血清同型半胱氨酸水平与颈动脉粥样硬化的关系及干预后的变化

目的探讨血清同型半胱氨酸(Hcy)水平与颈动脉粥样硬化(CAA)的关系,及叶酸、维生素B12干预后的变化。方法测定169例脑梗死患者(脑梗死组)及110名正常对照者(正常对照组)血清Hcy、叶酸、维生素B12水平;应用彩色多谱勒显像仪对脑梗死患者颈动脉进行检测;分析血清Hcy与叶酸、维生素B12水平以及与CAA程度的关系;观察叶酸、维生素B12干预4周后伴有高Hcy血症的脑梗死患者血清Hcy水平的变化。结果与正常对照组比较,脑梗死组血清Hcy水平明显增高(P<0.01);随着CAA程度增加,血清Hcy水平增高,叶酸、维生素B12水平下降;血清Hcy水平与叶酸、维生素B12水平呈负相关(r=-0.31,P<0.05;r=-0.47,P<0.01),与CAA程度呈正相关(r=0.58,P<0.05);干预治疗后血清Hcy水平显著下降(P<0.01)。结论血清Hcy水平增高是CAA危险因素之一;补充叶酸、维生素B12可降低血清Hcy水平。     

高同型半胱氨酸血症与颅内外血管狭窄的相关性研究

目的 探讨缺血性脑血管病患者高同型半胱氨酸(Hcy)血症与颅内外血管狭窄的关系.方法 应用全自动生化分析仪,用循环酶法检测405例缺血性脑血管病患者血清Hcy水平,同时检测血清叶酸、维生素B12水平,应用经颅多普勒(TCD)检测所有患者的颅内血管,应用双功能彩色多普勒检测颅外血管.根据检测结果将颈内动脉(ICA)分为:正常、轻度狭窄(＜50%)、中度狭窄(50%～69%)、重度狭窄(70%～99%)、闭塞;大脑中动脉(MCA)分为:正常、中度狭窄(50%～69%)、重度狭窄(70%～95%)、极度狭窄(＞95%).结果 有颅内外血管狭窄组血清Hcy水平显著高于无颅内外血管狭窄组(P<0.01),血清叶酸水平显著低于无颅内外血管狭窄组(P<0.05),血清维生素B12水平两组间差异无统计学意义(P>0.05);ICA、MCA不同程度狭窄患者间血清Hcy水平差异有统计学意义(均P<0.01),血清叶酸水平差异有统计学意义(均P<0.05),维生素B12水平差异无统计学意义(均P>0.05);Hcy水平与ICA、MCA狭窄程度呈正相关(r=0.356 ,P<0.01;r=0.345 ,P<0.01);血清叶酸水平与ICA、MCA狭窄程度呈负相关(r=-0.272 ,P<0.05;r=-0.265,P<0.05).结论 高Hcy血症与颅内外血管狭窄程度密切相关,高Hcy血症可能是缺血性脑血管病新的危险因素.     

川西北地区老年脑梗死与血浆同型半胱氨酸的相关性

目的 研究血浆同型半胱氨酸(Hcy)与川西北地区老年脑梗死发病的相关性.方法 测定川西北地区脑梗死患者60例和对照组60例的血浆Hcy水平.结果 观察组较对照组的血浆Hcy水平明显上升,有统计学意义(P<0.05),观察组的叶酸浓度及维生素B12水平较对照组低(P<0.05).结论 血浆同型半胱氨酸升高与川西北地区脑梗死的发病增加相关.     

精神分裂症血浆硫化氢、同型半胱氨酸、叶酸及维生素B6水平研究

目的:探讨精神分裂症患者血浆硫化氢(H2S)、同型半胱氨酸(Hcy)、叶酸(FA)和维生素B6(VitB6)水平的变化及其相关性.方法:检测66例精神分裂症患者和50名健康对照者的血浆H2S、Hcy、FA及VitB6水平.精神分裂症患者血浆H2S水平与Hcy、FA和VitB6水平的相关性用直线相关分析.结果:与正常对照...     

同型半胱氨酸在帕金森病患者血浆中的变化及临床意义

目的对比研究同型半胱氨酸(homocystein,Hcy)在帕金森病(Parkinson’s disease,PD)和脑梗死患者血浆中的变化,探讨其临床意义。方法检测PD、脑梗死患者及对照组血浆Hcy水平,检测PD、脑梗死患者及对照组血浆叶酸和维生素B_(12)水平。对PD患者血浆Hcy水平与叶酸及维生素B_(12)水平进行相关性分析,对血浆Hcy水平与PD严重程度、病程、临床类型、情绪、认知功能及是否服用美多芭进行相关性分析。结果 (1)PD组、脑梗死组及对照组血浆Hcy水平分别为20±11μmol/L、16±7μmol/L及11±2μmol/L,PD组和脑梗死组血浆Hcy水平均高于对照组,差异有统计学意义(P0.05或0.01),PD组血浆Hcy水平明显高于脑梗死组(P0.01);(2)PD组血浆叶酸和维生素B_(12)水平分别为6±5μg/L和514±345ng/L。PD组血浆叶酸和Hcy水平呈明显负相关(r=-0.453,P0.01);血浆维生素B_(12)和Hcy水平无明显相关性(r=-0.268,P0.05)。(3)按照Hoehn-Yahr分期对PD严重程度进行分组,轻、中、重度PD组血浆Hcy水平分别为16±8μmol/L、21±9μmol/L和35±3μmol/L,三组之间差异有统计学意义(P0.05);(4)血浆Hcy水平与病程、临床类型、情绪、认知功能及是否服用美多芭无关。结论 PD组和脑梗死组血浆Hcy水平明显增高,PD组Hcy水平与疾病严重程度密切相关,PD组血浆叶酸和Hcy水平呈明显负相关。     

血浆同型半胱氨酸与颅内动脉瘤的关系

目的 探讨血浆同型半胱氨酸(Hcy)、血清叶酸、维生素B12水平与颅内动脉瘤的关系.方法 采用化学发光法检测80例颅内动脉瘤患者和60例对照者血浆Hcy、血清叶酸、维生素B12水平,相关危险因索用logistic回归分析.结果 颅内动脉瘤组平均血浆Hcy水平明显高于对照组(P=0.005),两组中血浆Hcy升高分别有38例(48%)和9例(15%)(X2=16.239,P＜0.001);颅内动脉瘤组平均血清叶酸、维生素B12水平明显低于对照组(P=0.01;P=0.005);颅内动脉瘤患者血浆Hcy水平与血清叶酸、维生素B12水平呈负相关(P＜0.05).多因素logistic回归分析显示:血浆Hcy是颅内动脉瘤发病的独立危险因素,比值比(OR)=3.961[P=0.019,95%可信区间(CI):1.255～12.500].结论 高Hcy血症与颅内动脉瘤发病有密切关系,可能是颅内动脉瘤发病的一个独立危险因素;血浆Hcy水平升高可能与血清叶酸、维生素B12水平降低有关.     

同型半胱氨酸、叶酸和维生素B12与精神分裂症的关系

目的 探讨精神分裂症患者血浆同型半胱氨酸、血清叶酸和维牛素B12水平的改变及其可能的意义.方法 采用病例对照研究,精神分裂症患者组122例,正常对照组122例.循环酶法测定两组血浆同型半胱氨酸水平;电化学发光仪测定叶酸和维生素B12水平.结果 ①精神分裂症患者组血浆间型半胱氨酸水平[(27.23±21.41)I.Lmob/L]明显高于正常对照组[(14.34±7.45)tunol/L],差异有统计学意义(P<0.001);②精神分裂症患者组维牛素B12水平[(328.93±157.52)pg/mL]明显低于正常对照组[(464.02±166.29)pg/mL],差异有统计学意义(P<0.05);③血浆同型半胱氩酸水平与叶酸水平(r=-0.44,P<0.001)和维生素Bi2水平(r=-0.36,P<0.001)均呈负相关;④Ligistic回归分析结果 显示,同型半胱氨酸与精神分裂症有关(P<0.001),其优势比(OR)为1.14(95%CI:1.08-1.21).结论 血浆同型半胱氨酸水平增高可能是精神分裂症的危险因素;叶酸和维生素B12缺乏与精神分裂症患者血浆同型半胱氨酸水平增高有关.     

急性脑梗死患者血浆同型半胱氨酸、叶酸、维生素B12水平的测定及其临床意义

目的 探讨血浆同型半胱氨酸(Hcy)在急性脑梗死发病过程中的临床意义以及与病情、伴发症、叶酸、维生素B_(12)之间的关系。方法 采用化学发光法测定急性脑梗死患者血浆Hcy、叶酸、维生素B_(12)水平,并与对照组进行比较。结果急性脑梗死组血浆Hcy水平明显高于对照组(P<0.001),叶酸明显低于对照组(P<0.001);重型患者血浆Hcy水平明显高于中型及轻型患者(P<0.01,0.01),叶酸明显低于中型及轻型患者(P<0.01,0.05);伴发高血压病的患者血浆Hcy水平明显高于非高血压病的患者(P<0.05);急性脑梗死组血浆Hcy与叶酸、维生素B_(12)呈负相关(P<0.01,0.01);对照组血浆Hcy与叶酸呈负相关(P<0.05)。结论高Hcy血症是脑梗死的一个新的重要危险因素;Hcy水平与病情密切相关,与叶酸、维生素B_(12)呈负相关。     

血浆同型半胱氨酸与迟发性运动障碍患者认知功能的相关性研究

目的 探讨血浆同型半胱氨酸(homocysteine,Hcy)与迟发性运动障碍(tardive dyskinesia,TD)患者认知功能的关系.方法 对33例伴TD的精神分裂症患者进行血浆Hcy与血清维生素B12、叶酸水平检测以及韦氏记忆测定(WMS)、连线测验(TMT)和威斯康星卡片分类测验(WCST).结果 血浆Hcy水平与触觉、TMT(A、B)呈显著负相关,而与WCST未显示出明显的相关性;血清维生素B12水平与触觉、TMT-B及WCST中持续性应答数、概念化水平百分数呈显著正相关,血清叶酸水平与WMS、MT及WCST未显示出显著相关性.结论 TD患者认知损害可能与血浆Hcy水平及血清维生素B12水平有关.     

叶酸、Vit B_(12)干预对高Hcy的急性脑梗死近期预后的影响

目的观察叶酸、维生素B12干预治疗是否能降低高同型半胱氨酸血症的急性脑梗死患者的Hcy水平以及对患者近期预后的影响。方法根据血浆Hcy水平将急性脑梗死患者分为正常组(92例),干预组(39例)及对照组(37例),干预组除常规治疗外给予叶酸5mg.d-1和维生素B12500ug.d-1,其他两组仅予常规治疗。随访患者1年,观察血浆Hcy水平以及患者预后(NIHSS以及不良预后事件)。结果干预组Hcy水平显著降低(P=0.008),但是NIHSS评分较对照组无显著改善,不良预后事件发生率无差异。结论叶酸及维生素B12治疗能显著降低患者血浆Hcy水平,但是不能改善患者预后,考虑可能与维生素治疗不能改善炎症反应有关。维生素治疗能否降低心脑血管病的发生及复发需要进一步研究。     

Diphenylhydantoin, Phenobarbital, and Primidone in Saliva, Plasma, and Cerebrospinal Fluid

Diphenylhydantoin, primidone, and phenobarbital were determined in saliva and plasma of 164 patients by gas-liquid chromatography. The saliva ratio was about one-tenth in patients on diphenylhydantoin, 0.32-0.38 on phenobarbital alone and with other drugs, 0.97 and 0.96 on primidone alone and with other drugs. The S/P ratio of phenobarbital was similar in patients treated with primidone alone or with co-medication. For diphenylhydantoin and primidone, the S/P and CSF/plasma ratio were similar; for phenobarbital the S/P ratio was lower due to the difference in pH of saliva and CSF. Thus the concentration in saliva serves as a measure of the nonprotein-bound or free concentration in plasma with the advantage that saliva is easy to obtain. Co-medication does not change the S/P ratio for the three drugs studied. The high correlation between levels in plasma and in saliva allows the plasma levels to be predicted from the concentration in saliva.     

Fasciitis, perimyositis, myositis, polymyositis, and eosinophilia

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, and/or muscle fibers; eosinophilia in blood and/or in muscle biopsy. The following classification of 24 cases is suggested: at one end of the spectrum are fasciitis with eosinophilia: diffuse fasciitis (Shulman syndrome): 10 cases (3 with hematological complications); 2 cases of diffuse fasciitis with muscle atrophy; 3 cases of restricted fasciitis. Relapsing perimyositis with eosinophilia belong to the same spectrum, either diffuse (5 cases) with myalgias, or localized (2 cases). Other cases are focal myositis or multiple myositis, polymyositis with eosinophilia. The relationship among these cases is discussed. There is a continuum among the different groups. The pathophysiology remains unknown.     

Caspases, apoptosis, and Alzheimer disease: causation, correlation, and confusion

Extensive neuron loss occurs in Alzheimer disease (AD) brain and some authors have speculated that dysregulation of apoptotic death pathways is etiologically responsible for the disease. Apoptosis is regulated in mammalian cells by a family of cysteine proteases called caspases. At least 7 different caspases (caspases 1, 2, 3, 6, 8, 9, and 12) have been implicated in regulating neuronal cell death in response to amyloid beta (A beta) exposure in vitro, in animal models of neurodegenerative diseases, and in AD brain itself. Despite this seemingly impressive array of data implicating caspases and apoptosis as etiologic factors in AD, the direct involvement of caspase-dependent neuronal apoptosis in AD pathogenesis remains uncertain. Alternative explanations for some findings, contradictory experimental observations, and lack of morphologically convincing apoptotic neurons in the vast majority of AD brains has led to the revised hypothesis that apoptosis-associated molecular events cause neuronal dysfunction in the absence of, or prior to, neuronal death. Unfortunately, this new view renders the term "apoptosis-associated" functionally meaningless since it bears no relationship with apoptotic death and fails to focus scientific investigation on the molecular insults that trigger the "apoptosis-associated" response in AD neurons. On balance, an etiologic role for caspases in AD is far from proven. It remains possible, however, that caspase-dependent neuronal death contributes to AD neuron loss and thus, caspase inhibition offers some hope for extending AD neuron survival so that other agents, targeting upstream events, may delay or reverse primary AD pathology.