不同时期儿童精神科门诊初诊病人分析

目的 :探讨近 2 0年来儿童精神科门诊初诊的病种变化 ,就诊趋势 ,为儿童精神科门诊提供参考。方法 :查阅 1980、 1986、 1999年儿童 ( 3-15岁 )精神科门诊病历 ,做就诊人数、疾病分类统计。结果 :1、三个时期初诊就诊人数呈增长趋势 ,1980年 386人次 ,1986年 6 5 0人次 ,1999年 1198人次。疾病分布以儿童多动症、精神发育迟滞、待诊、癫痫、精神分裂症、抽动障碍、情绪障碍为主要病种共涉及 36个诊断。 2、 1986年出现新的症状诊断 :智力边缘状。 3、 1999年咨询病人增多 ,占初诊的 2 4 70 %。 4、孤独症成为 1999年的初诊首位病种 ,占 17 30 %。结论 :儿童精神卫生的需求在提高 ,应针对此需求做出相应的调整。     

青少年心理门诊服务模式的探讨

目的：了解上海市心理咨询中心少儿心理门诊2年来就诊患儿的情况,以探讨少儿心理卫生的服务模式。方法：按10：1的比例随机抽取1999年1月－2000年12月来就诊患儿的1012份门诊病历进行分析。结果：结果显示就诊患儿以小学生和初中生占大多数,男性多于女性,男女之比为近3：1,来自上海的患儿明显多于来自外地的患儿;治疗方法以药物治疗为主,心理咨询和心理治疗所占比例明显增加;就诊次数在6次以下者点89．8％;就诊患儿诊断按多少为序排列如下：行为障碍、情绪障碍、发育性障碍、其它障碍、精神疾病、抽动障碍、学习困难和适应障碍。结论：少儿心理卫生服务的主要对象是中小学生,心理卫生问题主要是行为障碍和情绪障碍,药物治疗结合心理治疗是受患儿欢迎的服务模式。     

郑州大学附属儿童医院小儿轮状病毒的感染状况及病原学特征分析

目的:探究郑州大学附属儿童医院小儿轮状病毒的感染状况及病原学特征。方法:选取2018年5月至2019年10月在本院进行治疗的272例腹泻患儿,分析其轮状病毒感染状况和病原学特征。结果:在272份腹泻样本中,134份轮状病毒抗体检测呈阳性,占腹泻患儿人数的49.26%。其中月龄小于12个月的患儿比例显著高于其它年龄段的患儿(P<0.05)。体温>37℃患儿所占比72.39%显著高于其它体温患儿所占比例(P<0.05)。腹泻次数4-6次患儿所占比60.45%显著高于其它腹泻次数患儿所占比例(P<0.05)。呕吐次数0患儿所占比85.82%,显著高于其它呕吐次数患儿所占比例(P<0.05)。脱水程度0%患儿所占比83.58,显著高于其它脱水程度患儿所占比例(P<0.05)。冬季轮状病毒感染患儿所占比45.52%显著高于其它季节患儿所占比例(P<0.05)。结论:小儿轮状病毒发病率较高,一般在冬季多发,病原学特征较多,一般以轻症为主。     

10岁以下住院烧伤儿童的临床分析

目的了解10岁以下儿童烧伤住院的特点,为儿童烧伤的预防与控制提供科学依据。方法收集部队医院2007年收治的10岁以下烧伤住院儿童病例资料,对其烧伤原因、发生时间、年龄、伤情等信息进行分类进行回顾性统计分析。结果共收治了10 163例10岁以下烧伤患儿,男女比例为1.69？1,5岁以下儿童烧伤占86.9%,其中1岁年龄段的占40.3%;5月份发生率最高,占10.1%;致伤因素多为热液烫伤,占85.9%;3岁以下年龄组中重度烧伤所占比例高于5岁以上各组（P〈0.05）。结论应加强对4岁以下儿童的监护和看管,加强对儿童生活环境的烧伤安全意识和措施的提高,从多方面入手预防儿童烧伤的发生。     

2009甲型H1N1流感大流行期间北京儿童的流感监测

目的 了解2009年甲型H1N1流感大流行期间北京地区儿童中流感流行的情况.方法 采用WHO推荐的实时荧光定量RT-PCR和国家流感中心推荐的分型方法,对2009年甲型H1N1流感大流行期间因流感样症状来首都儿科研究所附属儿童医院就诊患儿的咽拭子标本进行流感病毒核酸检测.结果 2009年6月1日至2010年2月28日期间共检测了4363份咽拭子标本,其中623例为甲型H1N1阳性,阳性率为14.3%,657例为其他甲型流感病毒阳性(15.1%),所有甲型流感病毒的总阳性率为29.3%.623例中有23例为危重症病例(占阳性患者的3.7%),其中5例死亡.618例信息完整的甲型H1N1病例中,患儿年龄为14天～16岁,性别比例为男比女为1.3:1.1～3岁儿童占25.2%,3～6岁学龄前儿童和6～12岁学龄儿童所占比例相近,各约占30%.在监测期间,仅呈现了一个甲型H1N1的流行波.2009年11月达到最高峰,随后减弱,2010年2月快速下降至2.7%.对监测期间每周20～30份临床标本同时进行季节性流感的监测显示,季节性H3N2、甲型H1N1和乙型流感交替流行.呼吸道合胞病毒(RSV)在甲型H1N1流行趋势减缓后逐渐流行成为流行优势株.结论 2009年6月至2010年2月北京地区儿童中出现甲型H1N1的流行,主要累及学龄前和学龄儿童.季节性流感和RSV与甲型H1N1交替流行.     

2016—2020年我国儿童疱疹性咽峡炎住院病例流行特征及疾病负担分析

目的分析我国2016—2020年儿童疱疹性咽峡炎(herpangina, HA)的流行特征及疾病负担, 为我国儿童HA的诊疗及防控提供基础参考数据。方法通过福棠儿童医学发展研究中心收集2016—2020年我国23个省份的27家儿童医院或妇幼保健院中HA住院患儿的病历首页信息, 对我国儿童HA进行流行病学、重症情况以及疾病负担等进行描述性统计分析。结果 2016—2020年全国27家儿童医院或妇幼保健院共报告HA住院病例24 099例;其中, 男女比为1.46∶1, 年龄≤6岁的住院患儿为23 432例(97.23%)。除2020年外, 每年HA发病都集中在4～9月份, 6～7月份为发病高峰期;华东地区统计住院患儿最多, 为8 520例(35.72%)。在研究期间, 全国HA患儿的住院占比是0.42%(24 099/5 790 910);东北地区的住院占比最高, 为0.69%(1 720/249 244)。本研究中一共有1 510例(6.27%)患儿表现为重症, 男女比为1.35∶1;其中, 1 326例(87.81%)患儿年龄≤3岁, 且年龄在28天-≤1岁的患儿重症率最高(7.47%...     

湖北省孤独症儿童就诊、康复服务的现况调查研究

目的 了解湖北省孤独症儿童就诊及康复机构现状，为孤独症儿童就诊及康复服务提供参考和建议。方法 在湖北省东西南北中选取具有代表性的5个市区，并在这5个市区的孤独症康复机构进行整群随机抽样，共选中26个康复机构，将选中机构就诊的孤独症儿童作为研究对象，自行设计两份问卷向康复机构负责人和孤独症家长进行调查，收到有效问卷252份。结果 患儿家长最先获取孤独症知识途径，医院就诊过程中了解的占74.20%。患儿第1次采取康复措施的平均年龄为3.25岁。患儿在康复期间就医总支出平均值是2741.87元。康复机构采用的干预方法中孤独症健康教育、言语训练等相对较多，在治疗中专项评估周期为3～6月的占65.40%。结论 孤独症儿童家长对孤独症的知识及相关信息了解严重不足，应设立孤独症康复咨询机构，患儿每次接受干预时的花费较高，需比较完善的医疗保障体系和社会的支持，就诊机构的专业人员需要增加，机构的干预方法需要统一标准，康复机构需要缩短随访和专业评估周期。     

儿童精神障碍住院临床资料的20年回顾分析

目的回顾分析新疆精神卫生中心近20年儿童精神障碍住院患儿一般临床资料的变化情况。方法对1991年9月至2011年8月间住院的年龄≤12岁的病历共123份进行回顾性分析。结果近20年精神障碍患儿住院人数先缓慢增加,2003年后增加明显并趋于平稳。随年龄增长住院人数递增。男性74例(60.2%),女性49例(39.8%)。诊断前6位为:癫痫或癫痫所致精神障碍(以下统称癫痫)、心境障碍、精神分裂症、癔症、精神发育迟滞及应激相关障碍。后10年组少数民族患儿住院及治疗有效比例显著高于前10年组(χ2=4.676,6.532;P<0.05)。结论儿童精神问题日益突出,需进一步关注西部儿童心理健康。     

15年来1176例孤独症门诊病例回顾性分析

目的:研究儿童孤独症患者的一般资料特点.方法:收集门诊就诊的1176例孤独症患者一般资料,使用SPSS统计软件进行描述性统计分析.结果:在1176例患者中,于3岁后才被家长发现症状者多达35.10%,3岁以下初诊患儿仅占21.43%,发现症状与前来求治平均间隔时间长达35.03±27.86个月.结论:加强健康教育,提高对本病的认识,以期早发现,早治疗.     

2006-2009年南山区学生肺结核病例情况分析

目的分析近年南山区校园结核病的发病情况,为有效预防和控制学校结核病疫情提供依据。方法将2006-2009年在深圳市南山区慢性病防治院就诊的学生肺结核初诊病例182例作为研究对象,收集病例的相关资料,采用描述性分析方法分析病例发现、分布特征和治疗转归等情况。结果 2006-2009年南山区学生肺结核病例占全区同期活动性肺结核病例的比例逐年递增,分别为0.99%、1.64%、1.88%和3.99%;因症就诊方式发现的病例分别占初诊、确诊和涂阳病例的70.9%、67.9%和90.0%,是发现学生病例的主要方式;小学、中学、大学初诊病例确诊率分别为5.56%、27.3%和35.8%,差异有统计学意义（P=0.029）。结论应采取多种措施继续加强学校肺结核预防控制工作,并将工作重点放在大学生群体。     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

Class II HLA in Georgia Caucasus Tbilisi Georgians and their Mediterranean ancestry: The Usko Mediterranean languages

Georgia (or Sakartvelo in its own language) is a South Caucasus Mts. country with its easternmost part is enigmatically named Iberia, like the Iberian Peninsula, which may refer to rivers “Kura” and “Ebro” or their valleys respectively. Most of their inhabitants speak Georgian which is included within Dene-Caucasian group and Usko-Mediterranean subgroup of languages. The latter includes Basque, Berber, ancient Iberian-Tartessian, Etruscan, Hittite, Minoan Lineal A and others. In the present paper, HLA class II -DRB1 and -DQB1 alleles has been studied and extended haplotypes calculated. Most frequent haplotypes are also of Mediterranean origin (i. e.: (A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*51)-DRB1*13:01-DQB1*06:03, or (A*24-B*35)-DRB1*01:01-DQB1*05:01) and DA genetic distances show that closest world populations to Georgians are Mediterraneans. Georgians also show common extended haplotypes ((A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*13)-DRB1*07:01-DQB1*02:01 and (A*03-B*35)-DRB1*11:01-DQB1*03:01) with Svan people, a secluded population in North Georgia mountains. We can conclude that Georgians belong to a very old Mediterranean substratum according to both linguistics (Usko Mediterranean languages) and HLA genetics.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.