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Published on: April 13, 2010
Characteristics of asthma and airway hyper-responsiveness after premature birth
Thomas Halvorsen1, Britt Torunn Skadberg, Geir Egil Eide
1Department of Clinical Medicine, Section of Pediatrics, University of Bergen, Bergen, Norway. thomas.halvorsen@pedi.uib.no
Insights
Children born extremely prematurely often develop asthma-like symptoms and airway hyper-responsiveness (AHR). These conditions in pre-term infants are linked to neonatal factors, not typical asthma triggers like allergies.
Area of Science:
- Pediatric Pulmonology
- Neonatology
- Allergy and Immunology
Background:
- Premature birth and bronchopulmonary dysplasia (BPD) are associated with asthma-like symptoms and airway hyper-responsiveness (AHR) in children.
- Mechanisms underlying these respiratory issues in pre-term infants are not well understood.
- Typical childhood asthma is linked to genetics, allergies, inflammation, and smoking.
Purpose of the Study:
- To investigate the factors associated with current asthma and AHR in extremely pre-term children.
- To compare these factors with those in a matched term-born control population.
- To explore the relationship between neonatal respiratory morbidity and asthma/AHR in pre-term infants.
Main Methods:
- A population-based cohort study of 81 extremely pre-term infants (gestational age ≤28 wk or birth weight ≤1000 g) and matched term-born controls.
- Assessment of current asthma and AHR at follow-up.
- Analysis of factors including inheritance, allergy, airway inflammation, smoking, and neonatal respiratory morbidity (e.g., BPD, oxygen requirement).
- Measurement of urinary leukotriene metabolite E4 (U-LTE4) and forced expiratory volume in the first second (FEV1).
Main Results:
- Pre-term children had higher rates of asthma and significantly increased AHR compared to controls.
- Pre-term infants showed reduced FEV1 and elevated U-LTE4 levels.
- In controls, asthma and AHR were linked to typical factors (genetics, allergy, inflammation, smoking).
- In pre-terms, asthma and AHR were less related to these typical factors.
- Neonatal history of BPD and prolonged oxygen treatment strongly correlated with AHR in pre-term infants.
Conclusions:
- Asthma and AHR in extremely pre-term children present differently from typical childhood asthma.
- Neonatal variables, particularly BPD and oxygen dependency, are key determinants of AHR in this population.
- These respiratory manifestations in pre-term infants may represent a distinct clinical entity.
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 < or = 28 wk or birth weight < or = 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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