Obesity and asthma

Obesity and asthma

Oral Presentations / Paediatric Respiratory Reviews 14S2 (2013) S1–S53 [7] Sudfeld CR, Dasenbrook EC, Merz WG, et al. Prevalence and risk factors for...

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Oral Presentations / Paediatric Respiratory Reviews 14S2 (2013) S1–S53

[7] Sudfeld CR, Dasenbrook EC, Merz WG, et al. Prevalence and risk factors for recovery of filamentous fungi in individualsnwith cystic fibrosis. Journal of Cystic Fibrosis 2010; 9: 110–116. [8] Elborn JS. Identification and management of unusual pathogens in cystic fibrosis. J R Soc Med 2008; 101: 2–5. [9] Nagano Y, Millar BC, Johnson E, et al. Fungal infections in patients with cystic fibrosis. Rev Med Micro 2007; 18: 11–16. [10] Tomee JF, Wierenga AT, Hiemstra PS, Kauffman HK. Proteases from Aspergillus fumigatus induce release of proinflammatory cytokines and cell detachment in airway epithelial cell lines. J Infect Dis 1997; 176: 300–303. [11] Bakare N, Rickerts V, Bargon J, et al. Prevalence of Aspergillus fumigatus and other fungal species in the sputum of adult patients with cystic fibrosis. Mycoses 2003; 46: 19–23. [12] Amin R, Dupuis A, Aaron SD, Ratjen F. The effect of chronic infection with Aspergillus fumigatus on lung function and hospitalization in cystic fibrosis patients. Chest. 2010; 137: 171–176. [13] de Vrankrijker AM, van der Ent CK, van Berkhout FT, et al. Aspergillus fumigatus colonization in cystic fibrosis: implications for lung function?. Clin Microbiol Infect. 2011; 17: 1381–1386. [14] Aaron SD, Vandemheen KL, Freitag A et al. Treatment of Aspergillus fumigatus in patients with cystic fibrosis: a randomized, placebocontrolled pilot study. PLoS One. 2012; 7(4): e36077. doi: 10.1371/journal.pone.0036077. Epub 2012 Apr 30. [15] Stevens DA, Moss RB, Kurup VP, et al. Allergic bronchopulmonary aspergillosis in cystic fibrosis – state of the art: Cystic Fibrosis Foundation Consensus Conference. Clin Infect Dis. 2003; 37 Suppl 3:S225–264. [16] Cohen-Cymberknoh M, Blau H, Shoseyov D et al. Intravenous monthly pulse methylprednisolone treatment for ABPA in patients with cystic fibrosis. J Cyst Fibros. 2009; 8: 253–257. [17] Shoseyov D, Brownlee KG, Conway SP, Kerem E. Chest. 2006; 130: 222– 226. [18] Persistence of Candida species in the respiratory tract of cystic fibrosis patients. Medical Mycology 2010; 48: 56–63. [19] Chotirmall SH, O’Donoghue E, Bennett K et al. Sputum Candida albicans presages FEV1 decline and hospital-treated exacerbations in cystic fibrosis. Chest. 2010; 138: 1186–1195.

IIO-11 Obesity and asthma J.A. Castro-Rodriguez. Pulmonology Unit, Departments of Pediatrics, School of Medicine, Pontificia Universidad Cat´ olica de Chile, Santiago, Chile Correspondence: Jose A. Castro-Rodriguez, MD, PhD, Lira 44, 1er. Piso, casilla 114-D, Santiago, Chile. Tel.: (56) 2 354 8189, fax: (56) 2 354 8122. E-mail address: [email protected] (J.A. Castro-Rodriguez). Keywords: obesity, asthma, phenotype, risk factor

Obesity as a risk factor for asthma: Asthma, overweight and obesity are the most common chronic morbidities in childhood from economically developed regions (and now in some middle developed countries) affecting up one in six and one in five children respectively [1,2]. And their prevalence is both increasing worldwide. Given that a rise in prevalence of obesity and asthma has paralleled westernization or urbanization (characterized by air pollution, environmental tobacco smoke, smaller family size, day care assistance, decreased exposure to infectious agents, and undesirable dietary or other lifestyle changes), it is also plausible that shared environmental factors are common to the rise of conditions in childhood [3]. Overweight and obesity is higher in children with asthma compared with general population [4]. Body mass index (BMI) is a practical and widely used measure of weight status in children and adults, although BMI may not be the ideal or the only measure to assess the influence of a high body weight on respiratory health. Indeed, a study showed that only central obesity, but not BMI, increases asthma risk in children [5]. The link between obesity and asthma is stronger in non-allergic asthma [3]. A recent study showed higher prevalence of non-eosinophilic asthma in female obese asthmatics compared to males [6]. A review confirmed the absence of atopy

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and bronchial hyperreactivity to methacholine in the association between asthma and obesity/overweight [7]. There are mixed results about the importance of gender in this relationship; however a tendency of females in the relation was more common [3]. Two recent analyses of large cohort reported that increased BMI and/or adiposity in children were associated with increased asthma symptoms, asthma exacerbations and emergency department presentation [8,9]. A prospective study showed decreased in inhaled corticosteroids efficacy in obese asthmatic children, suggesting steroid insensitivity may be present in children with a higher BMI [10]. Therefore, pharmacogenetic and randomized studies need to be done in order to know which will be the best controllers for obese asthmatic children. A recent study showed that dietinduced weight loss can achieve significant improvements in clinical outcomes for obese children with asthma. Hypertriglyceridemia and insulin resistance were positive associate with asthma, independent of BMI [11,12]. Adolescent males who were obese and also had mild persistent asthma had a significantly higher prevalence of metabolic syndrome than obese males without asthma [13]. Obesity as a risk factor for developing new asthma: Camargo et al. [14] carried out one of the first longitudinal studies in adults, showing that women who gained weight after 18 years of age ran a greater risk of developing asthma (incidence) in the next 4 years, regardless of caloric intake or physical activity. CastroRodriguez et al. [15], in the first longitudinal study of a pediatric population, showed that girls, but not boys, who became obese or overweight between 6 and 11 years of age ran a 7-fold greater risk of developing asthma (incidence) than those who maintained normal nutrition and growth, regardless of physical activity or allergic condition. Furthermore, the bronchodilatory reactivity (FEV1 ) and PEF variability were greater in obese and overweight girls compared to girls with proper nutrition. These findings led the authors to suggest that there may be an anomaly in the regulation of bronchial tone in females [15]. Even more, the prevalence of asthma was greater among obese girls with early menarche (before 11 years of age) than among those with a later menarche. This would indicate that obesity alters the production (or peripheral sensitivity) of the hormones associated with puberty in girls and that increased production of female hormones (or their sensitivity) alters lung development and regulation of airway tone in puberty-age girls (by enhancing bronchodilator reactivity) [15]. This association between obesity and asthma among women with early menarche was confirmed in independent studies in Mexico [16] and France [17]. It has also been reported that the use of exogenous estrogens is a risk factor for a higher incidence of asthma in women [18]. The mechanism by which estrogens cause increased airway responsiveness in asthma is still unknown, but in clinical practice cases of women with severe and refractory asthma associated with morbid obesity are not uncommon. Curiously, female sex is also associated with greater severity of irreversible airflow obstruction or chronic obstructive pulmonary disease. However, it is unknown whether resistance to inhaled corticosteroids in cases of severe asthma is associated with the metabolic effects of asthma, increased inflammation, or estrogenic effects. Therefore, we proposed a new phenotype of asthma: girls with early menarche before 11 yr who become obese during puberty, non-allergic, with high PEF variability and no hyperreactivity to methacholine [19]. Funding: none Competing Interest: None to declare. References [1] Lobstein T, Baur L, Uauy R; IASO International Obesity TaskForce. Obesity in children and young people: a crisis in public health. Obes Rev. 2004; 5 Suppl 1:4–104.

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[2] Masoli M, Fabian D, Holt S, Beasley R; Global Initiative for Asthma (GINA) Program. The global burden of asthma: executive summary of the GINA Dissemination Committee report. Allergy. 2004; 59: 469–78. [3] Papoutsakis C, Priftis KN, Drakouli M, Prifti S, Konstantaki E, Chondronikola M, Antonogeorgos G, Matziou V. Childhood overweight/obesity and asthma: is there a link? A systematic review of recent epidemiologic evidence. J Acad Nutr Diet. 2013; 113: 77–105. [4] Jensen ME, Wood LG, Gibson PG. Obesity and childhood asthma – mechanisms and manifestations. Curr Opin Allergy Clin Immunol. 2012; 12: 186–92. [5] Musaad SM, Patterson T, Ericksen M, Lindsey M, Dietrich K, Succop P, Khurana Hershey GK. Comparison of anthropometric measures of obesity in childhood allergic asthma: central obesity is most relevant. J Allergy Clin Immunol. 2009; 123: 1321–7. [6] Jensen ME, Gibson PG, Collins CE, Wood LG. Airway and systemic inflammation in obese children with asthma. Eur Respir J. 2013 Jan 24. [Epub ahead of print] PubMed PMID: 23349447. [7] Matricardi PM, Gruber ¨ C, Wahn U, Lau S. The asthma-obesity link in childhood: open questions, complex evidence, a few answers only. Clin Exp Allergy. 2007; 37: 476–84. [8] Kattan M, Kumar R, Bloomberg GR, Mitchell HE, Calatroni A, Gergen PJ, Kercsmar CM, Visness CM, Matsui EC, Steinbach SF, Szefler SJ, Sorkness CA, Morgan WJ, Teach SJ, Gan VN. Asthma control, adiposity, and adipokines among inner-city adolescents. J Allergy Clin Immunol. 2010; 125: 584–92. [9] Visness CM, London SJ, Daniels JL, Kaufman JS, Yeatts KB, Siega-Riz AM, Calatroni A, Zeldin DC. Association of childhood obesity with atopic and nonatopic asthma: results from the National Health and Nutrition ExaminationSurvey 1999–2006. J Asthma. 2010; 47: 822–9. [10] Forno E, Lescher R, Strunk R, Weiss S, Fuhlbrigge A, Celedon ´ JC; Childhood Asthma Management Program Research Group. Decreased response to inhaled steroids in overweight and obese asthmatic children. J Allergy Clin Immunol. 2011 Mar; 127:741–9. [11] Cottrell L, Neal WA, Ice C, Perez MK, Piedimonte G. Metabolic abnormalities in children with asthma. Am J Respir Crit Care Med. 2011; 183: 441–8. [12] Arshi M, Cardinal J, Hill RJ, Davies PS, Wainwright C. Asthma and insulin resistance in children. Respirology. 2010; 15: 779–84. [13] Del-Rio-Navarro BE, Castro-Rodriguez JA, Garibay Nieto N, Berber A, Toussaint G, Sienra-Monge JJ, Romieu I. Higher metabolic syndrome in obese asthmatic compared to obese nonasthmatic adolescent males. J Asthma. 2010; 47: 501–6. [14] Camargo CA Jr, Weiss ST, Zhang S, Willett WC, Speizer FE. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med. 1999; 159: 2582–8. [15] Castro-Rodriguez JA, Holberg CJ, Morgan WJ, Wright AL, Martinez FD. Increased incidence of asthmalike symptoms in girls who become overweight or obese during the school years. Am J Respir Crit Care Med. 2001; 163: 1344–9. [16] Herrera-Trujillo M, Barraza-Villarreal A, Lazcano-Ponce E, Hernandez ´ B, San´ın LH, Romieu I. Current wheezing, puberty, and obesity among Mexican adolescent females and young women. J Asthma. 2005; 42: 705–9. [17] Varraso R, Siroux V, Maccario J, Pin I, Kauffmann F. Asthma severity is associated with body mass index and early menarche in women. Am J Respir Crit Care Med. 2005; 171: 334–9. [18] Troisi RJ, Speizer FE, Willett WC, Trichopoulos D, Rosner B.Menopause, postmenopausal estrogen preparations, and the risk of adult-onset asthma. A prospective cohort study. Am J Respir Crit Care Med. 1995; 152: 1183–8. [19] Castro-Rodriguez JA. The relation between obesity and asthma. Arch Bronconeumol. 2007; 43: 171–75.

IIO-12 Vitamin D, bronchiolitis and asthma L. Bont. Pediatric Immunology and Infectious Diseases, University Medical Center Utrecht, Utrecht, The Netherlands The vitamin D receptor is a transcription factor expressed in most tissues. It is activated by vitamin D and regulates many metabolic pathways in the cell. In general, vitamin D inhibits cellular processes in which it is involved. Vitamin D is obtained through diet and produced upon sunlight exposure. There is

increasing appreciation that vitamin D contributes to healthy lung development. Epidemiological data show that vitamin D deficiency in utero or at very early age is associated with many acute and chronic diseases, including the risk of viral bronchiolitis. Several genetic studies have confirmed an association between a functional vitamin D receptor genetic polymorphism and the risk of severe bronchiolitis. The precise mechanisms by which vitamin D protects against severe viral bronchiolitis are not completely understood. In vitro studies show that vitamin D attenuates the host immune response without affecting viral clearance. Low vitamin D levels at early age predict asthma development and low vitamin D levels in asthmatic children are associated with more exacerbations, more use of medication and lower lung function. Despite epidemiological studies, genetic studies and basic studies point to a beneficial role of vitamin D to prevent bronchiolitis and asthma, trial data are far from conclusive. A placebo-controlled trial in Mongolia showed that vitamin D supplementation in vitamin D-deficient children prevents lower respiratory tract infections. However, other trials did not add evidence to use vitamin D supplementation to prevent or treat acute or chronic respiratory diseases during early childhood. Further studies are required to assess whether a target population exists that benefits vitamin D supplementation to prevent viral bronchiolitis or asthma development. References [1] Belderbos ME, Houben ML, Wilbrink B, Lentjes E, Bloemen EM, Kimpen JL, et al. Cord blood vitamin D deficiency is associated with respiratory syncytial virus bronchiolitis. Pediatrics 2011 Jun; 127(6): e1513-e1520. [2] Camargo CA, Jr., Ganmaa D, Frazier AL, Kirchberg FF, Stuart JJ, Kleinman K, et al. Randomized trial of vitamin D supplementation and risk of acute respiratory infection in Mongolia. Pediatrics 2012 Sep; 130(3): e561-e567. [3] Hansdottir S, Monick MM, Lovan N, Powers L, Gerke A, Hunninghake GW. Vitamin D decreases respiratory syncytial virus induction of NF-kappaB-linked chemokines and cytokines in airway epithelium while maintaining the antiviral state. J Immunol 2010 Jan 15; 184(2): 965–74. [4] Weiss ST, Litonjua AA. The in utero effects of maternal vitamin D deficiency: how it results in asthma and other chronic diseases. Am J Respir Crit Care Med 2011 May 15; 183(10): 1286–7. [5] Kumar GT, Sachdev HS, Chellani H, Rehman AM, Singh V, Arora H, et al. Effect of weekly vitamin D supplements on mortality, morbidity, and growth of low birthweight term infants in India up to age 6 months: randomised controlled trial. BMJ 2011; 342: d2975.

IIO-13 Nutritional interventions to prevent or treat bronchopulmonary dysplasia P. Manzoni1 , M. Mostert2 , C. Franco1 , M. Luparia1 , E. Tavella1 , M. Stronati3 , D. Farina1 . 1 Neonatology and NICU, A.O. Regina Margherita-S. Anna. S. Anna Hospital, Torino, Italy; 2 Department of Pediatrics, University of Torino, Italy; 3 NICU, IRCCS Policlinico San Matteo, Pavia, Italy Corresponding Author and address for proofs and reprints: dr. Paolo Manzoni, MD, Neonatology and Hospital NICU. Sant’Anna Hospital, Azienda Ospedaliera Regina Margherita-S. Anna, C. Spezia 60, 10126 Torino, Italy. Tel.: +39 011 3134304/5/8; fax: +39 011 3134888. E-mail address: [email protected] (P. Manzoni). Keywords: Bronchopulmonary Dysplasia; preterm neonates; nutrition; lactoferrin; lutein; prevention; respiratory; vitamin D

Abbreviations: VLBW = very low birth weight (below 1500 g.) NICU = neonatal intensive care unit NEC = necrotizing enterocholitis ROP = retinopathy of prematurity BPD = bronchopulmonary dysplasia Abstract: Nutrients in the prenatal and perinatal period play a major role in the development of the immune system as well as in the ability to contrast infections. A remarkable body of evidence supports the hypothesis that availability of specific,