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Differing associations of bmi and body fat with asthma and lung function in children.

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Differing associations of bmi and body fat with asthma and lung function in children.

Pediatr Pulmonol. 2013 Oct 25;

Authors: Wang R, Custovic A, Simpson A, Belgrave DC, Lowe LA, Murray CS

Abstract
BACKGROUND: Current evidence suggests that in children there is a significant, albeit weak, association between asthma and obesity. Studies generally use body mass index (BMI) in evaluating body adiposity, but there are limitations to its use.
METHOD: Children from a population-based study attending follow-up (age 11 years) were weighed, measured and had percent body (PBF) and truncal (PTF) fat assessed using bioelectrical impedance. They were skin prick tested and completed spirometry. Parents completed a validated respiratory questionnaire. Children were defined as normal or overweight according to BMI and PBF cut-offs. We tested the association between these adiposity markers with wheeze, asthma, atopy, and lung-function.
RESULTS: Six hundred forty-six children (339 male) completed follow-up. BMI z-score, PBF, and PTF were all positively associated with current wheeze (odds ratio [95% CI]: 1.27 [1.03, 1.57], P = 0.03; 1.05 [1.00, 1.09], P = 0.03; 1.04 [1.00, 1.08], P = 0.04, respectively). Similar trends were seen with asthma. However, when examining girls and boys separately, significant positive associations were found with PBF and PTF and asthma but only in girls (gender interaction P = 0.06 and 0.04, respectively). Associations between being overweight and wheezing and asthma were stronger when overweight was defined by PBF (P = 0.007, 0.03) than BMI (P > 0.05). Higher BMI was significantly associated with an increase in FEV1 and FVC, but only in girls. Conversely, increasing body fat (PBF and PTF) was associated with reduced FEV1 and FVC, but only in boys. No associations between adiposity and atopy were found.
CONCLUSION: All adiposity measures were associated with wheeze, asthma, and lung function. However, BMI and PBF did not have the same effects and girls and boys appear to be affected differently. Pediatr Pulmonol. © 2013 Wiley Periodicals, Inc.

PMID: 24166845 [PubMed - as supplied by publisher]

Think twice: Misleading food-induced respiratory symptoms in children with food allergy.

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Think twice: Misleading food-induced respiratory symptoms in children with food allergy.

Pediatr Pulmonol. 2013 Oct 25;

Authors: Ahrens B, Mehl A, Lau S, Kroh L, Magdorf K, Wahn U, Beyer K, Niggemann B

Abstract
Reported food-related symptoms of patients may sometimes be misleading. A correct delineation of food-induced symptoms is often difficult and various differential diagnoses have to be considered. We report on two cases of food-induced, predominantly respiratory symptoms (in one case life-threatening) in children with food allergy. First, a two-year-old boy with no history of allergies and suspected foreign body aspiration which was finally diagnosed as an anaphylactic reaction to fish, and secondly a six-year-old girl with multiple food allergies and allergic asthma who during an electively performed oral food challenge developed severe respiratory distress, drop in blood pressure, and asphyxia not due to an anaphylactic reaction but due to choking on an unnoticed sweet. These two cases represent challenging, life-threatening symptom constellations involving food-induced reactions in food allergic children, reminding us to question first impressions. Pediatr Pulmonol. 2013 9999:XX-XX. © 2013 Wiley Periodicals, Inc.

PMID: 24167079 [PubMed - as supplied by publisher]

Personalizing and targeting therapy for COPD - the role of molecular and clinical biomarkers.

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Personalizing and targeting therapy for COPD - the role of molecular and clinical biomarkers.

Expert Rev Respir Med. 2013 Oct 28;

Authors: Goh F, Shaw JG, Savarimuthu Francis SM, Vaughan A, Morrison L, Relan V, Marshall HM, Dent AG, O'Hare PE, Hsiao A, Bowman RV, Fong KM, Yang IA

Abstract
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by persistent airflow limitation. It is the third leading cause of death worldwide, and there are currently no curative strategies for this disease. Many factors contribute to COPD susceptibility, progression and exacerbations. These include cigarette smoking, environmental and occupational pollutants, respiratory infections and comorbidities. As the clinical phenotypes of COPD are so variable, it has been difficult to devise an individualized treatment plan for patients with this complex chronic disease. This review will highlight how potential clinical, inflammatory, genomic and epigenomic biomarkers for COPD could be used to personalize treatment, leading to improved disease management and prevention for our patients.

PMID: 24160750 [PubMed - as supplied by publisher]

Effectiveness of the influenza vaccine at preventing hospitalization due to acute exacerbation of cardiopulmonary disease in Korea from 2011 to 2012.

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There is a lack of targeted studies to validate the effectiveness of influenza vaccination on the reduction in influenza-related hospitalizations among patients with co-morbidities. In this study, we estimate the effectiveness of influenza vaccination on preventing hospitalizations in persons with cardiopulmonary disease and establish an evidence base for recommendations on influenza vaccination in this population.

During the influenza epidemic in 2011-2012, we performed a multicenter, retrospective case-control study. Cases were patients hospitalized due to acute exacerbation of asthma, COPD, ischemic heart disease (IHD), and congestive heart failure (CHF). Controls were selected from outpatients who visited study hospitals but who were not hospitalized. Cases and controls were matched 1:1 based on age, gender, and date of hospital visit. Conditional logistic regression analyses were used to determine the effectiveness of vaccination.

Between 25 December 2011 and 5 May 2012, 828 of each hospitalized and control subjects were identified. The influenza vaccination rate of the hospitalized and non-hospitalized patients was 54.2% and 60.4%, respectively (P = 0.006). The overall vaccine effectiveness for preventing hospitalization was 33.7% [95% confidence interval (CI) 14.0-49.0%; P = 0.002]. Conditional logistic regression analysis showed that influenza vaccination significantly reduced the risk of hospitalization, especially due to acute exacerbation of IHD and CHF, in patients aged 65 y and older. The estimated vaccine effectiveness in these patients was 56.0% (95% CI 32.1-71.4%, P = 0.002).

Influenza vaccination was associated with a reduction in the risk of hospitalization due to acute exacerbation of cardiopulmonary disease. We recommend the vaccine be given primarily to patients with underlying cardiovascular disease, particularly those 65 y of age and older.

Genetic susceptibility to lung cancer and co-morbidities.

Lung cancer is a leading cause of cancer death and disease burden in many countries. Understanding of the biological pathways involved in lung cancer aetiology is required to identify key biomolecules that could be of significant clinical value, either as predictive, prognostic or diagnostic markers, or as targets for the development of novel therapies to treat this disease, in addition to smoking avoidance strategies.

Genome-wide association studies (GWAS) have enabled significant progress in the past 5 years in investigating genetic susceptibility to lung cancer. Large scale, multi-cohort GWAS of mainly Caucasian, smoking, populations have identified strong associations for lung cancer mapped to chromosomal regions 15q [nicotinic acetylcholine receptor (nAChR) subunits: CHRNA3, CHRNA5], 5p (TERT-CLPTM1L locus) and 6p (BAT3-MSH5). Some studies in Asian populations of smokers have found similar risk loci, whereas GWAS in never smoking Asian females have identified associations in other chromosomal regions, e.g., 3q (TP63), that are distinct from smoking-related lung cancer risk loci. GWAS of smoking behaviour have identified risk loci for smoking quantity at 15q (similar genes to lung cancer susceptibility: CHRNA3, CHRNA5) and 19q (CYP2A6). Other genes have been mapped for smoking initiation and smoking cessation. In chronic obstructive pulmonary disease (COPD), which is a known risk factor for lung cancer, GWAS in large cohorts have also found CHRNA3 and CHRNA5 single nucleotide polymorphisms (SNPs) mapping at 15q as risk loci, as well as other regions at 4q31 (HHIP), 4q24 (FAM13A) and 5q (HTR4). The overlap in risk loci between lung cancer, smoking behaviour and COPD may be due to the effects of nicotine addiction; however, more work needs to be undertaken to explore the potential direct effects of nicotine and its metabolites in gene-environment interaction in these phenotypes.

Goals of future genetic susceptibility studies of lung cancer should focus on refining the strongest risk loci in a wide range of populations with lung cancer, and integrating other clinical and biomarker information, in order to achieve the aim of personalised therapy for lung cancer.

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