Airway responsiveness in low birthweight children and their mothers.

Chan, K N; Noble-Jamieson, C M; Elliman, Anthony D.; Bryan, Elizabeth; Aber, V. R.; Silverman, M

doi:10.1136/adc.63.8.905

Cited by 59 publications

(24 citation statements)

References 9 publications

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“…There were no differences in the gestational and postnatal age, birth weight, and height and weight at followup, between the CLD and control infants. Family history of atopy was equally common in the CLD and control infants, a finding similar to CHAN et al [23], (1988), but one which differs from NICKERSON et al [24], (1980).…”

Section: Discussionsupporting

confidence: 73%

Cysteinyl leukotriene involvement in chronic lung disease in premature infants

Cook

Yüksel²,

Sampson³

et al. 1996

Eur Respir J

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C Cy ys st te ei in ny yl l l le eu uk ko ot tr ri ie en ne e i in nv vo ol lv ve em me en nt t i in n c ch hr ro on ni ic c l lu un ng g d di is se ea as se e i in n p pr re em ma at tu ur re e i in nf fa an nt ts s A.J. Cook*, B. Yuksel*, A.P. Sampson**, A. Greenough*, J.F. Price* Cysteinyl leukotriene involvement in chronic lung disease in premature infants. A.J. Cook, B. Yuksel, A.P. Sampson, A. Greenough, J.F. Price. ERS Journals Ltd 1996. ABSTRACT: The pathophysiology of chronic lung disease (CLD) in premature infants who require mechanical ventilation and prolonged oxygen supplementation has been well-described but the underlying mechanisms are not understood. Our aim was to test the hypothesis that excess cysteinyl leukotriene (LT) production was a contributing factor in CLD. We compared LT production and lung function, at 7 months of age, in nine premature infants with CLD and in eight control infants without CLD. None of the control infants developed any neonatal respiratory problems, but two subsequently required bronchodilator therapy. Respiratory function was assessed by the measurement of thoracic gas volume (TGV), airways resistance (Raw) and functional residual capacity (FRC). Total cysteinyl LT production was quantified by measurement of leukotriene E 4 (LTE 4 ) in a spot urine sample.Although all patients were asymptomatic at follow-up, there was evidence of significant lung function abnormalities in infants with CLD. The CLD infants had significantly elevated TGV, Raw and FRC values reflecting airway obstruction when compared to the controls. Urinary LTE 4 levels were significantly higher in the CLD infants when compared to the controls (geometric mean: 741 and 337 pmol·mmol -1 creatinine, respectively). There was no direct correlation between urinary LTE 4 levels in the CLD group and TGV, Raw or FRC values.Although this study is small and a direct correlation between lung function and urinary leukotriene E 4 was not demonstrated, pathological lung function and an enhanced urinary leukotriene E 4 production in infants with chronic lung disease would tend to suggest that the cysteinyl leukotrienes were involved in the sequelae of this disease. Eur Respir J., 1996Respir J., , 9, 1907Respir J., -1912 Many of the pathological features of neonatal chronic lung disease (CLD) have been attributed to the pulmonary effects of mechanical ventilation and prolonged supplementary oxygen [1]. Infants developing CLD subsequently have repeated respiratory infections and wheezing attacks, and an increased rate of hospital admission [2]. Impairment of lung function, as evidenced by reduced dynamic compliance, airway hyperreactivity, increased airway resistance and hyperinflation, has also been described [1,[3][4][5][6][7]. These abnormalities are evident in the first few years of life [3][4][5], and may persist throughout childhood [6,7].Several mechanisms have been implicated in the pathogenesis of CLD. These include an imbalance of protease/antiprotease production [8], increased lipid mediator (platelet-a...

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Section: Discussionsupporting

confidence: 73%

Cysteinyl leukotriene involvement in chronic lung disease in premature infants

Cook

Yüksel²,

Sampson³

et al. 1996

Eur Respir J

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“…BERTRAND et al [94] initially suggested this mechanism after finding evidence of airway hyperreactivity in the mothers of premature infants, but this was not confirmed by another group examining airway responsiveness in mothers of premature or low birth weight children [95]. At least one study has suggested an additional risk of prolonged pregnancy in asthmatic females, which could not be explained by this same mechanism [15].…”

Section: Summary: Effect Of Asthma On Pregnancymentioning

confidence: 99%

Asthma during pregnancy: mechanisms and treatment implications

Murphy

Gibson²,

Smith³

et al. 2005

Eur Respir J

159

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Asthma is becoming increasingly prevalent worldwide. Numerous historical and prospective cohort studies have investigated the effects of maternal asthma on pregnancy outcome; however, the data has been conflicting and many studies have not used standard classifications for asthma severity. Overall, the literature suggests that asthmatic females are more at risk of low birth weight neonates, pre-term delivery and complications such as preeclampsia, especially in the absence of actively managed asthma treated with inhaled corticosteroids. Pregnancy with a female foetus may particularly increase the risk of these outcomes.In addition, pregnancy has an effect on the course of asthma. The risk of an exacerbation requiring medical intervention may be as high as 50% in females with severe asthma and this may further increase the risk of poor outcomes, particularly low birth weight and pre-term delivery.The mechanisms responsible for changes in asthma with pregnancy, or alterations in pregnancy outcomes due to asthma have not been thoroughly explored. Maternal inflammatory pathways may contribute to reduced foetal growth through alterations in placental function.Asthma treatment, by reducing maternal inflammation and preventing exacerbations, is safe for use in pregnant females and contributes to improved outcomes for both mother and foetus.

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“…Details are described elsewhere. 16 In order to examine the association between long term symptomatology and the level of neonatal intensive treatment, an oxygen score that reflected both the duration and intensity of treatment in the neonatal period was computed. This was derived by allocating one point for each hour of oxygen treatment with an inspired oxygen concentration between 22% and 40%, two points for each hour between 41 and 60%, three points for each hour between 61 and 80%, and four points for each hour between 81 and 100%.…”

Section: Protocolmentioning

confidence: 99%