脑出血患者血清可溶性细胞间黏附分子-1浓度的动态变化及其意义

目的　研究脑出血患者血清可溶性细胞间黏附分子 1(sICAM 1)浓度的动态变化及其意义。方法　采用酶联免疫吸附法 (ELISA)检测 5 0例脑出血患者发病后不同时间血清sICAM 1的含量 ,并与正常人比较 ,及出血量 >2 0ml与≤ 2 0ml患者的血清sICAM 1浓度比较。结果　脑出血组急性期不同时点血清sICAM 1浓度均明显高于对照组 (均P <0 0 0 1)。脑出血组血清sICAM 1浓度于发病后 2 4h升高 ,3～ 7d达高峰 ,病后14d明显下降 ,但仍明显高于对照组。出血量 >2 0ml患者血清sICAM 1浓度明显高于出血量≤ 2 0ml患者(P <0 .0 1～ 0 0 0 1)。结论　sICAM 1参与了脑出血的发生和发展过程 ;观察血清sICAM 1浓度 ,对判断病情及出血量有一定的帮助。     

32例脑干出血预后分析

目的研究脑干出血患者的预后与出血量、并发症之间的关系。方法观察我院经脑CT或MRI确诊的32例脑干出血患者。结果本组病例出血量为0．24～19．6ml，平均5．16ml。病死率40．6％，死亡病例出血量平均为8．21ml，是存活者的3倍。32例在发病过程中有9例出现肺部感染，其中死亡4例，有7例出现上消化道出血，其中死亡2例。结论脑干出血的预后与出血量密切相关，并发症是脑干出血死亡的危险因素之一，但并发症与出血量之间无明显因果关系。     

自发性脑干出血的临床分析

目的探讨脑干出血的病因、危险因素及出血量与预后的关系。方法对72例脑干出血的病人按出血量多少分为3组:A组27例,出血量<2ml;B组15例,出血量2～5ml;C组30例,出血量>5ml。分析各组的性别、年龄、原发性高血压人数、饮酒人数构成比及脑干出血量与临床特征、预后的关系。结果3组患者在性别、年龄、原发性高血压人数、饮酒人数构成方面无差别;部分临床特征及预后与出血量有关;原发性高血压及长期饮酒是脑干出血的主要病因。结论原发性高血压是脑干出血的最重要病因,长期大量饮酒是重要危险因素;并非年龄越大,脑干出血危险性越大;脑干出血量的大小决定着疾病的临床特征及预后。     

立体定向血肿抽吸术对小量基底核区出血患者血清基质金属蛋白酶-9水平及预后的影响

目的探讨立体定向血肿抽吸术治疗基底核区小量出血伴明显神经功能障碍患者的疗效及可能的治疗机制。方法分析2014年1月至2016年12月本院收治的自发性基底核区出血(出血量20~30ml)患者57例,分为手术组(30例,接受立体定向血肿抽吸术)和对照组(27例,内科治疗),比较2组患者发病24h内及治疗后3d、7d、14d血清基质金属蛋白酶-9(MMP-9)水平,并采用美国国立卫生研究院卒中量表(NIHSS)评定2组治疗前、治疗后14和30d的神经功能缺损程度,随访评估两组患者治疗后90d格拉斯哥预后评分(GOS)。结果发病24h内2组血清MMP-9水平差异无统计学意义;治疗后3d、7d、14d,手术组血清MMP-9水平均明显低于对照组(P0.01)。手术组治疗后14d、30d NIHSS评分低于对照组(P0.05)、治疗后90d GOS评分高于对照组(P0.05)。结论对基底核区出血量20~30ml伴有严重神经功能障碍的患者,早期行立体定向血肿抽吸术可明显降低血清MMP-9表达,减轻脑水肿,改善功能预后。     

补体系统激活变化趋势与急性脑梗死关系的临床研究

目的动态观察脑梗死患者发病后1月内补体C3和超敏C-反应蛋白（Hs-CRP）含量的变化趋势及其与梗死灶体积、神经功能缺损程度的相关性。方法分别在发病后12、24、48、72h、7、14d和1月,采用免疫散射比浊法测定56例脑梗死患者补体C3和Hs-CRP含量,观察并记录所有病例的病灶体积、神经功能缺损评分。同时选取46例健康受试者作为对照组。结果（1）病例组补体C3和Hs-CRP在不同测定时点浓度不同（F=163.456和97.622,P〈0.001）,表现为发病12h时补体C3和Hs-CRP浓度即有所增加,此后随着发病时间的增加浓度呈上升趋势,至发病7d达峰值,随后逐渐下降,至1月时趋于正常。（2）病例组血清C3、Hs-CRP的浓度于发病后12、24、48、72h、7、14d均高于对照组（P〈0.05）,1月时2组比较无明显差异（P〉0.05）;（3）病例组血清补体C3、Hs-CRP水平与梗死灶体积有关系,体积越大,血清补体C3、Hs-CRP水平越高。大、中病灶组血清补体C3、Hs-CRP浓度明显高于小病灶组（P〈0.05）;（4）病例组血清补体C3、Hs-CRP水平与神经功能缺损程度有关系,神经功能缺损越重,血清补体C3、Hs-CRP水平越高。重、中度神经功能缺损组血清补体C3、Hs-CRP浓度明显高于轻度缺损组（P〈0.05）。结论（1）急性缺血性脑卒中患者在急性期C3、Hs-CRP含量增高,存在补体系统激活。补体激活可能参与了急性缺血性脑卒中后脑组织的炎症过程;（2）急性缺血性脑卒中患者C3、Hs-CRP与脑梗死体积、神经功能缺损程度之间有密切关系,反映卒中时脑组织的损害程度。     

自发陛脑干出血的救治及影响其预后的因素分析

目的 探讨自发性脑干出血的救治并分析影响其预后的因素。方法 回顾性分析37例自发性脑干出血病人的临床资料，并结合文献对影响其预后的因素进行分析。结果 痊愈9例，好转15例，植物生存6例，死亡7例。结论 出血量、意识障碍程度是影响自发性脑干出血预后的主要因素。     

32例脑干出血预后分析

目的 研究脑干出血患者的预后与出血量、并发症之间的关系。方法 观察我院经脑CT或MRI确诊的32例脑干出血患者。结果 本组病例出血量为0.24-19.6ml,平均5.16ml。病死率40.6％,死亡病例出血量平均为8.21ml,是存活者的3倍。32例在发病过程中有9例出现肺部感染,其中死亡4例,有7例出现上消化道出血,其中死亡2例。结论 脑干出血的预后 与出血量密切相关,并发症是脑干出血死亡的危险因素之一,但并发症与出血量之间无明显因果关系。     

自发性脑干出血的临床分析

目的探讨脑干出血的病因、危险因素及出血量与预后的关系。方法对72例脑干出血的病人按出血量多少分为3组：A组27例，出血量〈2ml；B组15例，出血量2～5ml；C组30例，出血量〉5ml。分析各组的性别、年龄、原发性高血压人数、饮酒人数构成比及脑干出血量与临床特征、预后的关系。结果3组患者在性别、年龄、原发性高血压人数、饮酒人数构成方面无差别；部分临床特征及预后与出血量有关；原发性高血压及长期饮酒是脑干出血的主要病因。结论原发性高血压是脑干出血的最重要病因，长期大量饮酒是重要危险因素；并非年龄越大，脑干出血危险性越大；脑干出血量的大小决定着疾病的临床特征及预后。     

自发性脑干出血临床分析与预后

目的：研究自发性脑干出血患的预后及出血量、出血部位之间的关系。方法：观察了我院经脑CT或MRI确诊的、临床资料完整的100例自发性脑干出血的病人。结果：（1）发现脑干出血好发部位主要在桥脑基底被盖部、被盖部，其次为中脑，最少见于延髓。（2）本组死亡率为51％，其中桥脑被基部死亡率（62．2％）较高，其次为桥脑被盖部（43．7％）和中脑（42．8％）、桥脑基底部（30．7％）。（3）虽然延髓出血罕见，但因易累及生命中枢，即使出血量少，死亡率极高。（4）＞5ml组（分别为86．7％）死亡率最高，1－5ml组相对较低（28．9％），＜1ml组（6％）最小。（5）经统计死亡组出血量平均为5．8ml是存活平均值（2．3ml)的2．5倍。结论：脑干出血的预后因素受多因素影响，可与年龄、性别、体温、意识障碍、血压、出血部位和出血量有关，其中出血部位和出血量起主要作用。     

自发性重型脑干出血的治疗分析

目的探讨自发性重型脑干出血的有效治疗方法。方法复习我院1990～2004年88例自发性脑干出血中符合重型脑干出血入组条件的27例患者的临床资料,分为单纯内科治疗组(A组)、内科治疗+侧脑室穿刺持续引流组(B组)、外科手术治疗组(C组)。结果A组6例,好转、未愈各1例,死亡4例;B组19例,显效2例,好转8例,植物生存3例,未愈1例,死亡5例;C组2例,好转、植物生存各1例。A、B组治疗有效率(显效+好转)、死亡率经卡方检验无显著性意义(P>0.05)。结论重型脑干出血患者预后凶险,单纯内科治疗及内科治疗+侧脑室穿刺持续引流对改善患者预后价值可能均不大,但后者有可能延长患者的住院天数,外科手术治疗方法值得临床积极探索。     

帕金森病血抗氧化系统的变化及临床意义

探讨帕金森病（ＰＤ）患者体内抗氧化系统水平及其在ＰＤ发病中的可能作用。方法观测了７０例ＰＤ患者和７０例正常人的血浆维生素Ｃ、Ｅ浓度（Ｐ－ＶＣ，Ｐ－ＶＥ），血浆及红细胞膜超氧化物歧化酶（Ｐ－ＳＯＤ，Ｅ－ＳＯＤ）活性，血浆及红细胞过氧化脂质（Ｐ－ＬＰＯ，Ｅ－ＬＰＯ）水平的变化。结果与正常对照组相比，ＰＤ患者的Ｐ－ＶＣ、Ｐ－ＶＥ浓度及Ｐ－ＳＯＤ、Ｅ－ＳＯＤ活性均明显降低，而Ｐ－ＬＰＯ、Ｅ－ＬＰＯ水平则显著增高。并且Ｐ－ＶＣ、Ｐ－ＶＥ、Ｅ－ＳＯＤ水平与ＰＤ患者的病情和病程呈负相关。结论提示ＰＤ患者可能存在血抗氧化系统缺陷而使内源性氧自由基堆积，导致黑质神经元退变     

帕金森病血抗氧化系统变化及其临床意义

为探讨帕金森病（PD）患者体内抗氧化系统水平及其在PD发病中的作用，对70例PD患者血浆维生素C（P－VC）、维生素E（P－VE）、血浆及红细胞超氧化物歧化酶（P－SOD，E－SOD）、血浆与红细胞过氧化脂质（P－LPO，E－LPO）的水平进行了检测并与正常对照组比较。结果表明：PD组P-VC、P-VE水平及P-SOD、E-SOD活性均比正常对照组显著降低，而P-LPO、E-LPO则显著增高，并且P-VC、P-VE、E-SOD与病情和病程呈负相关，提示抗氧化系统缺陷及内源性氧自由基堆积与PD发病有密切关系。     

Antioxidants in Alzheimer's disease-vitamin C delivery to a demanding brain

Levels of several antioxidants and related markers were measured in cerebrospinal fluid (CSF) and plasma of 10 Alzheimer's disease (AD) patients and 10 controls. Daily dosage of vitamin C was significantly correlated with both plasma (R=0.662; p=0.0015) and CSF level (R=0.639, p=0.0024). Plasma and CSF vitamin C levels were also highly correlated R=0.793, p<0.0001). Similarly, daily dosage of Vitamin E was significantly correlated with plasma vitamin E (R=0.681; p=0.0009) and showed a trend toward correlation with CSF vitamin E (R=0.422, p=0.06). There were no significant differences between groups in absolute CSF or plasma levels of any analyte. However, the CSF: plasma ratio of vitamin C was significantly greater in the AD patients compared to the controls (p=0.048). In a subset of AD patients, hippocampal volume was significantly correlated with plasma (R2=0.833; p=0.004) and CSF (R2 =0.603; p=0.04) vitamin C levels, and inversely correlated with CSF:plasma vitamin C ratio (R2 =0.717; p=0.016). We conclude that oral vitamin C supplements are delivered to the brain, and speculate that the increased CSF: plasma ratio of vitamin C in AD reflects increased antioxidant consumption by the AD brain.     

Low plasma vitamin C in Alzheimer patients despite an adequate diet

Objective. To compare the vitamin C and E plasma levels in patients with Alzheimer's disease (AD) and to assess the vitamin C intake and nutritional status. Design. Case-control study. Four groups of sex- and age-matched subjects were compared: severe AD and moderate AD, in patients with moderate AD and controls. Setting. Community and hospitalized patients in the region of Toulouse, France. Participants. Patients with dementia who fulfilled criteria for Alzheimer's disease: severe Alzheimer group (N=20), Mini-Mental State Examination (MMSE) score range 0–9; moderate Alzheimer group (N=24), MMSE 10–23; hospitalized Alzheimer group (N=9), MMSE 10–23. Control group (N=19), MMSE 24–30. Measures. Plasma vitamin E and C were quantified by HPLC-fluorescence. Consumption of raw and cooked fruit and vegetables was evaluated in order to determine the mean vitamin C intakes. Mini Nutritional Assessment (MNA) and plasma albumin were used to measure nutritional status. Results. Institutionalized and community subjects were analysed separately. MNA scores were normal in home-living Alzheimer subjects with moderate dementia and significantly lower in those with severe disease, despite normal plasma albumin levels. In the home-living Alzheimer subjects, vitamin C plasma levels decreased in proportion to the severity of the cognitive impairment despite similar vitamin C intakes, whereas vitamin E remained stable. The hospitalized Alzheimer subjects had lower MNA scores and albumin levels but normal vitamin C intakes, but their plasma vitamin C was lower than that of community-living subjects. Institutionalized Alzheimer subjects had significantly lower MNA scores but normal vitamin C and albumin levels and vitamin C intakes compared with community-dwelling subjects of similar degree of cognitive impairment. Conclusion. Plasma vitamin C is lower in AD in proportion to the degree of cognitive impairment and is not explained by lower vitamin C intake. These results support the hypothesis that oxygen-free radicals may cause damage. Copyright © 1998 John Wiley & Sons, Ltd.     

Examination of free radical metabolism and antioxidant defence system elements in patients with obsessive-compulsive disorder

Free radicals and oxidative stress are involved in the pathogenesis of various diseases. Malondialdehyde (MDA) is a natural product of lipid peroxidation in all mammalian cells. Vitamins C and E are nonenzymatic antioxidant structures. Our study investigated the role of free radicals in the obsessive-compulsive disorder (OCD). The participants were 30 patients with OCD that were drug-free at least for a month and a control group of 30 healthy subjects, matched with respect to age and sex. In both groups, the levels of erythrocyte malondialdehyde and the plasma vitamin C and E concentrations were measured. The levels of malondialdehyde were significantly higher in the patient group than in the control group (p<.01). The levels of plasma vitamin E were significantly lower in the patient than in the control group (p<.02). Although our patient group had slightly lower concentrations of plasma vitamin C compared to our control group, the difference between these two groups was not statistically significant. There was a significant correlation between increasing malondialdehyde levels and decreasing vitamin E concentrations. This study shows the presence of a significant relationship of OCD and oxidative stress, and consequently, an involvement of free radicals and of the antioxidant defence. Biochemical studies may contribute to the understanding of OCD and its treatment.     

Plasma antioxidant status, immunoglobulin g oxidation and lipid peroxidation in demented patients: relevance to Alzheimer disease and vascular dementia

A large body of evidence supports a role of oxidative stress in Alzheimer disease (AD) and in cerebrovascular disease. A vascular component might be critical in the pathophysiology of AD, but there is a substantial lack of data regarding the simultaneous behavior of peripheral antioxidants and biomarkers of oxidative stress in AD and vascular dementia (VaD). Sixty-three AD patients, 23 VaD patients and 55 controls were included in the study. We measured plasma levels of water-soluble (vitamin C and uric acid) and lipophilic (vitamin E, vitamin A, carotenoids including lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha- and beta-carotene) antioxidant micronutrients as well as levels of biomarkers of lipid peroxidation [malondialdehyde (MDA)] and of protein oxidation [immunoglobulin G (IgG) levels of protein carbonyls and dityrosine] in patients and controls. With the exception of beta-carotene, all antioxidants were lower in demented patients as compared to controls. Furthermore, AD patients showed a significantly higher IgG dityrosine content as compared to controls. AD and VaD patients showed similar plasma levels of plasma antioxidants and MDA as well as a similar IgG content of protein carbonyls and dityrosine. We conclude that, independent of its nature-vascular or degenerative-dementia is associated with the depletion of a large spectrum of antioxidant micronutrients and with increased protein oxidative modification. This might be relevant to the pathophysiology of dementing disorders, particularly in light of the recently suggested importance of the vascular component in AD development.     

Plasma antioxidant vitamins in brain tumors

Plasma levels of vitamins A, E and C were analyzed in 102 patients with different types of brain tumors. A follow-up study was done with 27 postoperative patients. On comparison with plasma from normal individuals, vitamin A and E were decreased, but the decrease was statistically insignificant. Vitamin C levels remained in the normal range. In a comparative study of preoperative and postoperative cases, plasma vitamin A levels in postoperative glioma patients were significantly higher than those in the pre-operative state. There was no significant difference in the plasma level of vitamins C and E. The results of the present study suggest that the plasma antioxidant vitamins are not altered effectively in brain tumor cases.     

Lymphocyte oxidative DNA damage and plasma antioxidants in Alzheimer disease

CONTEXT: A large body of experimental evidence suggests that in Alzheimer disease (AD) pathogenesis an important role is played by oxidative stress, but there is still a lack of data on in vivo markers of free radical-induced damage. OBJECTIVES: To evaluate levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative damage to DNA, in peripheral lymphocytes; to measure plasma concentrations of several nonenzymatic antioxidants; and to assess the relationships between any observed changes in lymphocyte DNA 8-OHdG content and plasma antioxidant levels in patients with AD and healthy aged control subjects. SUBJECTS: Forty elderly outpatients with AD and 39 healthy age- and sex-matched controls were studied. MAIN OUTCOME MEASURES: The level of 8-OHdG was determined in DNA extracted from lymphocytes and plasma levels of vitamin C, vitamin A, vitamin E, and carotenoids (zeaxanthin, beta-cryptoxanthin, lycopene, lutein, and alpha- and beta-carotene) were measured by high-performance liquid chromatography. RESULTS: Lymphocyte DNA 8-OHdG content was significantly higher and plasma levels of antioxidants (with the exception of lutein) were significantly lower in patients with AD compared with controls. In patients with AD, a significant inverse relationship between lymphocyte DNA 8-OHdG content and plasma levels of lycopene, lutein, alpha-carotene, and beta-carotene, respectively, was observed. CONCLUSIONS: Markers of oxidative damage are increased in AD and correlate with decreased levels of plasma antioxidants. These findings suggest that lymphocyte DNA 8-OHdG content in patients with AD reflects a condition of increased oxidative stress related to a poor antioxidant status.     

Uric acid administration in patients with acute stroke: a novel approach to neuroprotection

Uric acid (UA) is the end product of purine catabolism in humans and is a powerful antioxidant whose generation is increased under ischemic conditions. However, both clinical and experimental studies reveal a gradual exhaustion of the antioxidant capacity after transient cerebral ischemia, and the magnitude of this consumption seems to be correlated with the extent of brain tissue injury, growth of the infarction, severity of neurological impairment in the acute phase, and long-term functional outcome. Growing evidence supports the neuroprotective effect of UA administration after brain ischemia. In experimental conditions, the administration of UA is neuroprotective both in mechanical models of brain ischemia (transient or permanent intraluminal occlusion of the middle cerebral artery) and in thromboembolic models of autologous clot injection. The administration of UA is feasible and safe in healthy volunteers. In acute stroke patients treated with recombinant tissue plasminogen activator (rt-PA), co-administration of UA has proven to reduce lipid peroxidation and to prevent the fall in UA blood levels that occur very early after stroke onset. Currently, a multicentric Phase III clinical trial is testing whether the administration of UA increases the clinical benefits of rt-PA, which represents the only approved therapy in patients with acute ischemic stroke. This review summarizes the available information justifying such a novel therapeutic approach in this devastating clinical condition.     

Dietary supplementation with vitamin E in hyperlipoproteinemias: effects on plasma lipid peroxides, antioxidant activity, prostacyclin generation and platelet aggregability

In a placebo-controlled trial healthy volunteers and patients with hyperlipoproteinemias types II and IV received orally vitamin E at doses of 300 mg and 600 mg daily for 2 weeks. Serum tocopherol levels increased two-fold, but serum concentrations of total lipids, cholesterol, triglycerides, ceruloplasmin and transferrin remained unchanged. Dietary supplementation with vitamin E suppressed elevated concentrations of plasma lipid peroxides and this effect was correlated with an increase in serum antioxidant activity. In patients a mild platelet suppressant effect of vitamin E (600 mg daily) was observed. Feeding an atherogenic diet to rabbits for a week resulted in elevation of plasma lipid peroxides and a 90% decrease in arterial generation of prostacyclin. Enrichment of the atherogenic diet with 100 mg vitamin E daily prevented the increase in plasma lipid peroxides and protected the prostacyclin generating system in arteries. Thus, in hyperlipoproteinemias vitamin E corrects certain abnormalities of lipid metabolism which might predispose to atherosclerosis.