空气污染与儿童哮喘

空气污染在儿童哮喘发生、发展中扮演着重要的角色,是哮喘的危险因素之一.日常生活中,空气污染物种类繁多,来源较为广泛.它们可通过各种机制和信号通路增加儿童哮喘发病风险和急性加重次数,损伤儿童肺功能,导致免疫学紊乱,增强过敏原致敏性,降低对治疗的反应性.儿童的年龄、性别、肥胖、致敏状态、抗氧化物质补充、防护措施等因素影响着污染物对机体的不良效应.尽管空气污染与儿童哮喘研究已取得一定进展,但仍有许多问题需要进一步探讨.该文就常见空气污染物对儿童哮喘的发生、发展的影响进行具体阐述.     

居室空气污染与儿童哮喘关系探讨

目的 观察室内装修后空气甲醛浓度以及室内被动吸烟与儿童哮喘的关系。方法 测量室内装修（小于5年）后居住发生哮喘儿童88例和104例健康对照儿童寝室空气甲醛浓度，并调查室内被动吸烟情况。结果 哮喘儿童居室内甲醛浓度以及被动吸烟率均高于对照组，差异有统计学意义（P均〈O．01）。结论 装饰材料中污染物甲醛及室内被动吸烟危害儿童健康，与儿童哮喘发生有关，调查结果有助于哮喘发作的预防。     

被动吸烟与儿童哮喘

被动吸烟对于儿童哮喘的发生及发展进程有着极大的负面影响.被动吸烟可导致发生儿童哮喘的风险上升.对于已经发展为哮喘的儿童,被动吸烟会影响哮喘控制,包括加重现有哮喘症状,诱发哮喘发作,降低生活质量,影响药物治疗.被动吸烟影响儿童哮喘发生及发展的机制还在进一步探索中,目前提出的相关机制主要有免疫功能异常、肺功能损害、气道高反...     

间歇与每日吸入布地奈德对轻度持续性哮喘儿童肺功能及呼出气一氧化氮的影响

目的 探讨间歇与每日吸入布地奈德对轻度持续性哮喘儿童的肺功能及呼出气一氧化氮（FeNO）的影响。方法 选择2016年1月至2018年1月就诊的6~14岁轻度持续性哮喘儿童共120例，采用分层随机法分为间歇吸入组60例（出现哮喘征兆时吸入布地奈德200?μg/d，持续6周）和每日吸入组60例（持续吸入布地奈德200?μg/d）。于治疗第3、6、9、12月进行随访，比较两组患儿基线资料、FeNO及肺功能指标的变化、激素用量、哮喘发作次数及哮喘病情控制情况。结果 两组患儿在治疗起始时，基线资料及FeNO、肺功能指标比较差异均无统计学意义（P > 0.05）。随着治疗时间的延长，两组患儿FeNO逐渐降低，肺功能指标逐渐改善（P < 0.001）。与间歇吸入组比较，每日吸入组在降低FeNO和提高1秒呼气量占预计值百分比（FEV1% pred）上具有优势（P < 0.001）。吸入方式和治疗时间对FeNO及肺功能指标的影响具有交互作用（P < 0.001），每日吸入组在治疗3个月后FeNO及肺功能指标迅速改善并趋于平稳，而间歇吸入组6个月后趋于平稳。治疗12个月后，两组患儿身高、体重增长及病情控制程度比较差异均无统计学意义（P > 0.05），间歇吸入组患儿布地奈德吸入量要明显少于每日吸入组（P < 0.05），但哮喘发作次数要多于每日吸入组（P < 0.05）。结论 间歇和每日吸入布地奈德对轻度持续性哮喘儿童能够达到相同的哮喘控制水平，且对患儿身高、体重增长均无影响；每日吸入布地奈德能够更加快速有效地降低FeNO和提高FEV1% pred；虽然间歇吸入能够减少激素用量，但有更高的哮喘发作风险。     

儿童哮喘缓解期维持临床控制的干预研究

目的探讨哮喘缓解期儿童伴发急性上呼吸道感染（AURI）时维持临床控制的干预措施。方法选取100例达到临床控制的哮喘儿童,随机分为观察组和对照组,均以最低剂量吸入性糖皮质激素和长效β2受体激动剂复合制剂（ICS/LABA）每晚吸入维持临床治疗。伴发AURI时均予常规处理;观察组除常规处理外同时给予早期短期升级治疗,即在维持治疗基础上每日早晨加吸等量ICS/LABA复合制剂,维持升级治疗7~10 d。两组急性发作时均根据其病情严重程度按哮喘指南诊治。治疗3、6、9、12个月后观察两组哮喘控制水平、哮喘急性发作严重程度、肺功能指标变化和不良事件发生情况等。结果治疗3、6、9、12个月各随访时间点,观察组哮喘控制率均在90%以上,对照组为80%左右,两组控制率比较差异有统计学意义（P < 0.05）。各随访时间点观察组哮喘急性发作严重程度明显低于对照组（P < 0.05）。与对照组相比,观察组肺功能大、小气道指标均明显改善（P < 0.05）。与对照组相比,观察组吸入糖皮质激素量以及对家庭生活的影响均明显减少（P < 0.05）。结论哮喘缓解期儿童伴发AURI时早期短期升级治疗可预防哮喘急性发作,提高哮喘控制率,改善肺功能。     

口服螨免疫疗法辅助治疗儿童哮喘疗效观察

目的　观察口服螨免疫疗法对哮喘儿童的辅助治疗作用。方法　应用螨口服脱敏液安慰剂双盲试验对２３ 例哮喘患儿进行１２ 个月的临床观察,并测定血清螨特异性ＩｇＥ（ＳＩｇＥ） 、螨皮肤变应原试验和肺功能检查。结果　服用螨脱敏液的患儿,血清螨ＳＩｇＥ在用药后６ 个月时下降并持续到１２ 个月,治疗１２ 个月时肺功能明显改善,咳嗽发作次数减少,无用药不良反应。结论　口服螨免疫疗法作为吸入激素的辅助疗法治疗螨过敏的哮喘患儿有一定效果。     

快速脱敏治疗变应性哮喘近期疗效观察

目的　观察快速脱敏疗法治疗儿童变应性哮喘的近期疗效。方法　将 45例哮喘患儿随机分为快速脱敏组 (A组 ) 2 4例和常规脱敏组 (B组 ) 2 1例 ,选用皮试阳性反应最明显的一种为脱敏变应原进行脱敏治疗。全部患儿在治疗前及治疗 6个月后进行气道反应性和肺功能测定。结果　A组总有效率为 83.33% ,B组为 46 .72 %。两组疗效比较有显著性差异 (P <0 .0 5 )。两组治疗后气道反应性和肺功能结果比较差异有显著性 (P <0 .0 5 )。结论　快速脱敏疗法治疗儿童变应性哮喘的近期疗效、气道反应性的降低和肺功能的改善均优于常规脱敏法 ,更能尽快控制哮喘发作。     

脉冲振荡法用于儿童肺功能检测

】　目的　探讨脉冲振荡法对儿童肺功能检测特别是哮喘的应用价值。方法　采用脉冲振荡法，对哮喘发作组121例、哮喘缓解组147例患儿和正常对照组217例进行肺功能测定，组间比较5 Hz时、20 Hz时的气道阻力（R     

儿童支气管哮喘过敏原测定及肺功能的变化

目的了解广州地区儿童支气管哮喘的过敏原及哮喘发作和缓解时肺功能的变化。方法应用MAST过敏原测定仪测定73例哮喘儿童的血清总IgE和35种过敏原，然后分别应用F2600型和303型肺功能促进行测定其哮喘发作和缓解时的肺功能变化。结果73例哮喘儿童中血清总IgE升高68例，占93．1％，这68例中可检出过敏原46例，占67．6％，46例中对尘螨过敏43例，占93．5％，对豚草、动物毛、蟑螂过敏3例，占6．5％。0～3a组哮喘发作时75％潮气量与最高呼气流速之比（25－PF）值为0．424±0．089，与正常预定值（0．6±0）比较显著降低．P＜0．01：而哮喘缓解时25－PF值为0．603±0.021，与正常预定值比较差异无显著性，P＞0．05。4～6a组和7a以上组哮喘发作时最大肺活量（FVC）、ls最大呼气量（FEV1）与正常预定值比较差异无显著性，P＞0．05．FEV1／FVC、FEF25％～75％与正常预定值比较差鼻有显著性，P＜0．05；而哮喘缓解时上述参数正常。结论广州地区儿童支气管哮喘与外源性过敏原密切相关．其中尘螨是诱发哮喘最主要的过敏原。肺功能仪测定哮喘儿童的肺功能变化可用来判断哮喘的严重程度，指导治疗和评价预后。     

儿童哮喘缓解期患儿小气道功能观察：附30例报告

本文对6岁以上的哮喘患儿进行了缓解期治疗,治疗后第8周检测肺功能,并设置对照组。结果表明缓解期治疗组的肺功能明显优于对照组。 资料与结果 一、临床资料1994年10月～1996年6月,我院哮喘门诊根据1987年全国小儿呼吸道疾病会议制定的支气管哮喘诊断的分型标准,确诊为哮喘急性发作的患儿,将控制了急性发作进入缓解期的6岁以上患儿随机分为治疗组及对照组,两组患儿各30例。治疗组患儿在哮喘急性发作控制后立即接受缓解期治疗,对照组未接受缓解期治疗。两组患儿     

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   

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.     

A profile of respiratory symptoms in urban and rural South Australian school children

This report describes the cross-sectional analyses of data from the first year of a longitudinal study using questionnaire and respiratory function data over a 5 year period from a sample of rural South Australian school children. The cumulative or lifetime prevalences of respiratory symptoms were estimated in 825 rural and 1261 urban school children aged between 5 and 15 years in order to determine if the prevalence rates differed between rural and urban school children. The study found the overall cumulative prevalence of asthma and/or wheezy breathing (AWB) to be 24.1% in the rural school children compared to 27.6% in the urban school children. Most children developed AWB symptoms before the age of 7 years, with 20% reporting moderately severe symptoms and 10% having more than one attack per fortnight. The cumulative prevalence of bronchitis, loose/rattly cough (BLRC) differed significantly between the rural school children (34.1%) and urban school children (47.9%). The BLRC symptoms preceded the development of AWB in many cases. Urban school children also reported a higher prevalence of atopic conditions.     

Hauttemperaturen verschiedener Körperoberflächenareale des Rumpfes bei Säuglingen

Summary In two groups of infants (3–53 weeks old) skin temperatures were controlled in different areas of the trunk—i.e.: regions of sternum, lungs, heart, liver, spleen, kidneys—at different room-temperatures (group I: 21–25°C; group II: 29–32°C). Rectal temperatures of some probands in both groups also had been controlled simultaneously. A definite change in the reaction to heat was proofed in different periods of the first year of life. In higher environmental temperatures the skin temperature was almost constant at every controll-point of the skin, even in older infants. In lower environmental temperatures the skin temperatures lowered continuously with age till 7. to 9. moth. From 10. to 12. month the lowering of skin temperature discontinued. The rectal temperatures were relatively constant in all infants. Only in infants from 7. to 12. month, whose skin temperatures were controlled in lower as well as in higher environmental temperatures, a tendency to higher rectal temperatures was proofed in warmer environmental temperatures.The significance of these results is discussed.

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Untersuchungen mit Unterstützung durch die Deutsche Forschungsgemeinschaft.     

Psychopathologie du syndrome d’Asperger et « aspérigisation » de la société contemporaine

The author has attempted here to point out, just for a start, the characteristics of Asperger syndrome from the point of view of psychopathology through a rereading of Hans Asperger's original paper (1944). This thesis merits reevaluation, if for no other reason than to fill the gaps in operational diagnostics based on the DSM. It is found by rereading that Asperger's view of the principal disturbances of autistic psychopathy include a “disturbance of natural evidence” or a “crisis of common sense”. This question of natural evidence that he evokes with regard to autistic psychopathy corresponds to W. Blankenburg's natural evidence, which constitutes a key concept for comprehending schizophrenia in the form poor-symptom (“symptomarme Schizophrenie”) that he observes in the speech of his patient Anne Rau. One can deduce from this that in terms of fundamental disturbances, Asperger syndrome and this “symptom-poor” schizophrenia overlap at the level of loss of natural evidence. It is moreover possible to classify Asperger syndrome among the disturbances of spacing in the sense meant by the evolutionary psychiatry of A. Stevens and J. Price. The author then develops our comprehension of Asperger syndrome from the point of view of the perspective proposed by the notion of resilience in people with Asperger syndrome and of the possibility for them, through these mechanisms of adaptation, to find in the organization of the personality of the “as if” type a position of relative equilibrium. They concur or overlap in the creation of crutches, of borrowed personalities secondarily legitimated by the reaction of the socius. This will end up in the production of inventions and œuvres (works). Clearly, one rarely encounters several cases that one could consider pertinently to be “successful” Asperger syndrome. Finally, the author notes that one can find a sort of isomorphism between Asperger syndrome and contemporary society when he proposes the term “asperigisation” to characterize our society, given that the equilibrium between emotion and logic is strongly disturbed in these patients, in whom logic undergoes hypertrophy while emotion is impoverished. From this perspective, the author hopes to suggest reasons for the increase in the number of cases of Asperger syndrome in the clinical setting and in society in general in our contemporary era.     

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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     

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.     

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.