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Asthma is a respiratory disease with both strong genetic and environmental influences. It is important for health care providers to recognize the role that atopy (allergies) play in the diagnosis, pathophysiology, and treatment of asthma in children and adults.


A 14 year old adolescent with a history of asthma since she was a toddler presents to your office for an annual checkup. As a child her asthma flares were much worse in the winter and she was admitted to the hospital at age 6 months with respiratory syncytial virus (RSV) bronchiolitis. She uses albuterol by metered dose inhaler (MDI) or nebulizer to control her asthma. She reports more problems with her asthma over the past 2 years and complains of increased symptoms during the spring track season.



Routine physical exams are an excellent opportunity for medical providers to help patients with asthma gain better control of their disease. There are many factors to consider when an adolescent has worsening asthma symptoms and the medical history can be a helpful tool. Younger patients who may be genetically susceptible to asthma often report RSV or another severe viral infection as an initial trigger of their diseasei. Adolescents entering puberty may experience worsening of both allergy and asthma symptoms. It is important to note that environmental exposures often change with the age and activities of patients as they grow. New pet exposure, seasonal pollens, sporting activities, air pollution, and cockroach infestations at home for inner city populations are all important details to address. Approximately 70% of patients with asthma have allergies, making atopy an important consideration in the care of a majority of asthmaticsii.

Case Continued:


The patient also reports frequent sneezing and nasal congestion. Her medical history includes eczema (atopic dermatitis). Her twin also has mild asthma. The patient uses about one inhaler a month for sports and reports some night time cough (two nights a week).

What is the next most appropriate step or test?

a) Start an antihistamine
b) Perform allergy testing
c) Start a nasal steroid
d) Start a low to medium dose inhaled steroid



Inhaled corticosteroids (ICS) are potent mediators of allergic inflammation in the airways. They work by modulating transcription of inflammatory proteins at the nuclear level of the cell. Inhaled steroids suppress the production of inflammatory cytokines, the recruitment of allergic cells such as eosinophils, and have the ability stabilize mast cells. This usually allows inhaled steroids to control inflammation at the airway level within a relatively short time period. The clinical effect of ICS, however, is dependent on compliance and the inflammatory pattern and symptoms of asthma usually return within one to two weeks after they have been discontinuediii.

The science behind the genetic influence on the development of asthma and allergic disease has become increasingly strong over the past few decades. Monozyogotic twin studies show an increased concordance of asthma and the incidence of allergic disease may double depending if one or both parents are atopic. It also appears that asthma and allergic diseases are not caused by a singular genetic mutation. Research has been focusing on genes controlling IgE production, interleukins such as IL-4 and IL-13 and certain receptors for bacteria present in the innate immune system (toll receptors). These genetic factors most likely interact with an individual’s environmental exposure as they grow and develop and may influence the development of atopic disease.iv

It is important to note that over one-third of patients who have atopic dermatitis as children will go on to develop asthma. It is possibly one of the strongest risk factors for asthma. New evidence suggests genetic factors such as mutations in proteins that are present in both the airway and skin may play a role in allergic sensitizationv. Although allergy testing may be helpful in a patient with this history, the best immediate step to take in her therapy according to NHLBI guidelines would be to start an inhaled steroid for moderate persistent asthma.

Case Continued:


The patient’s wheezing during track practice improves after 2 weeks of using her inhaled steroid. She still has night time cough. In the interval, she reports some throat tightness after eating pistachios at a party

What is the next most appropriate step in her management?

a) Prescribe and teach her how to use an epinephrine autoinjector
b) Allergy testing for tree nuts
c) Spirometry with flow volume loops
d) Start a nasal steroid



Treating her upper airway with nasal steroids and identifying her allergic triggers along with environmental control measures would be a part of her long term managementvi. Although adding a nasal steroid would probably help this patient due to allergic rhinitis and post nasal drip contributing to her night time cough, having the epinephrine autoinjector is the priority for patient safety.

Poorly controlled asthma is factor for mortality in patients who have both asthma and food allergies. The most common fatal reactions involve peanuts or tree nuts. It is imperative that providers provide education, injectable epinephrine, and strongly consider a referral to an allergy specialist in patients with concomitant food allergy and asthma.vii



Atopy should not be considered a disease of any one organ system. The genetics of individuals and their environment interact in a complex fashion that may lead to the signs and symptoms of respiratory allergy, asthma, food allergy, or atopic dermatitis. A thorough understanding of atopic disease will assist providers in coordinating their care of the upper and lower airways, gastrointestinal tract, and skin as it relates to patients with allergic disease of all ages.


i  Kusel MM, de Klerk NH, Kebadze T, et al. Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent asthma. J Allergy Clin Immunol. 2007;119:1105–1110.

ii  World Health Organization. Global surveillance, prevention and control of chronic respiratory diseases: a comprehensive approach, 2007. Available: Accessed: 2-20-2012.

iii  Leone FT, Fish JE, Szefler SJ, et al. Systematic review of the evidence regarding potential complications of inhaled corticosteroid use in asthma : collaboration of American College of Chest Physicians, American Academy of Allergy, Asthma, and Immunology, and American College of Allergy, Asthma, and Immunology. Chest. 2003 Dec;124(6):2329-40.

iv  Bjornsdottir US, Holgate ST, Reddy PS, et al. Pathways activated during human asthma exacerbation as revealed by gene expression patterns in blood. PLoS One. 2011;6(7):e21902.

v  van den Oord RA, Sheikh A. Filaggrin gene defects and risk of developing allergic sensitisation and allergic disorders: systematic review and meta-analysis. BMJ. 2009 Jul 9;339:b2433.

vi  National Asthma Education and Prevention Program. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Institutes of Health, National Heart, Lung, and Blood Institute, August 2007. NIH Publication 08-4051. Available: Accessed 12/27/2011.

vii  Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007 Apr;119(4):1016-8.

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