Introduction

Irrefutable clinical evidence exists demonstrating the involvement of platelets in allergic diseases, including asthma, allergic rhinitis and eczema. Experimental models of allergic disease suggest that platelets may play a fundamental role in the pathogenesis of the inflammatory response that follows exposure to allergens. Of importance are the observations that, despite being anucleate, platelets share many characteristics of inflammatory cells and, of particular interest in allergy, undergo chemotaxis, express adhesion molecules, release a wide variety of proinflammatory mediators, enzymes, cationic proteins, and themselves become activated by mediators released by other cell types involved in inflammation.

Clinical evidence of platelet involvement in allergic diseases

Numerous studies have revealed an alteration in the character and function of platelets from patients with allergic diseases, and these alterations may be dissociated from the well-characterized involvement of platelets in thrombosis and hemostasis, illustrating a dichotomy in platelet function (Fig. 56.1). Evidence is manifested as heightened platelet activation in vivo, whilst platelets from the same allergic patients are found to be refractory to a variety of stimuli ex vivo, a phenomenon possibly resulting from platelet ‘exhaustion’, where platelets are over stimulated in vivo and subsequently respond poorly to stimuli in vitro. In support of this concept, platelet aggregation has been observed to be abnormal in asthmatic patients. The ability of proaggregatory mediators such as noradrenaline and adenosine diphosphate (ADP) to induce aggregation is seen to be impaired, with no second phase aggregation, an occurrence that has also been correlated with increased serum immunoglubulin E (IgE) in asthmatic patients.