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1.
目的 分析初发1型糖尿病 (T1DM) 患儿的血脂状态,并对其影响因素进行研究。方法 将 2012-01-01—2017-12-31于中国医科大学附属盛京医院新确诊的 348 例 T1DM 患儿临床资料进行收集和汇总,比较T1DM 患儿与 40 例对照组儿童的血脂差异。对 T1DM 患儿根据血脂水平分为血脂正常组(n=153)与血脂异常组(n=195),比较两组患儿血脂各项指标差异。根据 糖化血红蛋白(HbA1c)值分为<11.5%(n=116)、11.5%~13.5%(n=109)、>13.5%(n=123)3组,比较3组患儿间的血脂差异等。结果 (1)T1DM 患儿的总胆 固醇( TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、载脂蛋白B(ApoB)等显著高于对照组,而高密度脂蛋白( HDL)、载脂蛋白A1(ApoA1)显著低于对照组。结果为 TC(mmol/L)(4.29±1.07 vs. 3.85±0.67,P<0.05)、 TG(mmol/L)(1.29±1.40 vs. 0.82±0.50,P<0.01)、LDL(mmol/L)(2.61±0.91 vs. 2.17±0.57,P<0.01)等。(2)T1DM 患儿血脂异常发生率为 56.03%,血脂异常组患儿 HbA1c (%)显著高于血脂正常组(12.93±2.16 vs. 12.10±2.37,P<0.01)。(3)HbA1c 越大的患儿其 TC、TG、LDL等越高。结果为 TC(mmol/L)(3.96±0.78 vs. 4.12±0.94 vs. 4.75±1.25,P<0.01)、TG(mmol/L)(0.91±0.50 vs. 1.38±1.72 vs. 1.56±1.60,P<0.01)、LDL(mmol/L)(2.34±0.72 vs. 2.38±0.73 vs. 3.05±1.03,P<0.01)。结论 T1DM患儿的血脂异常发病率较正常儿童明显增高;血糖越高的患儿其血脂异常状态越明显。  相似文献   

2.
目的:回顾浙江大学医学院附属儿童医院10年来住院儿童 1 型糖尿病的发病状况并探讨白介素-10(IL-10)在儿童 1 型糖尿病酮症酸中毒(DKA)中的临床意义。方法:对1999年1月至2009年2月在该院住院的263例334例次1型糖尿病患儿的临床资料进行回顾性分析;并对其中48例1型糖尿病患儿进行血脂、细胞因子等检查,根据有无酮症酸中毒分为 DKA组和非DKA组,24例正常健康儿童作为对照组,比较各组间血脂、细胞因子等参数的差异。结果:儿童1型糖尿病患儿中,女性多见(56.3%),发病年龄以6~11.9岁多见。32.7% 的患儿以酮症酸中毒为就诊表现。DKA组血脂、血糖及糖化血红蛋白均高于非DKA组,二分类logistic 回归分析示上述指标水平的升高均为酮症酸中毒的危险因素。IL-10水平在DKA组明显升高,余细胞因子在DKA组和非DKA组无明显差异。糖尿病组各细胞因子水平明显高于正常对照组。结论:1型糖尿病患儿酮症酸中毒发生率较高,糖、脂代谢紊乱是酮症酸中毒的危险因素。IL-10可能为酮症酸中毒的敏感指标。[中国当代儿科杂志,2010,12(11):849-854]  相似文献   

3.
目的 分析初发1型糖尿病(T1DM)患儿伴发糖尿病酮症酸中毒(DKA)的严重程度与甲状腺功能状态的相关性。方法 回顾性分析2015年1月至2020年12月内分泌遗传代谢科收治的167例初发T1DM患儿临床资料,比较T1DM患儿中非DKA,轻度、中度、重度DKA四组临床特点、实验室指标、甲状腺功能状态差异,分析血清游离三碘甲状腺原氨酸(FT3)水平的影响因素。结果 167例初发T1DM患儿中,男81例、女86例,中位年龄6.5(4.0~9.9)岁,中位病程14.0(7.0~28.0)d,非DKA组104例、轻度DKA组20例、中度DKA组16例、重度DKA组27例。各DKA组(FT3)、总三碘甲状腺原氨酸(TT3)、总甲状腺素(TT4)、pH值及HCO-3显著低于非DKA组,而阴离子间隙(AG)、血糖水平显著高于非DKA组;重度DKA组的白细胞计数、中性粒细胞百分比显著高于其他三组,差异均有统计学意义(P<0.05)。167例初发T1DM儿童中,甲状腺...  相似文献   

4.
目的 研究儿童青少年1型糖尿病(type 1 diabetes mellitus, T1DM)发生糖尿病酮症酸中毒(diabetic ketoacidosis, DKA)的危险因素,并建立DKA风险预测模型,以期降低该类患儿DKA的发生率,提高患儿生存质量。方法 回顾性选择2018年1月—2021年12月宁夏医科大学总医院收治的217例T1DM患儿,其中169例发生DKA患儿为DKA组,48例未发生DKA患儿为非DKA组。分析T1DM患儿发生DKA的危险因素,并建立预测T1DM患儿发生DKA风险的列线图模型。结果 217例T1DM患儿中DKA发生率为77.9%(169/217)。多因素logistic回归分析显示,T1DM患儿入院随机血糖高、糖化血红蛋白高(hemoglobin A1c, HbA1c)、血酮高、甘油三酯高与发生DKA密切相关(分别OR=1.156、3.203×1015、20.131、9.519,P<0.05)。列线图预测模型C-统计量为0.95,列线图模型预测T1DM患儿发生DKA的风险与实际发生DKA的风险平均绝对误差为0.004,说明模型整体预测能力较好。结论...  相似文献   

5.
目的探讨血清25-羟维生素D[25-(OH)D]水平与儿童1型糖尿病(T1DM)及酮症酸中毒(DKA)的相关性。方法选取2006年1月—2009年12月期间152例住院患儿,其中52例为首次发病的T1DM患儿,包括酮症酸中毒(DKA组)21例,以及非酮症酸中毒(非DKA组)31例,其余100例为非T1DM组。检测并比较三组患儿的血清25-(OH)D水平,分析血清25-(OH)D水平与儿童T1DM及DKA的相关性。结果 DKA组患儿的血清25-(OH)D平均为(53.6±27.8)nmol/L,显著低于非DKA组的(69.7±27.9)nmol/L和非T1DM组的(81.8±28.3)nmol/L(P<0.05);非DKA组患儿的血清25-(OH)D水平显著低于非T1DM组(P<0.05)。结论 T1DM患儿的血清25-(OH)D水平低,尤以DKA患儿最为明显,维生素D在儿童T1DM发病中的潜在保护效应值得关注。  相似文献   

6.
目的 调查已确诊的1型糖尿病(T1DM)患儿病程中糖尿病酮症酸中毒(DKA)的发生情况。方法 以首都医科大学附属北京儿童医院、上海交通大学附属儿童医院、南京医科大学附属南京儿童医院、郑州市儿童医院、江西省儿童医院、西安交通大学第一附属医院、昆明医科大学第一附属医院、武汉市妇女儿童医疗保健中心、苏州大学附属儿童医院、聊城儿童医院、福建省福州儿童医院、成都市妇女儿童中心医院12家医院登记系统为基础调查多中心1995年12月至2014年6月胰岛素治疗下的已确诊T1DM患者病程中发生DKA的频度和诱发原因。其中,T1DM确诊后发生的第1次DKA为组1A,第2次DKA为组1B。选择北京儿童医院2011年12月-至2012年5月T1DM患者血糖控制状况横断面调查病程中无DKA发生者为对照组,即组2。结果 12家医院共新诊断了1676例T1DM患儿,其中89例患者在病程中发生了100次DKA,发生比率为5.3%(89/1676),发生频率为5.9%(100/1676)。且各中心的DKA发生比率不同,波动在1.1%~24.1%之间。组1A的糖化血红蛋白(HbA1c)[(11.31±3.03)% vs.(8.26±1.53)%,P<0.01]及胰岛素剂量[(0.85±0.42)IU vs.( 0.71±0.31)IU,P<0.01]明显高于组2。组1A的胰岛素泵使用率高于组2(25.0% vs. 11.2%,P=0.01)。而且,前者的自我血糖监测达标率(12.1% vs. 40.1%, P<0.01)及复诊次数达标率(21.2% vs. 46.6%,P<0.01)明显低于后者。组1A的DKA诱因主要是感染(33.7%)、中断胰岛素注射(21.3%)、饮食异常(20.2%),1例患者为胰岛干细胞移植后DKA。组1B仍以感染为主要诱因(4/10),1例患者因为胰岛素泵故障而发生DKA(1/10)。不同病程内发生的DKA诱因分布不同(P<0.01),1年内主要以中断胰岛素注射为主,占39.3%(11/28);1年以上中断胰岛素注射仅占13.1%(8/61),主要以感染(22/61)和饮食异常(16/61)为诱因。DKA发生率高的医院主要是以感染为诱因,达50%(12/24),而DKA发生率低的医院感染诱因占28.1%(18/64)(P<0.01)。结论 已确诊T1DM患者病程中DKA发生率为5.3%,各中心不同,最高达24.1%。DKA者的血糖控制水平差,不能规律的进行自我血糖监测及门诊复诊,应该强化糖尿病教育。胰岛素泵使用者及胰岛干细胞移植的患者成为新的教育关注点。DKA发生率高的医院需要强化患者学习感染时的处理措施。  相似文献   

7.
目的 探讨糖尿病酮症酸中毒(DKA)患儿血清氧化应激指标的变化及其与代谢参数的相关性.方法 将受试者分为4组:即DKA组22例;血糖控制一般组18例,糖化血红蛋白(HbAlc)<9%;血糖控制较差组(HbAlc≥9%)22例;健康对照组36例.检测其血清丙二醛(MDA)、一氧化氮(NO)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)水平,并常规检测空腹血糖、血气、血清离子(K+,Na+,Cl-,P)、肾功能、尿常规、HbAlc.结果 DKA组血清MDA水平显著高于健康对照组(P<0.01)及血糖控制一般组(P<0.01),但与血糖控制较差组差异无显著性(P>0.05);3组糖尿病患儿血清NO水平均显著高于健康对照组(P<0.01),且血糖控制较差组NO显著高于血糖控制一般组(P<0.01);3组糖尿病患儿血清GSH-Px水平均显著低于健康对照组(P<0.01);4组间SOD水平差异无显著性(P>0.05).相关分析显示糖尿病患儿血清MDA水平与HbAlc呈极显著正相关(r=0.375,P<0.01),NO与HbAlc呈显著正相关(r=0.250,P<0.05),DKA患儿血清SOD水平与HbAlc呈显著负相关(r=-0.507,P<0.05),其他氧化应激指标与代谢参数问无相关性.结论 DKA患儿氧化应激产物显著增加,抗氧化能力降低,这些改变主要应归因于慢性高血糖而不是急性代谢紊乱.  相似文献   

8.
目的 探讨新发儿童1型糖尿病酮症酸中毒与重症儿童应激性高血精的鉴别诊断指标.方法 前瞻性研究30例1型糖尿病酮症酸中毒(DKA组)患儿[年龄(6.5±3.6)岁]和20例重症应激性高血糖(SHG组)患儿[年龄(5.8±3.1)岁]的鉴别诊断指标,分别比较两组糖化血红蛋白(HbAlc)、空腹血糖(FBG)、二氧化碳结合力(CO_2-CP)、阴离子间隙(AG)、空腹C-肽(FCP)、空腹胰岛素(FINS)、胰岛素抵抗指数(IRI)、皮质醇(COR)及是否依赖胰岛素治疗.对照组(C组)30例为健康体检儿童,年龄(6.1±3.4)岁.结果 DKA组和SHG组均有高血糖、AG和皮质醇升高.CO_2-CP降低.DKA组HbAlc显著高于正常对照和SHG组(P均<0.001),DKA组HbAlc>7.3%,SHG组HbAlc<6.5%.FINS、FCP及IRI在DKA组均显著低于SHG组和对照组(P均<0.001),DKA组FINS<2.6 U/L,FCP<0.16μg/L,IRI<2.7(mmol·U./L);SHG组FINS>9.3 U/L,FCP>0.9mg/L,IRI>5.3(mmol·U/L).SHG组对胰岛素无依赖性,而DKA组需依赖胰岛素才能控制血糖.结论 HbAlc、FINS、FCP及IRI是鉴别DKA和SHG的简便、良好的指标.DKA组HbAlc显著升高,FINS、FCP及IRI均显著降低;SHG组FINS、FCP及IRI均显著升高,HbAlc<6.5%.且DKA的治疗依赖胰岛素,而SHG组治疗不依赖胰岛素.  相似文献   

9.
目的探讨1型糖尿病(T1DM)酮症酸中毒(DKA)患儿缺氧诱导因子-1α(HIF-1α)与血管内皮细胞生长因子(VEGF)mRNA水平的变化。方法天津市儿童医院住院T1DM并DKA患儿30例,于确诊24 h内(DKA 1组)及DKA纠正后10 d(DKA 2组)采血,另选取同期住院的不伴感染、缺氧、肿瘤或结缔组织病的同年龄同性别患儿30例为对照组。实时荧光定量PCR(Real-time PCR)法测定其外周血CD4+T淋巴细胞HIF-1α与VEGF mRNA的相对表达水平。PCR产物行琼脂糖凝胶电泳鉴定特异性。采用SPSS 13.0软件进行统计学分析。结果 3组HIF-1α及VEGF mRNA相对表达水平比较差异均有统计学意义(Pa<0.01)。DKA1组HIF-1α及VEGF水平明显高于对照组,差异有统计学意义(Pa<0.01);DKA纠正后HIF-1α及VEGF水平恢复,差异有统计学意义(P<0.05,0.01),但直至DKA纠正后10 d(DKA2组)仍未恢复至对照组水平,差异有统计学意义(P<0.01,0.05)。Real-timePCR产物行琼脂糖凝胶电泳,产物位于预期位置,确定产物特异性。结论 T1DM并DKA患儿CD4+T淋巴细胞HIF-1α与VEGFmRNA水平升高,且DKA纠正后HIF-1α与VEGF mRNA水平不能恢复至正常,这可能与T1DM并发症的发生发展有关。  相似文献   

10.
目的探讨原发性肾病综合征(PNS)患儿不同尿蛋白排泄状态下血脂代谢特点,了解血脂代谢紊乱与尿蛋白定量的关系。方法根据尿蛋白排泄状态,将98例PNS患儿分成中度蛋白尿组[50mg/(kg.d)≤24h尿蛋白定量(24hUPr)〈100mg/(kg.d),33例]和重度蛋白尿组[24hUPr≥100mg/(kg.d),65例],收集45例表现为轻度蛋白尿[24hUPr〈50mg/(kg.d)]紫癜性肾炎患儿作为对照,检测血浆脂蛋白a(LPa)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL)、non-HDL、低密度脂蛋白(LDL)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)、ApoA1/B及24hUPr等指标。结果3组血浆LPa、TC、TG、non-HDL、LDL、ApoA1、ApoB及ApoA1/B水平具有显著性差异(Pa〈0.01);中度蛋白尿组血浆LPa、TC、non-HDL、LDL、ApoA1和ApoB水平显著高于轻度蛋白尿组;重度蛋白尿组血浆TC、TG、non-HDL和ApoB水平显著高于中度蛋白尿组,而ApoA1/B明显降低;重度蛋白尿组血浆LPa、TC、TG、non-HDL、LDL和ApoB水平显著高于轻度蛋白尿组,而ApoA1/B明显降低;中度蛋白尿组TC、HDL、non-HDL、LDL及ApoB分别与24hUPr呈高度正相关(r=0.84,0.54,0.84,0.83,0.70Pa〈0.01),而ApoA1/B与24hUPr呈高度负相关(r=-0.48P=0.01)。结论PNS患儿血脂代谢紊乱继发于蛋白尿,且随尿蛋白排泄状况不同而表现各异,在中度蛋白尿组二者关系最密切。  相似文献   

11.
儿童糖尿病198例   总被引:1,自引:0,他引:1  
目的 探讨儿童糖尿病(DM)的临床特点,为临床诊治提供理论依据.方法 对1999年1月-2009年3月在本院住院的198例DM患儿的临床表现和实验室检查进行回顾性临床分析.结果 198例DM患儿中,男97例,女101例.均为首诊病例;发病高峰年龄为5~6岁及9~11岁;首诊例数逐年增加,2008年较1999年增加了3.7倍;其中1型糖尿病(T1DM) 174例(占88.9%),2型糖尿病7例(占3.5%),新生儿DM 14例(占7.1%),其他3例(占1.5%).首诊的TlDM患者中,酮症酸中毒(DKA)的发生率为42.0%;发病前有感染史者55例,与无感染史者比较,DKA的发生率有统计学差异(P<0.01).有DM家族遗传史者23例.并甲状腺功能亢进症2例;并暂时性甲状腺功能减低症31例;并肝功能异常30例,肾功能异常12例,血脂异常48例,尿蛋白阳性27例.糖化血红蛋白为(12.0±1.8)%;共分析了25例T1 DM患者的自身抗体,胰岛细胞抗体阳性率为28%,胰岛素自身抗体的阳性率为20%,谷氮酸脱羧酶自身抗体(GADA)阳性率为72%.结论 首诊的儿童DM逐年增加,以T1DM为主;新生儿DM增加明显;DKA是T1DM患者就诊的重要原因;首诊的T1DM者中,感染是发生DKA的重要诱因;儿童DM常合并暂时性甲状腺功能减低症、肝肾功能异常及血脂异常;糖尿病自身抗体中GADA的阳性率最高.  相似文献   

12.
赵彦  杨斌  黄乐  吕玲 《实用儿科临床杂志》2012,27(8):594-595,610
目的探讨1型糖尿病(T1DM)及糖尿病酮症酸中毒(DKA)患儿并低三碘甲状腺氨酸(T3)综合征的临床特点。方法采用放射免疫分析法检测91例T1DM并DKA患儿(DKA组)及110例单纯T1DM患儿(非DKA组)血清T3、甲状腺素(T4)、促甲状腺激素(TSH)水平,观察2组T3、T4下降例数及水平,并将DKA组分为轻、中、重3个亚组,观察不同组别中甲状腺激素变化特点。结果 DKA组易发生T3、T4下降,DKA组T3[(0.54±0.51)μg.L-1]、T4[(5.65±2.80)μg.L-1]与非DKA组T3[(1.02±0.38)μg.L-1]、T4[(9.28±2.85)μg.L-1]比较,差异均有统计学意义(Pa<0.000 1)。中、重度DKA组与非DKA组T3比较,差异有统计学意义(Pa<0.000 1),轻、中、重度DKA组与非DKA组T4比较,差异均有统计学意义(Pa<0.000 4,0.000 1)。DKA组与非DKA组TSH比较,差异无统计学意义(P>0.05)。结论 T1DM患儿甲状腺激素检测的结果主要表现为T3降低,部分伴T4降低,其疾病的严重程度与甲状腺激素降低程度一致,T1DM并DKA患儿的T3、T4水平均有明显下降,提示T1DM患儿需重视甲状腺激素的检测,利于早期防治。  相似文献   

13.
Background: Diabetic ketoacidosis (DKA) development in children with new‐onset type 1 diabetes (T1DM) is often the main consequence of delayed diagnosis. The aim of the study was to estimate the frequency of difficulties in T1DM diagnosis and to investigate if and how the demographic factors (gender, patient's age at presentation, family history of T1DM, level of maternal education, place of residence, and health service unit the patient called at) have any influence on diagnostic delays. Subjects and methods: Retrospective analysis of 474 children (243 boys—51.27% and 231 girls ?48.73%) with new‐onset T1DM aged below 17 yr and living in the Pomeranian region of Poland was carried out. The delay in diagnosis was recognized if the patient was not diagnosed on the first visit because of omission, wrong interpretation of main diabetic symptoms, exclusive treatment of additional signs, or concomitant diseases. Results: Difficulties in diagnosing T1DM were found in 67 cases (14.13%) and they are the main cause of DKA development in these children (p = 0.00). Among the examined demographic factors, mainly the patient's age at presentation has a significant influence on diagnostic delays (p = 0.01), especially in children below 2 yr (p = 0.00). Most frequently family doctors were responsible for wrong preliminary diagnosis. Conclusions: Difficulties in diagnosing T1DM are a significant cause of DKA development in children with new‐onset disease. Patient's age at presentation is the main risk factor of delayed diagnosis, especially in children below 2 yr. The increase in awareness among pediatricians concerning the possibility of T1DM development in children is needed.  相似文献   

14.
ABSTRACT. Studies in identical twins have shown only a 50% concordance for type 1 diabetes, indicating that environmental factors are of major importance. Prospective studies in twins and siblings of type 1 diabetics provide evidence of a long pmdiabetic phase. Environmental factors, inducing a pathological immune response in genetically susceptible individuals, may thus act long before the clinical onset. In Sweden a high and increasing incidence of childhood diabetes has been shown, with peak incidence rates at puberty in both boys and girls. The incidence rate is higher for boys than for girls. Significant geographical and seasonal variations are clearly indicated. The epidemiology of lost beta-cell function shortly after clinical onset differs significantly from the epidemiology of clinical onset as to sex and geographical and seasonal distribution. Environmental factors that affect the clinical onset of type 1 diabetes may thus differ from factors affecting the beta-cell function after onset. Factors affecting the peripheral insulin sensitivity should therefore be taken into consideration also when discussing the natural history of type 1 diabetes. Key words: Type 1 akbetes, epidemiology, childhood, natural history, beta-cell function .  相似文献   

15.
目的探讨5岁以下婴幼儿糖尿病的临床特点、诊断及酮症酸中毒(DKA)的抢救措施。方法回顾性分析21例5岁以下婴幼儿糖尿病患儿的发病情况、临床特点、误诊情况,并探讨急救治疗体会。结果婴幼儿糖尿病临床症状不典型,糖尿病自身抗体阳性率低,初诊误诊率达52.4%,DKA发生率也高达52.4%。感染是诱发DKA的常见原因,患儿无1例死亡,1例放弃治疗,出院后治疗依从性不一。结论婴幼儿糖尿病多为特发性,临床症状不典型,易误诊、漏诊。感染可能导致患儿糖尿病的进展和临床表现出现。小剂量胰岛素持续静滴、调节酸碱平衡和纠正电解质紊乱是急救的关键。  相似文献   

16.
Diabetic ketoacidosis (DKA) has significant morbidity and mortality and is common at diagnosis in children. The aim of this study was to determine the frequency and clinical characteristics of DKA over a 20-year period among children diagnosed with type 1 diabetes mellitus (T1DM) at University children's hospital in Belgrade, Serbia. The study population comprised of 720 patients (366 boys) diagnosed with type 1 diabetes aged <18 years between January 1992 and December 2011. Of all patients diagnosed with T1DM, 237 (32.9 %) presented with DKA. The majority had either mild (69.6 %) or moderate (22.8 %) DKA. Sixty (55.0 %) of all children under 5 years had DKA compared to sixty-two (20.9 %) in the 5- to 10-year-old group and one hundred fifteen (36.6 %) in the 11- to 18-year-old patients (p?<?0.01), while 2.5 % of the entire DKA cohort were in real coma. During the later 10-year period, children less often had DKA at diagnosis compared with the earlier 10-year period (28.0 vs. 37.4 %) (p?<?0.01), but the frequency of severe DKA was higher in the age group <5 year and in the age group >11 year during 2002–2011, compared with the earlier 10-year period (12.9 vs. 3.4 %, p?<?0.01 and 17.1 vs. 3.8 %, p?<?0.01). Conclusion: The overall frequency of DKA in children with newly diagnosed type 1 diabetes decreased over a 20-year period at our hospital. However, children aged <5 years and adolescents are still at high risk for DKA at diagnosis.  相似文献   

17.
OBJECTIVE: To investigate whether pubertal development, duration of type 1 diabetes mellitus (DM1), or metabolic control play some role in the anomalies in growth observed in diabetic children. PATIENTS: We conducted a prospective evaluation of 83 patients (37 female, 46 male) who were followed from the onset of DM1 at the prepubertal stage until they reached final height. All patients were treated with a conventional regimen of insulin. METHODS: Height SDS, weight SDS, BMI SDS, duration of DM1 in years, and values of HbA1c were the study variables. RESULTS: In prepubertal (P1) girls (data for the initial vs the intermediate evaluations): weight SDS was -0.14 +/- 0.19 vs 0.11 +/- 0.20, p = ns; BMI SDS -0.25 +/- 0.15 vs 0.01 +/- 0.13, p = ns. In postpubertal (P3) girls, weight SDS was 0.49 +/- 0.2 vs 1.2 +/- 0.32, p <0.01; BMI SDS 0.09 +/- 0.16 vs 1.03 +/- 0.24, p <0.01, whereas in P1 boys, height SDS was 0.16 +/- 0.30 vs -0.20 +/- 0.27, p <0.05; and in P3 boys: 0.09 +/- 0.21 vs -0.28 +/- 0.26, p <0.05. Thus pubertal development influenced changes observed in girls with DM1, but did not do so in boys. The anomalies described in children with DM1 were observed from the third year of DM1 duration in both girls and boys. We did not observe any correlation between HbA1c values with height SDS, weight SDS or BMI SDS. CONCLUSIONS: The anomalies in growth observed in girls with DM1 are related to pubertal development, but this is not the case in boys. Alterations in children with DM1 were found from the third year of DM1 duration. Furthermore, the present data also indicate that the degree of metabolic control observed in our patients treated with modern but conventional regimen did not play a major role in the anomalies observed.  相似文献   

18.
This study evaluates the clinical profiles and outcomes of children with infantile-onset diabetes mellitus (IODM) (onset at <1 year). Twelve infants with IODM presenting to our hospital from January 2003 to December 2007 are analyzed. All undergo thorough history, clinical examination, and investigations and are managed as per hospital-approved protocol and periodically followed up. Of 12 infants (3 boys and 9 girls), 9 have a family history of DM. The median age at onset is 2.5 months. Six infants have features suggestive of Wolcott-Rallison syndrome (WRS), 4 infants have type 1 DM, and 1 infant each has Fanconi-Bickel syndrome and maturity-onset diabetes of young. None have pancreatic agenesis or calculi. Human leukocyte antigen (HLA) typing shows DQ3 and DR15 alleles predominating. Two children with WRS died; the rest are being followed up. The incidence of IODM is increasing, with multiple syndromic associations rather than a single perspective.  相似文献   

19.
目的调查初发1型糖尿病患儿酮症酸中毒(DKA)的发生情况。方法以224例初发1型糖尿病患儿为研究对象,进行回顾性分析,分为DKA组和未合并DKA组,各112例。DKA组患儿根据年龄分为≥5岁组(65例)和5岁组(47例),并根据酸中毒情况分为轻度(26例)、中度(29例)、重度(57例)3组。分析DKA发生的影响因素以及不同年龄DKA患儿的临床及实验室特点。结果 224例初发1型糖尿病患儿中最常见的症状为多饮(86.2%)、多尿(78.6%)及体重下降(57.1%)。与未合并DKA患儿比较,DKA组5岁、低收入、父母教育程度高中及以下所占的比例均较高,随机血糖、Hb A1C水平较高,pH、HCO_3~-及C肽水平更低,差异均具有统计学意义(P0.05)。≥5岁组与5岁组的轻、中、重度DKA所占比例的差异无统计学意义(P0.05)。与5岁组相比,≥5岁组DKA患儿的症状持续时间较长,随机血糖较低,HbA1C、C肽水平较高,差异具有统计学意义(P0.05)。结论 1型糖尿病患儿DKA发生率高,DKA的发生与年龄、父母文化程度及家庭收入有关。  相似文献   

20.
The objectives of the present work were to present a new reference for the age at childhood onset of growth and to investigate the secular trend in the timing of puberty in a community‐based normal population in Sweden. A total of 2432 children with longitudinal length/height data from birth to adulthood were used to determine the two measures by visual inspection of the measured attained length/height and the change in growth velocity displayed on a computer‐generated infancy‐childhood‐puberty (ICP) based growth chart. The series represents a sample of normal full‐term children born around 1974 in Göteborg, Sweden. We found about 10% of children were delayed (>12 mo of age) in the childhood onset of growth based on the previous reported normal range, i.e. 14% in boys and 8% in girls. Distribution of the age at childhood onset of growth was skewed. The medians were 10 and 9 mo for boys and girls, respectively. After natural logarithmic transformation, the mean and standard deviation (SD) were 2.29 (anti‐log 9.9 mo) and 0.226 for boys, 2.23 (anti‐log 9.3 mo) and 0.220 for girls, respectively. The 95% normal ranges were 6.3‐15.4 and 6.0‐14.3 for boys and girls, respectively. The distribution of the timing of PHV was close to the normal distribution. The mean values were 13.5 y for boys and 11.6 y for girls with 1 y SD for both sexes. Conclusion: A downward secular trend in the onset of puberty was clearly shown in the population. The age at childhood onset of growth did not correlate with the timing of puberty (r=?0.01 and 0.05, p > 0.7 and 0.1 in boys and girls, respectively). Normal ranges of the age at childhood onset of growth are in need of revise, as this study indicates. The new reference presented here could be a reliable indicator in further studies.  相似文献   

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