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与早产儿童相关的问题。

Issues relating to children born prematurely.

作者信息

Speer C P, Silverman M

机构信息

University Children's Hospital, Tübingen, Germany.

出版信息

Eur Respir J Suppl. 1998 Jul;27:13s-16s.

PMID:9699778
Abstract

Preterm infants suffer increased risk of acute and chronic respiratory disorders. In patients with chronic lung disease or severe bronchopulmonary dysplasia, long-term respiratory morbidity and pulmonary dysfunction into late childhood and early adulthood have been reported. This includes symptomatic morbidity (recurrent cough and/or wheeze) and lung function abnormalities such as increased resistance to airflow, airway hyperresponsiveness, and increased propensity to air-trapping. To date, no clinically significant association between prematurity and classical atopic asthma has been demonstrated. Therefore, interventions should primarily focus on the reduction of wheezing disorders and lung function abnormalities in children born prematurely. In order to design interventions in the foetal and early neonatal period or during childhood the potential risk factors for long-term morbidity need to be carefully identified at different age groups: factors which affect pre- and postnatal lung growth, airway inflammation, viral infections, air pollution and others. Future research issues should include well-conducted prospective follow-up programmes which will identify major risk factors in specific populations. Early intervention will provide information on disease mechanisms and on new prophylactic as well as therapeutic strategies.

摘要

早产儿患急性和慢性呼吸系统疾病的风险增加。在患有慢性肺病或严重支气管肺发育不良的患者中,已有报道称其在儿童晚期和成年早期会出现长期呼吸疾病和肺功能障碍。这包括有症状的疾病(反复咳嗽和/或喘息)以及肺功能异常,如气流阻力增加、气道高反应性和气体潴留倾向增加。迄今为止,尚未证实早产与典型特应性哮喘之间存在临床上显著的关联。因此,干预措施应主要侧重于减少早产儿童的喘息性疾病和肺功能异常。为了在胎儿期、新生儿早期或儿童期设计干预措施,需要在不同年龄组仔细识别长期发病的潜在风险因素:影响产前和产后肺生长、气道炎症、病毒感染、空气污染等因素。未来的研究问题应包括精心开展的前瞻性随访计划,以确定特定人群中的主要风险因素。早期干预将提供有关疾病机制以及新的预防和治疗策略的信息。

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Low-dose hyperoxia primes airways for fibrosis in mice after influenza A infection.低剂量高氧预处理可增强甲型流感病毒感染后小鼠气道的纤维化。
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Pulmonary mechanics and structural lung development after neonatal hyperoxia in mice.
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