Reactive airway disorders in children. Role of respiratory virus infections.

The knowledge of pathogenetic mechanisms of reactive airway disorders of children has advanced to complex interactions that involve respiratory virus infection, both antigen-specific and nonspecific chemical mediation, and neurogenic bronchoconstriction. Most of the clinical correlations have been derived from fragmentary studies which involved groups of children defined by one or only a few variables. To progress beyond this point, longitudinal studies are needed of infants and children for whom all of the variables are defined so that the interrelationship of these factors can be unraveled. Essential components of these studies would be that the subjects be tested for evidence of atopy, that the etiology of lower respiratory infections be determined, and that methods to follow pulmonary function be employed. These studies would require that relatively large numbers of children be followed from early infancy through childhood and that noninvasive procedures be employed for testing the various parameters in order to maintain compliance. Some investigators have suggested that the T-lymphocyte regulation of the immune response to certain antigens is altered in persons with atopy. Further research is needed to determine the genetic basis of this response. Furthermore, patients with asthma appear to have altered function of the autonomic nervous system. More information is needed to determine if this altered response (beta adrenergic subsensitivity versus alpha adrenergic and cholinergic hypersensitivity) is a cause, or a coexistent defect, or a result of atopic asthma. Finally, does hyperresponsiveness of the airways to non-specific irritants exist without underlying atopy? Most of the data presented above indicate that in its severe forms it, at least, coexists with allergen-induced asthma.(ABSTRACT TRUNCATED AT 250 WORDS)