Characteristics of asthma and airway hyper-responsiveness after premature birth

Authors

  • Thomas Halvorsen,

    1. Department of Clinical Medicine, Section of Pediatrics, University of Bergen, Bergen, Norway
    2. Department of Pediatrics, Haukeland University Hospital, Bergen, Norway
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  • Britt Torunn Skadberg,

    1. Department of Clinical Medicine, Section of Pediatrics, University of Bergen, Bergen, Norway
    2. Department of Pediatrics, Haukeland University Hospital, Bergen, Norway
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  • Geir Egil Eide,

    1. Department of Public Health and Primary Health Care, Centre for Clinical Research, Haukeland University Hospital and Section for Epidemiology and Medical Statistics, University of Bergen, Bergen, Norway
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  • Ola Røksund,

    1. Department of Pediatrics, Haukeland University Hospital, Bergen, Norway
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  • Lage Aksnes,

    1. Department of Clinical Medicine, Section of Pediatrics, University of Bergen, Bergen, Norway
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  • Knut Øymar

    1. Department of Clinical Medicine, Section of Pediatrics, University of Bergen, Bergen, Norway
    2. Department of Pediatrics, Stavanger University Hospital, Stavanger, Norway
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Thomas Halvorsen, Department of Pediatrics, Haukeland University Hospital, N-5021 Bergen, Norway
Tel.: +47 5597 5200
Fax: +47 5597 5147
E-mail: thomas.halvorsen@pedi.uib.no

Abstract

Asthma-like symptoms and airway hyper-responsiveness (AHR) are frequently reported in children subsequent to premature birth and bronchopulmonary dysplasia (BPD). There is limited knowledge on the mechanisms underlying these respiratory manifestations. Generally, childhood asthma and AHR is described within a context of inheritance, allergy and eosinophilic airway inflammation, and often in relation to cigarette exposures. We investigated these factors in relation to current asthma and AHR in a population-based cohort of 81 young people, born with gestational age ≤28 wk or birth weight ≤1000 g, and in a matched term-born control population. In the pre-term population, asthma and AHR were additionally studied in relation to neonatal respiratory morbidity. At follow up, more pre-term than control subjects had asthma. Forced expiratory volume in first second (FEV1) was reduced, AHR was substantially increased, and the level of the urinary leukotriene metabolite E4 (U-LTE4) was increased in the pre-term population compared to the term-born. In control subjects, asthma and AHR was associated with a pattern consistent with inheritance, allergy, airway inflammation, and cigarette exposures. In the pre-terms, asthma and AHR was either unrelated or less related to these factors. Instead, AHR was strongly related to a neonatal history of BPD and prolonged requirement for oxygen treatment. In conclusion, asthma and AHR subsequent to extremely premature birth differed from typical childhood asthma with respect to important features, and AHR was best explained by neonatal variables. These respiratory manifestations thus seem to represent a separate clinical entity.

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