Late phase reactions.
Our current understanding of LPR has evolved over the past 10-12 years, and there are still many areas where our information is still incomplete and cannot provide solid support for several of the hypotheses presented herein. Each suggestion presented is testable, however, and answers to many of the questions raised should eventually be available. The hypotheses presented provide a framework for understanding how airway inflammation contributes to airway reactivity and how certain irritant exposures can cause delayed-onset asthma. More importantly, they provide a rationale for the use of many of the specific drugs used to treat allergies and asthma. Indeed, if LPR and airway inflammation are as important in asthma (and other allergic diseases) as these hypotheses suggest, the use of agents specifically designed to prevent or treat LPR should increase. Thus, mast cell stabilizing compounds such as cromoglycate, ketotifen, and tranilast and anti-inflammatory agents like GCS might be viewed as specific therapy for asthma (and other allergic diseases), while bronchodilators (like antihistamines, decongestants and antipruritic drugs in other allergic diseases) might be considered as supportive agents. These concepts therefore suggest the early and aggressive use of specific agents in asthma while employing supportive drugs to help maintain lung function.
Kaliner
M A
MA
D000818:Animals; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000188:drug therapy; D008407:Mast Cells / Q000502:physiology; D012130:Respiratory Hypersensitivity / Q000188:drug therapy* / Q000503:physiopathology; D013997:Time Factors
D005938:Glucocorticoids