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Preterm birth, infant weight gain, and childhood asthma risk: A meta-analysis of 147,000 European children

Background: Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results.Objectives: We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years).Methods: First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age <37 weeks) and low birth weight (<2500 g) with childhood asthma outcomes.Results: Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P < .05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27).Conclusion: Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.

Common variable immunodeficiency is associated with a functional deficiency of invariant natural killer T cells

Background: Common variable immunodeficiency (CVID) is the commonest symptomatic primary antibody disorder, with monogenic causes identified in less than 10% of all cases. X-linked proliferative disease is a monogenic disorder that is associated with hypogammaglobulinemia and characterized by a deficiency of invariant NKT (iNKT) cells. We sought to evaluate whether a defect in iNKT cell number or function was associated with CVID.Objective: An evaluation of the function and number of iNKT cells in CVID.Methods: Six-color flow cytometry enumerated iNKT cells in 36 patients with CVID and 50 healthy controls. Their proliferative capacity and cytokine production (IFN-γ, IL-13, IL-17) was then investigated following activation with CD1d ligand alpha-galactosylceramide.Results: A reduction in the number of iNKT cells (31 iNKT cells/105 T cells) in patients with CVID compared with healthy controls (100 iNKT cells/105 T cells) was observed (P < .0001). Two cohorts could be discerned within the CVID group: group 1 with an abnormal number of iNKT cells (n = 28) and group 2 with a normal number of iNKT cells (n = 8). This segregation coassociated with the proliferative capacity of iNKT cells between the 2 groups. However, differences in the function of iNKT cells were noted in group 2, in which an increase in IFN-γ (P = .0016) and a decrease in IL-17 (P = .0002) production was observed between patients with CVID and controls. Finally, a significant association was seen between the number of iNKT cells and the percentage of class-switched memory B cells and propensity to lymphoproliferation (P = .002) in patients with CVID.Conclusion: iNKT cells are deficient and/or functionally impaired in most of the patients with CVID.

Integrating longitudinal information on pulmonary function and inflammation using asthma phenotypes

Unsupervised clustering approaches have recently provided a better understanding of asthma syndrome. Several studies have consistently identified new asthma phenotypes such as benign asthma, early-onset atopic asthma, and obese noneosinophilic asthma. Moore et al and others identified a neutrophilic-predominant phenotype with fixed severe airflow obstruction. Late-onset eosinophilic asthma with few symptoms was identified by 2 research groups as an emerging phenotype. However, analyses on biomarkers and longitudinal information of these phenotypes are limited. We aimed to determine whether longitudinal information on pulmonary function and inflammation was associated with distinct asthma phenotypes.

Obesity in asthma: Location or hormonal consequences?

Obesity has reached epidemic proportions worldwide. In US children and adolescents aged 2 to 19 years, the prevalence of obesity, as defined by a body mass index (BMI) of the 95th percentile or greater of the BMI-for-age/sex standard US Centers for Disease Control and Prevention charts, increased to 16.9% in 2010. Obesity has been linked to the development of cardiometabolic diseases (ie, atherosclerosis, dyslipidemia, hypertension, and type 2 diabetes). In addition, numerous studies in adults and children have demonstrated a strong positive relationship between obesity and asthma. Prospective studies have shown that obesity predates asthma and that the relative risk of asthma increases with increasing BMI. These studies demonstrated causality and dissociate the notion that the more sedentary lifestyle of asthmatic patients caused by their increased respiratory symptoms with exercise led to obesity. Obese asthmatic patients are reported to have a 5-fold higher risk of hospitalization compared with nonobese asthmatic patients, and obesity leads to 250,000 new cases of asthma per year in the United States. Another consequence of obesity is that obese asthmatic patients are less responsive to inhaled corticosteroids.

Classification of childhood asthma phenotypes and long-term clinical responses to inhaled anti-inflammatory medications

Background: Although recent studies have identified the presence of phenotypic clusters in asthmatic patients, the clinical significance and temporal stability of these clusters have not been explored.Objective: Our aim was to examine the clinical relevance and temporal stability of phenotypic clusters in children with asthma.Methods: We applied spectral clustering to clinical data from 1041 children with asthma participating in the Childhood Asthma Management Program. Posttreatment randomization follow-up data collected over 48 months were used to determine the effect of these clusters on pulmonary function and treatment response to inhaled anti-inflammatory medication.Results: We found 5 reproducible patient clusters that could be differentiated on the basis of 3 groups of features: atopic burden, degree of airway obstruction, and history of exacerbation. Cluster grouping predicted long-term asthma control, as measured by the need for oral prednisone (P < .0001) or additional controller medications (P = .001), as well as longitudinal differences in pulmonary function (P < .0001). We also found that the 2 clusters with the highest rates of exacerbation had different responses to inhaled corticosteroids when compared with the other clusters. One cluster demonstrated a positive response to both budesonide (P = .02) and nedocromil (P = .01) compared with placebo, whereas the other cluster demonstrated minimal responses to both budesonide (P = .12) and nedocromil (P = .56) compared with placebo.Conclusion: Phenotypic clustering can be used to identify longitudinally consistent and clinically relevant patient subgroups, with implications for targeted therapeutic strategies and clinical trials design.

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