Pediatric asthma: a different disease

Abstract

Asthma currently affects the lives of more than 30 million Americans from infancy to the elderly. In many ways, pediatric asthma differs from adult asthma, including childhood-onset adult asthma. Despite many advances in our understanding of the disease, the natural history of asthma is not well defined, especially in different subsets of patients. For many with allergic asthma the disease has its origins in early childhood, associated with early sensitization to aeroallergens and exposure to repeated viral infections. These early life exposures, coupled with genetically determined susceptibility, have a major impact on the natural history of the disease. A number of risk factors during the critical early stages in the initiation of asthma have been associated with subsequent outcomes. In addition, protective factors linked to early life experiences have also been delineated which may impact the development of atopy and asthma and reduce the prevalence of these diseases. Cumulatively, the data highlight the critical nature of this early period in which immune/inflammatory responses in the lung are initiated and serve to maintain the disease in subsequent years.

Figure 1.

Models of disease progression from childhood to adulthood. (A) Normal: remains normal, (B) begins normal: steep slope resulting in severe obstruction over time, (C) begins normal: rapid decline early on resulting in severe obstruction, and (D) Begins with low values and continues with low lung function. Adapted by permission from Reference .

Figure 2.

Stages of asthma. Asthma may be divided into two main stages: an initiation or inception phase, and a maintenance or progression phase. The triggers and pathways activated may differ in the different stages. In the initiation phase, early allergen exposure and repeated viral infections coupled with genetic susceptibility may be important in setting the outcomes in the second stage.

Figure 3.

Importance of gene–environment interaction on the origins of asthma. Gene–environment interactions contribute to the development of altered airway function and airway inflammation. Host factors and the age at initial exposure to allergen and/or virus are important determinants of the specific immune responses to the exposure. The development of allergen-specific and virus-specific IgE enhances the immune/inflammatory responses in the lung.