Clinical allergy and immunology最新文献

Mast cells and basophils contribute to induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes. The latter include a variety of stimuli that have only recently been elucidated, including mechanisms triggered by bacteria, virus, fungi, complement, or autoantibodies. MCs, and basophils contribute to inflammation both directly through the release of inflammatory mediators, cytokines and growth factors and indirectly through the activation of structural cells. Accumulating evidence places MCs (and most probably basophils) in a position of importance in the pathogenesis of CRS, particularly in the pathogenesis and progression of NP (Fig. 1). Mechanisms other than conventional IgE-dependent activation of MCs are intriguing as potential mechanisms of eosinophilic inflammation in non-allergic CRS/NP. Although it is not possible using current pharmacologic approaches to completely isolate the effects of MCs or basophils in CRS and NP pathogenesis, it seems most likely that such approaches will eventually be available. It might be expected that one or both of these cells will be shown to play important roles, particularly considering their potential for activation by IgE and non-IgE mechanisms, their production of a broad array of inflammatory mediators, cytokines and growth factors, and their unique assortment of proteases.

Incomplete resolution of acute rhinosinusitis leading to CRS is associated with a corresponding change in the microbiology of the disease. The shift in microbiology from acute to CRS favors infection with S. aureus, S. epidermidis, anaerobic bacteria (including beta-lactamase-producing strains), and gram-negative bacteria. With the exception of S. epidermidis, there is substantial evidence supporting the role of these organisms in the pathogenesis of CRS. It is worth noting that not all CRS patients are chronically infected. In fact, other inflammatory factors in the disease may predominate in the clinical presentation. This creates a clinical conundrum in which it is difficult to ascertain whether bacteria are involved. In general, a chronic bacterial infection is more likely if there is: underlying immune deficiency, one or more opacified sinuses on sinus CT in the absence of polyps, the presence of frank purulence draining from one or more sinus cavities, or the presence of gram-negative or antibiotic-resistant organisms (e.g., MRSA) on sinus culture. For patients seen for the first time, the approach to antibiotic treatment is usually empiric, following the guidelines outlined in this chapter and directing treatment at both aerobic and anaerobic bacteria. Whenever possible, the choice of antibiotics should be guided by properly obtained sinus cultures. In cases where empiric antibiotics have failed, the need for bacterial cultures is even more critical to assure proper treatment and to minimize antibiotic side effects.

By clinical experience, rhinitis has been suggested as caused by some endocrine disorders, but the evidence for this is vague, and the few descriptions almost anecdotal. Rhinitis of the menstrual cycle has been more described, although a solid picture is still lacking. Pregnancy rhinitis is therefore so far the only clearly defined "hormonal rhinitis." However, the cause of pregnancy rhinitis is not simply estrogen or progesterone, but seems multifactorial, and may possibly be associated with the PGH. Treatment consists mainly of information, physiological measures, and nasal saline washings.

A growing body of scientific evidence supports the link between nonallergic upper airway disorders and asthma. Multiple studies have demonstrated that most patients with nonallergic asthma have chronic nasal symptoms as well as radiographic evidence of sinus mucosal disease. Equally important, preexisting symptoms of rhinitis place nonallergic patients at higher risk for developing asthma. Experimental studies demonstrate that the upper and lower airways may be connected via a number of paths, and that the systemic circulation may play a key role in amplifying inflammation in other portions of the respiratory tract. Finally, given this complex relationship between localized and systemic inflammation, it behooves all physicians to assess and treat rhinitis and sinusitis when they are present in patients with asthma.