婴幼儿法洛四联症围手术期血糖与动脉血乳酸变化的相关性

目的研究婴幼儿法洛四联症围手术期血糖与动脉血乳酸变化的相关性及干预血糖对预后的影响。方法收集2014年1月至2020年12月在山西省儿童医院行法洛四联症根治手术的127例患儿的临床资料, 其中男73例, 女54例;年龄为(6.1±4.5)个月, 范围在2～12个月, 体重为(7.4±2.9) kg, 范围在4～10.5 kg, 术前经皮血氧饱和度为80.2%±10.3%, 范围在69%～91%, 血红蛋白为(155.2±30.5) g/L, 范围在118～212 g/L, MaGoon指数为1.30±0.34(1.10～1.70)。记录围手术期9个时间点的血糖及动脉血乳酸值, 按术后2 h血糖值分为3组:高血糖组(血糖值≥11.1 mmol/L)61例, 可接受血糖组(4.5 mmol/L≤血糖值<11.1 mmol/L)63例, 低血糖组(血糖值<4.5 mmol/L)3例, 其中高血糖组按照控制目标血糖分为两小组:常规控制血糖组(8.0～11.1 mmol/L)35例, 严控血糖组(4.5 mmol/L≤血糖值<8.0 mmol/L)26例。比较各组间动脉血乳酸值...     

早产儿低血糖与C肽、胰岛素、皮质醇关系的研究

目的 探讨早产儿低血糖的特点及与C肽、胰岛素、皮质醇的关系.方法 对我院收治的150例早产儿进行血糖及C肽、胰岛素及皮质醇监测.结果 胎龄小于34周早产儿(63例)与胎龄34～37周(87例)早产儿低血糖发生率分别为47.6％、28.7％,差异有统计学意义(x2=19.704,P＜0.05).低血糖组(55例)生后24h和生后3d皮质醇水平明显低于正常血糖组(95例),差异有统计学意义(P＜0.05),生后7d两组比较差异无统计学意义(P＞0.05).患儿胰岛素、C肽在各时间点比较差异无统计学意义(P＞0.05).结论 早产儿低血糖发生率较高,应加强早产儿血糖监测.     

218例无追赶生长的小于胎龄儿儿童期糖代谢分析

目的 探索无追赶生长的小于胎龄儿在儿童期的胰岛素敏感性.方法 收集2008年8月至2016年8月于北京大学第三医院儿科门诊就诊的身材矮小患儿439例,分为小于胎龄儿组(small for gestational age,SGA)218例和特发性矮小组(idiopathic short stature,ISS)221例.比较两组之间的空腹胰岛素、空腹血糖、空腹血糖与胰岛素比值、胰岛β细胞功能(HOMA%)和胰岛素抵抗指数(HOMA-IR)特点.结果 两组患儿均根据青春期分期及性别分组,SGA组与ISS组,青春期前男性患儿的空腹血糖分别为(4.7±0.6)mmol/L和(4.8±0.6)mmol/L,P=0.678,空腹胰岛素(5.1±4.0)mU/L和(4.3±4.7)mU/L,P=0.345,血糖胰岛素比值、HOMA%及HOMA-IR的差异均无统计学意义;青春期前女性患儿的空腹血糖分别为(4.5±0.5)mmol/L和(4.6±0.5)mmol/L,P=0.828,空腹胰岛素分别为(4.7±3.5)mU/L和(4.5±3.3)mU/L,P=0.603,血糖胰岛素比值、HOMA%及HOMA-IR的差异均无统计学意义;青春期男性患儿的空腹血糖分别为(5.0±0.8)mmol/L和(4.9±0.5)mmol/L,P=0.176,空腹胰岛素分别为(5.9±4.3)mU/L和(6.0±4.5)mU/L,P=0.958,血糖胰岛素比值、HOMA%及HOMA-IR的差异均无统计学意义;青春期女性患儿的空腹血糖分别为(4.9±0.6)mmol/L和(4.8±0.4)mmol/L,P=0.141,空腹胰岛素分别为(7.5±6.4)mU/L和(7.4±8.6)mU/L,P=0.448,血糖胰岛素比值、HOMA%及HOMA-IR的差异均无统计学意义.     

重症儿童高血糖与胰腺β细胞功能障碍的研究

目的 分析重症儿童高血糠发生与胰岛素抵抗和胰腺β细胞功能障碍之间的关系,探讨胰腺β细胞功能障碍与胰腺损伤的关系.方法 分析2012年6月至2013年3月湖南省儿童医院PICU收治的736例危重症患儿,以入住PICU 24 h内选择空腹时间点采集血标本,静脉血糖≥11.1mol/L为重度升高组（n=67）;6.1～ 11.1 mmol/L为轻度升高组（n=361）;≤6.1 mmol/L为血糖正常组（n =308）,比较血清胰岛素、C肽、血清淀粉酶、脂肪酶、尿淀粉酶、HOMA-β指数、HOMA-IR指数、按脓毒症严重程度分非脓毒症组（n =414）、脓毒症组（n=237）、严重脓毒症组（n=64）、脓毒性休克组（n=21）,比较血糖、血清胰岛索、C肽、HOMA-β指数、HOMA-IR指数差异.结果 （1）胰岛素、C肽、血淀粉酶、脂肪酶、尿淀粉酶的总体趋势随血糖升高而逐渐升高（rs值分别为0.235、0.142、0.142、0.119、0.093,P＜0.05）,三组间比较差异有统计学意义（P＜0.05）,血糖重度升高组血清淀粉酶（IU/L）[102.81（10.48-191.69）]、脂肪酶（U/L）[69.75（10.67-121.85）]高于正常值上限.重度升高组HOMA-β指数下降至18.75％,HOMA-β指数随血糖水平升高而下降（rs=-0.108,P ＜0.05）,HOMA-IR指数随血糖升高而逐渐升高（rs=0.455,P ＜0.05）.（2）非脓毒症组、脓毒症组、严重脓毒症组、脓毒性休克组患儿的血糖、胰岛素、C肽水平和HOMA-β指数差异有统计学意义（P＜0.05）,HOMA-IR指数比较差异无统计学意义（P＞0.05）.脓毒性休克组血糖为9.21 （6.21-19.60） mmol/L,HOMA-β指数降低至10.52％,血糖、胰岛素、C肽、HOMA-β指数与其他三组比较差异有统计学意义（P＜0.05）.结论 重症儿童高血糖与胰岛素抵抗和胰岛β细胞功能障碍有关,危重症继发胰腺损伤是导致胰岛β细胞功能障碍的原因;在脓毒症儿童,胰腺β细胞功能障碍使血糖升高的作用比胰岛素抵抗更加显著.     

窒息新生儿血糖变化与窒息程度的关系探讨

目的探讨新生儿窒息血糖监测的临床意义。方法收集2010年1月至2012年12月我院新生儿科收治的100例确诊为新生儿窒息的新生儿,根据Apgar评分分为轻度窒息组和重度窒息组,分别于生后3 h、24 h釆末梢血监测血糖,对比观察两组窒息患儿血糖变化。结果轻度窒息组64例,重度窒息组36例。生后3 h轻度窒息患儿血糖异常35例（54.69％）,明显低于重度窒息患儿的33例（91.67％）;生后24 h轻度窒息患儿血糖异常7例（10.94％）,也明显低于重度窒息患儿17例（47.22％）;轻度窒息组患儿3 h平均血糖（3.56±1.98）mmol/L,24 h平均血糖（3.57±1.52）mmol/L,重度窒息组患儿3 h平均血糖（6.93±1.57）mmol/L,24 h平均血糖（7.21±3.44）mmol/L,重度窒息明显高于轻度窒息组,差异均有统计学意义（ P＜0.05）。结论窒息程度越重,血糖异常发生率越高;轻度窒息新生儿血糖异常以低血糖为主,重度窒息以高血糖为主。对窒息患儿生后要定期监测血糖,特别是重度窒息患儿应把血糖的变化作为常规判断病情与对症治疗的重要辅助指标。     

脐动脉插管可能导致难治性低血糖

本文报告2例安置脐动脉导管(UAC)的新生儿,诱发了难治性低血糖。例1 男婴,体重2500g,妊娠39周后顺产。母亲健康,25岁,其母系有非胰岛素依赖性糖尿病史,但本人糖耐量试验正常。婴儿产后1小时,显示极度紧张不安,此时血糖1.57mmol/L(28mg/dl)。在经口喂养的同时,静滴10%葡萄糖液、其后血糖升至3.9mmo1/L(70mg/dl)。停止静滴葡萄糖后,又发生低血糖,乃于脐动脉内插入一根导管,持续滴注10%葡萄糖液,因患儿持续性低血糖,给予输注20%     

53例危重新生儿高血糖症

目的：　报道53例危重新生儿血糖监测结果,对危重新生儿高血糖的发生因素及与预后进行分析。方法：　 53例按有无器官功能衰竭分为单衰组,多衰组,无衰组;微量全血血糖>7mmol/L诊断高血糖。对检出的高血糖病例,在控制原发病的同时,降低葡萄糖输入浓度及速度,复查血糖,如未恢复正常予正规胰岛素治疗,直至血糖水平恢复正常。并对高血糖症的新生儿行头颅B超检查。结果：　单衰组与多衰组患儿血糖水平明显高于无衰组,多衰组血糖为(22.4±3.78)mmol/L ,单衰组血糖为(19.9±9.53)mmol/L ,无衰组血糖为(11.1±2.73)mmol/L ,单衰组、多衰组与无衰组比较均P<0.05。血糖越高,死亡率亦越高。 43例高血糖患儿中血糖24h之内恢复正常的有31例,其中24例治愈或好转,好转率77.4%,>24h恢复的有12例,5例好转,好转率41.7%,两者比较P<0.05。共有11例患儿发生颅内出血,其中1例血糖>10mmol/L,10例血糖>15mmol/L。结论：　危重症患儿血糖的变化可作为判断其病情及预后的辅助指标。     

危重新生儿血糖和胰岛素水平的变化及其临床意义

目的 探讨危重新生儿血糖和血清胰岛素的变化及其临床意义.方法 选择2006年12月-2009年1月在本院住院的危重新生儿60例.男36例,女24例;体质量2 300～4 200 g;胎龄35～41周;日龄1～27 d.采用微量血糖仪测定危重新生儿标本中血糖水平;对于高血糖和低血糖新生儿给予相应治疗;用化学发光免疫法检测危莺患儿血清胰岛素水平.健康对照组30例按上述同样方法测定相应指标.并进行二组比较.结果 危重60例患儿中糖代谢紊乱26例(43%),其中高血糖21例,低血糖5例.危重新生儿血糖、胰岛素水平[(6.37±4.11)mmol/L、(25.73±14.32)mIU/L]较健康足月新生儿[(4.13±1.73)mmol/L、(4.01±1.73)mIU/L]显著升高(t=2.32,4.76 Pa<0.01),经治疗后血糖均恢复正常.结论 危重新生儿可出现糖代谢紊乱及高胰岛素血症,对危重患儿应密切监测血糖变化,尽早发现血糖异常,及时诊断并合理处理.     

危重患儿血糖与胰岛素水平的临床分析

目的 分析危重患儿血糖和胰岛素水平变化,探讨危重患儿高血糖发生相关机制.方法 检测2007年1至12月我院PICU收治的51例危重患儿入院时血糖和胰岛素水平变化,并与15例健康体检儿检测结果进行对照分析.结果 (1)各种基础疾病下的危重患儿入院24 h内血糖均值均高于正常范围,以感染性休克组为最高[(11.35±6.21)mmol/L];患儿入院5 d内每日血糖均值波动情况以入院当天为最高,其后持续高于正常.(2)人院24 h内肺部感染、颅内感染和感染性休克患儿血胰岛素水平分别为(17.65±16.85)mU/L、(13.45±7.33)mU/L、(16.24±12.41)mU/L,均高于对照组[(8.70±6.57)mU/L],而先天性心脏病组[(6.75±3.22)mU/L]略低于正常组,但各组间差异无显著性(F=0.356,P=0.127);入院当天和第3天、第5天患儿血胰岛素平均水平均高于正常对照组[(8.70±6.57)mU/L];根据血糖水平,将患儿分为血糖正常组和高血糖组,两组血胰岛素水平分别为(5.44±3.38)mU/L、(14.22±12.29)mU/L,高血糖组胰岛素水平明显高于对照组.(3)患儿危重评分(PIM Ⅱ)均值为12.69±16.82,共死亡8例,病死率为15.6%;死亡患儿血糖和胰岛素水平均明显高于存活患儿(P＜0.05).(4)血糖和血胰岛素水平间无明显线性关系;危重症评分和血胰岛素水平无线性相关性;血糖和危重症评分间线性相关性不显著.结论 危重症患儿常出现高血糖和高胰岛素血症,两者在一定程度上间接反映疾病严重程度,也是判断预后的间接指标;高血糖与胰岛素相对不足或(和)胰岛素抵抗有关,至于其确切的关系需要进一步研究证实.     

手足口病患儿血糖测定的临床意义

目的 探讨手足口病患儿空腹血糖的变化及其在预测病情进展中的价值.方法 观察80例患儿空腹血糖的变化,其中普通型手足口病40例,重型手足口病40例.结果 40例普通型手足口病患儿血糖均值为(5.18 ±2.34) mmol/L;40例重型手足口病患儿血糖均值为(6.80 ±3.12) mmol/L.重型手足口病与普通型患儿比较,血糖水平明显升高,差异有统计学意义(P＜0.05).病情稳定的65例患儿血糖水平较低,为(4.52 ±2.25) mmol/L,而普通型手足口病(10例)和重型手足口病(5例)病情恶化的患儿血糖水平较病情稳定的患儿明显升高,分别为(6.32±2.34)mmol/L、(7.14±2.29) mmol/L,差异有统计学意义(P＜0.05).结论 手足口病发生时伴有应激反应增高表现,空腹血糖增高可以作为手足口病重症病例早期识别的一个危险因素.     

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.