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1.
MTHFR基因多态性及同型半胱氨酸与青年脑血管病的关系   总被引:4,自引:0,他引:4  
目的:研究Ns,N10-亚甲基四氢叶酸还原酶(MTHFR)基因多态性及血浆同型半胱氨酸(Hcy)水平与青年脑血管病的关系。方法:研究对比40例青年脑血管病患者(首次发病年龄≤50岁)及32例健康青年人的MTHFR基因多态性及血浆Hcy水平。结果:(1)对照组及病例组T/T纯合子率分别为37.5%和22.5%;T等位基因频率分别为60.9%和51.3%,差异均无显著统计意义(均P>0.05)。(2)病例组血浆Hcy几何均值(11.0±2.3μmol/L)显著高于对照组(8.0±1.4μmol/L,P<0.05)。(3)所有受试者中T/T组Hcy值高于C/C组(10.4μmol/L和7.6μmol/L),但差异无显著性(P>0.05)。结合叶酸考虑,进一步将所有受试者按叶酸中位数水平分组。叶酸中位数以下组中,T/T组Hcy值显著高于C/C组(P<0.05);而叶酸中位数以上组中,T/T组Hcy值与C/C组无显著差异。(4)血浆Hcy与叶酸、维生素B12呈显著负相关,与肌酐呈显著正相关。吸烟者血浆Hcy水平显著高于不吸烟者(P<0.05)。结论:(1)本组人群MTHFR基因C677T突变的纯合子在低叶酸状态下可引起血浆Hcy水平显著增高,但与青年脑血管病无显著关系。MTHFR基因677TT纯合突变可能为健康青年人脑血管的保护因素。(2)血浆Hcy水平与青年脑血管病的发生密切相关。(3)叶酸、维生素B12肌酐、吸烟是Hcy的非遗传影响因素。  相似文献   

2.
目的 探讨持续气道正压通气(CPAP)治疗在脑梗死恢复期合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者脑梗死二级预防中的作用及临床意义。方法 选取94例脑梗死恢复期合并OSAHS患者,根据其是否接受CPAP治疗分为治疗组和对照组,分别测定治疗组CPAP治疗前后及对照组相应时间的空腹血糖、空腹胰岛素及血浆同型半胱氨酸(Hcy)水平,计算出胰岛素抵抗指数(HOMA-IR),比较治疗前后两组血浆Hcy水平、HOMA-IR的差异,分析CPAP治疗对脑梗死恢复期合并OSAHS患者HOMA-IR、血浆Hcy水平的影响。结果 CPAP治疗前治疗组的HOMA-IR、血浆Hcy水平与对照组比较,差异不具有统计学意义[(5.47±177;2.43 umol/L)vs(5.68±177;2.53 umol/L),P>0.05;(19.25±177;10.03 umol/L)vs(19.52±177;9.86 umol/L),P>0.05],CPAP治疗后治疗组的HOMA-IR、血浆Hcy水平较对照组显著降低,差异具有统计学意义[(1.94±177;1.23 umol/L)vs(5.59±177;2.51 umol/L),P<0.05;(13.35±177;6.52 umol/L)vs(19.57±177;9.29 umol/L),P<0.05]。结论 CPAP治疗可以降低脑梗死恢复期合并OSAHS患者胰岛素抵抗、血浆Hcy水平,在预防脑梗死恢复期合并OSAHS患者的梗死复发方面有特殊的作用。  相似文献   

3.
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。  相似文献   

4.
青年脑梗死患者血浆同型半胱氨酸水平及影响因素研究   总被引:1,自引:0,他引:1  
目的分析青年脑梗死患者血浆同型半胱氨酸(homocysteine,Hcy)的水平特点,并探讨其相关因素。方法采用高效液相色谱法检测55例青年脑梗死患者、316例老年脑梗死患者和40名健康青年对照者血浆Hcy水平,对青年脑梗死患者血浆Hcy的分布特征及相关因素进行统计学分析。结果青年脑梗死组血浆Hcy水平(几何均数17.35μmol/L)高于健康青年对照组(几何均数11.88μmol/L),差异有统计学意义(P〈0.01);与老年脑梗死组(几何均数17.60μmol/L)比较差异无统计学意义(P〉0.05);青年脑梗死患者Hcy水平与叶酸水平以及性别相关,回归系数分别为~0.513(P〈0.01)和-0.242(P〈O.05)。结论青年脑梗死患者血浆Hcy水平显著增高,男性高于女性,Hcy水平与叶酸水平呈负相关。  相似文献   

5.
联合维生素治疗对脑卒中病人高同型半胱氨酸血症的影响   总被引:3,自引:0,他引:3  
目的:研究联合维生素治疗对脑卒中病人高同型半胱氨酸血症的影响。方法:对450例脑卒中(包括短暂性脑缺血发作、脑梗死、脑出血)患者进行血清同型半胱氨酸(Hcy)水平的测定,联合维生素(叶酸、维生素B6、维生素B12)治疗高同型半胱氨酸血症的病人。结果:联合维生素治疗平均15.07±5.57天,Hcy水平从28.90±12.21umol/l降到15.63±9.52umol/l,P<0.01。结论:联合维生素治疗可以明显降低血浆同型半胱氨酸水平。  相似文献   

6.
同型半胱氨酸与脑卒中及相关因素分析   总被引:7,自引:0,他引:7  
目的:研究同型半胱氨酸和脑梗死、短暂性脑缺血发作(TIA)及脑出血的关系。方法 对450例脑卒中(包括短暂性脑缺血发作、脑梗死、脑出血)患者及149例对照组进行血清同型半胱氨酸(Hcy)水平的测定,经颅超声多普勒(TCD)检测颅内外血管。结果 发现脑梗死、TIA组和脑出血组血浆Hcy水平(分别为20.82±11.86,20.61±13.73,24.78±12.75umol/L)非常显著高于对照组(9.84±2.25umol/L,p<0.01);脑梗死组与脑出血组HCY水平有显著差异,P=0.041,高同型半脱氨酸血症在脑出血组的比例(75.5%)明显高于脑梗死组(56.5%)和TIA组(48.6%),p<0.05,高同型半胱氨酸血症对脑梗死、TIA、脑出血的相对危险度分别为1.670(95%的可信区间为1.089,2.562)、1.654(95%的可信区间0.828,3.302)、2.454(95%的可信区间1.479,4.071)。未发现缺血性脑卒中血管狭窄与高同型半胱氨酸血症比例间的统计学上的显著差异。病例组中有糖尿病的患者HCY的水平16.14±7.82(umol/l)明显低于无糖尿病者22.55±12.66(umol/L),p<0.01。结论 血浆Hcy水平不但与缺血性脑卒中有关,而且对脑出血也有显著影响,高同型半胱氨酸血症与脑出血的关系更密切。血管狭窄和同型半胱氨酸水平及比例间无显著差异,无糖尿病的脑卒中患者中,同型半胱氨酸水平对脑卒中有重要影响?  相似文献   

7.
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。  相似文献   

8.
目的 探讨脑梗死患者血浆硫化氢、同型半胱氨酸(Hcy)、叶酸和维生素B6水平的变化及其相关性.方法 检测60例脑梗死患者和40名正常对照者血浆硫化氢、Hcy、叶酸及维生素B6水平.脑梗死患者血浆硫化氢水平与Hcy、叶酸和维生素B6水平的相关性采用直线相关分析.结果 与正常对照组比较,脑梗死组血浆Hcy水平显著增高,血浆硫化氢、叶酸、维生素B6水平显著降低(P<0.05~0.001).血浆硫化氢水平与Hcy水平呈负相关(r=-0.6271,P<0.01),与叶酸及维生素B6水平呈正相关(r=0.5341,P<0.005;r=0.4615,P<0.05).结论 脑梗死患者血浆硫化氢、叶酸和维生素B6水平明显降低,Hcy水平升高.血浆低硫化氢水平可能参与了高Hcy血症致脑血管病的发病机制,可能是脑血管病的危险因素.  相似文献   

9.
同型半胱氨酸与脑血管病的临床研究   总被引:27,自引:4,他引:23  
目的探讨血清总同型半胱氨酸(tHcy)增高与脑血管病的发病、类型及传统危险因素的关系.方法采用高效液相色谱荧光检测法(HPLC-FD)测定99例脑血管病患者(28例TIA、46例动脉硬化性脑梗死和25例脑出血)及52例对照者的血清Hcy水平.结果 (1)脑血管病组的血清Hcy平均水平(17.5±7.3 μmol/L)显著高于对照组(10.2±3.7 μmol/L);(2)TIA、脑梗死和脑出血 3组间的血清Hcy水平无显著性差异(均P>0.05);(3)血清叶酸及Vit B12 与血清Hcy 均呈负相关;(4)血清Hcy水平>15.0 μmol/L,经校正性别、年龄、吸烟、高血脂、高血压、糖尿病及冠心病等危险因素后,脑血管病的相对危险度(OR)为3.2[95%可信区间(CI)为1.0~6.9].结论 (1)血清Hcy浓度升高可增加脑血管病的发病危险度,且与传统的脑血管病的危险因素及脑血管病的类型无关.(2)叶酸、VitB12是Hcy的非遗传性影响因素.  相似文献   

10.
目的探讨不同水平的同型半胱氨酸和脑梗死相关危险因素及脑梗死TOAST分型之间的相关性。方法选取我院卒中单元2010年1月~2011年3月急性脑梗死患者,根据患者血浆同型半胱氨酸(Hcy)水平首先将急性脑梗死患者分为正常(〈15umol/L)及轻度增高组(15umol/L~30umol/L)及中重度增高组(≥30umol/L);根据患者的卒中危险因素、临床特点及影像学资料对所有患者行TOAST分型。结果①Hcy轻度增高组与Hcy正常相比,血浆维生素B12水平明显降低(P〈0.001),余危险因素之间比较无统计学差异;而Hcy中重度增高组与正常组与相比,中重度增高组男性比例(P=0.014)及吸烟率(P=0.019)明显高于正常组、高血压患病率(P=0.004)及血浆维生素B12水平(P=0.002)明显低于正常;②Hcy正常组、Hcy轻度增高组的TOAST分型均以大动脉粥样硬化性卒中(LAA)型比例最高、其次为小动脉闭塞性卒中(SAO)型,而Hcy中重度增高组以SAO型比例最高,其次为心源性脑栓死(CE)型,Hcy中重度增高组LAA型比例明显低于Hcy正常组(P=0.007),具有统计学差异;结论脑梗死患者不同水平的Hcy伴有不同的卒中危险因素及不同的TOAST构成,Hcy中重度增高伴有高的男性比例及吸烟率,伴有低的高血压比例及低血浆维生素B12水平;Hcy中重度增高组TOAST分型以SAO型。  相似文献   

11.
目的:了解石家庄地区青年脑梗死和TIA患者(年龄≤45岁〉血清同型半胱氨酸(homocysteine,HCY)水平及给予叶酸、B族维生素治疗后HCY含量的变化。方法:采用荧光偏振免疫分析法,对80例脑梗死患者,80例TIA患者及80例健康人进行血清HCY的检测,同时测定其叶酸、维生素B12水平后,各组均随机分成干预治疗组与非干预治疗组,每组40例,干预治疗组给予叶酸5mg,隔日1次,维生素B12250ug,1日1次,维生素B610mg,1日1次,口服6个月后复查上述各指标。结果:治疗前三组血清HCY水平各不相同,脑梗死组为(16.5±5.4)mmol/L,TIA组为(14.4±5.0)mmol/L,与正常对照组(12.1±2.9)mmol/L比较,具有显著性差异(P<0.01)。相关分析发现,血HCY水平与叶酸、维生素B12呈负相关。干预治疗后,治疗组患者的血HCY水平均有下降。结论:高HCY血症是青年脑梗死及TIA患者的独立致病因素,补充营养元素有助于降低血HCY水平。  相似文献   

12.
帕金森病患者伴发高同型半胱氨酸血症的相关因素分析   总被引:1,自引:0,他引:1  
目的探讨帕金森病(Parkinson’s disease,PD)患者伴发高同型半胱氨酸血症(hyperhomocysteinemia,Hhcy)与左旋多巴(levodopa,L-dopa)治疗的关系。方法收集门诊154例PD患者,检测其同型半胱氨酸(Homocysteine,Hcy)的水平。高于正常值者列为研究组,正常值范围内为对照组,2组就年龄、性别、病程、L-dopa治疗情况、叶酸和维生素B12水平等进行对照分析。结果研究组使用L-dopa治疗者比例(62/76))明显高于对照组(44/78)(P0.01),而其他因素包括性别、年龄、病程、叶酸和维生素B12浓度对Hcy的升高而无明显影响(P0.05);治疗组血浆Hcy浓度(24.34±8.67)umol/L明显高于未治疗组(14.26±6.11)umol/L(P0.01)。结论L-dopa治疗可以导致PD患者的血浆Hcy水平升高,可能是PD患者伴发Hhcy的独立危险因素。  相似文献   

13.
目的 探讨同型半胱氨酸(homocysteine,Hcy)水平及亚甲基四氢叶酸还原酶(methylenetetrahydrofolate reductase,MTHFR)基因多态性与缺血性卒中(ischemic stroke,IS)的关系,并分析Hcy与叶酸、 VitB12之间的相关性。 方法 运用酶循环法和聚合酶链式反应(polymerase c hain r eaction,PCR)-芯片杂交法分别检测217 例IS患者和223例对照者血浆Hcy与MTHFR C667T基因型,并对照分析两组的基因型频率和等位基因 频率分布差异及血浆Hcy水平;运用免疫分析法检测两组中既往未服用过含叶酸和VitB12药物的88例 I S患者和125例对照者血清叶酸、Vi tB12水平,并与Hcy水平进行相关性分析。 结果 IS组Hcy浓度高于对照组,差异有显著性([ 23.95±12.13)μmol/L vs(17.31±7.20)μmol/L, t =29.61,P<0.001],IS组与对照组MTHFR 基因型频率CC、CT、TT型分别为14.3%、44.7%、41.0%和 18.4%、48.9%、32.7%,等位基因C与T的频率分别为36.6%、63.4%和42.8%、57.2%,无显著性差 异(基因型频率:χ 2=3.59,P =0.166;基因频率:χ 2=3.52,P =0.061)。MTHFR基因TT型(162例)、CT 型(206例)和CC型(72例)的血浆Hcy水平分别为(25.19±12.53)μmol/L、(18.21±8.08)μmol/L和 (16.65±6.90)μmol/L,其中TT型显著高于CT型和CC型,CT型显著高于CC型(P 均<0.001)。I S组和对 照组血浆Hcy水平与VitB12呈负相关(I S组和对照组分别为r =-0.431,P<0.001和r =-0.507,P<0.001), 与叶酸亦呈负相关(IS组和对照组分别为r =-0.489,P<0.001和r =-0.446,P<0.001)。 结论 IS患者血浆Hcy水平较正常人偏高;MTHFR C667T基因突变、叶酸和VitB12水平降低是血浆Hcy 水平升高的影响因素;MTHFR C667T基因突变可能与缺血性卒中无关。  相似文献   

14.
同型半胱氨酸与阿尔茨海默病及血管性痴呆   总被引:2,自引:0,他引:2  
目的研究同型半胱氨酸(Homocysteine,Hcy)及叶酸、维生素B_(12)与阿尔茨海默病(Alzheimer Dis- ease,AD)和血管性痴呆(Vascular dementia,VaD)的关系,并通过Hcy揭示AD发病的血管危险因素。方法用美国国立神经病学、语言障碍和卒中-阿尔茨海默病和相关疾病学会(NINCDS-ADRDA)标准的可能标准严格筛选AD患者35例,用ADDTC诊断标准筛选VaD患者30例,并同期选择31例无临床脑血管病史、无认知功能障碍的健康查体中心志愿者为对照组。取肝素抗凝的血浆用循环酶法进行Hcy的测定。取血清由全自动化学发光免疫检测仪进行叶酸和维生素B_(12)的测定。结果AD组和VaD组血浆Hcy水平显著高于对照组,血清叶酸和VitB_(12)水平显著低于对照组。VaD组存在痴呆程度越高血浆Hcy水平越高这一显著正相关关系,而AD组这一正相关关系无统计学意义;且发现VaD组患者MMSE评分越低其血浆Hcy水平越高这一显著负相关关系,而AD组这一关系仍无统计学意义。在所有研究对象中存在血浆Hcy水平与血清叶酸及VitB_(12)水平的显著负相关关系。结论提示高Hcy血症可能是引起AD和VaD的一个重要危险因素,Hcy作为一个新的血管因素加强了AD与血管危险因素之间的联系,并且提示积极治疗高Hcy血症在预防AD和VaD方面可能有积极意义。  相似文献   

15.
目的 探讨急性脑梗死患者给予维生素B_(12)制剂(甲钴胺)和叶酸(Fa)治疗前后血浆同型半胱氨酸(Hcy)、叶酸和维生素B_(12)水平变化及其对预后的影响.方法 检测152例急性脑梗死患者和132例正常人血浆同型半胱氨酸(Hcy)、叶酸、维生素B_(12)水平,并对急性脑梗死患者进行神经功能缺损评分(NIHSS);将急性脑梗死组随机分为干预组和非干预组,干预组给予维生素B_(12)制剂(甲钻胺)联合叶酸治疗,治疗4周后复测血浆同型半胱氨酸(Hcy)、叶酸和维生素B_(12)水平,并再次进行神经功能缺损评分(NIHSS).结果 急性脑梗死组和正常健康对照组之间血浆Hcy水平、叶酸和维生素B_(12)水平存在明显差异(P<0.01),予以补充叶酸和维生素B_(12)(甲钴胺)治疗后,干预组血浆Hcy水平明显下降,神经功能缺损评分显著升高,与非干预组相比有显著性差异(P<0.05).结论 急性脑梗死患者血浆Hcy水平升高,补充叶酸、维生素B_(12)制剂有助于降低血浆Hcy水平,有利于脑梗死疾病的转归.
Abstract:
Objective To explore the changes of the levels of plasma homocysteine ( Hcy), folate and vitamin B_(12) and the relationship between the changes and the prognosis in patients with acute cerebral infarction who were treated with vitamin B_(12) preparation (methylcobalamin) and folate. Methods The plasma level of Hcy, folate and vitamin B_(12) ( VitB_(12)) of 152 patients with cerebral infarction and 132 healthy people were measured, and the patients with acute cerebral infarction were given a mark with the evaluation of neurological impairments (NIHSS). The patients with acute cerebral infarction were randomly divided into intervention group and non-intervention group. The intervention group was treated with vitamin B_(12) preparations (methylcobalamin) and folate. After 4 weeks, retested the plasma homocysteine (Hcy), folate and vitamin B_(12) levels, and carried out NIHSS score once again. Results In the plasma level of Hcy, folate and vitamin B_(12), there were significant differences between the acute cerebral infarction group and the healthy control group (P < 0.01 ). In intervention group, the plasma homocysteine levels decreased significantly, and the evaluation scores increased significantly after intervention treatment, and there was significant differences between intervention group and non-intervention group (P <0.05). Conclusion The levels of plasma Hcy increased in the patients with acute cerebral infarction. Being added with folate and vitamin B_(12) preparations was well to reduce the levels of plasma Hcy, and it was also conducived to the prognosis of acute cerebral infarction.  相似文献   

16.
High levels of homocysteine (Hcy) were suggested to contribute to the pathogenesis of schizophrenia. Recent investigations have shown that treatment with folic acid, vitamin B-12 and pyridoxine are effective in reducing Hcy levels while concomitantly reducing the score of positive and negative symptoms in schizophrenic patients. In addition to the availability of nutrients (mainly folate, vitamins B6 and B12), plasma Hcy concentrations are dependent on complex metabolic regulation that could be disrupted in schizophrenia.This study was designed to test the influence of disease activity on plasma Hcy levels. Plasma Hcy concentrations were measured in male chronic schizophrenic patients with a predominantly positive (SCH (+)) or predominantly negative (SCH (−)) syndrome in schizophrenia immediately upon admission to the hospital (exacerbation phase) and one month later (remission phase). During this period patients received antipsychotic medications without vitamin therapy. The effects of age, duration of illness, folate and B12 concentrations, as well as smoking and coffee consumption habits on the observed changes were evaluated. Age- and sex-matched subjects were included in the control group. In the control group plasma Hcy concentration was 8.75 ± 1.84 μmol/L. In the exacerbation phase plasma Hcy concentrations were significantly increased both in SCH (+) (14.91 ± 6.19 μmol/L) and SCH (−) groups (12.8 ± 3.27 μmol/L). There was no difference in plasma Hcy concentrations between SCH (+) and SCH (−) patients. Serum folate and B12 concentrations were not significantly different in any of the investigated groups of subjects. The plasma Hcy concentrations could not be correlated with age, duration of illness, the score of positive symptoms or the concentration of folate and vitamin B12. A positive correlation was found between plasma Hcy level and score of negative symptoms in both groups of patients. No correlation was found between smoking or coffee consumption habits and plasma Hcy concentrations. All patients exhibited decreased plasma Hcy levels in the remission phase of the illness, with a mean decrease of 2.68 ± 1.57 μmol/L. Folate and B12 levels did not differ in the exacerbation and remission phases of the illness.The significant decrease of plasma Hcy levels, without changes in folate and vitamin B12 concentrations in the remission phase of schizophrenia, could indicate an influence of a pathogenetic process involved in schizophrenia on Hcy metabolism.  相似文献   

17.
IntroductionPrevious studies have suggested a significant increase in plasma homocysteine (Hcy) levels in levodopa-treated Parkinson’s disease (PD) patients, and vitamin B12 and folate supplementation may decrease Hcy levels. However, the effects of catechol-O-methyltransferase inhibitors on levodopa-induced increase in Hcy levels were conflicting. The aim of this study was to evaluate whether Hcy levels are increased in levodopa-treated PD patients and to evaluate the effects of vitamin B12 and folate or entacapone on Hcy levels in levodopa-treated PD patients.MethodsWe analyzed and compared plasma Hcy levels in 20 levodopa-naïve PD patients and 42 levodopa-treated PD patients, followed by randomized assignment of 42 levodopa-treated patients to treatment groups with either vitamin B12 and folate, entacapone, or no medication.ResultsPlasma Hcy levels in levodopa-treated PD patients were higher than those in the control group, but the difference was not statistical significant (15.25 ± 6.70 and 13.13 ± 4.68, P = 0.216). Patients treated with vitamin B12 and folate had a significant decrease in plasma Hcy levels (P < 0.001). In the entacapone group, Hcy levels were mildly decreased, but the change did not reach statistical significance.ConclusionLevodopa-treated PD patients had higher plasma Hcy than levodopa-naive PD patients. Unlike entacapone, combination supplementation with vitamin B12 and folate was associated with significantly decreased plasma Hcy. We suggest that plasma Hcy levels should be monitored during levodopa treatment, and supplementation with inexpensive vitamin B12 and folate is beneficial for levodopa-treated patients.  相似文献   

18.
目的:探讨血浆同型半胱氨酸(Hey)与迟发性运动障碍(TD)的关系.方法:对33例伴TD的精神分裂症患者(TD组)与33例不伴,TD的精神分裂症患者(非TD组)进行血浆Hey与血清维生素B12、叶酸水平检测.结果:TD组血浆Hey水平显著高于非TD组,而血清叶酸水平显著低于非TD组.两组血浆Hey水平均与血清维生素B1...  相似文献   

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