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Background: longitudinal studies of the natural history of childhood and adolescent rhinitis are lacking. Objectives: to investigate the natural history of rhinitis up to 18 years of age, and how that is influenced by gender and atopy. Methods: the Isle of Wight birth cohort was recruited in 1989 (n=1456). Questionnaire data on nasal symptoms (rhinitis) were collected at 1, 2, 4, 10 and 18 years of age. To define atopy, skin prick tests were conducted at 4, 10 and 18 years. The 12-month period prevalence plus positive and negative transitions (defined as change in disease status in two consecutive study assessments) were stratified by gender and atopic status. Results: overall rhinitis prevalence increased from 5.4% at 4 years to 35.8% at 18 years (P Conclusion: atopic rhinitis becomes increasingly common as children grow into adolescents, with stronger associations to male gender. Non-atopic rhinitis shows a female predominance at 18 years as girls ‘grow into’ it more during adolescence. Our findings suggest differential gender effects on the increasing prevalence of both atopic and non-atopic rhinitis in adolescence. Clinical Relevance: a better understanding of how gender and atopic status influence rhinitis during adolescence emerges from this study. Application of such knowledge could help to improve clinical recognition, judge prognosis and ultimately improve management of this common condition.

Summary Background The pathophysiology of idiopathic rhinitis is unknown although evidence is accumulating to suggest that many patients may have a localized form of allergic rhinitis in the absence of other atopic symptoms and markers. This study compares detailed nasal challenge results obtained from patients with idiopathic rhinitis to those of atopic and normal controls. Methods Patients with idiopathic rhinitis (n = 23), perennial allergic rhinitis (n = 8) and normal controls (n = 8) underwent a normal saline challenge to exclude hyper-reactivity and then bilateral nasal allergen challenges. Nasal patency was assessed by anterior active rhinomanometry. Results All of the patients with atopic rhinitis demonstrated positive bilateral allergen challenges. All normal control subjects had bilateral negative challenges. Two patients in the idiopathic group tested positively to saline and were excluded from further study with 62% of the remainder testing positive to allergens. Of the idiopathic patients testing positive, 85% were sensitive to house dust mite. Conclusion A significant proportion of patients with idiopathic rhinitis have positive nasal challenges, the vast majority to house dust mite allergen. These findings add to the weight of evidence that suggests ‘localized allergy’ may exist in the absence of systemic atopic markers.

Background There is increasing evidence for the role of basophils in the pathogenesis of atopic diseases such as bronchial asthma, atopic dermatitis and atopic rhinitis. Recently, it has been reported that basophils derived from healthy donors produce the immunoregulatory cytokines interleukin (IL)-4 and IL-13 after cross-linking of cell surface IgE. In addition to well-known inflammatory mediators, such as histamine and leukotriene C4, these cytokines produced by basophils are also considered to be associated with atopic diseases. Objective Our first objective was to determine whether or not mite-sensitive atopic asthmatic basophils produce IL-4 and IL-13 in response to mite antigens. Our second objective was to investigate the relationship between antigen-specific or nonspecific IgE in the serum and the production of these cytokines in order to determine the association of basophil-derived cytokines with the pathogenesis of atopic asthma. Our final objective was to study how production of these cytokines could be regulated by some anti-asthma drugs. Methods Basophils were purified from peripheral venous blood of 67 atopic asthma patients with elevated RAST for the house dust mite. Cells were stimulated with mite antigens for 6 hours and then IL-4 and IL-13 levels in the supernatants were measured by enzyme-linked immunosorbent assay (ELISA). Results Mite-sensitive asthmatic basophils produced IL-4 and IL-13 when stimulated with mite antigens. Mite-induced IL-4 production peaked at 6 hours after the stimulation, whereas IL-13 production continued up to 24 hours. The higher the concentration of mite-specific IgE but not total IgE released in the serum, the more IL-4 and IL-13 were produced by basophils in response to mite antigens. The production of these cytokines was significantly suppressed by the anti-asthma drugs theophylline (IL-4, p