胰岛素泵治疗儿童1型糖尿病并酮症或酮症酸中毒26例

目的观察胰岛素泵持续皮下注射胰岛素对儿童1型糖尿病并酮症或酮症酸中毒(DK/DKA)的疗效。方法本院内分泌科2003~2005年收治的1型糖尿病并DK/DKA患儿43例,分为治疗组26例和对照组17例。治疗组予胰岛素泵治疗,对照组予小剂量胰岛素持续静脉滴注。比较二组患儿血糖、尿酮体、血pH值变化,住院时间长短。结果1.治疗组血糖下降相对稳定,纠正酸中毒后无反复。2.治疗过程中治疗组未出现低血糖,对照组2例出现。3.住院时间治疗组[(11.92±4.72)d]较对照组[(17.35±4.83)d]治疗组较对照组明显缩短(P<0.001)。结论胰岛素泵持续皮下注射胰岛素治疗儿童1型糖尿病并DK/DKA是安全有效的。     

胰岛素泵在1型糖尿病患儿的合理使用

目的 探讨胰岛素泵强化治疗对1型糖尿病(T1DM)患儿的疗效,并分析影响疗效和胰岛素用量的因素.方法 本院内分泌科2003-2008年收治的T1DM患儿68例.对其进行短期胰岛素泵强化治疗,将其分为初诊组和复诊组、感染组和非感染组,并酮症酸中毒(DKA)和非DKA组,观察影响使用胰岛素泵治疗效果的因素,在年龄、初诊、感染和并DKA等情况下胰岛素泵的使用情况.结果 68例患儿均予胰岛素泵强化治疗,血糖达标天数为(4.37±1.60) d,达标时胰岛素用量为(1.22±0.34) U/(kg·d);初诊组和复诊组血糖达标时间、胰岛素用量比较均无显著差异(Pa>0.05);非感染组达标时间明显均较感染组、并DKA组短(Pa<0.05);与非感染组比较,感染组、并DKA组基础胰岛素用量大(Pa<0.01),小年龄组胰岛素输注管堵塞和发生低血糖例次明显多于大年龄组儿童.结论 胰岛素泵的使用在T1DM患儿存在着差别,小年龄组胰岛素泵使用要慎重.     

应用胰岛素泵治疗儿童1型尿病合并酮症酸中毒

目的 探讨使用胰岛素泵持续皮下输注胰岛素治疗儿童１型糖尿病合并酮症酸中毒的可行性。方法 将在我院住院的１型糖尿病合并酮症或酮症酸中毒的患儿１２例,分为胰岛素泵治疗组和对照组,每组６例,分别使用胰岛素泵皮下输注胰岛素和小剂量胰岛素静脉滴注,常规胰岛素的用量为０．０５～０．１０ＩＵ／（ｋｇ．ｈ）,观察血糖、β－羟丁酸、尿酮体的变化,结果 ⑴两组患儿的血糖在使用量为０．０５～０．１０ＩＵ／（ｋｇ．ｈ）经     

新发儿童1型糖尿病酮症酸中毒与重症儿童应激性高血糖的鉴别诊断

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.     

儿童1型糖尿病的10年回顾及白介素-10在糖尿病酮症酸中毒中的临床意义

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］     

儿童1型糖尿病胰岛素泵治疗长期随访的疗效观察

目的 比较1型糖尿病(T1DM)患儿应用持续皮下胰岛素输注(CSII)与每日多次皮下胰岛素注射(MDI)治疗对血糖控制的疗效差异.方法 回顾性收集91例应用CSII方式治疗1年以上T1DM患儿的临床资料,评估其糖化血红蛋白(HbA1C)水平、糖尿病酮症酸中毒(DKA)再发生情况,通过与75例应用MDI治疗的T1DM患儿...     

儿童1型糖尿病90例

目的探讨儿童1型糖尿病(IDDM)的发病情况、临床特点、远期并发症及酮症酸中毒(DKA)的治疗。方法回顾性分析1993～2003年我院90例IDDM患儿的发病情况,临床特点,远期并发症,并探讨DKA的治疗。结果10～16岁儿童发病率最高,感染是诱发DKA的常见原因,未长期坚持胰岛素治疗易导致IDDM远期并发症的发生。结论小剂量胰岛素持续静滴、纠正水电解质紊乱、调节酸碱平衡是抢救DKA的关键;坚持长期胰岛素治疗是防治远期并发症IDDM的关键。     

25-羟维生素D与儿童1型糖尿病及酮症酸中毒的相关性研究

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。     

胰岛素泵应用失败原因分析及对策

目的 纠正带泵患儿的误区,充分发挥胰岛素泵的优越性.方法 分析7例T型糖尿病患儿带泵并发酮症酸中毒(DKA)的原因,查找原因并作出相应对策.结果 7例患儿均出现高血糖,最高血糖＞30mmol/L,HbAIc 9.7%.发生DKA原因,4例机器原因(堵管,机器无报警,皮下软管折曲,滑脱);1例因饮食不控制,随意增加胰岛素用量;1例未及时更换注射部位致皮肤感染;另1例并发全身感染,未及时就诊.结论 佩带胰岛素泵也会并发DKA,应积极查找原因并作出相应对策.加强心理及健康教育,进行饮食控制,注意运动疗法,带泵期间多检查泵的工作状态,并积极处理并发症,才能使泵发挥最佳疗效.     

儿童糖尿病酮症酸中毒17例临床分析

目的 分析儿童糖尿病酮症酸中毒(diabetic ketoacidosis,DKA)的临床特点及其相关治疗,以减少临床上的误诊、误治.方法 回顾性分析2003年1月至2007年12月我院收治的17例DKA的临床资料.结果 儿童DKA以原发性糖尿病为多见,伴有少数继发性药物性糖尿病,但疾病初期易误诊(47.1%).针对DKA的治疗以液体复苏、纠正酸中毒和控制血糖为原则,其中液体复苏应首选等张的生理盐水,纠正酸中毒应补充适量的碳酸氢钠,控制血糖以小剂量胰岛素静滴为宜.17例患儿中15例经上述处理均治愈出院,仅2例放弃治疗.结论 及时确诊、小剂量胰岛素静滴调控血糖、液体复苏纠正水电解质紊乱、维持酸碱平衡是救治DKA的关键.     

Allergic factors associated with the development of asthma and the influence of cetirizine in a double-blind, randomised, placebo-controlled trial: First results of ETA®

There is a common progression known as the allergic march from atopic dermatitis to allergic asthma. Cetirizine has several antiallergic properties that suggest a potential effect on the development of airway inflammation and asthma in infants with atopic dermatitis. Methods. Over a two year period, 817 infants aged one to two years who suffered from atopic dermatitis and with a history of atopic disease in a parent or sibling were included in the ETAC^® (Early Treatment of the Atopic Child) trial, a multi-country, double-blind, randomised, placebo-controlled trial. The infants were treated for 18 months with either cetirizine (0.25mg/ kg b.i.d.) or placebo. The number of infants who developed asthma was compared between the two groups. Clinical and biological assessments including analysis of total and specific IgE antibodies were performed. Results. In the placebo group, the relative risk (RR) for developing asthma was elevated in patients with a raised level of total IgE (≥ 30 kU/I) or specific IgE (≥ 0.35 kUA/I) for grass pollen, house dust mite or cat dander (RR between 1.4 and 1.7). Compared to placebo, cetirizine significantly reduced the incidence of asthma for patients sensitised to grass pollen (RR = 0.5) or to house dust mite (RR = 0.6). However, in the population that included all infants with normal and elevated total or specific IgE (intention-to-treat - ITT), there was no difference between the numbers of infants developing asthma while receiving cetirizine or placebo. The adverse events profile was similar in the two treatment groups. Discussion. Raised total IgE level and raised specific IgE levels to grass pollen, house dust mite or cat dander were predictive of subsequent asthma. Cetirizine halved the number of patients developing asthma in the subgroups sensitised to grass pollen or house dust mite (i.e. 20% of the study population). In view of the proven safety of the drug, we propose this treatment as a primary pharmacological intervention strategy to prevent the development of asthma in specifically sensitised infants with atopic dermatitis.     

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孤独症谱系障碍(autistic-spectrum disorders,ASDs)近年来患病率逐年攀升至1%左右,其症状往往伴随终生,成为严重威胁儿童健康和发展的神经发育性疾患;注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是儿童期最常见的精神障碍,国内报道患病率为4.13%～5.83%,其症状可延续至青少年期,甚至到成年期[1]。这两类精神障碍在成年期的临床表现、共患病、治疗策略和预后与儿童期有哪些不同呢?本文通过回顾相     

EXCITING NEW TREATMENT APPROACHES FOR PATHYPHYSIOLOGIC MECHANISMS OF SICKLE CELL DISEASE

During the past several decades, our understanding of the complex pathophysiology of vasoocclusion associated with sickle cell disease has improved greatly. Interaction of genes, hemoglobin molecules, red cell membrane and metabolic changes, cell-cell interactions and cell-plasma interactions, red cell adhesion to vascular endothelium, activation of coagulation, and vascular reactivity play a role in vaso occlusion. Penicillin prophylaxis of pneumococcal infections and appropriate use of blood transfusions and other supportive measures improved survival of sickle cell patients. Hydroxyurea made a major impact on sickle cell therapy when it was shown to decrease acute painful episodes, acute chest syndrome, and the need for blood transfusion in adults. Significant experience in the use of hydroxyurea has been accumulated in older children. The benefits and risks of hydroxyurea for younger children and long-term risks in all patients will be evaluated in future investigations. Other promising therapies include butyrate compounds, clotrimazole, magnesium supplementation, poloxamer 188, antiadhesion agents, anticoagulant approaches, and nitric oxide. Hemopoietic transplantation remains the only curative therapy. However, several transgenic mouse models are available for studies of gene therapy or other treatment approaches on biochemical, cellular, and pathologic effects of mutant genes.     

Infiltrations of Epstein-Barr virus-carrying cells in granular lymphocyte-proliferative disorders corresponding to chronic active Epstein-Barr virus infection

A 21-year-old man with granular lymphocyte-proliferative disorders (GLPD) associated with chronic active Epstein-Barr virus (EBV) infection is described. Chromosomal analyses revealed several clonal abnormalities and two of them were mainly repetitious. High copy numbers of monoclonal EBV genome were also detected in the proliferative large granular lymphocytes (LGLs), indicating the monoclonal expansion of EBV-infected LGLs. The patient had an indolent course for several years, and there was no evidence of infiltrations of his bone marrow until the end stage. At autopsy, microscopic studies revealed marked infiltrations of LGL in the liver and spleen, and the infiltrating cells were NK-cell immunophenotype. The infiltrated LGLs showed latency I.     

LUTEINIZING HORMONE RECEPTOR MUTATIONS IN DISORDERS OF SEXUAL DEVELOPMENT AND CANCER

Human male sexual development is regulated by chorionic gonadotropin (CG) and luteinizing hormone (LH). Aberrant sexual development caused by both activating and inactivating mutations of the human luteinizing hormone receptor (LHR) have been described. All known activating mutations of the LHR are missense mutations caused by single base substitution. The most common activating mutation is the replacement of Asp-578 by Gly due to the substitution of A by G at nucleotide position 1733. All activating mutations are present in exon 11 which encodes the transmembrane domain of the receptor. Constitutive activity of the LHR causes LH releasing hormone-independent precocious puberty in boys and the autosomal dominant disorder familial male-limited precocious puberty (FMPP). Both germline and somatic activating mutations of the LHR have been found in patients with testicular tumors. Activating mutations have no effect on females. The molecular genetics of the inactivating mutations of the LHR are more variable and include single base substitution, partial gene deletion, and insertion. These mutations are not localized and are present in both the extracellular and transmembrane domain of the receptor. Inactivation of the LHR gives rise to the autosomal recessive disorder Leydig cell hypoplasia (LCH) and male hypogonadism or male pseudohermaphroditism. Severity of the clinical phenotype in LCH patients correlates with the amount of residual activity of the mutated receptor. Females are less affected by inactivating mutation of the LHR. Symptoms caused by homozygous inactivating mutation of the LHR include polycystic ovaries and primary amenorrhea.     

Resurgence of measles in Singapore: profile of hospital cases

OBJECTIVE: To ascertain the profile of cases of measles seen at a general hospital during a recent outbreak that occurred despite a measles vaccination program. METHODOLOGY: A retrospective study from January 1991 to March 1998. All patients with measles (ICD code 055. 9) seen at the emergency unit or as inpatients were included. RESULTS: There were 87 cases identified. The diagnosis was clinical in all and proven serologically in 71%. Eighty-five per cent of the cases occurred between January 1997 and March 1998. There was a bi-modal age distribution with peaks in the very young (相似文献   

Personality profiles and heart rate variability (vagal tone) in children with recurrent abdominal pain

The aim of the study was to explore psychological factors and autonomic activity in children with recurrent abdominal pain and to compare them with those in a control group of healthy children. The Personality Inventory for Children was used for assessment of developmental, emotional and psychosocial factors in 25 children with recurrent abdominal pain (age, 7-15 y). Parasympathetic and sympathetic functions in these children and in 23 healthy control subjects (age, 7-13 y) were also investigated, non-invasively using a computerized polygraph. Vagal tone (parasympathetic function) was indexed by calculation of respiratory sinus arrhythmia in beats/min. Skin conductance (sympathetic function) was recorded by the constant current method. On the Personality Inventory for Children, 16 patients had high scores on somatic concern. Several patients had scores in the clinical range for depression, withdrawal and anxiety, but the mean scores for these personality profile scales were well within the normal range of healthy children. Interestingly, there was a spike on the L (Lie)-scale for most of the patients and 15 patients had scores above or close to the clinical cut-off value. As compared with the scores in healthy children, vagal tone and sympathetic tone were normal. Conclusion: Many children with recurrent abdominal pain have scores in the clinical range for depression, withdrawal, anxiety and L-scale indicating coping problems, denial and a trend towards somatic concern that may contribute to the evolution of abdominal pain. Autonomic nerve activity was not disturbed in these children.     

Understanding infant formula

The World Health organisation recommends breast feeding infants for the first six months of life. When this breast feeding does not occur either through parental choice or medical need, infant formulas will be required. There is a bewildering array of formulas on the UK market for many different requirements. When faced with an unsettled infant many parents (and healthcare professionals) will experiment with the infant formula available and then attend the paediatric clinic looking for help and advice. It is therefore essential that paediatricians understand what milks are available and what the key differences between different products are. This review attempts to provide a simple guide through many of the formulations currently available in the UK; and offers advice for the dietary management of the child with extra calorie requirements, infants with cow's milk protein allergy, gastro oesophageal reflux disease, apparent unresolved hunger and infantile colic. Whatever the underlying condition, there is likely to be an infant formula that is suitable in this generation of ever expanding formulations.     

Overcoming surfactant inhibition with polymers

Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextran and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration.