癫癎和热性惊厥患儿血清褪黑素水平的变化及其临床意义

目的：探讨癫癎和热性惊厥患儿血清褪黑素水平的变化及其临床意义,为褪黑素用于癫癎和热性惊厥的治疗提供依据。方法：该研究分为对照组,即上呼吸道感染发热无惊厥患儿;热性惊厥组,其中又分为单纯性热性惊厥(SFS组)和复杂性热性惊厥(CFS组);癫癎组。采用酶联免疫吸附法(ELISA)分别测定各组血清褪黑素水平。结果：癫癎和复杂性热性惊厥患儿血清褪黑素水平分别为8.66±1.38和14.91±2.61 ng/L,均显著低于对照组的23.93±2.01 ng/L,差异有显著性(P<0.01),单纯性热性惊厥患儿血清褪黑素水平为20.72±2.54 ng/L,低于对照组,但差异无显著性意义(P>0.05);癫癎患儿血清褪黑素水平明显低于热性惊厥患儿,差异有显著性(P<0.01)。结论：癫癎和复杂性热性惊厥患儿血清褪黑素水平降低。补充外源性褪黑素可能是治疗儿童癫癎和热性惊厥的一个新途径。［中国当代儿科杂志,2009,11（4）：288-290］     

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目的探讨网织红细胞平均血红蛋白质量在小儿缺铁性贫血中的诊断价值。方法采用拜耳ADVIA120全自动血液分析仪检测50名健康儿童和59例临床诊断为缺铁性贫血患儿的外周血细胞和网织红细胞血红蛋白质量,同时用BeckmanCx9测定血清铁蛋白质量浓度,将所得数据进行统计学分析。结果血红蛋白(Hb)、平均红细胞体积(MCV)、单个网织红细胞平均血红蛋白(CHr)质量、血清铁蛋白(SF)在缺铁性贫血患儿明显低于健康儿童,而平均红细胞体积分布宽度(RDW)在缺铁性贫血患儿明显高于健康儿童。结论CHr质量作为诊断儿童缺铁性贫血的指标,具有重要的临床价值。     

铁缺乏和婴幼儿惊厥的关系

为探讨铁缺乏和婴幼儿惊厥之间的关系 ,我们对 1996～1998年门诊 6个月～ 3ａ的患儿 10 0例进行观察 ,现报告如下。临床资料10 0例随机分成惊厥组和对照组各 5 0例 ,惊厥组男 2 8例 ,女 2 2例 ,平均年龄 1.8ａ。对照组男 2 6例 ,女 2 4例 ,平均年龄 2 .1ａ。患儿母亲年龄、出生体重、分娩类型、喂养史等均无差异。惊厥组发生惊厥的次数 1～ 5次 ,有热惊厥 6 0次 ,无热惊厥 2 0次 ,均采用全自动血球计数仪测定血红蛋白含量、红细胞计数、红细胞平均容积、红细胞平均血红蛋白含量、红细胞平均血红蛋白浓度 ;全自动生化分析仪测定血清铁、钙含…     

缺铁性贫血伴幽门螺杆菌感染68例的治疗

目的：缺铁性贫血目前在我国仍是最常见的贫血类疾病,该研究旨在了解缺铁性贫血伴幽门螺杆菌感染的患儿抗幽门螺杆菌加铁剂治疗的疗效。方法：143例缺铁性贫血病例均做13C-呼气试验,其中阳性68例,将68例患者随机分为A,B二组。A组(35例):口服硫酸亚铁加2周治疗幽门螺杆菌的三联疗法;B组(33例):口服硫酸亚铁。结果：接受治疗的68例患者中,A,B二组在疗程结束后第8周复查血红蛋白、血清铁及血清铁蛋白均较治疗前有明显上升,且A组患者治疗后血红蛋白、血清铁及血清铁蛋白上升明显高于B组,差异有显著性,均P<0.01。结论：幽门螺杆菌感染与缺铁性贫血关系密切,与单独铁剂治疗相比较,加用抗幽门螺杆菌的治疗可加快提高血红蛋白的水平,二者配伍才是治疗缺铁性贫血伴幽门螺杆菌感染患者的最佳方案。     

低锌血症与热性惊厥的关系

目的探讨低锌血症与热性惊厥(FC)的关系。方法热性惊厥患儿(FC组)96例,健康体检儿童(对照组)90例。均抽取空腹静脉血5mL,应用原子吸收法测定二组儿童血锌水平,比较二组低锌血症的发生率。结果FC组22例为低锌血症,其发生率为22.9%;而对照组仅10例为低锌血症,发生率为11.1%,二组比较有显著性差异(χ2=4.54 P<0.05)。结论锌缺乏可能与FC的发生有关;FC患儿应积极纠正低锌血症。     

珠蛋白生成障碍性贫血并缺铁性贫血患儿的临床特征

目的观察珠蛋白生成障碍性贫血(地贫)高发区小儿地贫并缺铁性贫血(IDA)的临床特征。方法回顾性分析25例地贫并IDA的地贫突变类型和治疗效果。比较地贫并IDA组与单纯地贫组、单纯IDA组的血常规参数。结果 25例患儿中,轻型β-地贫14例,轻型α-地贫7例,中间型α-地贫3例,中间型β地贫1例。补铁治疗有效,血红蛋白升高(21.24±7.62)g.L-1。单纯地贫组红细胞容积、红细胞分布宽度和血小板计数较地贫并IDA组与单纯IDA组稍高(P<0.05),2组平均血红蛋白水平无明显差异(P>0.05)。结论在地贫高发区地贫患儿并IDA较常见,对地贫患儿需进行常规铁代谢指标测定。     

小儿热性惊厥与低铁血症

为进一步探讨小儿热性惊厥 (ＦＣ)与缺铁性贫血及低铁血症的关系 ,我们于 1997～ 1998年观察了 85例ＦＣ患儿的血清铁及缺铁性贫血情况 ,现报告如下。对象与方法一、对象　 1.观察组 85例为ＦＣ住院的患儿。ＦＣ的诊断根据《关于小儿高热惊厥诊断和治疗的建议》[1] 。引起发热的原发病为呼吸道感染、肠道感染。 2 .对照组 :随机选择同期因ＦＣ住院的 85例为对照组。两组性别、年龄比较 ,均有可比性 ;两组均为呼吸道感染 70例 ,消化道感染 15例。二、方法　入院后均取血做以下项目检查 :1.使用瑞典产ＡＣ─ 92 0型全自动血球计数仪测定血红蛋…     

616例小儿热性惊厥首次发作的临床特点及危险因素分析

目的了解热性惊厥患儿首次发作的临床特点及危险因素,指导临床医师对有危险因素的患儿采取相应干预措施,降低热性惊厥的发生。方法选取我院2016年8月至2018年8月收治的616例首次热性惊厥患儿为研究对象,回顾性分析患儿的临床特征及首次发作危险因素,并随机抽取同期发热但无惊厥发作(既往也无惊厥病史)的601例患儿为对照组。结果616例热性惊厥患儿,男344例,女272例,汉族584例,蒙古族32例。1岁以下126例(20.5%),~3岁405例(65.8%),3岁以上85例(13.7%)。发作病因中以急性上呼吸道感染[53.6%(330/616)]、疱疹性咽峡炎[25.9%(160/616)]及幼儿急疹[10.5%(65/616)]居前3位。惊厥发作时体温在38.0℃及以上者570例(92.5%),16例(2.6%)患儿惊厥发作后出现发热。534例(86.7%)患儿在发热24 h内出现惊厥发作。608例(98.7%)患儿表现为全面强直阵挛性发作。惊厥持续时间<5 min 548例(89.0%)、~14 min 48例(7.8%)、~29 min 16例(2.6%)及≥30 min 4例(0.4%)。572例(92.9%)患儿在单次热程中仅1次惊厥发作。临床类型中单纯性热性惊厥占88.3%(544/616),复杂性热性惊厥占11.0%(68/616),惊厥持续状态占0.7%(4/616)。危险因素分析显示首次惊厥时年龄、低钠、低铁、低锌、剖宫产、异常出生史、抽搐前1周疫苗接种史及热性惊厥家族史在热性惊厥组和对照组中差异有统计学意义(P<0.05)。Logistic回归分析发现首次发热惊厥年龄、低铁、剖宫产、低钠及热性惊厥家族史是热性惊厥首次发作的独立危险因素(P<0.05)。结论热性惊厥首次发作多见于3岁以内婴幼儿,以单纯性热性惊厥为主,惊厥发作时体温高,易发生于发热后24 h内,病毒感染是最常见病因。引起热性惊厥首次发作的危险因素依次为首次发作年龄、低铁、剖宫产、低钠及热性惊厥家族史,针对危险因素采取相应的干预措施可降低热性惊厥的发生。     

小儿热性惊厥T淋巴细胞及红细胞免疫功能的研究

目的：探讨热性惊厥患儿外周血T淋巴细胞和红细胞免疫功能的变化。方法：对82例热性惊厥患儿、40例上呼吸道感染患儿及40例正常小儿进行有关免疫检测。用微量全血氚标记胸腺嘧啶核苷掺入法,测T淋巴细胞增殖反应;用McAb-APAAP法测T淋巴细胞亚群的分布和CD25抗原、HLA-DR抗原表达;用生物素 亲和素双抗夹心酶联免疫吸附测定法,测γ-干扰素(γ-IFN)水平;用酵母花环实验,测红细胞免疫粘附功能。结果：单纯型热性惊厥的每分钟脉冲数(CPM)及刺激指数(SI)分别为5 609.4±3 587.4,20.5±15.6;复杂型的CPM及SI分别为 2 817.3±2 422.8,11.0±8.40,均分别显著低于正常对照组(20 305.9±12 810.3,69.2±45.2)及上感组(9 785.2±7 509.8,44.5±39.8),差异有显著性(P0.05)。RBC 3bR花环形成率复杂型为(9.1±4.4)%,显著低于正常对照组(15.8±5.7)%及上感组(13.5±5.1)%,差异有显著性(P<0.05)。RRC IC花环形成率单纯型为(3.0±1.0)%,复杂型为(2.6±0.7)%,均显著低于正常对照组(3.7±1.3)%及上感组(3.9±1.4)%(P<0.05)。结论：热性惊厥患儿的T淋巴细胞及红细胞免疫功能均受损,尤以复杂型热性惊厥患儿更明显。     

缺铁大鼠肠道铁调节蛋白信使核糖核酸表达研究

目的探讨肠道铁调节蛋白信使核糖核酸(IRP2 mRNA)的表达及其对肠道铁代谢的调节作用 方法 选择健康成年Wistar大鼠40只,随机分为对照组(10只)和缺铁组(30只),建立缺铁动物模型 根据血清铁(SI)、sFn、血红蛋白(Hb)测定结果进行分组 火焰法测定SI,放射免疫分析法测定sFn。参照组织/细胞总RNA提取试剂盒提取十二指肠黏膜总RNA逆转录聚合酶链反应(RT-PCR)法检测不同贫血状态下十二指肠中IRI2 mRNA表达、结果 IRP2 mRNA表达:对照组为0.38±0.12,隐性缺铁组为0.39±0.16,轻度缺铁性贫血组为0.51±0.08,中度缺铁性贫血组为0.51±0.14隐性缺铁组与对照组比较无差异(P>0.05);轻度缺铁性贫血组和中度缺铁性贫血组与对照组比较均有显著差异(P均<0.05);轻度缺铁性贫血组与隐性缺铁组及中度缺铁性贫血组比较均无差异(P均>0.05);中度缺铁性贫血组与隐性缺铁组比较有显著差异(P均<0.05)随缺铁程度增加,IRP2 mRNA表达总体上呈上升趋势结论 IRP2是体内铁代谢的重要调节蛋白     

Serum transferrin receptor in children: usefulness for determinating the nature of anemia in infection

OBJECTIVES: To know the variations of serum transferrin receptor (sTfR) and its indices depending on the status of body iron and the presence of infection in children, to evaluate their usefulness for recognizing the nature of anemia in infection, and to know the role of erythropoietic activity in these conditions. DESIGN AND METHODS: Three hundred and sixty-eight children between 1 and 10 years were included: 206 healthy children; 60 iron deficient anemic children (IDA); 102 with anemia and infectious disease, 58 of them meeting criteria for IDA. We measured hemoglobin, red cell indices, reticulocytes, transferrin saturation, serum ferritin, erythrocyte protoporphyrin, serum erythropoietin, and sTfR. Statistic method: ANOVA test, multiple linear regression, and ROC curve. RESULTS: sTfR, sTfR/ferritin ratio, and sTfR-logferritin index values were found to increase significantly in IDA children. These values were significantly lower in infectious anemia than iron deficiency states. Serum erythropoietin only was elevated significantly in iron deficiency states. In children without infection, mean corpuscular hemoglobin, erythrocyte protoporphirin, erythropoietin logarithm, and total-iron-binding-capacity logarithm predicted 81% of sTfR variability. sTfR and its indices showed a very high sensitivity and specificity for recognizing iron deficiency states. In children with IDA and infection sensitivity for sTfR/ferritin ratio was low (area under the curve: 0.71; 95% confidence interval: 0.64-0.88). For discriminating the nature of anemia in infection the cut-off point obtained for sTfR, sTfR/ferritin ratio, and sTfR-F index were 3, 70, and 1.8, respectively, and their sensitivity and specificity were also very high. CONCLUSIONS: sTfR, sTfR/ferritin ratio, and sTfR-F index are useful parameters for recognizing iron deficiency and the nature of anemia in infection. In IDA+infection, sTfR/ferritin ratio should not be recommended in the diagnosis of iron deficiency. In iron deficiency, erythropoietic activity has a secondary role as predictor factor of sTfR levels.     

东莞市学龄前儿童维生素A缺乏现状及维生素A对血清铁蛋白及红细胞参数的影响

目的 了解东莞市学龄前儿童维生素A缺乏现状,探讨维生素A对血清铁蛋白、红细胞及网织红细胞参数的影响。方法 于2015年4月至2016年12月通过整群抽样方法,选取东莞市无现患疾病的学龄前儿童（3~6岁）2 085例,对所选儿童进行血常规、网织红细胞计数、血清铁蛋白、血红蛋白电泳及维生素A浓度检测。分析年龄、性别与维生素A浓度及血清铁蛋白浓度的关系,维生素A浓度对血清铁蛋白、红细胞及网织红细胞参数的影响以及维生素A缺乏加重储存铁减少对红细胞参数的影响。结果 储存铁减少的儿童占比为6.71%（140/2 085）;维生素A缺乏儿童占比为32.52%（678/2 085）,其中亚临床缺乏占维生素A缺乏总人数的95.4%（647/678）,临床缺乏占维生素A缺乏总人数的4.6%（31/678）。不同性别组儿童维生素A浓度比较差异无统计学意义（P > 0.05）,但女性儿童血清铁蛋白浓度高于男性（P < 0.05）。维生素A临床缺乏组儿童血清铁蛋白浓度高于亚临床缺乏组和正常组（P < 0.05）。维生素A缺乏时,储存铁减少组平均红细胞体积和平均红细胞血红蛋白含量较储存铁正常组降低（P < 0.05）。维生素A缺乏组血红蛋白浓度、平均红细胞血红蛋白浓度、红细胞计数、红细胞压积、网织红细胞绝对值、网织红细胞百分比、网织红细胞血红蛋白含量均低于维生素A正常组,而平均红细胞体积高于维生素A正常组（P < 0.05）。结论 东莞市学龄前儿童维生素A缺乏状况仍较严重;维生素A缺乏可对血清铁蛋白、红细胞以及网织红细胞参数产生影响。     

Thalassemia major may decrease the frequency of febrile convulsions in children

Aim: We aimed to determine the relative frequency of febrile convulsion in children with major thalassemia to theorize that higher serum iron levels could reduce the incidence of febrile convulsion. Background: Febrile convulsion is the most common type of seizure in childhood that its causes are not fully understood. However, some risk factors have been cited such as the serum iron level. Materials and methods: Three hundred and fifty-nine children aged more than 5 years with major thalassemia who were receiving blood were enrolled as the case group. The control group consisted of 357 children without thalassemia aged 4–7 years (151 boys, 206 girls) who were referred to healthcare centers for routine health monitoring. Included data were the history of febrile convulsion, age of onset and type and the frequency of convulsions. Results: Children in control group significantly experienced more febrile convulsions than thalassemic children [4/359 (1.1%) in the thalassemic children and 14/357 (3.9%) in the control group had experienced febrile convulsions (P = 0.017)]. Conclusion: The frequency of febrile convulsion in children with major thalassemia is less than that of normal children. Children with thalassemia major may have higher serum levels of iron and such high serum iron levels might have a protective role in the children who have a vulnerability for febrile convulsions.     

THE DIAGNOSIS OF IRON DEFICIENCY BY ERYTHROCYTE PROTOPORPHYRIN AND SERUM FERRITIN ANALYSES

ABSTRACT. Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r=-0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 μg/l. In a group of apparently hematologically normal children between the age of 10–14 years (hemoglobin≥ 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 μmole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.     

The diagnosis of iron deficiency by erythrocyte protoporphyrin and serum ferritin analyses

Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r = -0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 microgram/l. In a group of apparently hematologically normal children between the age of 10--14 years (hemoglobin greater than 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 mumole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.     

Iron deficiency as a risk factor for first febrile seizure

We conducted this study to determine the role of iron deficiency as a risk factor for first febrile seizure in children. Fifty children between 6 months to 6 years with first febrile seizure (Cases) and 50 children with febrile illness but without convulsions (Controls) were enrolled from the pediatric ward of a tertiary care hospital. Iron deficiency was determined by estimation of hemoglobin, red blood cell indices and serum ferritin. The mean serum ferritin level (μg/L) was significantly low in Cases (31.9 ± 31.0) as compared to Controls (53.9 ± 56.5) with P = 0.003. Iron deficiency could be a potential risk factor for febrile seizure in children.     

The role of erythrocyte protoporphyrin in the diagnosis of iron deficiency anemia of children

The values of erythrocyte protoporphyrin, ferritin and mean corpuscular volume (MCV) measurements in diagnosing iron deficiency anemia were investigated in 72 iron deficient and in 25 healthy control infants. Receiver operator curve, sensitivity and specificity of erythrocyte protoporphyrin, ferritin and mean corpuscular volume were compared between the study and control groups. In the study group mean corpuscular volume, hemoglobin and ferritin concentrations were significantly lower, and erythrocyte protoporphyrin was significantly higher when compared to the control group. In the iron deficient study group, erythrocyte protoporphyrin was the most sensitive test and ferritin was the most specific test, whereas ferritin was the most diagnostic test and mean corpuscular volume was the least diagnostic test. A significant correlation between erythrocyte protoporphyrin and hemoglobin values was determined. We conclude that erythrocyte protoporphyrin is a more sensitive but less specific test than ferritin, and it can be used as a first-line diagnostic test in the evaluation of iron deficiency and in diagnosing iron deficiency anemia in infants.     

Leukocyte DNA damage in children with iron deficiency anemia: effect of iron supplementation

Iron deficiency is frequently associated with anemia. Iron is a transition-metal ion, and it can induce free radical formation, which leads to formation of various lesions in DNA, proteins, and lipids. The aim of this study was to investigate baseline oxidative DNA damage and to clarify the role of the administration of a therapeutic dose of iron on DNA oxidation in children with iron deficiency anemia (IDA). Twenty-seven children with IDA and 20 healthy children were enrolled in the study. Leukocyte DNA damage (strand breaks and Fpg-sensitive sites) was assessed using comet assay before and after 12 weeks of daily iron administration. Before the iron administration, the frequency of DNA strand breaks in the children with IDA was found to be lower than those in the control group (P < 0.05), but there was not a significant difference for frequency of Fpg-sensitive sites. After 12 weeks of iron administration, the frequency of both DNA strand breaks and Fpg-sensitive sites were found to be increased (P < 0.01). No significant association was determined between DNA damage parameters and hemoglobin, hematocrit, serum iron, total iron binding capacity, and ferritin. In conclusion, basal level of DNA strand breaks is at a low level in children with IDA. After iron administration, DNA strand breaks and Fpg-sensitive sites, which represent oxidatively damaged DNA, increased. However, this increase was unrelated to serum level of iron and ferritin.     

热性惊厥患儿血清细胞因子水平的变化及临床意义

目的 了解6月～2岁单纯性和复杂性热性惊厥患儿血清IFN-α,IL-8和TNF-α水平的异常变化。方法 应用ELISA法检测64例单纯性热性惊厥和52例复杂性热性惊厥患儿血清IFN-α,IL-8和TNF-α的含量,并对IL-8和TNF-α进行了相关性研究。结果 单纯性热性惊厥组血清TFN-α,IL-8和TNF-α的含量分别为467.68±112.46 ng/L,74.38±18.74 ng/L和812.36±232.38 ng/L,其含量明显高于正常对照组（P﹤0.01）,也明显高于单纯性热性惊厥组（P﹤0.01）。IL-8和TNF-α在这两组疾病中分别呈正相关（r1=0.565,r2=0.64,P ﹤0.01）。结论 ①在单纯性热性惊厥和复杂性热性惊厥中,细胞因子明显增加,在增强机体免疫系统抗感染的同时,也激发了免疫性炎症反应,对组织细胞可能产生损伤。②IL-8和TNF-α在两组疾病中形成一对辅助因子,并参与了整个病理过程。     

Measurement of reticulocyte hemoglobin content to diagnose iron deficiency in Saudi children

Iron deficiency and iron deficiency anemia are common conditions in children, especially in developing countries. It is often difficult for the pediatrician to know which indices should be used in the diagnosis of these conditions in children. Reticulocyte hemoglobin (Hb) content (CHr) has been shown to be an accurate indicator of anemia, however whether its use suits the situation in developing countries or not is unclear. The aim of this study was to evaluate the value and effectiveness of using CHr as a method to diagnose iron deficiency and iron deficiency anemia in Saudi children. The samples for the study were collected from 305 children suspected to have anemia. Complete blood count, transferrin saturation (Tfsat), ferritin, circulating transferrin receptor (TfR) and CHr were measured. Three groups were defined, iron deficiency (Tfsat <20%, Hb >11 g/dL; n=120), iron deficiency anemia (Tfsat <20%, Hb <11 g/dL; (n=73) and controls (Tfsat >20%; n=112). The anemic group had significantly lower macrocytic anemia (MCV), mean corpuscular hemoglobin (MCH) and CHr. All of the variables in the anemia group were significantly lower than those of the control group except for the ferritin level. Compared to the control group, the iron deficiency group also showed significantly lower values except for transferrin receptor and the ferritin levels. CHr levels of <26 pg correlated well with anemic states. CHr together with a complete blood count may provide an alternative to the traditional hematologic or biochemical panel for the diagnosis of iron deficiency and iron deficiency anemia in young children and is cost-effective in developing countries. A CHr cut-off level of 26 pg is considered to be a reasonable indicator of anemic states.