Asthma, Breathlessness, and Obesity in School Age Children

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Asthma, Breathlessness, and Obesity in School
Age Children

• Autumn Ford, MD
• Allergy Fellow
• Study Coordinator
• Clinical Immunology Society
• 2007 School in Hypersensitivity and Allergic
  Diseases
• Estes Park, Colorado
• September 6-10th

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Introduction

• We suspect that breathlessness in obese children
  is often from physical deconditioning alone and
  misdiagnosed as asthma.

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Background

• The incidence of obesity and asthma has risen to
  epidemic proportions in children.
• Obesity may precede asthma, and the risk of
  asthma increases with increasing obesity.
  (Camargo et al, 1999 Guerra et al, 2004.)
• Sedentary lifestyle and obesity could contribute
  to the development or worsening of asthma, rather
  than asthma causing sedentary lifestyle and
  eventually obesity.

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Background

• In the absence of deep inspiration, the airways
  of nonasthmatics behave similarly to those of
  asthmatics.
• Deep inspiration has a bronchoprotective effect
  in healthy individuals, and this is absent in
  asthma.
• Obesity may restrict deep inspiration and prevent
  the ability to stretch the airways.
• Furthermore
• Obesity leads to systemic inflammation.

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Hypothesis

• 1 Breathlessness in obese children with
  physician diagnosed asthma is often from
  deconditioning rather than asthma.
• 2 The inflammatory mediator profiles in the
  children with breathlessness from deconditioning
  are different than those with breathlessness from
  asthma.

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Study design

• case controlled cross-sectional pilot study
• enrolling 50 adolescents (ages 12-19)
• 10 normal wt controls
• 10 obese nonasthmatics
• 30 obese asthmatics
• 23 enrolled to date
• 18 with data analysis

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Inclusion Criteria

• 30 obese (BMIgt95th tile for age) adolescents
  with MD dx asthma in past 12 months
• 20 nonasthmatics (10 obese, BMIgt95 and 10
  non-obese, BMIlt85)
• Hgbgt12 females
• Hgbgt13 males

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Methods

• Breathlessness/physical activity Questionaire
• Treadmill Exercise Challenge
• Spirometry and eNO
• /- Methacholine Challenge

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Questionaire

• History of Asthma
• History of Eczema
• History of Allergic Rhinitis (symptom scale
  out of 4)
• Sneezing
• Nasal Itching
• Anterior Rhinorrhea
• Nasal Congestion
• Tobacco Exposure

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CONTROL n8
OBESE-NA n4
OBESE- A n6
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Aim

• Primary
• To determine if the subjects breathlessness is
  associated with cardiopulmonary abnormalities or
  deconditioning.
• Secondary
• To compare the inflammatory mediator profiles of
  asthmatics and nonasthmatics.

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Primary Outcome

• Graded exercise challenges
• --VO2 at maximal exercise
• -- pulmonary reserve
• Airway hyperresponsiveness
• --Methacholine challenges

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Secondary Outcome

• Immunologic and inflammatory biomarker
  measurements
• Total and specific IgE to common indoor/outdoor
  aeroallergens
• Exhaled Nitric Oxide
• Eosinophil count
• Serum and urinary prostaglandins and leukotrienes
• Fasting blood for lipids
• Blood sugar and Hemoglobin A1c

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VO2 max

• The rate of oxygen uptake or consumption at
  maximal exercise
• Addresses Is exercise capacity normal?
• Max VO2 is expressed per kg as ml/kg/min (based
  on ht, age, sex, activity level, /- wt)
• Lower limit 83 of predicted

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Pulmonary Reserve

• PR 1- Ve/MVV
• (nl is gt38)
• Addresses is ventilatory function
  normal?
• Ve-Minute Ventilation
• RR x Vt
• MVV-Maximal Voluntary Ventilation (L/min)
• FEV1x40

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In theory..

• Asthma
• Reduced exercise capacity, VO2 max
• Normal Cardiovascular responses
• Ventilatory limitation, decreased pulmonary
  reserve
• Deconditioned
• Cardiovascular responses borderline abnormal,
  improve w/ conditioning
• Decreased exercise capacity, VO2 max
• No ventilatory limitation
• Obesity
• Nl cardiovascular response
• Decreased exercise capacity VO2 max/kg
• No ventilatory limitation, nl Pulm reserve

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Results
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Conclusions

• Our exercise testing was able to detect the
  presence of pulmonary insufficiency at peak
  exercise in breathless obese adolescents.
• Three out of six obese asthmatics had no evidence
  of significant pulmonary impairment at peak
  exercise, possibly disputing prior physician
  diagnosis of asthma.

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Additional Findings..

• Two of the 3 obese nonasthmatics, and 2 of the 3
  obese asthmatics with low PR, had elevated
  eosinophilia and eNO.
• Inflammatory mediators could help distinguish
  asthmatics from poorly conditioned obese teens.