ABSTRACT
I. Introduction The pharmacology of cough may be considered in two separate paradigms: either as a specific treatment of the cause or as a general modulation of cough reflex hypersensitivity. If the origin of the cough can be determined, for example, an inhaled foreign body, specific treatment (by removal of the foreign body) may be curative. Alternatively, ameliorating the consequences of the specific cause, such as reducing the eosinophilic inflammation of cough-variant asthma with corticosteroids, may be the next preferred option. Indeed, current guidelines on the management of chronic cough recommend therapeutic trials of individual agents based on the most likely suspected cause (1-3) (Fig. 1). The second strategy is based on suppression of the cough reflex. The rationale for such a strategy is that in many disease states the cough reflex is hyperresponsive (4); in addition, treatment of the primary associated cause of the cough may not be entirely successful. Cough suppression is the major option used in the treatment of acute cough (1). However, the efficacy of agents used in much of the multimillion pound over-the-counter market in acute cough has a poor scientific base. In intractable chronic cough, which is either treatment resistant or undiagnosed (or “idiopathic”), cough suppression remains the only valuable option. The main thrust of drug development is in the area of cough suppression, with the holy grail of cough therapeutics being the normalization of the cough reflex, suppressing the abnormal cough while retaining this vital reflex, whose main function is to protect the airways against aspiration.
