有心肌梗塞家族史儿童血清脂蛋白（a）的研究

为探讨有心肌梗塞家族史的少年儿童血脂的改变，特别是脂蛋白（ａ）的改变，采用单克隆抗体酶联免疫吸附实验，对３３例有心肌梗塞家族史的少年儿童测定其脂蛋白（ａ）［Ｌｐ（ａ）］。结果：血清Ｌｐ（ａ）＞３００ｍｇ／Ｌ：心肌梗塞家族史阳性的３３例中有１６例（４８％），而对照组３３例中只有５例（１５％）（χ２＝８．５４０，Ｐ＜０．０５）；有心肌梗塞家族史儿童的血清Ｌｐ（ａ）含量明显高于对照组。提示：对有心肌梗塞家族史的后代，应适时检测Ｌｐ（ａ），及早施行干预措施，以达到预防的目的。     

风湿热患儿血清脂蛋白(a)和胆固醇变化的临床意义

目的：研究风湿热（RF）患儿血清脂蛋白（a) [Lp(a)]和胆固醇（TC）变化的临床意义。方法：分别采用克隆抗体ELISA法和酶法对RF患儿63例，正常对照组70例测定Lp(a)和TC水平。结果：RF患儿血清Lp(a)较正常对照组高，差异有显著性（P＜0．01），RF患儿各组间的Lp(a)差异无显著性（P均＞0．05），但均高于对照组，差异均有显著性（P＜0．05或P＜0．01）。RF患儿血清TC较对照组低，差异有显著性O（P＜0．05），而RF患儿各组间TC也均低于对照组，但差异均无显著性（P均＞0．05）。结论：RF患儿TC下降机制尚未清楚。血清Lp(a)增高可作为RF患儿风湿活动的参考指标，而其持续增高可能是使RF向风湿性心脏病发展的危险因素之一。     

有急性脑血管病家族史儿童血清脂蛋白(a)和载脂蛋白E基因多肽检测

1999年 3～ 8月我们研究了有急性脑血管病家族史的少年儿童血清脂蛋白 (ａ) [ＬＰ(ａ) ]和载脂蛋白Ｅ(ＡｐｏＥ)及基因多肽 ,所得结论与现有报道各有异同。对象 :观察 1组 :有急性脑血管疾病家族史的少年儿童。按第二届全国神经精神会议推荐的符合动脉硬化性脑血栓形成 (15例 )及脑出血 (15例 )的诊断标准 ,均为我院神经内科住院的患者的第二代亲属共 30例 ,男 16例 ,女14例 ,年龄 7～ 15岁。观察 2组 :有心肌梗死家族史的少年儿童。依照国际心脏病学会及世界卫生组织制定的心肌梗死诊断标准 ,均经我院心血管内科确诊为心肌梗死患者的后代 3…     

肥胖儿童的脂蛋白、纤溶指标的变化及意义

目的　分析肥胖儿童脂蛋白(a)[Lp(a)]、纤溶指标的变化及其相关性,探讨儿童期肥胖是否存在动脉粥样硬化的高危因素及脂代谢与血栓形成间的相互作用。方法　应用免疫比浊法检测60 例肥胖儿童及60 例正常体重健康儿童的血清Lp(a)、纤溶酶原(Pg)含量。以发色底物法测定血浆纤溶酶(Plm )的活性。以酶联免疫吸附双抗体夹心法(ELISA)检测血浆纤溶酶原激活抑制物-1(PAI-1)水平。结果　与正常对照组相比,肥胖儿童血循环Lp(a)、Pg、PAI-1 水平显著增加(P分别< 0.001,0.002,0.001),血浆Plm 活性显著降低(P< 0.02)。Lp(a)与Pg 和PAI-1 有显著正相关(r分别为0.950 和0.328　P< 0.001 和0.02)。Lp(a)和Plm 显著负相关(r= - 0.302　P< 0.02)。结论　肥胖儿童血脂增加、纤溶受抑,存在致动脉粥样硬化的高危因素。高水平Lp(a)与纤溶受抑密切相关     

思密达治疗小儿病毒性肠炎：附150例分析

目的评价思密达治疗婴幼儿急性轮状病毒肠炎的效果。方法选择3年间秋冬季来我院儿科就诊的患儿，具备：≤2岁，居住在银川地区，急性起病，病程在5天内，24h大便4次以上，稀水样。并随机分为思密达治疗组96例，对照组54例，进行统计学分析。结果治疗组96例，显效49例(51．0％)，有效35例(36．5％)，无效12例(12．5％)；对照组54例，显效18例(33．33％)，有效20例(37．04％)，无效16例(29．63％)。治疗组总有效率(87．5％)高于对照组(70．4％)。结论应用思密达治疗婴幼儿急性轮状病毒肠炎能缩短病程。     

有高血压家族史青少年血浆内皮素及相关因素分析

目的 研究有高血压家族史的正常血压青少年及有肥胖症时血浆内皮素（ET）和饮食习惯，体重、身高，克托莱指数，心率、血压等相关因素。方法 采用放射免疫法检测有高血压家族史青少年及正常对照组血浆ET浓度。结果 有高血压家族史青少年的体重、身高、克托莱指数，心率，血压与正常对照组比较无显著性差异，而饮食习惯中喜食咸肥者明显高于对照组，血浆ET有增高趋势，但无统计学意义，有高血压家族史正常血压肥胖症者血浆ET明显增高。结论 原发性高血压的发生可能与不良饮食习惯有关。有高血压家族史肥胖症者血浆ET增高表明有发生原发性高血压的危险。需积极干预。     

牛初乳短链胰岛素样生长因子对脂蛋白(a)诱导的肾小球系膜细胞增生与转化生长因子-β1表达的影响

目的探讨牛初乳短链胰岛素样生长因子(Bct-IGF)对脂蛋白(a)[Lp(a)]诱导的肾小球系膜细胞(GMCs)增生与转化生长因子-β1(TGF-β1)表达的影响。方法将GMCs分为6组培养:对照组,Lp(a)组和不同浓度的Bct-IGF组,后5组培养时均加入5.0 mg.L-1Lp(a),后4组培养时分别加入100μg.L-1、200μg.L-1、400μg.L-1、800μg.L-1Bct-IGF。利用四甲基偶氮唑蓝(MTT)法测定细胞增殖率,末端转移酶介导的dUTP缺口末端标记法(TUNEL)测定GMCs凋亡率;ELISA法测定培养上清TGF-β1水平,反转录-PCR法检测TGF-β1 mRNA表达。结果与400μg.L-1Bct-IGF组比较,Lp(a)组、100μg.L-1Bct-IGF组、200μg.L-1Bct-IGF组GMCs细胞增殖率均明显增高,差异有统计学意义(Pa<0.05);800μg.L-1Bct-IGF组较之降低,但差异无统计学意义(P>0.05)。与400μg.L-1Bct-IGF组比较,LP(a)组、100μg.L-1Bct-IGF组、200μg.L-1Bct-IGF组GMCs细胞凋亡率均明显降低,差异有统计学意义(Pa<0.05);800μg.L-1Bct-IGF组较之增高,但差异无统计学意义(P>0.05)。Lp(a)组培养上清中TGF-β1水平显著高于400μg.L-1Bct-IGF组(P<0.01);Lp(a)组培养细胞TGF-β1 mRNA表达显著高于400μg.L-1Bct-IGF组(P<0.01)。结论 Lp(a)可以促进GMCs增生及TGF-β1的过表达,Bct-IGF可以抑制Lp(a)诱导的GMCs的异常增生,促进Lp(a)诱导的GMCs的凋亡。     

喘息性疾病血清胸腺活化调节趋化因子测定及其意义探讨

目的了解血清胸腺活化调节趋化因子(TARC)在不同喘息性疾病免疫学发病机制中的作用。方法收集2008年3月至2008年12月在贵阳医学院附属医院门诊和急诊诊断为喘息性疾病的患儿67例,包括毛细支气管炎患儿20例、喘息性支气管炎20例、支气管哮喘27例。其中男33例,女34例。年龄平均(4.66±1.26)岁。对照组18例,男11例,女7例。年龄平均(4.96±1.81)岁。采用酶联免疫吸附(ELISA)双抗体夹心法,检测喘息性疾病患儿及对照组血清中TARC。结果 (1)喘息性疾病患儿血清TARC显著高于正常对照组(t=3.669,P<0.05)。(2)3种喘息性疾病之间血清TARC两两相比差异无统计学意义(P>0.05),在3种喘息性疾病患儿中,毛细支气管炎患儿血清TARC最高。(3)喘息性疾病患儿血清TARC增高率(53.7%)与正常对照组增高率(0%)相比,差异具有统计学意义(t=16.82,P<0.05);不同喘息性疾病患儿之间血清TARC水平增高率两两相比,差异无统计学意义(t=2.575,P>0.05)。结论血清胸腺活化调节趋化因子(TARC)可能参与了这3种喘息性疾病的发病过程。     

早产儿低血糖与胰岛素、C肽、瘦素及皮质醇的关系研究

目的 探讨胰岛素(Ins)、C肽(C-ep)、瘦素(Lp)及皮质醇(Cor)水平与早产儿低血糖的关系.方法 采用放射免疫分析法检测47例发生低血糖早产儿和55例正常血糖早产儿(对照组)在生后24 h内、生后3d、7 d血清中的Ins、C.ep、Lp、Cor含量,并进行分析比较.结果 两组各时段Ins、C-ep、Lp差异无统计学意义(P>0.05),而生后24 h内、生后3 d血清中Cor含量低血糖组明显低于正常血糖组,两者比较差异有统计学意义(P<0.05),生后7 d则两组差异无统计学意义(P>0.05).结论 早产儿胰岛B细胞分泌胰岛素功能基本成熟;胎龄>32周的新生儿体内可能已开始存在脂肪一胰岛素内分泌轴;早产儿低血糖与Cor激素有关,通过调节作用而影响早产儿血糖水平.     

白细胞介素-4基因启动子多态性与广西壮族支气管哮喘患儿易感性和血清总免疫球蛋白E水平的相关性

目的研究IL-4基因启动子区域-589C/T和-33C/T位点多态性在广西壮族儿童中的分布及与壮族儿童支气管哮喘(哮喘)易感性及血清总IgE水平的相关性。方法采用聚合酶链反应-限制性片段长度多态性方法对健康儿童102例和哮喘患儿72例IL-4基因-589位点和-33位点进行分析,ELISA方法检测2组血清总IgE水平。采用SPSS 14.0软件进行统计学分析。结果1.IL-4-589位点在健康对照组中基因型分布频率为CC 5.9%、CT 23.5%、TT 70.6%,哮喘组为CC 2.8%、CT 19.4%、TT 77.8%;健康对照组等位基因频率为C 17.6%、T 82.4%,哮喘组为C 12.5%、T 87.5%。2.IL-4-33位点在健康对照组和哮喘组中基因型分布和等位基因频率与IL-4-589位点频率分布一致,连锁不平衡值△=0.978。3.哮喘组与健康对照组之间基因型频率和等位基因频率比较差异均无统计学意义(Pa>0.05)。4.哮喘组血清总IgE水平较健康对照组明显增高(P<0.01);各组不同基因型间血清总IgE水平比较差异均无统计学意义(Pa>0.05);3种相同基因型不同组间比较哮喘组血清总IgE水平均较健康对照组高(Pa<0.05)。结论在广西地区壮族儿童人群中,IL-4基因启动子-589位点和-33位点存在多态性,两位点存在连锁不平衡,其多态性与壮族儿童哮喘的易感性无关联,与血清总IgE水平无相关性。     

Lipoprotein (a) and apolipoprotein A-1 and B in schoolchildren whose grandparents had coronary and cerebrovascular events: A preliminary study of 12–13 year old Japanese children

The aim of this study was to evaluate the relationship between the serum levels of lipoprotein (a) [Lp (a)] and apolipoproteins (apo A-1 and apo B) in schoolchildren with a history of coronary and cerebrovascular events in their grandparents. We measured serum concentrations of Lp (a) and apoliproteins immunochemically in 289 schoolchildren aged 12–13 years and questioned parents about coronary and cerebrovascular events in the children's grandparents. In boys and girls, mean ± s.d. levels of apo A-1, apo B and Lp (a) were 134 ± 20.3 and 136 ± 17.4 mg/dL, 61 ± 16 and 66 ± 15 mg/dL and 12.5 ± 15.3 and 12.5 ± 15.1 mg/dL, respectively. There were no significant sex differences in the levels of apo A-1, apo B, and Lp (a). The Lp (a) levels (mean ± s.d., 12.5 ± 15.2 mg/dL; median 7.5 mg/dL, n = 289) were not affected by other variables. The Lp (a) distribution was strongly positively skewed and 75% of schoolchildren had very low levels. In the total 289 schoolchildren, thirty-two grandparents who had had coronary vascular events (21 myocardial infarction, 11 angina pectoris) and twenty-three grandparents who had had cerebrovascular events were recorded. By the boxplot statistical analysis, no difference was found in Lp (a) levels in children whose grandparents had myocardial infarction compared with those whose grandparents had no such history, or compared with those whose grandparents had suffered cerebrovascular events. Analysis also showed that the values of log Lp (a) in children whose grandparents had myocardial infarction tended to be higher than the values in children whose grandparents had no such history (P = 0.09). No significant differences in the levels of apo A-1 and apo B and in the apo B/A-1 ratio could be seen between children grouped according to the presence or absence of coronary and cerebrovascular events in their grandparents. These results suggest that high levels of Lp (a) in schoolchildren aged 12–13 years may partly reflect the existence of coronary vascular disease in older family members. Lp (a) may account for the strongest index of family history to disease risk in comparison with other apolipoproteins. Further study is needed to clarify the appropriate mass measurement method for Lp (a) in schoolchildren.     

Lipoprotein(a) and cardiovascular risk factors in a cohort of 6-year-old children. The Rivas-Vaciamadrid Study

We have studied the distribution of lipoprotein(a) (Lp(a)) and its relation to lipid profiles and a family history of cardiovascular disease in grandparents in a cohort of 673 6-year-old Spanish children. Lp(a) levels were highly skewed, showed no differences between sexes and had no relevant relations with anthropometric variables. When compared with children without a family history of stroke, children with a family history of this disorder showed significantly higher levels of Lp(a) (median 13 mg/dl, range 2–110 mg/dl versus 9 mg/dl, range 2–120 mg/dl, P =0.02). Also the percentage of children with a family history of stroke was higher in the group of children with Lp(a) levels above 30 mg/dl than in the group who exhibited lower levels (20.9% versus 10.4%, P =0.002). Children with a family history of coronary heart disease had higher levels of Lp(a) than children without such history (median 14 mg/dl, range 2–120 mg/dl versus 8 mg/dl, range 2–62 mg/dl, P =0.03). Finally, when compared with children with Lp(a) levels <30 mg/dl, those with Lp(a) levels above 30 mg/dl showed significantly higher mean levels of total cholesterol (174.9 versus 169.4 mg/dl, P <0.05), low-density lipoprotein-cholesterol (109.1 versus 102.4 mg/dl, P <0.05), and apolipoprotein B (81.9 versus 74.6 mg/dl, P <0.05). Conclusion: our study shows the existence of an association between high levels of lipoprotein (a) in 6 year-old children and a family history of both cerebrovascular and coronary disease in grandparents. High levels of lipoprotein (a) were also associated with high levels of low-density lipoprotein-cholesterol and apolipoprotein B.Abbreviations Apo apolipoprotein - LDL low-density lipoprotein - Lp(a) lipoprotein(a)     

Correlation of toddlers' serum lipoprotein(a) concentration with parental values and grandparents' coronary heart disease: the STRIP baby study

The correlation between lipoprotein(a) (Lp(a)) concentrations in children aged 7-24 months and their family members was determined and the association between the Lp(a) values of the children and a family history of coronary heart disease (CHD) was assessed. The Lp(a) values of the children correlated strongly with midparent Lp(a) values as early as at 7 months of age ( r = 0.54 to 0.59, p < 0.0001). This correlation was stronger than the correlation of serum total cholesterol and total cholesterol corrected for Lp(a) - cholesterol between children and parents. None of the parents had CHD. The median Lp(a) concentration of the parents with a family history of CHD was significantly higher than that of parents with no such history (111 vs 87 mg/l,p = 0.024). However. the children's Lp(a) levels were not associated with CHD in their grandparents. The genetic dependence of the Lp(a) concentration is already evident in infancy. The Lp(a) concentration in young parents, but not in their 24-month-old children, is associated with CHD in grandparents. This may be explained by a dilution of the genetic influence on Lp(a) over two generations.     

Influence of family history of morbid cardiovascular events on blood pressure levels of school children

The influence of family history of hypertension, myocardial-infarction and/or stroke on the blood pressure levels of 3,194 children in the age group 5-15 years was studied. Compared to children of normotensive parents, subjects coming from families with history of uncomplicated hypertension, complicated hypertension (hypertension plus myocardial infarction or stroke) and myocardial infarction or stroke without history of hypertension tended to have significantly higher levels of both systolic and diastolic pressures (p less than 0.001) in both the sexes in all age groups studied. Further, 15 (4.83%) of the children coming from families with positive history of one of the aforesaid morbid cardiovascular events had persistent hypertension (BP greater than mean +2 SD for age and sex). On the contrary only one (0.03%) of the 2,884 children belonging to normal parents had persistent hypertension. All the 16 children with sustained hypertension had only mild hypertension and were asymptomatic. Ten (62.5%) of them were obese (weight/height2 greater than 2.26). Baseline investigations failed to detect underlying cause to account for raised blood pressures in 9 of the 16 cases that could be investigated. These findings suggest that children of people with hypertension or other morbid cardiovascular events are more likely to have persistently elevated blood pressures than children from families without such a history.     

ApoB-100 and ApoB/ApoA-1 ratio in children and adolescents from families with very early myocardial infarction

AIM: The relationship between apolipoprotein B, LDL/ApoB, ApoB/ApoA-1, lipids and a family history of very early myocardial infarction (parent and/or grandparent <45 years) was studied in 46 children compared with 64 controls. METHODS: 19 children came out of families with a myocardial infarction (MI) of the father and 27 children with MI of a grandparent. RESULTS: In the whole risk group LDL-C, ApoB and ApoB/ApoA-1 ratio showed the most significant relationship, whereas in children from families with MI of the father ApoB level showed the strongest association with family history of MI. No relationship could be found for ApoA1, HDL-C and LDL/ApoB. CONCLUSION: Our results show that levels of ApoB, LDL-C and ApoB/ApoA-1 might be better predictors in children from families of very early MI as compared with ApoA-1, HDL-C and LDL/ApoB.     

Cardiovascular risk factors in children with obesity,hypertension and diabetes: lipoprotein(a) levels and body mass index correlate with family history of cardiovascular disease

The aims of the study were to compare atherosclerosis risk factors in obese, hypertensive and diabetic children with positive and negative family history (FH) of cardiovascular disease (CVD) and to find which of the new atherosclerosis risk factors may be of clinical value in predicting future cardiovascular events. A total of 285 children and adolescents were divided into groups: obese, obese and hypertensive, hypertensive, and diabetic. Each group was further segregated into children with positive or negative FH of CVD. Positive FH groups were analysed according to FH of CVD before or after 55 years of age, and in parents and grandparents separately. We assessed lipids, body mass index (BMI) and new risk factors: lipoprotein(a) Lp(a), apolipoprotein A-I (apo A-I) and apolipoprotein B (apo B), homocysteine (Hcy), fibrinogen (FB), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1). A positive FH of CVD was found in 28% of the children and in 8.7% it was premature CVD. Children with a positive FH had higher BMI (25.4 versus 23.7 kg/m(2), P<0.05) and highest BMIs were found in those with FH of CVD <55 years (26.8 kg/m(2), P<0.05) or in parents (27.4 kg/m(2), P<0.05). Lp(a) levels were higher in children with a positive FH (0.38 versus 0.28 g/l, P<0.05) and highest in children with a FH of premature CVD (0.44 g/l, P<0.05). Differences were also found in apo B levels (0.90 versus 0.84 g/l, P<0.05). In logistic regression analysis only BMI and Lp(a) were significant in predicting future cardiovascular events. CONCLUSION: obese, hypertensive and diabetic children often originate from families with cardiovascular disease. Children with a family history of cardiovascular disease have a higher body mass index. Levels of lipoprotein(a) and apolipoprotein B may be predictive of future cardiovascular disease in predisposed children.     

Cholesterol screening in children during office visits

Elevated blood cholesterol levels, a major risk for coronary artery disease in adults, has been associated with atherosclerotic disease in children. More than 10% of North American children have blood cholesterol levels higher than the desirable levels for adults. Current guidelines recommend screening only in children who have a family history of hyperlipidemia or myocardial infarction at an early age; however, this method fails to identify most children with hypercholesterolemia. Office-based cholesterol screening is an effective means to identify children and family members for dietary assessment and counseling. Should these measures be insufficient to lower the child's cholesterol level, referral for pharmacologic treatment is indicated.     

Cholesterol screening of seven-year-old children. How to identify children at risk

An inquiry was distributed to the parents of 1052 seven-year-old school beginners, concerning three issues, i.e. a known family history of myocardial infarction, angina pectoris before the age of 55 years and hyperlipidemia. A total of 147 children with a known family history were included in the study and compared with 148 classmates as control subjects. The proband children were subgrouped according to heredity factors and subjected to multivariate analysis at the 5% significance level for serum cholesterol fractions and triglycerides vs the control group. Statistically significant increased levels of total cholesterol and low density lipoprotein cholesterol, as well as an increased low density lipoprotein cholesterol and high density lipoprotein cholesterol ratio were found for all groups with hereditary for hyperlipidemia (p less than 0.001). However, no statistically significant difference was observed in the groups with heredity for myocardial infarction or angina pectoris exclusively. Also, there was no difference in any of the risk groups for high density lipoprotein cholesterol and triglycerides. The serum cholesterol levels in the present study were, to our knowledge, higher than those found elsewhere, except for Finland.     

Hereditary dyslipidemias and combined risk factors in children with a family history of premature coronary artery disease.

AIM: Schoolchildren aged 10-11 with a family history of premature coronary artery disease (CAD), were examined in order to identify children with genetically determined dyslipidemias and a combination of risk factors. METHODS: A total of 4000 questionnaires were distributed by the school; 55% of the families answered and returned the questionnaire. Blood lipids, apolipoprotein B, and Lp(a) lipoprotein were analysed in high risk children and their parents. RESULTS: A family history of premature CAD in parents or grandparents was identified in 208 families; 175 agreed to take part in a clinical examination and laboratory tests. Normal blood lipid tests were found in 89 children. Another 48 had an isolated increase of Lp(a) lipoprotein of minor clinical importance. Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations. In addition, possible FH was detected in eight of the parents. CONCLUSION: It is worthwhile asking parents about the occurrence of premature CAD among their child's closest relatives.