参与了ACI并发SIRS、MODS,并具有重要作用。     

癫痫持续状态并发全身炎症反应综合征致多器官功能障碍综合征的临床研究

目的探讨癫痫持续状态(SE)并发全身炎症反应综合征(SIRS)致多器官功能障碍综合征(MODS)的可能机制,揭示肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)在SE并发SIRS及向MODS转化机制中的作用及病理生理意义。方法观察78例SE患者并发SIRS及MODS的发生率;应用双抗体夹心(ELISA)法测定其血清TNF-αI、L-1β的动态变化,并与32名健康人进行对照比较。结果SE时并发SIRS的发生率为47.44%(37/78),其中56.76%(21/37)诱导发生MODS。单纯SE组、SE致SIRS组和SE致MODS组患者血清TNF-α、IL-1β水平均明显高于正常对照组(均P<0.01),并呈逐渐升高趋势,与病情的严重程度相关。结论SE并发SIRS是导致MODS的主要机制,TNF-αI、L-1β参与了SE并发SIRS及导致MODS发生、发展的病理生理过程,并具很高的预警价值。     

脑梗死患者血清中TNF-α、sICAM-1的变化及其临床意义

目的 :探讨 TNF- α与 s ICAM- 1在急性脑梗死发病中的作用及其相互关系。方法 :采用双抗体夹心酶联免疫吸附法 (EL L SA)测定 5 1例脑梗死患者及 16例有卒中危险因素的患者、 2 3例正常对照者血清 TNF- α与 s ICAM-1的含量。结果 :急性期脑梗死患者血清 TNF- α与 s ICAM- 1含量显著高于正常对照组 (P均 <0 .0 1) ;恢复期脑梗死患者 TNF- α与 s ICAM- 1含量明显下降 ,与卒中危险因素对照组的水平接近 ,但仍显著高于正常对照组 (P<0 .0 5 ) ;急性期脑梗死患者 TNF- α与 s ICAM- 1呈正相关 (r- 0 .6 3,P<0 .0 1)。结论 :TNF- α与 s ICAM- 1作为免疫因素参与了缺血性脑血管疾病炎症 /免疫反应的发生、发展全过程 ;推测临床脑缺血后 ICAM- 1的上调可能与 TNF- α有关     

急性脑梗死患者血清肿瘤坏死因子及循环内皮细胞含量变化的对比研究

目的　研究急性脑梗死 (ACI)患者血清肿瘤坏死因子 (TNF)及循环内皮细胞 (CEC)含量的变化 ,探讨 TNF与 CEC的关系及其临床意义。方法　采用放射免疫分析法检测 6 0例 ACI患者血清 TNF- α和 CEC的含量 ,并与 2 0例健康人作对照。结果　 (1)脑梗死患者急性期血清 TNF- α和 CEC含量明显高于恢复期 (P<0 .0 1)。恢复期血清 TNF- α及 CEC则高于正常水平 (P<0 .0 1)。 (2 )脑梗死急性期血清 TNF- α和 CEC升高的程度与梗死灶大小密切相关 (P<0 .0 1)。 (3)急性期血清 TNF- α与 CEC呈正相关 (r=0 .6 9,P<0 .0 1)。结论　 ACI患者血清TNF- α及 CEC含量升高 ,提示 TNF- α及血管内皮细胞的损伤共同参与脑梗死的发生发展过程。保护血管内皮细胞 ,降低 TNF- α的水平 ,对于缺血性脑血管病的防治将具有重要意义。     

Cardio-facio-cutaneous syndrome and moyamoya syndrome

We reported a patient with cardio-facio-cutaneous (CFC) syndrome associated with moyamoya syndrome. The patient was referred at 6 years 5 months with left hemiplegia and right-sided eye deviation. He had an apparently short stature, macrocephaly, left ptosis and atopic skin, and was odd looking. He exhibited an incomplete right bundle branch block on electrocardiogram and an atrial septal defect on ultrasound cardiography. He was diagnosed as having CFC syndrome. Head magnetic resonance imaging showed a flow void in the bilateral basal ganglia, but did not show any ischemic changes. Magnetic resonance angiography showed bilateral stenosis with an internal carotid artery at the Willis artery ring level and bilateral moyamoya. Contrast angiography demonstrated occlusion of both middle cerebral arteries. Cerebrovascular anomalies have not previously been reported in CFC syndrome. This is the first case of CFC syndrome associated with moyamoya syndrome.     

Reye syndrome and reye-like syndrome

Reye syndrome is an acute metabolic encephalopathy, largely affecting children and adolescents. In Reye-like syndrome, because of inborn errors of metabolism, hypoglycemia, hypoketonemia, elevated ammonia, and organic aciduria are often evident. It is well-known that fatty-acid oxidation defects can present as Reye-like syndrome. The most commonly diagnosed metabolic disorder in association with Reye syndrome has been medium-chain acyl coenzyme A dehydrogenase deficiency. The present consensus seems to be that Reye syndrome is very rare, and that any child suspected of manifesting this disorder should undergo investigations for inborn errors of metabolism. We recently treated a child with "Reye-like illness" who possibly manifested a long-chain acyl dehydrogenase deficiency, and who had also ingested aspirin. We discuss the possible pathogenesis of the disorder in this child. The end results of mitochondrial dysfunction in Reye syndrome and Reye-like illness may be similar.     

Leigh syndrome associated with West syndrome

Leigh syndrome (LS) (sub-acute necrotizing encephalomyelopathy) is characterized by symmetric brain lesions occurring mainly in the basal ganglia and associated with variable clinical manifestations such as hypotonia, psychomotor retardation, and feeding difficulties. Patients with LS may develop seizures. Only three patients with LS have been identified in the literature as having West syndrome (WS). We have seen 12 children with LS in the past 20 years, and noticed that as many as five of them developed WS. This report discusses five LS children with WS, comparing them with seven LS children without WS. In all five patients, infantile spasms developed after LS had become evident, in addition to other type(s) of seizures. The onset of LS in all the patients with WS was before 10 months of age. Although not statistically proven, early onset of LS, spasticity, nystagmus, apnea, poor feeding, and cardiac problems seemed to be associated with the development of WS. We were not able to conclude that certain types of symptoms or examination results of patients with LS indicated the development of WS. The association of LS with WS did not markedly influence the prognoses of the children. WS may not be a rare complication of LS, especially in infants under 12 months of age. This report is the first review of LS associated with WS.     

Moebius syndrome in Kallmann syndrome.

A girl born with congenital paresis of cranial nerves III, IV, and VII (Moeblus syndrome) subsequently developed a progressive peripheral neuropathy. There was suggestive evidence of a familial neuropathy with autosomal dominant inheritance in three family members. The patient also had hypogonadotrophic hypogonadism and anosmia (Kallmann syndrome).     

Catatonic syndrome and neuroleptic malignant syndrome

Several clinical reports suggest that neuroleptic malignant syndrome (NMS) is not a distinct clinical entity but an acute form of catatonic syndrome (CS). They both share many clinical features and it is impossible to differentiate them on the basis of biochemical findings. Both respond similarly to treatment. The article describes some case reports from the literature and our own case report of NMS as a form of CS.     

Carpal tunnel syndrome and metabolic syndrome

Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy. Many factors such as diabetes mellitus, hypothyroidism, hormonal replacement therapy, corticosteroid use, rheumatoid arthritis and wrist fractures may cause CTS. Metabolic syndrome includes abdominal obesity, dyslipidemia, hyperglycemia, and hypertension that may cause CTS. In this study, we aimed to evaluate the relation between CTS and metabolic syndrome. We studied 107 (96 female and 11 male) right-handed patients who had a clinical and electrophysiologically confirmed diagnosis of CTS. We then divided the patients into two groups (patients with and without metabolic syndrome) according to the criteria of ATP III definition. Eighty (75%) of the patients with CTS had metabolic syndrome. Among the 80 patients with metabolic syndrome, CTS was found in 150 hands (43 mild, 58 moderate and 49 severe cases). Among the 27 patients without metabolic syndrome, CTS was found in 43 hands (27 mild, 14 moderate and 2 severe cases). The electrophysiological parameters (median nerve distal motor latency, median nerve motor amplitude, median nerve motor conduction velocity, median nerve sensory onset latency, median nerve sensory amplitude and median nerve sensory conduction velocity) were worse in patients with metabolic syndrome (P < 0.05). In conclusion, metabolic syndrome was found to be three times more common in patients with CTS and CTS was more severe in patients with metabolic syndrome when compared with those without metabolic syndrome.     

Cobb syndrome and Klippel-Trenaunay-Weber syndrome]

We reported two patients with neurocutaneous angiomatosis. Patient 1, a 36-year-old woman of Cobb syndrome had cutaneous portwine angiomas in the high back and spinal arteriovenous malformations at the level of Th4-11. She had also atrophy and livedo reticularis presenting during standing position in the left lower extremity. Patient 2, a 47-year-old man of Klippel-Trenaunay-Weber syndrome had varices in the bilateral lower extremities, cutaneous portwine angiomas in the high back and bilateral lower extremities, and hypertrophy of the bilateral legs. Neuroradiological examination revealed abnormal vessels in the spinal canal at the level of C5 and Th4. These syndromes may have no essential difference because of the presence of neural and cutaneous angiomas at the corresponding level, venous system disorders and trophic changes (hypertrophy/atrophy).