Introduction

Bronchial asthma is a disease of the airways that is characterized by increased responsiveness of the tracheobronchial tree to a multiplicity of stimuli. A number of causes have been postulated for the increased airway responsiveness; however, the basic mechanism remains unknown. The most popular hypothesis at present is that of airway inflammation, in which allergic mechanisms seem to play a key role. Therefore, the modulation of allergic mechanisms should be a fruitful approach to treating asthma.

Allergic reaction are dependent on an IgE response controlled by T- and B-lymphocytes and are activated by the interaction of antigen with mast cell-bound IgE molecules. After that, eosinophil recruitment into the airways occurs via cytokine- and adhesion molecule-dependent mechanisms. Thus, for the modulation of allergic responses there are many possible approaches, including interfering with IgE production, modulation of inflammatory cell activation, and antagonism to mediators.

In this book, IgE modifiers and mediator antagonists, namely receptor antagonists for lipid mediators, tachykinins, and bradykinin, are described elsewhere. Therefore, in this chapter I will discuss cromones and some other agents which are used for the clinical treatment of asthma as antiallergic drugs.

Chromones

The drugs cromolyn sodium and nedocromil sodium, traditionally referred to as mast cell stabilizing agents, comprise an important group of anti-inflammatory drugs useful in the treatment of bronchial asthma. Although cromolyn sodium is a chromone, whereas nedocromil sodium belongs to the structural class of pyranoquinolines, they share many clinical characteristics.