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目的探讨单纯性肥胖儿童载脂蛋白(apolipoprotein,Apo)E基因多态性的分布及其对血脂、脂蛋白、载脂蛋白的影响,及其与冠状动脉、心电图改变的关系。并对其早期预测和疾病预防提供理论依据。方法选择2002年12月至2004年12月潍坊医学院附属医院儿科的6～14岁单纯性肥胖儿童89例和健康儿童76例。抽取外周静脉血,测定血清中甘油三酯(TG),总胆固醇(TC),高密度脂蛋白胆固醇(HDLC),低密度脂蛋白胆固醇(LDLC),载脂蛋白A1(ApoA1),载脂蛋白B100(ApoB100)浓度。应用改良的聚合酶链式反应限制性片段长度多态性(PCRRFLP)分析及聚丙烯酰胺凝胶电泳测定儿童ApoE基因型。结果共检出4种ApoE基因型,E3/3、E4/3、E2/3、E4/2,以ε3为最常见。与健康儿童比较,肥胖儿童ε4等位基因频率增高,差异有显著性(P<0.05)。结论单纯性肥胖儿童有ApoE基因多态性的变化,且明显影响小儿血浆脂类代谢,肥胖儿童ApoE4与冠心病有密切相关性。     

肾病综合征患儿血载脂蛋白E变化及与中分子尿蛋白关系的研究

目的　研究原发性肾病综合征 (INS)患儿血载脂蛋白E(ApoE)的变化及与中分子尿蛋白的关系。 方法　检测 5 0例INS患儿血ApoE及血胆固醇 (TC)、甘油三酯 (TG)、高密度脂蛋白胆固醇 (HDL C)、低密度脂蛋白胆固醇 (LDL C)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)及血清总蛋白 (TP)、白蛋白 (Alb)、2 4h尿蛋白 (TUP)。用HYDRASYSLC(Sebia)全自动电泳分析系统测定INS患儿尿蛋白分子质量大小以确定其尿蛋白类型。以 5 0例年龄、性别相匹配的健康儿童为对照组。结果　活动期INS患儿血ApoE及血TC、TG、HDL C、LDL C、ApoB显著高于对照组 (均P <0 0 1)。 92 %INS患儿有高ApoE血症。血ApoE及血TC、TG、LDL C、ApoB与血TP、Alb呈显著负相关 (P <0 0 1) ,而血ApoE、TC、TG、LDL C、ApoB与TUP无相关。选择性中分子蛋白尿 (SMUP)组血ApoE显著高于非选择性蛋白尿 (NSUP)组 (P <0 0 1)。结论　INS患儿血ApoE明显升高 ,高ApoE血症广泛存在于INS患儿 ,血ApoE升高不能作为脂蛋白肾小球病的特异性诊断指标。中分子尿蛋白是INS患儿血ApoE升高的一个重要原因。     

单纯性肥胖症儿童动脉硬化的研究

为探讨单纯性肥胖症儿童颈总动脉、股动脉是否具有早期动脉硬化的形态学改变、变化的程度以及相关因素，采用高分辨率彩色多普勒超声检测仪分别检测肥胖组和对照组儿童的双侧颈总动脉、股动脉的内膜—中层厚度(IMT)和血流速度(PSV和EDV)，并检测两组儿童的血脂。结果显示，肥胖组儿童动脉内膜呈现不同程度的毛糙、不光滑、连续性差、限局性增厚，有的形成局部强回声斑块，动脉IMT明显高于对照组(P＜0．001)；中度肥胖组和重度肥胖组、病史＜5年组和≥5年组、男孩组和女孩组之间，动脉IMT差异有显著性(P＜0．01)，且与血甘油三酯(TG)和总胆固醇(TG)水平成正相关(r＝0．705和0．56)。提示中、重度单纯性肥胖症儿童颈总动脉、股动脉具有不同程度的早期动脉硬化改变，其变化程度与肥胖程度、肥胖病史长短、性别以及血脂水平有关。     

单纯性肥胖外周血单核/巨噬细胞趋化因子与胰岛素抵抗的相关性研究

了解单纯性肥胖儿童外周血单核/巨噬细胞趋化因子与胰岛素抵抗相关参数的关系。方法　2006年5月至2008年5月广西医科大学第一附属医院儿科70 例确诊为单纯性肥胖儿童作为研究对象,30名健康体检儿童作为健康对照组。流式细胞仪测定外周血单核细胞CD68阳性率;酶联免疫吸附（ELISA）法测定血浆巨 噬细胞炎性蛋白-1α（MIP-1α）、单核细胞趋化蛋白-1（MCP-1）水平;放射免疫分析（RIA）法测定血浆脂联素（ADPN）、血浆胰岛素（Ins）浓度,计算体质 指数（BMI）,按HOMA模型计算胰岛素抵抗指数（InRI）,并与相关变量进行Pearson相关分析或偏相关分析。结果　单纯性肥胖组血浆MIP-1α、MCP-1水平高于 健康对照组,两组比较差异有统计学意义（P < 0.05）。两组外周血CD68阳性率比较差异无统计学意义（P > 0.05）。两组InRI比较差异有统计学意义 （P < 0.05）。单纯性肥胖组血浆MIP-1α、MCP-1水平分别与BMI、腰围（WC）和InRI呈正相关 （P < 0.05）。血ADPN分别与BMI、WC和InRI呈负相关（P < 0.05）。外 周血单个核细胞CD68阳性率与BMI、WC和InRI无相关性（ P > 0.05）。结论　单纯性肥胖患儿体内存在低程度炎症反应,肥胖儿童外周血单核/巨噬细胞趋化因子 与胰岛素抵抗及中心性肥胖相关,可以作为肥胖相关疾病的早期预测指标之一。     

肥胖儿童载脂蛋白E基因多态性的研究

目的 探讨单纯性肥胖儿童载脂蛋白Ｅ（ＡｏｐＥ）基因多态性的分布及其对血脂、脂蛋白、载脂蛋白的影响。方法 采用改良的聚合酶链式反应－限制性片段长度多态性方法分析肥胖及健康儿童ＡｐｏＥ基因型。结果 肥胖儿童Ａｐｏε４等位基因频率（０．１２２９）较健康儿童（０．０６１８）增高（Ｐ〈０．０５）。ＡｐｏＥ基因多态性影响健康儿童的血脂水平。在单纯性肥胖儿童,ε２,ε３,ε４等位基因携带者的血甘油三酯（ＴＧ）、     

原发性肾病综合征患儿血清胆红素、尿酸水平与脂质代谢紊乱的关系

目的 探讨原发性肾病综合征(PNS)患儿血清胆红素、尿酸(UA)水平与脂质代谢紊乱的关系.方法 检测PNS患儿和健康儿童各50例血清总胆红素(TBIL)、结合胆红素(DBIL)、未结合胆红素(IBIL)、UA、脂蛋白a(LPa)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A1(ApoA1)及载脂蛋白B(ApoB)水平,并计算血脂综合指数.结果 1.肾病组UA、LPa、TC、TG、HDL.C、LDL-C、ApoB、TC/(HDL-C TBIL)和LDL-C/(HDL-C TBIL)明显高于健康对照组(Pа=0),而TBIL、DBIL和IBIL与健康对照组比较均无显著性差异(Pа>0.05);2.健康对照组血清胆红素、UA水平与血脂代谢无明显相关(Pа>0.05),而肾病组HDL-C与TBIL呈正相关(r=0.31 P=0.04),LDL-C分别与TBIL、IBIL呈负相关(r=-0.36 P=0.03,r=-0.33 P=0.04);3.肾病组UA分别与TBIL、IBIL呈正相关(r=0.37 P=0.02,r=0.45 P:0).结论 血清胆红素及UA水平变化对健康儿童血脂代谢不构成影响,但对PNS患儿,TBIL、IBIL降低,UA升高与脂质代谢紊乱密切相关.血脂综合指数可用于评价PNS患儿脂质代谢紊乱的严重程度及可能并发心血管疾病的危险性.     

单纯性肥胖儿童血脂类、内皮素、糖耐量变化的意义

目的研究不同程度单纯性肥胖儿童血总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白(LDL)、内皮素(ET)及糖耐量变化。方法选择单纯性肥胖儿童436例,其中轻度单纯肥胖242例、中度单纯肥胖138例、重度单纯肥胖56例。对照组儿童80例。检测各组儿童血TC、TG、LDL、ET、糖耐量。结果单纯肥胖患儿血TC、TG、LDL、ET明显高于对照组,各项之间均有显著性差异,且增高程度与体质量呈正相关;重度单纯肥胖患儿中4例糖耐量异常,对照组无异常。结论单纯性肥胖儿童血脂类和ET表达水平均有增高,个别重度肥胖患儿有糖耐量下降情况,应对单纯性肥胖儿童进行早期干预。     

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目的探讨单纯性肥胖儿童血浆同型半胱氨酸(HCY)、血脂的变化及其与心脑血管疾病的关系,为儿童单纯性肥胖及成年期心脑血管疾病的防治提供新的思路。方法收集2008年12月至2009年12月大连医科大学附属第一医院34例单纯性肥胖患儿及25例同期健康体检儿童,利用彩色多普勒超声探查肝脏形态结构;同时取禁食12h以上的静脉血,检测血浆HCY、血浆总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-Ch)、低密度脂蛋白(LDL-Ch)及血浆脂蛋白(α)[LP(α)]。结果肥胖组18例出现肝脏形态改变,对照组中仅1例;肥胖组血浆TC、TG、LDL-Ch明显高于对照组,差异有统计学意义(P均<0.05);HDL-Ch、LP(α)与对照组比较,差异无统计学意义(P>0.05);肥胖组血浆HCY为(10.91±2.57)μmol/L,对照组为(5.13±1.12)μmol/L,前者较后者明显增高(P<0.05);血浆HCY与血脂水平间无明显相关性。结论单纯性肥胖儿童较健康儿童更易患有脂肪肝或脂肪肝倾向,其发生与患儿脂质代谢异常密切相关;单纯性肥胖儿童血浆HCY明显增高,且HCY与血脂水平无相关性,是心脑血管疾病的独立危险...     

单纯性肥胖儿童和非肥胖儿童脂肪细胞基础凋亡率的研究

目的　探讨单纯性肥胖儿童和非肥胖儿童脂肪细胞的基础凋亡状况及其相关因素。方法　应用DNA原位末端标记技术 (terminaldeoxynucleotidyltransferase mediateddUTPnickendlabeling,TUNEL)检测 15例单纯性肥胖儿童 (男 11例 ,女 4例 )和 15例非肥胖儿童 (男 9例 ,女 6例 )腹壁皮下脂肪细胞的基础凋亡状况 ,计算凋亡指数 (apoptosisindex,AI)并进行对比和相关性分析。结果　单纯性肥胖儿童和非肥胖儿童腹壁皮下脂肪细胞存在很低的凋亡率 ,肥胖组AI为 (0 2 3± 0 18) % ,非肥胖组为 (0 6 5± 0 5 9) %。单纯性肥胖儿童脂肪细胞的凋亡率明显低于非肥胖儿童 (P <0 0 2 ) ;儿童腹壁皮下脂肪细胞的AI与体块指数 (bodymassindex ,BMI)、体脂百分数 (percentbodyfat,BF % )和体脂含量(fatmass,FM)呈负相关 ,与性别和年龄则无明显相关性。结论　儿童腹壁皮下脂肪细胞的AI与BMI和FM呈负相关 ,单纯肥胖儿童脂肪细胞的凋亡率明显低于非肥胖儿童 ,这种异常有可能参与了肥胖症的发生过程     

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目的 探讨β3-肾上腺素能受体基因(p3-AR)Trp64Arg变异与新疆哈萨克族儿童肥胖的相关性.方法 选取乌鲁木齐周边地区95例6-12岁哈萨克族学龄肥胖儿童及87名非肥胖儿童,用限制性片段长度多态性方法检测被调查儿童的基因型,生化方法检测血清甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDLC)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A(ApoA)、载脂蛋白B(ApoB)水平,并测量身高、体重.结果 变异型等位基因(C)在被调查对象中出现的频率为0.194,其中男0.210,女0.160.肥胖儿童中变异等位基因(C)、Trp64Arg变异基因型的出现频率明显高于非肥胖者(P＜0.05).单纯性肥胖儿童与非肥胖儿童比较,血清TG、TC、LDL-C、ApoB水平均明显升高(P＜0.05).B3-AR不同基因型间血脂比较,差异无统计学意义(P>0.05).结论 哈萨克族学龄儿童中存在一定的B3-AR Trp64Arg变异,可能与哈萨克族儿童肥胖有关.     

The usefulness of measuring body fat deposition for detecting obesity and atherogenesity in Japanese school children

Body fat deposition was measured in overweight and non-overweight children using a bioelectrical impedance method, and its relationship with serum lipids and apolipoproteins was investigated in 90 overweight children (over 120% of their ideal weight) and 241 non-overweight children aged 10–15 years in Niigata Prefecture. The results were as follows. Overweight boys had significantly higher levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), atherogenic index (AI), RLP-cholesterol (RLP-C), apoA1, apoA2, apoB, apoC2, apoC3, apoE and the ratio of apoB to apoAl than non-overweight boys. Overweight girls had significantly higher levels of TC, LDL-C, AI, remnant-like lopoprotein cholesterol (RLP-C), apoA2, apoB, apoC2, apoC3, apoE and the ratio of apoB to apoA1 than non-overweight girls. It has been reported that of all children studied 2.1% had higher levels of RLP-C than its upper limit known for adults (12 mg/dL). Of the overweight children in the present study, 4.4% had a high level of RLP-C whereas only 1.2% of non-overweight children had a high RLP-C level. No difference in the lipoprotein levels was found between overweight and non-overweight children. In both boys and girls, relative weight, body fat, skinfold thickness and body mass index (BMI) were correlated with the lipoprotein levels. Non-overweight boys whose body fat was over 20% had significantly higher levels of TC, LDL-C, apoA2, apoB, apoC2, apoE and apoB/A1 than those whose body fat was less than 20%. It was concluded that the measurement of body fat deposition, together with relative weight, was useful for detecting obesity and atherogenesity in Japanese school children.     

载脂蛋白E基因多态性与原发性肾病综合征脂质代谢紊乱的关系

目的研究原发性肾病综合征(PNS)患儿载脂蛋白E(apoE)主要等位基因和基因型的分布规律,探讨apoE基因多态性与PNS脂质代谢紊乱的关系。方法检测PNS患儿46例和正常小儿39例血清总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、apoA1、apoB和apoA1/B,同时用聚合酶链反应-单链构象多态性(PCR-SSCP)结合测序的方法确定apoE基因型,并根据平衡法计算出各等位基因频率。结果1.肾病组TC、TG、HDL-C、LDL-C、apoB、apoA1/B均明显高于对照组(P均<0.01);2.肾病组apoE2/2频率显著高于对照组(χ2=4.50 P<0.05);3.肾病组不同基因型和等位基因各项血脂指标均未见明显差异。结论PNS患儿存在明显脂质代谢紊乱,apoE2/2频率显著增高,apoE基因多态性对PNS患儿血脂水平未见明显影响。     

Obesity and lipid profiles in children and adolescents

Childhood obesity is associated with unfavorable lipid profile, suggesting that obese children should be screened for hypercholesterolemia. However, the prevalence of hypercholesterolemia in childhood obesity, and the effect of the degree of obesity on lipid profile, are unknown. Eighty-nine obese children and adolescents (BMI >85%, mean age 10.4 +/- 2.5 years) and 53 non-obese control children matched for age, gender and pubertal stage participated in the study. Early morning blood samples for serum lipids were collected in all children after a 12-h fast. Mean serum cholesterol and triglycerides (TG) levels were significantly higher (p <0.05) among the obese children (cholesterol: 175.2 +/- 31.4 vs 143.3 +/- 24.3 mg/dl; TG: 122.8 +/- 69.7 vs 94.3 +/- 37.8 mg/dl in obese and control children, respectively). Among the obese children, 52% had elevated serum cholesterol levels (>170 mg/dl) compared to 16% in the controls. The degree of obesity (BMI 85-95% vs BMI >95%) had no effect on serum lipids. Unfavorable lipid levels were relatively common among obese children, suggesting that obesity should be considered a risk factor for hypercholesterolemia, and that screening obese children for hypercholesterolemia should be considered.     

Apolipoprotein E phenotypes and plasma lipids in diabetic children and adolescents

Apolipoprotein E (apoE) polymorphism is a genetic determinant of serum lipoprotein levels and coronary heart disease risk. ApoE appears in three major isoforms E2, E3 and E4, coded by corresponding alleles 2, 3 and 4. These give six different phenotypes. Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. We studied the frequencies of apoE phenotypes and their association with plasma lipids in 201 diabetic children, aged 2–17 years, and in 216 healthy controls with the same age range. Phenotyping was performed directly from plasma by iso-electric focusing and immunoblotting. Plasma total and high density lipoprotein (HDL) cholesterol (C) and triglycerides were determined by routine laboratory methods. Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. There were no differences in apoE phenotype or allele distributions between the diabetic and control subjects. The frequencies of 2, 3, and 4 in the diabetic and control children were 0.08 versus 0.07, 0.73 versus 0.72 and 0.19 versus 0.21. The difference in apoE2/2 frequencies (2.0 in diabetic and 0.5% in normal children) was not statistically significant. In the diabetic children, there was a distinct relation between apoE phenotype and plasma lipids; presence of apoE2 was associated with the lowest and that of apoE4 with the highest concentrations of total and low density lipoprotein (LDL) C, and apoB. Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. The influence of apoE polymorphism on plasma lipids was less clear in the controls. ApoE polymorphism did not relate to body mass index, glycohaemoglobin A1c or daily insulin dosage. As compared to controls, diabetic children had significantly lower concentrations of total and LDL-C and apoB as well as higher ratios of HDL-C/LDL-C and apoA1/apoB. In conclusion, there was no difference in distribution of apoE phenotypes or alleles between diabetic and non-diabetic children. ApoE polymorphism proved to be an important genetic determinant of plasma lipid levels in patients with IDDM.     

Cardiometabolic risks vary by weight status in pediatric kidney and liver transplant recipients: A cross‐sectional,single‐center study in the USA

There is an increasing need to understand long‐term metabolic changes and resultant comorbidities because life expectancy is increasing after pediatric kidney and liver transplants. We evaluated differences in classic and novel cardiometabolic biomarkers among obese and normal weight adolescent transplant recipients. We enrolled a total of 80 adolescent (mean±SD, 14.8 years ±3.0) transplant recipients (63 kidney, 17 liver) with mean duration from transplantation of 6.0 (±4.1) years. Among kidney transplant recipients, overweight and obese individuals had higher leptin (16.7 vs 7.5 μg/mL, P<.001), lower HDL (1.1 vs 1.3 mmol/L, P=.02), higher free fatty acid (0.6 vs 0.5 mmol/L, P=.03), higher apoB‐to‐apoA1 ratio (0.8 vs 0.6, P=.03), and higher glucose (5.8 vs 4.3 mmol/L, P=.03) concentrations compared to normal weight individuals. Regardless of obesity status, over half of all participants (57.5%) were considered at high cardiometabolic risk using consensus guidelines, and this was more pronounced for kidney transplant recipients (61.9%). Post‐transplantation adolescents have increased cardiometabolic risk characterized by traditional risk factors of obesity and diabetes. The presence of obesity significantly worsens biomarkers of cardiometabolic risk. Future studies should explore whether treatment of obesity can improve the health and long‐term outcomes for children undergoing solid organ transplant.     

Postprandial hyperlipidemia after a fat loading test in minority adolescents with type 2 diabetes mellitus and obesity

The continuing increase in the incidence of type 2 diabetes mellitus (DM2) and obesity in children and adolescents is attributable to excessive caloric intake. Abnormal lipid metabolism in the postprandial state leads to long exposure of the vasculature to hyperlipidemia. Most children and adolescents with DM2 are obese, and many have fasting hypertriglyceridemia. Clustering of hyperlipidemia, DM2 and obesity increases the risk for cardiovascular disease. We therefore studied lipids, insulin, C-peptide, and glucose in response to an oral fat load simulating the fat content of a high-fat, fast-food meal in 12 type 2 diabetic obese, 15 non-diabetic obese, and 12 non-diabetic non-obese (control) adolescents (aged 10-19 yr; 87% African-Americans). All three groups were age-, sex-, and sexual maturation-matched. Mean body mass indices were similar in the diabetes and obese groups (32.7 +/- 1.1 vs 35.8 +/- 1.6 kg/m2). All patients with DM2 had fasting C-peptide > 0.2 nmol/l (0.7 ng/ml) and negative diabetes-associated autoantibodies. Serum total cholesterol, triglyceride, high- and low-density lipoprotein cholesterol, insulin, C-peptide, and plasma glucose levels were measured at 0, 2, 4, and 6 h after the fat load. The area under the curve (AUC) was calculated by trapezoidal estimation. Triglyceride AUC was significantly greater in the diabetes group than in the other two groups (15.7 +/- 2.9 vs 9.2 +/- 0.7 and 7.5 +/- 0.7 mmol x h/l [1389 +/- 258 vs 819 +/- 60 and 663 +/- 62 mg x h/dl]; p < 0.02 and <0.004, respectively), as were insulin, C-peptide, and glucose AUCs. Incremental triglyceride response (delta triglyceride = peak - fasting) in the diabetes group was significantly higher than that in the control group (2.1 +/- 0.7 vs 0.8 +/- 0.1 mmol/l 189.7 +/- 58.4 vs 71.2 +/- 11.1 mg/dl]; p < 0.04). Insulin resistance was estimated using the homeostasis model assessment (HOMA), which was greater in the diabetes group than in the obese and control groups (14.4 +/- 2.8 vs 5.2 +/- 0.8 and 3.2 +/- 0.4; p < 0.001 and < 0.0001, respectively). The diabetes group was divided into subgroups of high and normal fasting triglycerides on the basis of triglyceride levels above and below the 95th percentile. The delta triglyceride in the subgroup with high fasting triglycerides was substantially greater than in the subgroup with normal fasting triglycerides (3.4 +/- 1.1 vs 0.8 +/- 0.2 mmol/l [305.2 +/- 96.8 vs 74.2 +/- 18.0 mg/dl]; p < 0.001). Total cholesterol and triglyceride AUCs were much greater in the high vs normal fasting triglycerides subgroup (33.0 +/- 2.9 vs 24.2 +/- 1.9 and 23.6 +/- 3.5 vs 7.8 +/- 0.6 mmol x h/l [1274 +/- 113 vs 934 +/- 72 and 2085 +/- 309 vs 692 +/- 49 mg x h/dl]; p < 0.02 and <0.0001, respectively), as were insulin and C-peptide AUCs. HOMA was greater in the high vs normal fasting triglycerides subgroup (20.8 +/- 4.0 vs 8.0 +/- 1.6; p < 0.0001). In addition to elevated plasma glucose levels, there were no significant differences in either insulin or lipid parameters among the diabetes subgroup with normal fasting triglycerides, the obese group, and controls. Our data suggest that postprandial hyperlipidemia in response to a fat loading test is present in adolescents with DM2 who already have fasting hypertriglyceridemia. The degree of insulin resistance as an underlying abnormality--not DM per se--determines the degree of postprandial lipemia.     

Hypercalcitoninemia and hypocalcemia in acutely ill children: studies in serum calcium, blood ionized calcium, and calcium-regulating hormones

We studied the hypotheses that serum calcium and blood ionized calcium would be low in acutely ill children and would rise with clinical improvement. In 15 children admitted to the pediatric intensive care unit, the blood ionized calcium level was 4.45 +/- 0.06 mg/dl (1.11 +/- 0.015 mmol/L) on entry versus 5.17 +/- 0.03 mg/dl (1.29 +/- 0.01 mmol/L) in control subjects (p less than 0.005), rose significantly on days 2 and 3, and was 5.12 +/- 0.04 mg/dl (1.28 +/- 0.01 mmol/L) at discharge (p less than 0.005). Changes in serum calcium level were similar, whereas serum magnesium and phosphorus levels were normal and did not change. Basal serum parathyroid hormone concentrations were elevated, rose further during the study, and were normal at discharge. Serum parathyroid hormone levels correlated inversely with blood ionized calcium levels, indicating that compensatory hyperparathyroidism occurs with low blood ionized calcium concentrations. Basal serum calcitonin values were evaluated on entry and decreased with clinical improvement. Serum calcitonin levels correlated significantly with low blood ionized calcium levels, indicating that hypercalcitoninemia may play a role in the pathogenesis of hypocalcemia in these children. Urine calcium excretion was not increased in the four children studied. We speculate that with clinical improvement, a rise in serum parathyroid hormone levels and a decline in serum calcitonin levels may help restore normocalcemia in these acutely ill children.     

Effect of polyclonal anti-TNFalpha antibody on endotoxic shock in suckling rats

The aim of this study was to evaluate the effect of anti-tumor necrosis factor alpha (TNFalpha) antibodies on the TNFalpha gene expression in a neonatal septic shock model. Ten-day-old Sprague-Dawley rats were divided into four groups and given intraperitoneal (ip) injection as follows: group 1: 0.1 ml saline; group 2: 0.1 mg/kg Salmonella enteritidis lipopolysaccharide (LPS); group 3: 1 mg/kg of anti-TNFalpha antibodies (Ab); group 4: 0.1 mg/kg of LPS and 1 mg/kg of Ab. We found that in group 2, LPS induced shock, demonstrating hypoglycemia and lactacidemia (p < 0. 05) and death (81.8%). Ab decreased the mortality significantly (35%) and attenuated the hypoglycemia (35 +/- 8 mg/dl in group 2 vs. 53 +/- 3 mg/dl in group 4) and lactacidemia (5.40 +/- 0.63 vs. 2.35 +/- 0.45 mmol) at 8 h in group 4 when compared to group 2. Northern blot demonstrated a significant decrease in TNFalpha mRNA expression in group 4 as compared to group 2, at 2 h after LPS injection. We conclude that the beneficial effects of anti-TNFalpha antibodies on LPS-induced shock may be due to decreased TNFalpha gene expression.     

Serum cholesterol levels during and after Kawasaki disease

Serum total cholesterol and high-density lipoprotein (HDL) cholesterol concentrations were studied in paired sera from 23 patients (16 boys) with Kawasaki disease (KD) during acute illness and in 35 patients (21 boys) 5.4 to 7.7 years after KD. Total cholesterol and HDL cholesterol concentrations were significantly lower (paired t test, p = 0.0001) in samples taken within 30 days of the onset of illness (3.32 +/- 0.85 mmol/L (128 +/- 33 mg/dl) and 0.54 +/- 0.25 mmol/L (20.8 +/- 9.7 mg/dl) than in the second samples taken 2 to 16 months after onset of disease (4.16 +/- 0.93 mmol/L (161 +/- 35 mg/dl) and 1.24 +/- 0.35 mmol/L (47.2 +/- 13.9 mg/dl). The lowest total cholesterol levels were observed in samples taken 6 to 9 days after the onset of KD (p = 0.019). No correlations were seen between the highest erythrocyte sedimentation rate, C-reactive protein, or thrombocyte counts and the acute or convalescent cholesterol levels. In patients studied 5.4 to 7.7 years after recovery from KD, the mean total cholesterol concentrations were still lower than in healthy Finnish children. In girls the HDL cholesterol concentrations were similar, whereas 3 of the 18 boys studied had HDL cholesterol values more than 2 SDs below the mean for healthy boys. There was no correlation between the serum cholesterol concentrations and coronary artery abnormalities. These data lead us to infer that KD does not cause such permanent changes in cholesterol metabolism as to be considered a risk factor for atherosclerosis beyond that caused by the disease itself.     

瘦素受体基因20外显子突变对儿童脂质代谢影响的临床研究(英文)

目的：探讨瘦素受体基因(LEPR)第20外显子突变对脂质代谢的影响及肥胖儿童基因型与血脂的关系。方法：用聚合酶链反应限制性片段长度多态性(PCRRFLP)方法及聚丙烯酰胺凝胶电泳分析20外显子的基因突变频率,并测定单纯型肥胖儿童(102例)和健康儿童(81例)血清中甘油三脂(TG)、总胆固醇(TC)、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)水平。两组分别测量身高、体重,计算体重指数(BMI)及脂肪百分比。结果：肥胖儿童瘦素受体基因的20外显子经PCRRFLP及聚丙烯酰胺凝胶电泳分析,检测出3种基因型G/G,G/A和A/A型。肥胖儿童20外显子3057位G→A突变频率较健康儿童增高(P<0.05)。A/A基因型的肥胖儿童其血清TG(1.8±0.5mmol/Lvs1.0±0.4mmol/L,P<0.01)、BMI(33±5kg/m2vs25±4kg/m2,P<0.05)水平和脂肪百分比(30±8vs20±3,P<0.01)均明显高于G/G基因型者,而血清HDL水平则低于后者(1.08±0.23mmol/Lvs1.38±0.22mmol/L,P<0.01)。G/A型肥胖儿童,除其血清TG浓度高于G/G基因型者外(1.6±0.4mmol/Lvs1.0±0.4mmol/L,P<0.05),余各项指标均与另外两种基因型无明显差别。心电图检查显示部分A/A型血脂增高儿童有ST段和T波改变。结论：单纯型肥胖儿童瘦素受体基因第20外显子存在基因多态性,且该多态性明显影响肥胖儿童的脂质代谢及体脂分布。该研究为临床上开展对肥胖儿童的早期干预提供了理论依据。