摘要:

Purpose of reviewNasal polyposis is a chronic inflammatory disease of the upper airway characterized histologically by the infiltration of inflammatory cells like eosinophils or neutrophils. Several hypotheses have been put forward regarding the underlying mechanisms including chronic infection, aspirin intolerance, alteration in aerodynamics with trapping of pollutants, epithelial disruptions, epithelial cell defects/gene deletions (CFTR gene), inhalant or food allergies. The present review is an update on the pathomechanisms of nasal polyposis.Recent findingsIn the majority of nasal polyps, eosinophils comprise more than 60% of the cell population. Besides eosinophils, mast cells and activated T cells are also increased. An increased production of cytokines/chemokines like granulocyte/macrophage colony-stimulating factor, IL-5, RANTES and eotaxin contribute to eosinophil migration and survival. Increased levels of IL-8 can induce neutrophil infiltration. Increased expression of vascular endothelial growth factor and its upregulation by transforming growth factor-β can contribute to the edema and increased angiogenesis in nasal polyps. Again, transforming growth factor-β can modulate fibroblast function and thus contribute to eosinophil infiltration and stromal fibrosis. Other mediators like albumin, histamine and immunoglobulins IgE and IgG are also increased in nasal polyps. In addition, the local production of IgE in nasal polyps can contribute to the increased recurrence of nasal polyps via the IgE-mast cell-FcεRI cascade. Finally, mast cell/T cell-epithelial cell/fibroblast interactions can contribute to the persistent eosinophilic inflammation seen in polyps.SummaryThus although nasal polyposis is a multifactorial disease with several different etiological factors, chronic persistent inflammation is undoubtedly a major factor irrespective of the etiology.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewSensitization to pets is a risk factor for asthma and it was assumed that pet ownership was a risk factor for sensitization. Epidemiological studies failed to confirm this, some even suggesting that keeping pets decreased the risk of sensitization and asthma. In the last year, 10 studies have been published which have, at least in part, attempted to address the question. The results, however, are heterogeneous and it is still not clear how we should advise our patients on this issue of pet ownership.Recent findingsResults of studies of the association between exposure to cat or cat allergen and the development of sensitization are such that almost any view on the relationship could be supported by evidence from the literature. For dogs, there are fewer data, but there is little to suggest that keeping a dog increases the risk of sensitization to dog. The majority of studies reviewed find either no association or a reduced risk of asthma amongst pet owners, but only one of these selectively excludes those who deliberately avoid pets from the analysis. There is evidence to suggest that amongst non-pet owners, the risk of sensitization and of asthma increases in areas with a high proportion of pet owners. There is evidence emerging that the effect of exposure to pets may be different in different relative risk groups, based on parental allergy. There is also evidence that asthma is more severe amongst pet sensitized pet owners.SummaryThere are several large birth cohort studies being conducted around the world designed to measure the development of asthma and allergies in children with prospective and objective measures of environmental exposures. The results of such studies are required before the association between pets and asthma can be determined.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe frequency of allergic diseases is increasing worldwide. Experimental and clinical studies have linked a reduced number of early infections to this trend. The gastrointestinal system, which comprises the largest lymphoid tissue and microbial reservoir of the body, has received more attention during the last few years as a potential determiner in the development of atopic disease.Recent findingsAlterations in intestinal microbiota have been detected both in infants suffering from allergic disease and in those later developing the disorder. Delay in the compositional development ofBifidobacteriumandLactobacillusin gut microflora was a general finding in allergic children. In a subsequent study, perinatal administration of lactobacilli halved the later development of atopic eczema during the first 2 years of life. Specific strains of the healthy gut microbiota have been shown to induce the production of IL-10 and transforming growth factor-β, which possess an important regulative role in the development of allergic type immune response. Probiotics also strengthen gut defence barrier mechanisms and reduce antigen load in the gut. Pattern recognition receptors in intestinal epithelial and antigen-presenting cells have been demonstrated to mediate a continuing dialogue between host and gut microbiota.SummaryDespite several promising findings, the exact role of gut normal microbiota in the development of allergy remains to be elucidated. For successful interventions, more data concerning a communication between host and specific microbial species are needed.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe increasing prevalence of allergic rhinitis, its impact on individual quality of life and social costs, as well as its role as a risk factor for asthma, underline the need for improved treatment options for this disorder. We reviewed the recent literature published in English, dealing with relevant and appropriately controlled clinical trials on the treatment of allergic rhinitis.Recent findingsIn addition to well established pharmacological therapies with antihistamines, corticosteroids, decongestants and mast cell stabilizers, new therapeutic options become increasingly important, including leukotriene modifiers, anti-immunoglobulin E antibodies, phosphodiesterase inhibitors and intranasal heparin; there also exist new developments in appropriate allergen specific immunotherapy.SummaryPromising results, both with established and novel treatment options, are communicated, but further studies are still necessary to confirm these data.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewIt has been hypothesized that asthma and allergic rhinitis are both manifestations of a single inflammatory process present throughout the airway and that control of the inflammatory response associated with allergic rhinitis may help to reduce inflammation throughout the airway and improve control of asthma. Although previous evidence has documented that therapy directed at allergic rhinitis can improve asthma symptoms and bronchial responsiveness, until recently, there was no evidence that the use of medication targeted at the upper airway can also reduce utilization of acute health care services due to asthma.Recent findingsWe identified studies published between August 2001 and July 2002 that examined the therapeutic link between allergic rhinitis and asthma. In particular, we concentrated on investigations that evaluated whether, among patients diagnosed with allergic rhinitis and asthma, treatment of the former resulted in significantly fewer asthma-related emergency department visits or inpatient hospitalizations. Two such studies were identified. Using observational study designs, both investigations established that among a population with asthma and allergic rhinitis, treatment for allergic rhinitis was associated with a decrease in the risk of subsequent asthma-related events by one-third to one-half compared with persons who did not receive treatment for this disorder.SummaryEffective management of allergic rhinitis with nasal steroids and possibly oral antihistamines reduces utilization of acute health care services due to asthma among persons with co-existent asthma.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewRhinosinusitis affects more than 10% of the US population. It results in high health care expenditure as well as decreased productivity through lost days of school or work. This review includes recent findings in diagnostics and pathophysiology, as well as recent advances in treatment.Recent findingsParameters used in the diagnosis of rhinosinusitis include patient symptomatology, physical and endoscopic findings, computed tomography scan scores, and culture results. There has been poor correlation between patient symptoms and computed tomography scan scores, but middle meatal cultures have been shown to correlate well with ethmoid sinus cultures obtained from chronic rhinosinusitis patients. Chronic inflammation with a predominance of eosinophils and T lymphocytes in the tissues is being recognized as a hallmark of chronic rhinosinusitis, especially in patients with asthma or allergic rhinitis. Th2 cytokines are prominent in sinus tissues of patients with chronic rhinosinusitis and allergic rhinitis. While antibiotics are used with greater frequency in the treatment of acute and chronic rhinosinusitis, adjuvant therapies, such as intranasal steroids, might affect patient symptoms and curb disease recurrence.SummaryClinical symptoms are important in making the diagnosis of rhinosinusitis and should be supported by objective findings on nasal endoscopy and, if necessary, computed tomography scans. The mainstay of treatment remains antibiotics, with a potential role for decongestants and intranasal steroids. The presence of chronic inflammation with a Th2 cytokine predominance in sinus tissues should be kept in mind, especially in patients with coexistent morbidities such as allergic rhinitis and asthma.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe present review focuses and comments on the increasing body of evidence correlating respiratory viral infections with asthma onset and exacerbations.Recent findingsRecent data suggest multiple and some time contrasting roles for viral infection in the origin of asthma. These data also indicate that the immune status of the host, including atopy, may interactively contribute to this process, conferring susceptibility or even resistance to the development of asthma in virus-infected individuals. In the presence of asthma, the role of viral infection in triggering exacerbations is clearly established. Chemokine and cytokine responses of the respiratory epithelium, a biased type 1/type 2 cytokine balance, defective costimulation, as well as abnormal neural control have been suggested as possible mechanisms. The importance of concurrent or synergistic effects of allergen exposure is currently under scrutiny.SummaryViruses may initiate and certainly exacerbate asthma. Mild repeated infections early in life could also stimulate type 1 immune responses conferring protection from atopy and asthma. The host's immune status, the type of viral infection and the timing of exposure to various environmental stimuli are probably the key factors in this process. Mechanistic insights deduced from recent work should allow for the development of intervening strategies in the near future.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewInterest in the role of the mast cell in bronchial asthma has waxed and waned over several decades, but there is now compelling evidence that mast cells make an important contribution to the pathophysiology of this disease. This review will discuss current advances in this field.Recent findingsMast cells, but not T cells or eosinophils, localize within the bronchial smooth muscle bundles in patients with asthma but not in normal individuals or those with eosinophilic bronchitis. Smooth muscle mast cell density correlates significantly with indices of bronchial hyperresponsiveness, and is likely to be an important factor determining the asthmatic phenotype. Tryptase induces proliferation in human airway smooth muscle, and the recently identified transmembrane form induces the development of bronchial hyperresponsiveness in mice. IL-4 and IL-13, known mast cell products, also induce bronchial hyperresponsiveness in the mouse, in the absence of an inflammatory response. There are therefore several pathways by which the close approximation of mast cells with airway smooth muscle cells might lead to disordered smooth muscle function. Mast cells also infiltrate the airway mucous glands in patients with asthma, showing features of degranulation, and a positive correlate with the amount of mucus obstructing the airway lumen. Taken together these observations suggest that mast cells also play an important role in regulating mucous gland secretion.SummaryThe development of potent and specific inhibitors of mast cell secretion, which remain active when administered long term to asthmatic airways, should offer a novel approach to the treatment of asthma.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewA close relationship has been described between atopy, allergic rhinitis and asthma. The purpose of this work was to review recent data that have become available on the interactions between these conditions and the ways in which they influence one another.Recent findingsRecent findings support previous observations suggesting that atopic dermatitis and rhinitis often accompany or precede the development of asthma. Further data support the notion that early-life exposure to domestic animals, a farming environment, passive smoking, and being raised in a large family, may be protective against the development of atopy and/or allergic diseases, although this seems modulated by genetic factors. Furthermore, the appearance of house-dust-mite-specific immunoglobulin E antibodies in early childhood has been identified as a major risk factor for the development of asthma in children with atopic dermatitis; and the association between sensitization to specific allergens and airway hyperresponsiveness was reported to be the strongest for indoor allergens such as house-dust-mite and cat. Allergen exposure can increase airway responsiveness in non-asthmatic subjects with allergic rhinitis and is associated with an increase in markers of lower airway inflammation, particularly with indoor allergens. Furthermore, nasal allergen provocation can induce bronchial inflammation and vice versa, suggesting close interrelations between upper and lower airways.SummaryIn summary, the recent observations on the relationships between atopy, rhinitis and asthma support the hypothesis of a unique systemic condition with variable manifestations, which may develop following an imbalance between T helper cell types 1 and 2 lymphocyte populations. The latter may be influenced by environmental exposure in early life. Upper- and lower-airway inflammatory events influence each other, supporting the concept of ‘united airways’. Further studies should look at the relationships between these conditions to identify individuals at high-risk of developing them and develop strategies to possibly prevent their onset.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewLeukotriene modifiers have recognized utility in the management of asthma. The aim of this review is to put into context recent research findings that extend our understanding of cysteinyl leukotriene synthesis and actions in the pathogenesis of asthma and allergic disease.Recent findingsPrevious literature has shown that T helper type 2 cytokines thought to favor asthma and allergic diseases upregulate leukotriene synthesis. Recent findings show that interleukins-4 and -13 also upregulate cysteinyl leukotriene 1 receptor expression. Conversely, the regulation of cytokine expression by leukotrienes has also been explored: cysteinyl leukotrienes upregulate type 2 cytokine expression and decrease type 1 cytokine expression, favoring an allergic phenotype. Genetic determinants of the expression of leukotriene-forming enzymes include polymorphisms of the 5-lipoxygenase and LTC4synthase promoters. Novel actions of leukotrienes continue to be recognized, and a role for leukotrienes in the development of airway remodeling accompanying chronic asthma is discussed. Mounting evidence implicates leukotrienes in the pathogenesis of asthma following viral infections. Finally, advances in the measurement of leukotrienesin vivoare reviewed.SummaryLeukotrienes and their receptors play an important role in the pathogenesis of asthma. Advances in our understanding of the synthesis and actions of these lipid mediators provide the scientific rationale for appropriate utilization of leukotriene modifiers and for envisioning novel leukotriene-based therapeutic approaches in the clinical management of asthma.

ISSN:1528-4050    

出版商:OVID    

年代:2003

数据来源: OVID