维生素干预治疗对阿尔茨海默病病人血浆同型半胱氨酸水平的影响

目的探讨阿尔茨海默病(AD)病人血浆同型半胱氨酸(Hcy)水平的变化及维生素干预治疗对AD病人血浆Hcy水平的影响。方法选取75例AD病人为病例组,71例同龄非痴呆老人为对照组,测定两组血浆Hcy、叶酸、维生素B12水平,并随机选取15例AD病人接受口服叶酸5mg及维生素B12500μg,每日晨服1次,干预治疗4周。结果AD病人血浆Hcy水平显著高于对照组(P<0.001),血浆叶酸水平、维生素B12显著低于对照组(P<0.001),接受维生素干预治疗的15例AD病人,4周后血浆Hcy水平下降(P<0.001),叶酸及维生素B12水平均升高(P<0.001)。结论AD病人存在血浆高Hcy水平;AD血浆Hcy水平升高与饮食中摄入维生素不足关系密切,维生素干预治疗能够有效地降低AD病人血浆Hcy水平。     

老年高血压并缺血性脑卒中患者血浆同型半胱氨酸变化的临床意义

对66例老年原发性高血压患者、68例高血压并缺血性脑卒中患者及65例老年健康人进行血浆同型半胱氨酸（Hcy）、叶酸及维生素B12检测。结果显示，高血压和高血压并缺血性脑卒中组患者血浆Hcy水平均高于健康者（P〈0．01），而叶酸、维生素B12低于健康者（均P〈0．05）。认为老年高血压病及伴缺血性脑卒中患者的发病与血浆Hcy水平升高及叶酸、维生素B12水平降低有关，补充叶酸、维生素B12可能有助于减少老年脑血管病的发生。     

叶酸、B族维生素对高同型半胱氨酸血症脑梗死患者血管内皮细胞功能的影响

将120例高同型半胱氨酸(Hcy)血症的脑梗死患者随机分为治疗组和对照组,治疗组口服叶酸、维生素B6、维生素B12,对照组不服用上述药物.治疗前和治疗4周后分别测定血浆Hcy水平及内皮素(ET)、一氧化氮(NO)水平.发现治疗组治疗4周后,血浆Hcy、ET水平明显降低,NO水平明显升高.提示叶酸、B族维生素干预治疗能降低血浆Hcy水平,对高Hcy血症脑梗死患者血管内皮细胞功能损害有一定的改善作用.     

叶酸和维生素B12、B6对阿尔茨海默症患者血浆Hcy、血脂水平的影响

目的观察叶酸和维生素B12、B6对阿尔茨海默症患者血浆同型半胱氨酸(Hcy)、血脂水平的影响。方法选择阿尔茨海默症患者42例,随机分为干预组和对照组,各21例。两组常规治疗相同,干预组同时服用叶酸和维生素B12、B6,均治疗30 d。治疗前后检测两组血浆Hcy、D-二聚体(D-D)、纤维蛋白原(FIB)和血脂,并进行长谷川痴呆量表(HDS)评分。结果干预组治疗后血浆Hcy、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、极低密度脂蛋白胆固醇(LDL-V)、D-D、FIB下降水平高于对照组(P均<0.05),HDS评分高于对照组(P<0.05)。结论补充叶酸和维生素B12、B6可降低阿尔茨海默症患者血浆Hcy和血脂水平。     

不同剂量叶酸、B族维生素对冠心病患者血浆同型半胱氨酸的影响

目的探讨不同剂量叶酸、B族维生素对冠心病患者血浆同型半胱氨酸(Hcy)水平的影响。方法对90例血浆同型半胱氨酸增高的冠心病患者随机分为A、B、C三组,每组30例,A、B组为治疗组,口服不同剂量的叶酸、B族维生素;C组为对照组,不服用上述药物。治疗前和治疗4周后分别测定血浆同型半胱氨酸的变化。结果A组、B组干预治疗4周后血浆Hcy明显下降,与C组比较P<0.001,A组、B组治疗前后自身比较P<0.001,A、B两组间比较差异无统计学意义(P>0.05)。结论冠心病患者用叶酸、B族维生素干预治疗后,血浆Hcy明显下降。其下降程度与药物剂量无明显关系,小剂量应用可达防治目的,可作为冠心病患者的早期预防药物。     

急性冠脉综合征高同型半胱氨酸血症与血叶酸等的关系

目的:测定急性冠脉综合征(ACS)患者中血浆高同型半胱氨酸(Hcy)水平,研究其与血浆叶酸、维生素B12的关系。方法:对52例ACS患者与46例对照组患者的血浆Hcy及叶酸、维生素B12水平进行比较分析。结果:ACS患者血浆Hcy含量明显高于对照组(P<0.01),而血浆叶酸和维生素B12水平明显低于对照组(P<0.01)。两组血浆Hcy含量与叶酸、维生素B12含量呈负相关(r=0.505,0.405,P<0.01)。结论:高Hcy血症通过加速动脉粥样硬化而导致急性冠脉综合征。补充叶酸、维生素B12或许对急性冠脉综合征的防治有益。     

叶酸、B族维生素对老年慢性心力衰竭伴高同型半胱氨酸血症患者心室重构及心功能的影响

目的 通过口服叶酸、B族维生素(VitB)治疗老年慢性心力伴高同型半胱氨酸(Hcy)血症患者,观察血清Hcy水平的改变对心室重构及心功能的影响.方法 选择87例血清Hcy水平增高的慢性心力衰竭患者(Hcy≥ 15μmo/L),随机分为对照组(41例,仅服用利尿剂、β受体阻滞剂、ACEI或ARB等基础药物)、干预组[46例,除基础用药外加用叶酸5mg(1次/d)、VitB12 0.5mg(1次/d)、B6 40mg(1次/d)],分别于治疗前、后4周测定患者空腹血清Hcy水平及查彩超评价心室形态学及心功能,所有数据进行统计学处理,最终84例完成了治疗计划.结果 干预组治疗4周后心室重构及心脏舒张功能相关指标均有改善,血清Hcy减低,与对照组比较差异有统计学意义(P＜0.05).结论 口服叶酸、VitB可降低老年慢性心力衰竭伴高Hcy血症患者血清Hcy水平,从而改善心室重构和心功能.     

急性冠状动脉综合征患者血浆同型半胱氨酸水平的变化及其主要影响因素

目的:探讨同型半胱氨酸(Hcy)及其代谢相关因子(叶酸、维生素B12)和血脂与急性冠状动脉综合征(ACS)之间的关系。方法:110例ACS患者(ACS组)及110例性别和年龄相匹配的非心脑疾病者(对照组),应用高效液相色谱荧光分析法测定血浆Hcy浓度,同时测定叶酸、维生素B12浓度及血脂水平,分析血浆Hcy与ACS有无相关性,并进一步分析Hcy与叶酸和维生素B12之间的关系。结果:①ACS组血浆Hcy浓度[(16.75±11.97)mmol/L]高于对照组[(13.15±5.65)mmol/L],(P<0.05)。②血浆Hcy浓度和血浆叶酸、维生素B12浓度呈明显的非线性负相关。③ACS组血脂与Hcy水平无明显相关。结论:高Hcy血症是ACS的一个新的危险因素,叶酸、维生素B12是影响ACS患者血浆Hcy水平的主要因素。     

血浆同型半胱氨酸、叶酸、维生素B_(12)水平与脑梗死及血管性痴呆的相关性

目的探讨血浆同型半胱氨酸(Hcy)、叶酸及维生素B12水平与脑梗死及血管性痴呆(VD)的相关性。方法采用直接化学发光技术测定32例VD患者,18例非痴呆性脑梗死患者及20例健康对照组血浆Hcy、叶酸及维生素B12水平。结果 VD患者血浆Hcy水平明显高于非痴呆性脑梗死组及正常对照组(P<0.01),其叶酸及维生素B12水平也明显低于非痴呆性脑梗死组及正常对照组(P<0.01)。但不同程度VD患者间Hcy、叶酸及维生素B12水平无显著差异(P>0.05)。结论高Hcy血症是脑梗死及VD的危险因素,但不能影响VD程度。     

高龄患者缺血性脑白质疏松症与血浆同型半胱氨酸的关系

目的 通过测定高龄缺血性脑白质疏松症(LA)患者的血浆同型半胱氨酸(Hcy),探讨高龄患者Hcy与缺血性LA发生、发展的程度、损害部位相关性及临床意义.方法 选择均经MRI证实的高龄男性(年龄≥80岁)患者99例,经LA影像学分级后,分为轻度脑白质损害组(轻度组,27例)、中度脑白质损害组(中度组,41例)、重度脑白质损害组(重度组,31例).测定空腹血浆总Hcy,并进行比较,并对血浆Hcy与血清叶酸及维生素B12水平进行相关分析.结果 与重度组比较,轻、中度组患者吸烟、腔隙性脑梗死、高Hcy比例明显降低(P＜0.05),轻度组患者高血压比例明显降低(P＜0.05);Hcy与叶酸、维生素B12水平呈负相关;各脑区损害程度以深部白质损害最为严重.结论 高龄患者血浆Hcy升高,血清叶酸、维生素B12降低与缺血性LA程度及部位密切相关.     

叶酸和维生素B6、B12对不稳定型心绞痛并高同型半胱氨酸患者预后的影响

近年来的研究表明,高同型半胱氨酸（homocys—teine,Hcy）血症可导致心血管疾病发病率和死亡率增高,与高脂血症、高血压、高血糖等因素同等重要,是动脉粥样硬化发生、发展的一个独立危险因素。     

Demonstration of vitamin B12 deficiency by a simple cytochemical reaction in the peripheral blood smear

Summary A simple, rapid and inexpensive cytochemical method for the detection of vitamin B 12 deficiency was applied in several types of anemias and matched with the levels of vitamin B 12 and folic acid in the serum of the patients. It was found that in patients with low vitamin B 12 levels the stained erythrocytes and the erythroid precursors showed a yellowish brown discoloration, which was not detected in folic acid deficiency and all other types of anemias. This test therefore may be used for differentiation between B 12 and folate deficiency whenever megaloblastic anemia is diagnosed.     

B族维生素在雄性小鼠高尿酸血症中的作用

目的研究B族维生素对高尿酸血症小鼠血尿酸水平的影响及其对高尿酸血症引起的内皮功能紊乱的作用。方法 SPF级昆明雄性小鼠63只,按体质量完全随机分成6组,A、B、C、D、E和F组。A组蒸馏水处理作为对照组,B组酵母膏+乙胺丁醇混合液灌胃处理建立小鼠高尿酸血症模型作为对照组;其余4组除建立模型外,还需在C组小鼠灌胃液中加入别嘌呤醇片,在D、E和F组中分别加入低、中、高剂量的叶酸+维生素B6+维生素B12混合溶液。3周后取血测定小鼠血尿酸水平及血清一氧化氮值。结果 3周后,6组小鼠的血清尿酸水平差异有统计学意义(F=14.7469,P<0.05)。与B组比较,D、E和F组小鼠的血清尿酸水平均能在一定程度上有所降低,且差异有统计学意义[D组(217.38±74.99)μmol/L,E组(228.19±65.25)μmol/L,F组(174.48±34.60)μmol/L比B组(302.93±56.99)μmol/L,均为P<0.05]。其中F组降低更显著,但其降低效果均低于C组[C组(105.52±49.32)μmol/L比F组(174.48±34.60)μmol/L,P<0.05]。6组小鼠的血清一氧化氮水平差异有统计学意义(F=7.0499,P<0.05)。与B组比较,E组和F组的血清一氧化氮水平均升高[E组(16.52±10.95)μmol/L,F组(18.63±10.77)μmol/L比B组(2.51±3.89)μmol/L,P<0.05],且与C组比较,F组升高更明显[C组(9.35±5.65)μmol/L比F组(18.63±10.77)μmol/L,P<0.05]。血清一氧化氮水平与尿酸水平呈负直线相关(r=-0.278,P<0.05)。结论叶酸、维生素B12及维生素B6可呈剂量依赖性降低高尿酸血症小鼠的血尿酸水平;同时较大剂量的B族维生素能够在一定程度上升高血清一氧化氮水平。     

Vitamin B12 deficiency and gastric histopathology in older patients

AIM: To compare upper gastric endoscopic and histopathologic findings in older adults in the presence and absence of B12 deficiency. METHODS: A prospective analysis of upper gastric endoscopic and gastric histopathologic findings from 30 newly identified B12-deficient patients (11 males, 19 females) and 16 controls with normal B12 status (6 males, 10 females) was performed. For all subjects, the indication for upper endoscopy and gastric biopsy were unrelated to B12 status. A single pathologist, blinded to B12 status, processed and interpreted the biopsy samples. Endoscopic and histopathologic findings were correlated with age, gender, hematocrit (Hct), MCV and B12 status. RESULTS: The B12-deficient group had significantly lower mean serum B12 levels compared to the controls (P<0.00005) while their mean Hct, MCV and serum albumin levels were similar. Iron deficiency (ferritin- based) was present in 21% of B12-deficient patients and intrinsic factor antibodies were present in 29% (5/17) of B12-deficient patients. The endoscopic findings revealed significantly different rates of gastritis and atrophy between the B12-deficient and control groups (P= 0.017). B12-deficient patients had significantly less superficial gastritis (62% vs 94%) and significantly more atrophic gastritis (28% vs 0%) as compared to the controls (P= 0.039). Intestinal metaplasia was similar in both groups. Hellcobacter pylori infection rates were similar in the B12-deficient patients and controls (40% vs 31%). CONCLUSION: Significantly different endoscopic findings and types of gastritis could often be observed in the presence and absence of B12 deficiency. Atrophy, based on endoscopy, and atrophic gastritis, based on histopathology, suggest the presence of B12 deficiency. Gastric histopathology is not influenced by the age, gender, Hct or MCV of the patients.     

Role of vitamins B6, B12 and folic acid on hyperhomocysteinemia in a Pakistani population of patients with acute myocardial infarction

BACKGROUND AND AIM: Pakistani people belong to an ethnic group which has the highest rate of coronary artery disease (CAD). We investigated the possible correlation between deficiency of vitamins B6, B12 or folic acid and hyperhomocysteinemia in Pakistani patients with acute myocardial infarction (AMI). A case-control study was carried out involving 224 AMI patients (age 30-70 years; 55 females and 169 males) and 126 normal healthy subjects (age 31-70 years; 35 females and 91 males). METHODS AND RESULTS: Fasting venous blood was obtained from cases and controls. Serum was analyzed for folic acid and B12 using radioassays. Plasma was analyzed for pyridoxal phosphate (PLP; coenzymic form of B6) using a radioenzymatic assay and for total homocysteine using a fluorescence polarization immunoassay. Mean serum B12 concentration in AMI patients was found to be significantly lower than the mean for controls (241+/-185 pg/ml vs 608+/-341 pg/ml; p < 0.001). Mean serum folate level in patients was also found to be lower than controls (3.35+/-3.78 ng/ml vs 4.93+/-2.93 ng/ml), however, the differences were not statistically significant. Similarly, mean PLP concentration in plasma of cases (19.4+/-24.4 nmol/l) was lower than the concentration in controls (23.2+/-17.6 nmol/l), but the difference was not statistically significant. Mean plasma homocysteine level in AMI cases (18+/-8.36 micromol/l) was higher than the mean level in controls (16.4+/-4.9 micromol/l), but not to a significant extent. However, this mean homocysteine concentration in normal healthy subjects was among the highest reported in the literature and was significantly more than mean values reported in most Eastern and Western studies. Compared to controls, there was significantly greater deficiency of folate (32.5% vs 67.1%), B12 (3.2% vs 63.4%) and PLP (49.2% vs 74.1%) in AMI patients. Deficiencies of folate, B12 and PLP were defined as serum folate levels less than 3.5 ng/ml, serum levels of B12 less than 200 pg/ml and plasma PLP levels less than 20 nmol/l. Mean plasma homocysteine levels in smokers were found to be significantly higher in both cases and controls. Similarly, mean serum folate levels in smokers (compared to nonsmokers) were significantly lower in both cases and controls. CONCLUSIONS: Substantial nutritional deficiencies of these three vitamins along with mild hyperhomocysteinemia, perhaps through an interplay with the classical cardiovascular risk factors (highly prevalent in this population), could be further aggravating the risk of CAD in the Pakistani population.     

Long term use of metformin leading to vitamin B 12 deficiency

Metformin is a commonly used oral hypoglycaemic agent worldwide. Gastrointestinal side effects and lactic acidosis related to metformin usage are commonly recognized. However, the associated vitamin B12 deficiency is less well known. We present a case of long term metformin use resulting in vitamin B12 deficiency     

Plasma homocysteine,dietary B vitamins,betaine, and choline and risk of peripheral artery disease

Objective

Few studies have examined the roles of homocysteine and related nutrients in the development of peripheral artery disease (PAD). We examined the associations between plasma homocysteine, dietary B vitamins, betaine, choline, and supplemental folic acid use and incidence of PAD.

Methods

We used two cohort studies of 72,348 women in the Nurses' Health Study (NHS, 1990–2010) and 44,504 men in the Health Professionals Follow-up Study (HPFS, 1986–2010). We measured plasma homocysteine in nested matched case–control studies of clinically recognized PAD within both cohorts, including 143 PAD cases and 424 controls within the NHS (1990–2010) and 143 PAD cases and 428 controls within the HPFS (1994–2008). We examined the association between diet and risk of incident PAD in the cohorts using a food frequency questionnaire and 790 cases of PAD over 3.1 million person-years of follow-up.

Results

Higher homocysteine levels were positively associated with risk of PAD in men (adjusted IRR 2.17; 95% CI, 1.08–4.38 for tertile 3 vs. 1). There was no evidence of an association in women (adjusted IRR 1.14; 95% CI, 0.61–2.12). Similarly, higher folate intake, including supplements, was inversely associated with risk of PAD in men (adjusted HR 0.90; 95% CI, 0.82–0.98 for each 250 μg increase) but not women (HR 1.01, 95% CI, 0.88–1.15). Intakes of the other B vitamins, betaine, and choline were not consistently associated with risk of PAD in men or women.

Conclusion

Homocysteine levels were positively associated and dietary folate intake was inversely associated with risk of PAD in men but not in women.     

Serum vitamin D and vitamin-D-binding protein levels in children with chronic hepatitis B

BACKGROUND Vitamin D is an essential fat-soluble secosteroid hydroxylated by the liver to form the intermediate metabolite calcidiol{25-hydroxy vitamin D[25(OH)D]},which is a reliable indicator to investigate individual vitamin D status.Vitamin-D-binding protein(VDBP)is a multifunctional glycoprotein mainly synthesized in the liver and the major transport protein for vitamin D and its metabolites.Serum vitamin D and VDBP are both associated with hepatitis B.However,few studies have reported the relationship and clinical significance of vitamin D and VDBP with hepatitis B virus(HBV)replication and hepatic fibrosis in children with chronic hepatitis B(CHB).AIM To explore vitamin D and VDBP serum levels in children with CHB and the association of vitamin D and VDBP with HBV replication and hepatic fibrosis.METHODS We enrolled 204 children with CHB admitted to Hunan Children’Hospital in summer and autumn between 2018 and 2019 and 170 healthy controls.CHB patients included:164 hepatitis B e antigen(HBeAg)positive and 40 HBeAg negative;193 hepatitis B surface antigen(HBsAg)positive and 11 HBsAg negative;164 with detectable HBV deoxyribonucleic acid(DNA)and 40 with undetectable HBV DNA;131 with HBV genotype B and 23 with HBV genotype C;and 27 without hepatic fibrosis and 97 with hepatic fibrosis.Serum levels of 25(OH)D,VDBP,liver function markers,and other clinical parameters were collected to analyze their association with vitamin D and VDBP.Mann-Whitney U test,Kruskal-Wallis H test,or t test was used to analyze serum 25(OH)D and VDBP levels in different groups.Spearman rank correlation test was utilized to analyze the correlation of 25(OH)D and VDBP with other markers.Statistically significant factors determined by univariate analysis were further analyzed by binary multivariate logistic regression analysis.P<0.05 was considered statistically significant.RESULTS Children with CHB had lower serum 25(OH)D(56.64±17.89 nmoL/L)and VDBP[122.40(70.74-262.84μg/L)]levels than healthy controls had(P<0.001).Serum 25(OH)D and VDBP levels were significantly different among the different grades of hepatic fibrosis(P<0.05).VDBP levels in children with HBV genotype C,HBsAg,HBeAg,and detectable HBV DNA were significantly lower than those in children with HBV genotype B,no HBsAg,no HBeAg,and undetectable HBV DNA(P<0.05).Serum 25(OH)D level was negatively correlated with age and serum total bilirubin level(r=-0.396 and-0.280,respectively,P<0.001).Serum VDBP level was negatively correlated with HBV DNA(log10 IU/mL)(r=-0.272,P<0.001).Serum 25(OH)D level was not correlated with VDBP level(P>0.05).Univariate(P<0.05)and multivariate logistic regression analysis showed that low level of 25(OH)D(odds ratio=0.951,95%confidence interval:0.918-0.985)and high level of HBV DNA(odds ratio=1.445,95%confidence interval:1.163-1.794)were independently correlated with hepatic fibrosis(P<0.01).CONCLUSION Serum levels of 25(OH)D and VDBP are decreased in children with CHB.Serum VDBP level is negatively correlated with HBV replication.Low level of 25(OH)D is independently associated with hepatic fibrosis in children with CHB.There is no significant association between serum levels of 25(OH)D and VDBP.