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Three different types of risk factors in asthma

Risk factors can be distinguished in hereditary and acquired factors and factors triggering acute exacerbation. Hereditary factors correspond to a genetic predisposition determining the development of asthma or allergic sensitization. Multiple genes may be involved in the pathogenesis of asthma but no particular gene or genes have been identified with certainty yet. Atopy, defined as the production of abnormal amounts of IgE antibodies, occurs in 30 to 50 percent of the population and is the strongest predisposing factor for asthma. Another factor with heritable component is airway hyperresponsiveness. It is associated with airway inflammation and remodelling indicating that it may precede the development of asthma.

In predisposed individuals "acquired" environmental factors modify the development of asthma. The allergen-specific IgE-mediated reaction probably simply represents one of several mechanisms triggering acute asthma exacerbations or maintaining chronic inflammation. Other extrinsic factors include irritants from plants, organic or inorganic chemicals, often referred to as occupational sensitizers, and other irritants like tobacco smoke and air pollution defined as the atmospheric accumulation of irritants.

Respiratory infections especially caused by viruses like respiratory syncytial viruses may act as triggers to asthma exacerbations. Concerning socio-economic status it has been shown that asthma prevalence is higher in developed countries and in affluent compared to poor regions. Besides allergens, irritants and respiratory infections other factors exist triggering acute exacerbations. These include e.g. exercise and hyperventilation which seems to be a specific stimulus since other subjects without asthma but even other respiratory diseases are not affected by airflow limitation following exercise.

Literature:

The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Worldwide variation in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. 1998. Lancet ; 351 (9111): 1225-1232

Laprise C, Boulet LP. Asymptomatic airway hyperresponsiveness: a three-year follow-up. 1997. Am J Respir Crit Care Med ; 156: 403-409

O'Byrne P. GINA Executive Commitee. Global strategy for asthma management and prevention. 2004. National Institutes of Health. Publication No 02-3659

von Mutius E. The environmental predictors of allergic disease. 2000. J Allerg Clin Immunol ; 105: 9-19

Suman OE, Beck KC, Babcock MA, Pegelow DF, Redden AW. Airway obstruction during exercise and isocapnic hyperventilation in asthmatic subjects. 1999. Journal of Applied Physiology ; 87: 1107-1113

Wiesch DG, Meyers DA, Bleecker ER. Genetics of asthma. 1999. J Allergy Clin Immunol ; 104: 895-901

Factors contributing to asthma development

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